Highest Pressure Human Body Can Survive In? One design for underwater human inhabited environments is to have equal pressure between the surrounding water and the submerged habitat, thus allowing a section of the floor to be open to the water and removing the necessity for strong plating to protect it.  This requires the air pressure within the environment to be greater than atmospheric pressure so that it can withstand the pressure of both the atmosphere and the pressure from the overlying water.

So how much pressure can the human body survive in without need for special suits and breathing apparatuses (as this would place a limit on how deep you could build such an environment without special accommodation)?

Edit: So far i've found an article about a man trapped in a sunken boat who survived for days in an air pocket trapped in the bathroom 100 feet down.  He couldn't resurface without the use of a diving bell and gradual decompression; but this case provides a lower bound for how high the highest pressure can be.

Calculations:  14.7 psi (atm pressure) + 1200 inches*0.037 psi/in^3 = 60 psi for the underwater pocket (roughly 4 times atmospheric pressure).
http://news.nationalgeographic.com/news/2013/12/131204-nigerian-air-bubble-survival-shipwreck-viral-video-science/

The deepest recorded simulated dive is still the on-shore French Hydra 10 experiment at 701 msw (meters salt water); at a pressure of 71 atm. Since breathing a mixture containing helium is required at such depths (to avoid the extreme narcosis produced by nitrogen at such depths), the new problem helium causes is

  High-pressure nervous syndrome (HPNS). HPNS, brought on by breathing helium under extreme pressure causes tremors, myoclonic jerking, somnolence, EEG changes, visual disturbance, nausea, dizziness, and decreased mental performance. Symptoms of HPNS are exacerbated by rapid compression, a feature common to ultra-deep "bounce" dives.

Actually that Wikipedia description is a bit misleading, the problem is caused by any gas mixture, not just helium, but other gasses like nitrogen or hydrogen have a narcotic effect that counteracts HPNS. HPNS sets in at about 120m:

  The high pressure
  neurological syndrome (HPNS) begins to show signs at about 1.3 MPa (120 m) and its effects intensify at greater depths.
  HPNS starts with tremor at the distal extremities, nausea, or moderate psychomotor and cognitive disturbances. More severe
  consequences are proximal tremor, vomit, hyperreflexia, sleepiness, and psychomotor or cognitive compromise. Fasciculations
  and myoclonia may occur during severe HPNS. Extreme cases may show psychosis bouts, and focalized or generalized
  convulsive seizures. Electrophysiological studies during HPNS display an EEG characterized by reduction of high frequency
  activity (alpha and beta waves) and increased slow activity, modification of evoked potentials of various modalities (auditory,
  visual, somatosensory), reduced nerve conduction velocity and changes in latency. Studies using experimental animals have
  shown that these signs and symptoms are progressive and directly dependent on the pressure. HPNS features at neuronal and
  network levels are depression of synaptic transmission and paradoxical hyperexcitability.

The problem with extreme helim pressure was partially alleviated in the Hydra experiments by mixing/replacing some of it with hydrogen, in the so-called Hydreliox mixture.

  For the Hydra VIII mission at 50 atmospheres of ambient pressure, the mixture used was 49% hydrogen, 50.2% helium, and 0.8% oxygen.

The French did this based on prior experiments which found that the narcotic effect of hydrogen reduces HPNS (or even completely eliminates it at lower depths):

  A H2-He-O2 mixture with 54 to 56% hydrogen was studied with 6 subjects (professional divers) during 2 dives to 450 m. The 38-h compression was the same as that used with other types of breathing mixtures (He-O2 and He-N2-O2). The results obtained during compression and during the stay at 450 m in H2-He-O2 show that the EEG changes (increase of theta activities in the anterior regions of the skull, decrease of alpha activities) are similar to those found with other respiratory mixtures. On the other hand, the other symptoms of high pressure neurologic syndrome (HPNS) were clearly improved for the same depths. Thus, neurologic symptoms (tremor, dysmetria, myoclonia, drowsiness) are nonexistent, and the performances during psychometric tests remain similar to those of the surface. Hydrogen, with its narcotic potency, suppresses some symptoms of HPNS and seems to open new perspectives for deep diving.

Of course, having hydrogen (in such large proportion) and oxygen in a gas mixture poses dangers of fire, explosion etc. This is avoided by decreasing the oxygen concentration; alas this cannot be a one-step process (for diving):

  The major problem with hydrogen-oxygen mixtures is the potential for explosion. Although the concentration of oxygen needed for combustion of oxygen-hydrogen mixes varies a bit with pressure, a general rule of thumb is that hydrogen-oxygen mixes above 5 %  O2 are at-risk.. So, to avoid nasty fires and explosions, hydrogen is only considered as a breathing gas component at pressures where a less-than 5% oxygen concentration in the breathing gas mix gives a partial pressure of oxygen great enough to sustain life. Perhaps the most common example of a hydrogen-fire related disaster is the destruction of the Hindenburg dirigible. [...]

  In 1944 Arne Zetterstrom discovered a way to breach the transition between compressed air and Hydrox without risking explosion. The technique was to descend to 100 feet and switch to a 4% oxygen / 96 % nitrogen mixture. After breathing this mix for sufficient time to allow the oxygen concentration in the lungs to drop below the "explosion threshold," the diver switched to Hydrox and continued descent. On ascent, the diver again used the Nitrox (4% O2 / 96% N2) as a transition between Hydrox and air. Using this technique, he descended to 363 feet. At that depth, the alteration in voice characteristics, coupled with excitement, made communication impossible and additional dives used a telegraph key.  [...]

  During the mid 1960's research into the use of hydrogen in breathing gases resumed with animals breathing Hydrox for up to 24 hours at 70 Ata. One interesting aspect of the animal research was the suggestion that hydrogen reduced the HPNS (high pressure nervous syndrome) often observed with helium based gas mixes on deep dives. Ultimately animals would be taken to 3500 feet on hydrox.

  In 1983 COMEX, the French deep diving concern (perhaps more famous in the US as the company providing the submersible used in the recovery of artifacts from the Titanic) began a series of dives to investigate the narcotic potential of hydrogen. Divers including H.G. DeLauze, President of COMEX, descended in open sea to approximately 300 feet for five minutes. The divers could not perceive a difference between Hydox and Heliox at that depth.  Chamber dives to 300 m (984 ft) demonstrated that hydrogen possessed a narcotic effect different from nitrogen. Hydrogen narcosis (the "hydrogen effect") had a tendency to be more psychotropic, i.e. more like LSD, while nitrogen narcosis had an effect similar to alcohol. This deeper work suggested that Hydrox as a binary gas mix would not be too useful at depths below about 500 feet.

Based on that COMEX developed a protocol of switching from heliox to hydreliox at 250msw.

A more recent (1994) COMEX paper reported that at 500m (on hydreliox), manual dexterity was about 80% of the surface one, while the arithmetic ability decreased to 60%. So not dying and being able to function as on the surface, aren't the same thing.

Also these experiments are time consuming and costly. In Hydra VIII, the whole thing took one month, of which only 10 days or so were spent at maximum depth. And in case "something bad happens" interventions aren't easy in such settings.

A 1984 American experiment with trimix at 650m was aborted after one of the three subjects (despite negative previous neuropsychiatric screening, as well having substantial commercial diving experience and successfully taking part in the previous experiments of the series) developed hallucinations and then full blown mania at 625-650m.

  The Atlantis IV dive was designed to test the ability of 5%
  N2 trimix breathing mixture (5% N2, 0.5 atmosphere
  oxygen, with the balance helium) to counteract the
  [high pressure nervous] syndrome without nitrogen narcosis. [...]

  The dive began with an initial compression rate of
  30 m/hour to 300 m (1000 ft) sea water equivalent
  pressure. By day 3 of the dive, at about 470 m, subject
  C had developed significant insomnia. On day 4 (540
  m), this subject became stressed and complained of
  mild auditory illusions of music and visual distortions
  consisting of a “halo effect” around the chamber’s
  apparatus. On day 5 (625 m) of the dive, the subject’s
  irritability, insomnia, and agitation worsened. He was medicated with temazepam, 60 mg, and achieved
  substantial relief of these symptoms after 15 hours’
  sleep. However, with further compression to 650 m,
  subject C experienced a recrudescence of auditory and
  visual illusions and developed rapid speech, racing
  thoughts, shortened attention span, and difficulty in
  focusing on tasks. Ankle clonus, marked hyperreflexia,
  and myoclonic jerking were documented, and he complained of nausea and weakness. In contrast, the other
  two subjects performed normally in almost all respects.
  On day 9 (650 m), the subject stated he felt “paranoid”
  and that he felt like “I’m going insane.” He
  began to carry a mirror to look at himself to “remind
  myself that I’m not a raving maniac.” He stated that
  colors were enhanced and vivid and he could see
  “unusual” mosaic patterns on the metalwork within
  the chamber. He was unable to comply with instructions
  to enable cognitive function to be tested because
  of extreme agitation and distractibility.[...]

  Early on day 9 (650 m), the decision was made to
  halt the dive, but decompression from 650 m is still
  experimental and could not be accelerated. Because the
  decompression process was expected to last as long as 30 days, it was necessary to consider medicating the
  subject more intensively. Since lithium had been shown
  to exacerbate symptoms of the high pressure nervous
  syndrome in animals and the effects of phenothiazines
  at such high pressures were virtually unknown,
  the decision was made to control the diver’s agitation
  with benzodiazepines. Accordingly, diazepam was used in doses up to 120 mg/day. This treatment only
  mildly sedated the subject and provided no real control
  of his behavior.
  The subject’s agitation persisted over the next 14
  days and was marked by decrements in his cognitive
  function and bursts of aggressive paranoia, grandiosity,
  and irritability. By day 24 of the dive (383 m), the
  subject’s irritable and aggressive behavior was becoming
  potentially dangerous and led to the decision to
  medicate with chlorpromazine, up to 300 mg/day.
  Within 48 hours of the beginning of chlorpromazine
  treatment there was dramatic improvement in the
  subject’s behavior. He became relatively calm and
  better organized. He denied having illusions or hallucinations. [...]

  Ten days after exiting the chamber, the subject again
  exhibited signs of hypomania including hyperactivity,
  insomnia, and irritability. Lithium carbonate therapy
  lessened these symptoms and was continued prophylactically
  for 6 months. It was then discontinued
  without any recurrence of symptoms.


DNA replication: How many DNA polymerase molecules work in parallel? Background research

I am aware that DNA polymerase works in pairs, at least. This is to process both opposite stands of a given chromosome. The 3'-to-5' "leading strand", and 5'-to-3' "lagging strand" simultaneously. This two-DNA-polymerase process is beautifully shown in this TED talk by Drew Berry.

I have not checked any non-online sources but simple Google queries failed to answer my questions below.

Question

Within a single Eukaryotic cell, is the process of DNA-replication carried out by just a single pair of DNA-polymerases? Or do multiple pairs of DNA-polymerases work in parallel?

In the (beautifully rendered) video you linked to, the green molecules are DNA polymerases. So you can already see that there are more than two DNA polymerases at work!

At each replication fork, there is generally one DNA polymerase working on the leading strand, but on the lagging strand, multiple DNA polymerases may be working at the same time (as depicted in the video). Note that different types of polymerase are thought to be primarily responsible for the leading (Pol ε) and lagging (Pol δ) strands in eukaryotes (but not prokaryotes, which use Pol III for both).

Next, note that at every origin of replication, there are two replication forks working simultaneously, one in each direction. So that's double the number of polymerase molecules.

On top of that, a single eukaryotic cell has multiple chromosomes. Each one must have at least one origin of replication of its own, which can operate in parallel. In reality, each eukaryotic chromosome has up to thousands of origins of replication (prokaryotic chromosomes generally only have one). Human cells have on the order of 100,000 origins of replication. So depending on how many origins are active simultaneously, there are likely many thousands of polymerase molecules acting at once to replicate the DNA of a single eukaryotic cell.

You could probably do a rough estimate of the number of polymerase molecules active simultaneously by taking the average duration of S phase in your cell of interest and dividing by the genome size and the speed of polymerase.


In an open circulatory system, how is blood moved? In the mollusks section, the powerpoint mentioned that gastropods and bivalves have an open circulatory system. According to the note, this means that the blood does not travel in vessels. How, then, does blood move? Does that mean that these organisms are simple enough to be able to survive by just pumping blood straight out into the body?

How does this type of circulatory system work?

Thanks!

evamvid

In a closed circulatory system, all of the blood stays within blood vessels or the heart itself.

Organisms that have open circulatory systems, such as arthropods, have hemolymph (a fluid that is essentially a mixture of blood and interstitial fluid). The hemolymph actually does travel in vessels for a very short amount of time, as it is leaving the heart. After this, it goes to the body cavities of the animal and directly bathes the tissues in the fluid in order to deliver oxygen, nutrients, etc.

Hemolymph moves throughout the body when the animal moves. Also, when the heart relaxes, hemolymph is drawn back toward the heart through ostia, or open-ended pores.

So to answer your question, yes, these animals can survive just by pumping hemolymph straight into the body. This is only effective because their body cavities are very small. In humans, an open circulatory system would never work because it would require an enormous amount of work to pump and circulate blood throughout our entire body cavity.


Where do B cells produce antibodies? I was recently at a Leukemia and Lymphoma Society conference where a particular oncologist lecturer claimed that all antibodies are created in the bone marrow (I won't mention his name, as he was a great lecturer, and I don't wish to sully his name if he happened to be wrong on this particular point).

Wikipedia seems to indicate that antigens are produced in "Secondary Lymphatic Organs" or occasionally in the bone marrow, but I've been misled by Wikipedia before.  It seems to me that evolution would favor creating antibodies close to the infection, and not far away in the bone marrow or lymphatic organs (how would the antibodies "know" how to get back to the original infection?  It would be very inefficient to send antibodies all over the body if the infection is localized.)

My questions is: Could someone "map out" the travel of a typical B-cell throughout the body from the time the B-cell detects an antigen up to the time it produces antibodies (and if it later stops producing anti-bodies, please include that)?

The oncologist seems to be incorrect.

Antibodies are created all over the body inside secondary lymphatic organs (lymphatic nodes) or any other mucosal associated lymphatic tissue (MALT).

B cells mature in the bone marrow and finish their maturity in the periphery, then they can live in lymph nodes, MALT, spleen, omentum or other structures and they can create antibodies in all of those structures.

In regard of your localized infection question, you are right. When a pathogen enters the body the B cells closer to it are in the lymph node that is closer to that site and thus there is where the antibody response will take place. That is why when you have a sore throat (throat infection) your tonsils are swollen (they are lymphatic organs too).


Is sequencing error a function of the nucleotide being read? Checking out on Google Scholar, I can see that for Illumina (just to consider one example) the sequencing error rate is of the order of 0.001-0.01 per nucleotide.

Talking about sequencing error, let's consider mismatches (substitution of one nucleotide by another) only. Knowing the "true" nucleotide at a given position, is it as likely to be read as any other specific nucleotide during a mismatch or are there bias? For example, if the true nucleotide is A, is it more likely to be found being as a G (as they both are purines) than a T or a C? Are some nucleotides more likely to be misread than others?

I am hoping the answer won't depend too much on the sequencing techniques.

Unfortunately, it does depend on sequencing techniques.

For example, in Illumina sequencing, each sequence fragment is amplified (in order to get a stronger signal) and forms a cluster on the microarray. Each cluster is sequenced by cycles of:

Adding fluorescent terminator nucleotides. These nucleotides are modified to contain an inhibiting/terminating group and prevents more nucleotides from being added. Theoretically, only one nucleotide is incorporated into every DNA fragment in this step.
Washing off excess nucleotides.
Capturing the incorporated nucleotide using imaging techniques and determining which base was incorporated (based on the colour of fluorescence).
Cleaving the terminator from the added nucleotides, so that the reaction can continue.

Image from Metzker, 2010.

This way, each fragment is synthesized, one nucleotide at a time, and each nucleotide that is incorporated gets detected. However, the first step is not flawless: sometimes more than one nucleotide gets incorporated into a certain DNA fragment, or no nucleotides get incorporated. Eventually, the DNA fragments in a cluster (all containing the same sequence) will fall out of sync ("phasing") and the fluorescent signal will become less clear, with a mixture of different colours. This is the main cause of sequencing error for Illumina machines, and also the reason why Illumina reads are relatively short (~300bp).

So to answer your question, in this example, nucleotides may be erroneously read as nearby nucleotides in that sequence. Errors will vary using other sequencing methods and how those methods work.

The article I linked earlier explains various sequencing methods in more detail. (Unfortunately, it's behind a paywall so some may not be able to view it.)


Pooling already extracted dna? I had ethanol precipitated a large amount of DNA (2ml) and had to split the sample in half to spin down because only the microcentrifuge has the correct rotor to spin that fast. I want to get as concentrated of a DNA sample as possible. Is it possible (correct) to combine the resuspended DNA? I wanted a total of 30 ul of extracted DNA. Could I resuspend each of the two sample in 15 ul and then combine them?

What is the best way to go about this. I realize just keeping them separate might be the best option. I also realized I could've lost DNA when transferring the sample to a smaller tube. I did this because I don't believe it is correct to spin for longer at a lower speed...

If it were me...

You can resuspend the two separate pellets (A and B) in 10ul each.
Collate in one tube (add A to B).
Use the remaining 10ul  from your desired volume to 'wash out' tube B and add the wash to tube A.

So long as the DNA is from the same sample this is a perfectly reasonable step that should not result in a substantial loss.


Can a cancerous cell from outside cause cancer in a healthy person? If a cancerous cell enters the body of a healthy person from someone else's blood or something, will that healthy person get cancer? In human beings.

Can a cancer cells from someone else's body cause cancer in a healthy person?

No. Cancer cells from another person cannot cause cancer in a healthy person. The rare cases of transmissible tumors all involve unhealthy or not yet developed persons.

Transmission of tumor cells from one individual to another happens, but is quite rare, and in all cases involves some compromise or reduced development of the immune system. Though tumor cells do metastasize in an individual, when this occurs, tumor seeds must be able to evade the immune system and find an environment suitable for adhesion and replication. Tumor associated cells (non cancerous cells that regulate the microenvironment to make it favorable for growth and replication) are discussed in this seminal paper on cancer biology by Hannahan and Weinberg.  There are similarities to infectious processes, but cancer is not measles. Tumor cells don't shed in comparable numbers, aren't adapted for immune escape in a separate host, and don't express appropriate adhesion proteins for portals of entry on a new host or readily induce tumor associated niches in a new host. The cases where person-to-person transmission of cancer via tumor cell inoculation does occur seem to demonstrate more how cancer cells are not infectious agents.

Donor-related tumors in transplant patients occur in immunosuppressed patients, but are still rare. The low frequency of transmission seems to be due, in part, to screening. The fact that we see this at all demonstrates the significance of transmission route and immune escape.
Maternal-fetal, and in utero twin-twin seem to be exceedingly rare, but have occurred, again, demonstrating the existence, but poor efficiency of transmission. Here, the fetus has an undeveloped immune system. I would not consider this case to be cancer cells causing cancer in a healthy person.
Inoculation of volunteers with tumor cells in a problematic series of experiments at Sloan Kettering in the 50s, transplantation of tumor cells into patients with other cancers, resulted in growth, recurrence after excision, and death in some cases. Transplantation into healthy volunteers (yes, they did this) resulted in nodules that spontaneously regressed. This experiment has since been interpreted as evidence for immune system control of transplanted tumor system in healthy individuals, as compared to growth and progression in a receptive niche in a cancer patient.

So person-to-person transmission of cancer cells is rare and requires an immunosuppressed or undeveloped host, or a host who already has cancer. There are no documented cases of person-to-person transmission to a healthy individual, and documented cases of failed transmission despite a surgical attempt. This is because, unlike an infectious microbe, in a healthy individual, there is not a suitable receptor for adhesion at an exposed or accessible site, a suitable environment for replication, and adaptations for immune escape by tumor cells in the original host are not effective in a new host.

As a side note, there are contagious cancers in other species, but this doesn't seem to be particularly relevant to a question about whether cancer can be transmitted between two humans. Many cancers have transmissible risk factors (e.g., human herpesvirus-8, hepatitis B and C viruses, human papilloma virus 16 and 18, and others)


What is this small tree? I found a dozen of these small trees in a local park that is just an overgrown homestead.  The leaves look something like an elder but the flower clusters surrounded by white, four petaled false flowers are completely unknown to me. What species is this?

Location:  Shenandoah valley in central Virginia, U.S.A.

Sandy soil on inside of a sharp curve of the South River,
just above the flood plain.
This area has been occupied by people, for a couple hundred years,
so this could very well be a cultivated plant.

This is very likely some species of Viburnum.

Viburnum is a genus of about 150–175 species of shrubs in the Adoxaceae family that are primarilly native throughout the temperate Northern Hemisphere.

All species of viburnum (as far as I know) have opposite leaves, as does the specimen in the picture.

Many species of Viburnums bloom in white in the last part of April through early May, and typically you have to pay attention to flower shape and often, more importantly, the leaf shape to differentiate species.

Without location information, an exact species ID is not guaranteed, but your specimen looks very similar to:

Doublefile Viburnum (Viburnum plicatum)

 Source: Dave's Garden

 Source: Missouri Botanical Garden

This species produces two rows of white flower clusters, with both small and large flowers, along the stem.

According to Wikipedia: Viburnum plicatum is a popular ornamental plant, both in its native area and in various temperate regions.

Based on the "double" flower types of your specimen, it's likely V. plicatum f. tomentosum:

  Cultivars with wild-type flowerhead structure are sometimes described as a separate botanical form V. plicatum f. tomentosum. They include 'Cascade', 'Lanarth' and 'Rowallane'.2[3] Two cultivars in this group, 'Mariesii'[5] and 'Pink Beauty',[6] have gained the Royal Horticultural Society's Award of Garden Merit.

Habit: A deciduous, multi-stemmed medium-sized shrub that typically reaches 2.5 3 m tall. [Source].

Leaf: ovate, 5-10 cm long, up to 5 cm wide; pointed apex and rounded leaf base; serrated leaf margin; 8 to 12 pairs of veins; pubescent underside; dark green leaf color. [Source].

Flowers: individual flowers form a large (up to 10 cm diameter) flat-topped cyme composed of showy infertile flowers surrounding unshowy fertile flowers. Blooms in May. [Source].


What is allele-specific gene expression? I read somewhere that the two different alleles which we (and other species) inherit from our parents are not expressed equally in our cells. Which genes show allele-specific expression? How and why?

There are a few well known examples of allelic exclusion (which is what you've described):

In females (human and probably other mammals too) one of the two X-chromosomes is silenced (shut down) during embryo development. This means that some cells have one allele (from maternal X) active, while other cells have the other one (from paternal X) active. The actual mechanism behind this is quite complex, but ultimately results in the complete epigenetically-controlled prevention of gene expression from one X-chromosome. This is necessary because otherwise females would produce twice the amount of all proteins on the X-chromosome compared to males.

Another well known example relates to the genes that lead to the building of the B-cell receptors and antibodies. During maturation of the B-cells different segments of these genes are rearranged in a process call VDJ recombination. In order to make sure that the cells produce only one kind of B-cell receptor/antibody one of the two alleles for these genes is silenced after a certain rearrangement step has taken place.


What is the difference between a response element and a enhancer? I have been confused as to the difference between a response element and an enhancer.

Wikipedia has the definition of response element as the following:

  Response elements are short sequences of DNA within a gene promoter region that are able to bind specific transcription factors and regulate transcription of genes.

Wikipedia's definition of enhancers:

  In genetics, an enhancer is a short (50-1500 bp) region of DNA that can be bound by proteins (activators) to increase the likelihood that transcription of a particular gene will occur.[1][2] These proteins are usually referred to as transcription factors.

They seem almost the same. What are the main differences?

The only difference I can see is that response elements can both halt transcription or allow for it. While enhancers only promote transcription if the transcription factor is present.

Is this the difference between the two, or is there something else that differentiates them?

Enhancers specifically bind transcription factors in an effort to obtain robust rates of transcription, in a very general fashion and may be upstream or downstream of a promoter. Remember that you don't need to receive a signal to produce housekeeping genes, regulated by general transcription factors, because they're always needed (in part). A response element can enhance or repress transcription depending on the stimulus.

Vitamin D response element (VDRE) is a fair example: In response to your extracellular calcitriol or 1,25(OH)2D, the vitamin D receptor will complex with a number of proteins that bind at the VDRE, controlling transcription of various vitamin D-controlled gene targets.

  Vitamin D activity is mediated through binding of 1,25(OH)2D3 to the vitamin D receptor (VDR), which can regulate transcription of other genes involved in cell regulation, growth, and immunity. VDR modulates the expression of genes by forming a heterodimer complex with retinoid-X-receptors (RXR).

Source: http://www.wikipathways.org/index.php/Pathway:WP1531

And just as well, other promoters such as that for pro-parathyroid hormone contain VDRE sequences that suppress it's transcription (ref).


How long do viruses, such as Zika, stay in the body? Can a virus stay in your body (after recovery) in a concentration that is sufficient to infect someone?

Is it known how long the Zika virus persists in the body?

According to the CDC the zika virus persists in the blood for around a week.

  Zika virus usually remains in the blood of an infected person for about a week but it can be found longer in some people. - CDC

I can't find much information on how long the Zika virus specifically can persist after recovery, it seems unknown just now. However, it is advised to be careful about sexual contact after infection, which suggests longer persistence is suspected in other fluids/tissues.

  British health authorities have suggested using condoms for at least 28 days. - NYTimes

Some viruses do persist for a while after recovery, including Ebola Virus Disease, which can be sexually transmitted for around three months after recovery:

  Some viruses, including Ebola, can linger for some time after recovery in parts of the body (for example, testes, eyes, spinal column fluid) not easily reached by the immune system. - CDC

These parts of the body have immune privilege. This means they can be infected by antigens without producing strong immune responses. This is thought to occur to protect vital tissues/areas which could be damaged by inflamation and the immune response, such as the brain, eyes, spinal column, testes, and fetuses.

Since I wrote this answer there have been several reported cases of sexually transmitted zika, highlighting the problems that can arise from immune privilege.


Aren't current explanations for the evolution of human cooperation a little too reductionist? Lately, I've become a believer in the limits of reductionist explanations especially in areas like complex systems and biology. So, without wasting any more time, I'll get to my question..

Whenever we think of something like cooperation, the most common explanation that comes up is that of genetic fitness. It is said that evolution would have selected for psychological mechanisms of cooperation because it is beneficial in a society in which reciprocity is possible. You scratch my back, and I scratch yours. Add to the mix the ability to name names, and reputation becomes a kind of proxy signal for fitness.

Now, the major problem I have with this is does it all have to boil down to fitness? Can't it be a phenomenon that is culture-specific? Different cultures go to different lengths to help a stranger. Yet, we all share the same evolutionary history. This seems like a strong indicator that cooperation can't be reduced to one's genetic or reputational fitness alone. Should the study of cooperation be handed off to the anthropologists?

Interesting question!

I think that in terms of 'tribal' fitness, altruism would be strongly selected for, as communities would tend to be quite small (relative to, say, a town today). In modern civilization cultures have developed differing levels of altruism, but I imagine this is a result of upbringing rather than inherent differences in tendency toward altruistic actions.

So in my opinion you cannot rule out altruism being selected for because it is clearly an advantage (in terms of survival / fitness) in smaller communities - we just don't live in that kind of society any more; people don't have to be altruistic to get by, and this kind of mind-set can 'evolve' culturally, outside genetics. But on the whole I would still argue that most people are inclined toward altruism - ether because they feel naturally inclined to help others, or feel that by helping others some benefit (such a reputation) would be bestowed upon them (the former may be the same as the latter, but at an unconscious level).


What is the point in the Neuromuscular Junction? Surely a direct connection (i.e. an electrical synapse) between motor neurone and the sarcolemma would allow for much faster neuromuscular transmission? It is my understanding that chemical synapses are only useful in facilitating spatial summation of action potentials from multiple presynaptic terminals... muscles have no need for this as they are innervated by a single motor neurone only?

After much searching on the internet I've found an answer to this question: the neuromuscular junction facilitates amplification of the motor neurone potential to generate a large enough current to depolarise a muscle fibre as muscle fibres have a much larger area of membrane (ie a larger capacitance) than neurons.
Source: Encyclopedia of Neuroscience: Volume One

The reason is the tremendous amplification of the neuromuscular junction. The amplification occurs since a small current is generated in a nerve can rekease large amounts of molecules of the transmitter acetyl-choline ($\require{mhchem} \ce{ACh}$), each of which can open channels in the much larger muscle membrane and can create much larger currents. In addition, a motor nerve fiber often branches profusely to innervate hundreds of muscle fibers, thus providing further amplification.
Finally, the capacitance of the muscular membrane has long been known to be much greater than the capacitance of the nerve membrane, because of the additional membranous systems, such as the transverse tubules in muscular fibers. Thus the capacity of the muscle to store charge is much greater than that of a nerve membrane and much more current must be supplied to depolarize muscle cells directly.


Can you freeze an ATP assay sample for later use? I am going to use adult Drosophila to do an ATP assay (ATP determination kit A22066). The most convenient for me is to freeze the samples and perform the experiment later.

However, the protocol provided by the kit producer keeps saying the assay is extremely sensitive, so I'm not sure if it's okay to keep the homogenized samples under -80°C for a short period of time.

Pure ATP can be stable when stored frozen but I would be worried, perhaps unjustifiably, about storing a homogenized sample. You should try dividing a homogenized sample in half and assaying one half right away and the other half after freezing to see how the signals compare.


Basic question about evolution I want to understand a mechanism how at the first times when the life began on earth evolution helped the new species to arise through selection while the same organism also continued to live as not evolved. If natural selection favors survival of the fittest, than why after a living evolves to a new fittest form, the older form still exists while it should be counted as unfit for survival and extinct, I am not sure but bacteria may be an example perhaps and I am not asking about the situations where the unfit form has extinct but both organisms continued to live.

I want to understand a mechanism how at the first times when the life began on earth evolution helped the new species to arise through selection while the same organism also continued to live as not evolved.

Well, this beginning is not grammatically correct so it is hard to make much comments on it.

  If natural selection favors survival of the fittest, [..]

Selection is the process by which fitter individuals increase in frequency in the population. survival of the fittest is a layman phrasing of the process that is natural selection. Natural selection therefore does not favour survival of the fittest, but it is represented by the phrasing survival of the fittest.

  [..] th[e]n why after a living evolves to a new fittest form, the older form still exists

It does not. The older form is called an ancestor. The ancestor does not exist today. If there was a speciation events, then the ancestral lineage would have giving rise to more than a single lineage today. Some of these modern lineages may 'look more' like the ancestors than others but it does not mean that any ancestor still exist.

For example, the chimpanzee is not an ancestor of humans. Chimpanzees (and bonobos) and humans share a common ancestor that is about 8 millions old. To consider another example, humans and an oak tree share a common ancestor. This ancestor was neither a human, nor an oak tree. This ancestor lived about 1.6 billions years ago.

If you want to know why I am using term 'lineage' rather than 'species', you can have a look at this post

See below linked Biology.SE posts for more information

  the older form still exists while it should be counted as unfit for survival and extinct

Don't forget that different lineages may (and will be at equilibrium due to the competitive exclusion principle) be adapted to different ecological niche. As such, one lineage will not necessarily outcompete the other one.

Source of information on StackExchange

There is a lot you can learn on the subject. You should start with an introduction to phylogenetics such as the one provided in the post

Why do the ancestors of birds still exist?

You can also have a look at

Extinction of species

You should also have a look at

How does Darwinian Evolution work?

Reading your post, it sounds like you may have too a pan-selectionist view of evolution. Related to this point, you might want to read

Why don't mammals have more than 4 limbs?

Source of information external to StackExchange

Understanding Evolution is a good introductory course to evolutionary biology.

Response to comment

  Thank you for the very descriptive answer, as you have figured out easily I am very new to evolution. I will read the references you have provided carefully

You're welcome!

  is after evolution of a specie through natural selection,

This show again that you have too a pan-selectionist view of evolution.

  unfit ancestor extinct and this is explained through phylogeny ?

From wikipedia

  Phylogenetics is the study of the evolutionary history and relationships among individuals or groups of organisms (e.g. species, or populations).

A phylogeny is a tree of life of a given taxon. For example here is a phylogeny of placental mammals.

To be able to fully answer your own question, you need to understand the relationships between lineages and therefore you need to have some understanding in phylogenetics.


How does a virus take control over the host cell? When the virus integrates its DNA with the hosts and enters the lytic pathway, do the viral proteins that produced destroy the cells DNA? Do they deactivate it? Also does the cell function in the same way as before?

A virus does not typically destroy its host's DNA. Rather, the virus makes the host cell express viral proteins at an elevated rate compared to the host's own proteins. This is usually achieved because the viral genome contains a strong constitutive promoter, possibly coupled to an enhancer sequence. The virus may also preferentially insert itself into transcriptionally active sections of the host DNA.

As I said earlier, expression of the host's own genes as a whole is not directly regulated by the virus, though specific genes may be up- or down-regulated (immune-system related genes are often primary targets). However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions.

Remember however, that the virus relies totally on the host's machinery to make viral proteins. So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against. This doesn't mean that the cell is healthy though. A significant chunk of the cell's resources have been hijacked by the virus, and a virus infected cell is typically just limping along, clinging to life, as it were.

Depending on the virus, once sufficient virions have been assembled inside the cell, the virus may enter a lytic phase, where the cell literally bursts to release the virions into the surrounding environment to infect new cells. At this point, the cell is obviously dead.


What is this yellow sticky excretion from a moth? Details in photos Saw this moth on some grass the other day and took some bad phone photos. I'd like to know what the yellow excretion is. I believe it is an excretion from the moth (as opposed to for example, some bubble gum someone dropped on the ground), because it was attached to the tail end of the moth instead of its whole body.

I tried to label the pictures as best I could, you may have to look closely. You can only see a tiny portion of the moth wing in the first picture, below.

The yellow thing was quite sticky but not as hard as bubble gum, as it stopped the moth from flying away. It was frantically flapping its wings trying to get away from some ants, which seemed to be very attracted to the yellow thing. At first I thought the swarm of ants were eating the dead moth, but the moth was alive and the ants were more interested in the yellow sticky thing. I got a thin stick and pulled away some of the sticky stuff and the moth was free enough to crawl away, taking the yellow sticky thing with it, leaving a thin trail behind, like when you stretch out bubble gum. It seemed to be very sticky to the moth and my stick, and very tensile, because unlike a spider's web, I was able to draw it out more when I tried to pull it away from the moth to free it.

I am so curious to know what it might be. I don't think it was made by ants, because it seemed to be attached to, or coming from the actual moth, although, the ants did not seem to be stuck to it.

Please add "moths" to the tags if you have enough 'reputation level' to do so.
Thank you

Some moths exude a yellow lymph excretion when they are threatened.
https://www.nature.com/articles/219747a0
The photo is not very clear, It's difficult to see the species of moth. what did the moth do after? did it fly away? If the moth was looking ill, it could be that it had a parasite.
https://www.insidescience.org/news/meet-moth-produces-both-bird-and-ant-repellants


Cardiac vs. skeletal muscle contraction For the heart muscles, it is the extracellular Ca2+ that is necessary for the contraction, but for the skeletal muscles, it is intracellular Ca2+.

One of my answers on a test was the following: "In cardiac muscles, an augmentation of the intracellular Ca2+ concentration is necessary for muscle contraction".

Therefore, I'm confused. For the heart, is it extracellular or intracellular Ca2+ that determines contraction?

Perhaps your confusion will be helped by separating for you 2 processes that occur in both skeletal and cardiac muscle contraction.  The first process is the electrical change (action potential) in the muscle cells membrane that triggers the contraction and the second is the contraction of the muscle cell itself.

The latter process, contraction of the muscle cell, is basically the same for both muscle types.  Simplistically this requires high intracellular Ca in both skeletal and cardiac muscle.  In short, when the intracellular Ca in the cell is high all muscle cells will contract and when it decreases they will relax.

The difference between the cell types is what triggers this increase in intracellular Ca when the cells are stimulated I.e. what causes the increase in intracellular Ca.  In skeletal muscles the action potential moving through structures called t tubules directly causes release of Ca from the sarcoplasmic reticulum.  In cardiac muscle this is different as the action potential here causes Ca to enter the cell from outside and it is this small amount of Ca coming from the extracellular space that triggers release of the far larger amounts of Ca in the cell that are needed for contraction.  This is called Ca Induced Ca Release or CICR.

Schematic pictures are the best way to understand the differences in the processes in the 2 muscle types so try these 2 links (Cardiac (https://courses.lumenlearning.com/boundless-ap/chapter/cardiac-muscle-tissue/) & Skeletal (https://opentextbc.ca/anatomyandphysiology/chapter/10-3-muscle-fiber-contraction-and-relaxation/)

You can also access the Textbook of Medical Physiology by Guyton and Hall online or at a school/university library which will give you more detail.


why is the cleavage in frogs holoblastic and not meroblastic? background information
The cleavage of the frog embryo during the embryo development is holoblastic (complete cleavage). However when we look at yolk-rich eggs we see a cleavage pattern which is meroblastic (partial cleavage).

Question
But the frog eggs are also yolk rich right? So why do frog embryo's use holoblastic cleavage?

Because:

Frog eggs are not yolk-rich. They are mesolecithal, they have an intermediate amount of yolk.
Yolk is concentrated within vegetal pole of the egg. That is why yolk-packed macromeres divide much slower than micromeres on the vegetal pole, which barely contain any yolk.

My sources:

https://kjcscientific.wordpress.com/project-excalibur/
Gilbert's Developmental Biology (2009)


What metabolic activities are performed by a developing human fetus's liver? I understand that organ function varies with the stages of development. Does a fetal liver EVER perform lipogenesis, gluconeogenesis, make bile, etc? Or does it only begin performing these actions postnatally?

I have heard that a fetus delivered between 24-26 weeks can potentially be "okay" with proper care and monitoring in a hospital. I would assume (please correct me if I'm wrong) that this implies the fetus's liver has developed at this time. So in the case of a fetus that was not delivered at 24-26 weeks, does it spend the remainder of the pregnancy in a fully functioning state? Or at least, which functions does it begin to perform?

I've been trying to find an answer on Google, but one walks a fine line when searching for human development information -- either the results are oversimplified "expecting mothers" websites, or journal articles speculating about the effect of X on the development of Y in the mouse/chick/zebrafish/giraffe/et cetera other nonhuman model.

It's old and I can't get access to this issue of the Annals of the New York Academy of Science, but it looks like it has some relevant information. Sifting through the abstracts it seems the vasculature of the fetal liver is completed at around 8 weeks although is still different to the adult vasculature because of the umbilical vein. The growth of the organ itself goes through different stages with each lobe growing different amounts:

They start the same size
12 weeks the left lobe is twice as large as the right
36 weeks the left is 10% larger than the right
at birth they are the same size
5days after birth the right is 10% larger
adults, they are the same size

And, studies have been conducted with dyes to look at liver function in both its capacity to concentrate the dyes and secrete it into the bile. The fetal liver can carry out bile acid synthesis, despite lacking digestive purposes, from very early on (Suchy et al. 1987). The fetus does however require help in removing the toxic cholephilic organic anions (COAs), which is done via the placenta. This review describes more.

There is also evidence to suggest the newborn's liver is not performing all the usual metabolic processes of children or adults (from looking at drug toxicity and delays in excretion/detoxification), as would be expected. More recent literature notes the fetal liver lobes (right and left) as having differnt biochemical capacities and independent function due to the right one getting less oxygen. Also, a layer of drug metabolising enzymes normally present in adults is missing in the fetal liver, although its capacity for drug metabolism is still better than that of rodents.

  In the adult liver, there is a clear zonation of metabolism of carbohydrates, proteins, lipids, and bile salts. In the livers of fetal rats, mice, and humans, this heterogeneous distribution of enzymes and metabolic function does not exist initially. Towards the end of gestation, the adult pattern of heterogeneity for these processes begins to emerge, and after birth, the adult pattern is rapidly established (Ring et al. 1999)

There is in vitro evidence for the activity of glutathione S-transferase and sulfotransferases in the human fetal liver. Returning to the asymmetry of fetal liver function (albeit in sheep..) it was found that levels of malondialdehyde, an index of lipid peroxidation, oxygen consumption, and CYP levels (a family of oxidative enzymes), are higher in the left lobe than the right lobe of the fetal liver which evens out after birth.

So in conclusion, looks like a variety of metabolic enzymes are present in the human fetal liver from very early on after the organ is formed. We know a varitey of metabolic enzymes are present and the drug/dye metabolism studies show there is some fetal liver activity, albeit reduced from that of an adult or child. The limitation with many of the studies that have been done is that they have to use in vitro data and extrapolate to the in vivo situation, so I guess we still don't really know for sure how metabolically active it is. It is clear though that it remains inefficient and unable to carry out all the functions required of it during childhood/adulthood until after further development after birth when it has stopped growing and adapted to ex utero conditions.

References

Ring JA, Ghabrial H, Ching MS, Smallwood RA, Morgan DJ. Fetal hepatic drug elimination. Pharmacol Ther. 1999 Dec;84(3):429-45.

Suchy FJ, Bucuvalas JC, Novak DA. Determinants of bile formation during development: Ontogeny of hepatic bile acid metabolism and transport. Semin Liver Dis 1987; 7(2): 77-84


Is there a word for the length of time an animal stays with parents before going off on their own? Gestation is a word describing the pregnancy for animals, and you can use 'gestation period' to describe how long a pregnancy generally takes for a species. I'd like to know if there's a corollary word for the time an animal stays with its parents before leaving.

For example, after birds are hatched, they stay in the nest for a while, but they eventually leave the nest. Is there a single word or phrase that is used to describe the time between hatching and leaving the nest? I imagine different bird species have different periods, and other animals (that don't stay within families their whole life) can also be describe in a similar matter. Perhaps 'puberty', though I'm guessing there's a more specific word.

As you talk about bird, most of the terminology I am suggesting below comes from the ornithology literature.

Fledging period

Defined on wikipedia:

  Fledging is the stage in a volant animal's life between hatching or parturition and flight.

Nestling period

Defined in Kouba et al. (2015):

  In altricial birds, the nestling period is an important part of the breeding phase because the juveniles may spend quite a long time in the nest, with associated high energy costs for the parents.

Rearing period

See its usage in for examples Yuan et al. (1994) and Brickell et al. (2009)

Juvenile

While the term juvenile does not refer to a period of time, you can refer to this concept as the period while children are still juvenile. From dictionary.com

  a young bird in the stage when it has fledged, if altricial, or has replaced down of hatching, if precocial.


What do you see when your eyes are closed? If you are in pitch black and you close your eyes, you sometimes can see strange shapes of various colors. A lot of the time these shapes and colors change as you observe them. This phenomenon still occurs if you are not in complete darkness.

I am wondering what this is that you are `seeing'? Is this phenomenon classified as seeing, as how can we be looking at something if our eyes are closed?

If you are not seeing these shapes and colors, then what you observe is pure darkness. What is this pure darkness that you are seeing? Since you are seeing it, is something stimulating the vision parts of your brain? Is it the back of your eyelid?

This is called a phosphene — the experience of perceiving light in the visual cortex without light actually entering the eye. This commonly happens due to stimulation of the retinal ganglion cells by something else. The most frequent source in normal individuals is pressure to the retina (e.g. rubbing a closed eye.) It is also possible for phosphenes to occur due to neuronal stimulation at the cortical level. Most people have had the experience of “seeing stars” when you stand up too quickly. This happens because orthostatic hypotension results in transiently decreased cerebral perfusion; it is the metabolic shift in oxygenation and/or glucose delivery to cortical neurons that causes the perception of light. Something similar occurs with brief rises in intracranial pressure that occurs with sneezing or coughing.* Magnetic stimuli can also induce this phenomenon.

Phosphenes can also be pathologic (i.e. disease-associated). Migraine headache sufferers may experience a visual “aura” prior to a headache, which is a type of phosphene, likely mediated at the cortical level. There is some evidence to suggest that preventing the phosphene may also reduce headache frequency. Other conditions associated with phosphenes include abnormalities of the optic nerve** and retina — just as stimulation of a peripheral somatic sensory nerve might cause a pain signal to arrive in the brain in the absence of true tactile stimulation, disorders of the optic nerve can generate disorganized signals that the brain perceives as light.

*Increased intracranial pressure leads to decreased perfusion due to the differential between peripheral and cerebral pressures.

**If you read nothing else linked to this question, take a look at that paper (free in PMC). It describes optic neuropathy associated with auditory-evoked phosphenes. The patients perceived sound as light!


Do chicks in eggs excrete? I want to know if, as a baby chick grows inside the egg, does it excrete waste?

If it does excrete waste, does the waste just sit inside the egg with the chick, until the chick cracks open the egg and gets out?

Yes they excrete uric acid which is stored in the allantois of the embryo; which acts as a reservoir of nitrogenous waste.

Uric acid is not very soluble in water, so it stays as a small solid mass.


If Evolution Is In Progress, Why Fight Extinction? Natural selection is a central tenet of evolution. However, most biologists seem determined to prevent the extinction of the species that have been selected against. Why is this? Preservation of genetic diversity?

I thought evolution was supposed to create diversity not destroy it. What am I missing?

First, a shorthand definition of Evolution is heritable change and not 'progress' (which is a rather loaded word). Also, evolution is not 'supposed' to do anything, and can lead to both an increase or a decrease in diversity, since (local) diversity is simply the net result of speciation rate and extinction rate (if we exclude colonization of new species from other areas). Therefore, I think the question is framed in the wrong way.

Second, there are many reasons why biologists might want to halt species extinctions, as hinted in the other comments and answers. Most obviously, conservation biologists want to prevent man-made extinctions which are due to how we have influenced/modified/destroyed the natural environments. I don't think conservation biologists in general are determined to halt all 'natural' extinction. However, most of the time it is really hard to pinpoint what would be a 'natural' extinction. Either way, the current rates of extinction, which have been estimated to lie 100-1000 times (IUCN, 2007) above background rates (some say it's closer to 10000 times higher), indicate that most extinctions are man-made.

The rationales people use for preserving biodiversity can however differ. Three distinct categories are:

1) For human survival and/or economy, e.g. through ecosystem services or resources we rely on.

2) For human welfare, e.g. recreation or esthetical reasons.

3) Ethical considerations, e.g. inherent value of species or to preserve the unique evolutionary history of the system.

Another way to structure these is to label 1) & 2) as instrumental values and 3) as inherent values. The instrumental values can then be subcategorized as services, goods/resources, information (e.g. genetic to be used in medical research), and esthetical/spiritual values.

Since the direct value of individual species are often (usually) uncertain (irrespectivly of the direct rationales used) the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. However, other aspects of biodiversity are functional diversity, which focus on preserving functional groups of species, or phylogenetic diversity, focusing on taxonomic coverage and uniqueness (evolutionary history), instead of 'overall' biodiversity (see e.g. Flynn et al, 2011 for a discussion of these concepts). Under these perspectives less focus is placed on individual species.


Why do flagella form a bundle only when they rotate counterclockwise during chemotaxis? During Chemotaxis in bacteria with flagella, the flagellar rotation dictates how the cell moves. If the flagella rotate counterclockwise, then they form a bundle at one end of the cell (---O) and propel it forward in a coordinated fashion. However, if the flagella rotate clockwise, then each flagella acts independently to push the cell in many different directions.

My question is, why doesn't clockwise flagellar rotation simply cause the bundle to form on the opposite end of the cell? (O---)

In principle this can happen, but you have to read up on flagellar dynamics and polymorphic transitions (Real-Time Imaging of Fluorescent Flagellar Filaments, Turner et al. 2000).

From Howard Bergs lab page:

  Runs can occur with filaments of any polymorphic form; although, the normal form predominates. For a cell to tumble, not every filament needs to change its direction of rotation. Different filaments can change directions at different times, or a tumble can result from the change in direction of only one.

If the whole bundle comes apart it can reform on either end of the cell body because E. coli has a random flagellation pattern (peritrichous) and thus no preferred direction of propagation of the cell body.

Also have  look here for some nice movies from the Berg lab.


Why does rabies cause hydrophobia? What feature of rabies pathophysiology causes hydrophobia? Why is hydrophobia unique to this one particular type of viral infection?

Rabies causes hydrophobia in the encephalitic stage which means when it affects the brain and causes swelling and inflammation of multiple areas of the brain. Hence, it affects the complex areas in the brain needed for swallowing. Initially into the course of the disease, the patient has involuntary contractions of neck muscles when he drinks water.  At later stages of disease, the patient starts contracting his muscles even at the thought of water. Rabies virus is a neurotropic virus which means that it travels through nerves because of its preference to attach to acetylcholine receptors in the neurons.  That is how the virus spreads from the bite site to the brain(via the nerves).


What type of animation software is used to create these molecular motor motions? Recently, I came across this video on molecular motor motion. Can someone suggest software that can do similar animations? I am not sure what they (at Harvard Medical School) used but the animations are really cool.

Most any reasonable animation/modeling software can handle this sort of animation. I have developed an educational iOS app with interactive biological macromolecules, including several animations. Here is how I would approach this, I suspect something similar was done here.

The models are likely built up from PDB files, or equivalent. These files allow viewing and manipulating large molecules in 3D with special viewers.  Many 3D modeling/animation apps can also view and convert these molecules into polygonal models that can be used as components and then animated within the app. I use Cinema 4D, not cheap. There is a free, downloadable program called Blender. I'm sure Blender can handle the animation but not certain whether it can read and convert the PDB file. If not, there may be other options for this.

This is not a challenge to be taken lightly. The person doing the animation you reference also knew how to assemble the parts as well as how the movement is effected. There is also a steep learning curve to using this type of software.


Can visual acuity be improved? Is it possible to completely cure myopia using natural methods (i.e. not with Lasik etc.)?.
I have seen websites claiming that exercising the eyes will help improve eyesight.

Is this true?

While there is no such thing as perfect vision, growing evidence from Asia shows that looking often at distant objects (which one does naturally when being outside) can stop myopia progression. Vice versa, progression appears to increase when myopic children mainly live indoors.

D. J. Park, N. G. Congdon: Evidence for an "epidemic" of myopia. In: Annals of the Academy of Medicine, Singapore. 33, 1, Jan 2004, 21–26. PMID 15008557. (Review).

K. A. Rose, I. G. Morgan et al: Outdoor activity reduces the prevalence of myopia in children. In: Ophthalmology. 115, 8, Aug 2008, 1279–1285. DOI:10.1016/j.ophtha.2007.12.019. PMID 18294691.


How sterile is sterile when working with nucleic acids to prevent contamination? I am reading up on preparatory work on working with nucleic acids and a lot of the instructions speak on excessive procedures on cleaning environments with high %ethanol and making sure the equipment is nuclease free, and autoclaved.

Are these sterilization steps really necessary when doing research /running gels? Buying all of this equipment seems very excessive, and given that just one nuclease could compromise my results why bother?

Short answer: Yes

Long answer: Depends what you are working with.

DNA: If you are working with DNA, its pretty stable and you can usually get away with a 70% ethanol wash/autoclave (mainly to prevent contamination and obtain consistent results). EDIT: Read Chris's answer also below

RNA: If you are working with RNA well.. whatever you did for DNA doesnt apply anymore. You have to take it to the next level.  You will need to replace everything, you'll need nuclease free water, tubes, reagents and whatnots. Throw out ethanol and bring in RNAZap, DEPC water or something like that.

  An RNase free environment is essential when working with RNA samples. There are two main reasons for RNA degradation during RNA analysis.

  First, RNA by its very structure is inherently weaker than DNA. RNA is made up of ribose units, which have a highly reactive hydroxyl group on C2 that takes part in RNA-mediated enzymatic events. This makes RNA more chemically labile than DNA. RNA is also more prone to heat degradation than DNA.

  Secondly, enzymes that degrade RNA, ribonucleases (RNases) are so ubiquitous and hardy; removing them often proves to be nearly impossible. For example, autoclaving a solution containing bacteria will destroy the bacterial cells but not the RNases released from the cells. Furthermore, even trace amounts of RNases are able to degrade RNA. Note that RNAses are present everywhere (skin, reagents, normal plastic etc).

  Therefore, it is essential to avoid inadvertently introducing RNases into the RNA sample during or after the isolation procedure.

Remember that following microbiological aseptical techniques is usually good practice (and a requirement) when working in a molecular biology lab.

There are excellent guides available online for working with RNA:

I took the above paragraph from here:
http://www.bioline.com/us/rna-hints-and-tips

Life tech has a few more tips for you: https://www.lifetechnologies.com/uk/en/home/references/ambion-tech-support/nuclease-enzymes/general-articles/working-with-rna.html

Here is a good pdf to have in your labbook as a reference sheet:http://genomics.no/oslo/uploads/PDFs/workingwithrna.pdf

If this scares you , that's good because when working with RNA there are a million things that can go wrong the first few times you try it. You have to be very careful, and adapting a cavalier attitude such as not bothering is going to come back and haunt you at night...


Is there a reason why human eyesight and plants make use of the same wavelength of light? The accepted range for the wavelengths of light that the human eye can detect is roughly between 400nm and 700nm.  Is it a co-incidence that these wavelengths are identical to those in the  Photosynthetically Active Radiation (PAR) range (the wavelength of light used for normal photosynthesis)?

Alternatively is there something special about photons with those energy levels that is leading to stabilising selection in multiple species as diverse as humans and plants?

Good question.

If you look at the spectral energy distribution in the accepted answer here, we see that photons with wavelengths less than ~300 nm are absorbed by species such as ozone. Much beyond 750 infrared radiation is largely absorbed by species such as water and carbon dioxide. Therefore the vast majority of solar photons reaching the surface have wavelengths that lie between these two extremes.

Therefore, I would suggest that surface organisms will have adapted to use these wavelengths of light whether it be used in photoreceptors or in photosynthesis since these are the wavelengths available; i.e., organisms have adapted to use these wavelengths of light, rather than these wavelengths being special per se (although in the specific case of photosynthesis there is a photon energy sweet spot).

For example this study suggests that some fungi might actually be able to utilize ionizing radiation in metabolism. This suggests that hypothetical organisms on a world bathed in ionizing radiation may evolve mechanisms to utilize this energy.


X-recessive disorder pedigree confusing me This is a pedigree of a family in which bleeder disease, an x-recessive disease, is present. I am asked which marker, A or B, the disease is linked to.
I've asked about this type of problem before: X-recessive disorders and genetic markers
The solution there was the fact that the families were unrelated so the disease being linked with a marker in one family did not correspond to the disease being linked to the same marker in another family.
The answer to this problem is "A". However this is ONE family and there are males in this family with the A marker on their only X-chromosomes who are unaffected and women with two A markers who are also unaffected. How would you explain that? They have the marker for the disease on both alleles but not the disease?

Remember: A and B are genetic markers that might be linked to the disease gene. Neither A nor B are actually the hemophilia disease mutation (or gene), A or B are proxies, or substitutes for the mutation in the disease gene.
Since it is an X-linked recessive, it is only the Mother's two X chromosomes that are candidates.  You can completely ignore the Father's copy of X that also happens to carry the A marker.
In the F1 generation every male who received the copy of the Mother's X marked with A died, and every male who received her X marked with B survived. Therefore her X marked with A is linked to the mutation.

Those other AA females are either heterozygotes, or outsiders who married into the family. The outsiders do not carry the mutation.

Perhaps your confusion is due in part to the fact that some key facts are not explicit in the pedigree diagram from your instructor's course materials? Try drawing the various genotypes out like this:


Can two protein secondary structures "overlap" in the PDB? I have a technical question regarding the syntax in Protein Data Bank files.  In the protein with PDB# 1AE9 (pdb file), there are two lines in the .pdb file:

HELIX    4   4 MET A 255  ILE A  265  1                                  11

SHEET    2   B 2 ILE A 253  MET A 255 -1  N  ILE A 253   O  ILE A 248

Now, as I understand the documentation, this means there is an alpha helix starting from residue "MET A 255" to the residue "ILE A  265".  There is also a beta strand from "ILE A 253" to "MET A 255".  We see that the alpha helix and beta strand share the residue "MET A 255".

The documentation describes these as:

"Name of the initial residue."
"Name of the terminal residue of the helix."

The wording suggests that the "initial" residue is included, but I'm unsure of whether or not the "terminal" residue would be included.

  Question:  Should I consider this residue as belonging to both the alpha helix and beta strand?  Or should I consider the "terminal" residue as not belonging to the secondary structure element?  (Or something else?)

TLDR; Answer: You could consider this particular residue to belong to both structural elements, but it's a tricky call and depends on the method of secondary structure assignment.

Ambiguous secondary structure allocation comes up fairly often. Whilst obviously, not many people will be able to use this protein specifically, the below approach could be useful for other proteins.
Default pymol assignment
In PyMol I used fetch 1ae9 and highlighted M at position 255 on the A chain in red. I can see why this isn't a satisfying representation: the beta sheet allocation is very short, and the residue in question is clearly the beginning of a helix.

DSS is more conservative
To run a more conservative secondary structure allocation run dss in pymol (watered down dssp). This reveals that the beta sheets were actually quite putative.

We can see why when we look at the stick model (below). There are only a few (2-4) residue pairs in proximity that would be available for hydrogen bonding, even assuming all 4 form H-bonds, calling this a bona fide beta sheet could be seen as a bit generous.

Dual assignment can be okay.
Looking at this example (1ae9), we see the potential for H-bonding with another putative beta sheet, as well as a backbone angle that starts to form a helix. It's a classic case of ambiguous dual assignment. @AlexanderDScouras draws a reasonable conclusion that both is okay and to directly answer the question: dual assignment is possible, and allowed. I would prefer to rule out beta sheets in this particular case, but on the condition that one highlights that there is plenty of hydrogen bonding in the hairpin loop.
So long as it's reasonable.
So long as you can reasonably justify the assignment it's probably okay. You can manually assign any residue and secondary structure.
# set residue 155 to be alpha-helical
alter 155/, ss='H'

# update the scene in PyMOL to reflect the changes.
rebuild

Evidence is always a good idea to support manual assignments. A quick and thorough way would be to run the sequence through a few secondary structure predictors, or use the genesilico metaserver to save yourself some hassle (you'll need an account) (this does feel like going back a step since you now have a structure, so exercise caution - if the sequence prediction doesn't look correct according to the structure, it's probably not). Another method as suggested by shigeta is running this through a Ramachandran plot (RAMPAGE is a favourite).

If it's very very unclear then discuss it thoroughly and clearly whenever this part of the protein is relevant. These secondary structure assignments have somewhat arbitrary cut-offs after-all, and when things get near the thresholds, it's important to approach the situation with clarity and specificity.

Ramachandran plot image source: By Dcrjsr - Own work, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=9105708


Why aren't we immune to the "cold" As far as I know, people suffer from the cold since ever. Why didn't and don't we evolve to resist it?

The main reason is that there really isn't any one "cold," but rather the word is used to describe many different infections that simply have the same symptoms. The reason for these same symptoms is that almost all of the symptoms that one experiences in a cold are actually the immune response to said infection. For instance, a fever is used to make the body less hospitable for the infection causing agent and throwing up is used to ensure that harmful substances are removed from the digestive system before they can cause too much harm.

The reason that the body can't simply evolve resistance to all of these possible infections is both because the infections evolve too and because there are simply too many of them that all need a separate method to be defeated. Therefore, curing the common cold is effectivley curing the majority of known ailments.


Can kit foxes and red foxes produce offspring? Can a kit fox (Vulpes macrotis) and a red fox (Vulpes vulpes) together produce offspring?

Would such a hybrid be fertile?

Yes, a red fox and a kit fox could produce hybrid offspring, but it would be sterile.

Sterile red fox / arctic fox (V. lagopus) hybrids have been bred for the fur trade for decades (source).

Arctic foxes are quite closely related to kit foxes, and both species are equally distantly related to red foxes, so since one can produce hybrids then the other should be able to as well. Here's a screenshot from onezoom.org showing their relation. (Arctic fox = Vulpes lagopus)

Red fox / kit fox hybrids have not been observed in the wild, and kit foxes are not widely kept in captivity except in zoos, so I am not aware of any record of such hybrids. It would likely take intentional effort on the part of a fox breeder to produce them.


List authors (scientists) by various attribute Is there an easy way to list authors of biology articles by

University
country
number of published articles
sum of citations of all articles he/she wrote
fields of study (population genetics)
...

For example, I want to know who are the 10 most popular/cited authors in population genetics in UK's universities. How can I achieve such search?

For example, do WebOfKnowledge provide such tools?

Please, let me know if this question should be asked on another SE website.

I don't think that you can do this systematically in Web of Science but you can do it in an exploratory way.

Initial search: Topic - "population genetics" + Address - UK

sort by Times cited is probably more useful than the default (newest to oldest)

open Authors in sidebar - this is a list of the top 100 names
can refine to the top 10, or whatever

For example consider Brian Charlesworth:

Open an item with his name in the author list (he has some single author items)
Click on the link of his name to see his papers
Click on Create citation report to see charts of published items per year and citations per year

It may be that you know all this.


Evolution of plants and chloroplasts? I am considering the evolution of plants, specifically considering the chloroplast. I am getting slightly confused and cannot seem to find the information I need to build a coherent picture in my head. Specifically, I have the following questions:

Is the defining feature of a plant cell that it has, or once had, chloroplasts? Is the group of plants all of the species which came from the single common ancestor eukaryotic cell which first acquired a photosynthesising bacterium as an endosymbiont?
In that case, the plants Alectoria sarmentosa (witch's hair lichen) and Monotropa uniflora (Indian Pipe), which are non-photosynthesising plants and do not have chlorophyll, must have some remanant of a chloroplast inside of them (unless they are not actually plants and are just plant-like fungi). My question here is, are these really plants? If so and it is true that plants are defined as all being descendant from this first photosynthesising eukaryote ancestor, then what is their 'remnant chloroplast'? I.e. what organelle do they have that used to be a chloroplast.
If it is true that there are plants which have organelles that used to be chloroplasts but not longer have chlorophyll and photosynthesise, then it is almost certainly the case that the chloroplasts carry out some function other than photosynthesis that is beneficial to the plant's survival (e.g. I know that remnant mitochondria- hydrogenosomes and mitosomes- are useful for fixing iron although they do not carry out respiration). What are the other functions of chloroplast-like organelles?

Modern biology attempts to group organisms by clades, that is, into groups that contain all descendants of a particular organism and no others.  A clade may be associated with characteristics that most or all members of the clade possess, but those characteristics do not define the clade.  Previously it was common to describe biological groups by particular defining characteristics, but that has been largely abandoned because it often does not reflect true relationships.

"Plants" (or Plantae) is a term that can mean several different things, which are outlined in this Wikipedia table.  In short, it might be (approximately) the clade of "land plants", the clade of "green plants", which includes land plants and green algae, or the clade containing those plus the red algae and the glaucophyte algae.  That last clade, also known as the Archaeplastida, is thought to include all descendant species of the initial organism which initially established the symbiosis leading to chloroplasts (although not some organisms that acquired chloroplasts by secondary ingestion of archaeplastida).  It seems like you are most concerned with that third group.

Alectoria sarmentosa (witch's hair lichen) is not a plant by any of these definitions.  It is a lichen, which are symbioses of a fungi with a cyanobacterium or a green algae.  Green algae of course have chloroplasts.

Monotropa uniflora (Indian Pipe) is a member of the heather family and so is a plant by any of the above three definitions.  It does not have chlorophyll; my guess is that it likely has degenerate chloroplasts.

I think a separate question would be appropriate to inquire about the chloroplast remnants of non-photosynthesizing plants like Monotropa uniflora.


How much does calcium reduce iron absorption? Generally calcium inhibits the absorption of iron, but to what extent? One atom of calcium will not block 100% of iron absorption, that clearly isn't feasible. On the other hand, if someone ate 10 pounds of calcium, they wouldn't absorb any iron. How can we quantitatively determine the inhibition of iron absorption for a given calcium intake?

In short: Calcium can inhibit absorption of iron, but this does not necessary have any significant effect on the long-term iron status in the human body.

Iron (Linus Pauling Institute):

  The presence of calcium decreases iron absorption from both nonheme
  (i.e., most supplements and food sources other than meat, poultry, and
  seafood) and heme sources (meat). However, calcium
  supplementation up to 12 weeks has not been found to change iron
  nutritional status, probably due to a compensatory increase in iron
  absorption. Individuals taking iron supplements should take them two
  hours apart from calcium-rich food or supplements to maximize iron
  absorption.

In various studies, calcium from food or supplements in usual amounts decreased iron absorption by about 50%, but the calcium dose/iron absorption relationship cannot be simply quantified, because it is affected by several factors, for example:

Phytates in food inhibit the absorption of both calcium and iron (BiomedCentral).
Calcium may inhibit the absorption of nonheme iron from plant foods less than heme iron from meat (academic.oup.com).
Different calcium supplements may differently affect the absorption of different iron supplements.

The inhibitory effect of calcium on iron absorption is not linear and one may not be able to express it as a simple formula. Below are some examples from studies.

A review of studies, American Journal of Clinical Nutrition, 2010

  The reported dose-effect relation between the amount of calcium given
  and the degree of inhibition of iron absorption differs from other
  factors influencing iron absorption.
  This dose-effect pitfall is illustrated by 2 studies...[Read more in the linked article ].

A review of studies, PubMed, 2010

  The quantitative effect, although dose dependent, was modified by the
  form in which Ca was administered and by other dietary constituents
  (such as phosphate, phytate and ascorbic acid) known to affect Fe
  bioavailability. The results of most multiple-meal human studies
  suggest that Ca supplementation will have only a small effect on Fe
  absorption unless habitual Ca consumption is very low.

A study, PubMed, 1991

  When taken without food, calcium carbonate did not inhibit the
  absorption of ferrous sulphate with doses of either 300 mg Ca and 37
  mg Fe or 600 mg Ca and 18 mg Fe. However, at the latter levels,
  calcium citrate and calcium phosphate reduced iron absorption
  significantly by 49% and 62%, respectively. All calcium supplements
  inhibited absorption of the iron supplement when taken with food. The
  absorption of dietary nonheme iron was also inhibited by all three
  supplements. This inhibition was less pronounced from a meal of high
  iron availability and low calcium content (28%) than from a breakfast
  meal of low iron availability and high calcium content (55%).

A study, American Journal of Clinical Nutrition, 2005

  Calcium supplementation reduced heme and total iron without
  significantly affecting nonheme-iron absorption, regardless of meal
  bioavailability.


what are examples of experimental designs on exposing materal for degradation if one wanted to compare how sources of DNA would degradate in various conditions(environmental) how would they do this in an experimental fashion but also be best comparable to real world examples of Enviromental conditions? Sorry if this question is worded poorly, any suggestions would be appricated.

For example, if I were to expose my own blood to various conditions such as a wet enviroment versus a dry ennviroment, how would I best replicate these enviroments in real life(ie: bloodly water in a cup versus dried blood on a floor) without introducing confounding varables?

I would need some type of "standard" yes? And if so, then would using sterile controled conditions be appropriate, or should I literally be using these real world situations for "better" results?

I tired finding papers, but I guess my research methods are too poor to get anything useful.

EDIT:

My facilities I have access to are a small academic institution, I know basic autoclave use and have access to gel rigs and pcr machines. My samples do not have to be blood, it could be any human tissue or sample, like hair or spit. I suppose I would use the same sample, but kept in a sterile condition for a controo, maybe a petri dish?

I guess my mental protocol would be to try different degradation conditions and extractions, but starting with a boiling DNA extraction to see how effective a certain condition was compared to a control.

I could set up a time table of like 2 weeks to perform the experiment, and every 3 days or so, extract DNA from the control and the sample to then pcr with some human primers(I think we are using the fbi's CODIS primers that they use in foriensics, but only a subset due to cost) and then run an agarose gel to determine degradation( poorer resolution meaning more degradation I suppose?).

Another wuestion that popped to mind, for my time table and my DNA extractions, would I have to perform the pcr and subsequent gel elecrrophorsis as soon as I am done with my extraction, or could I store the extraction samples until I am ready to run a large batch of pcr tubes and a large gel? Would they degrade in a -80°C freezer?

Have you heard of qPCR? This method quantifies the amount of DNA in the sample. Another quantitative PCR method you might look into is taqman PCR. Traditional PCR + agarose gel electrophoresis is not going to give you a quantitative measurement of the DNA in your sample.
Here are the wikis on taqman and qPCR.
taqman https://en.wikipedia.org/wiki/TaqMan
qPCR https://en.wikipedia.org/wiki/Real-time_polymerase_chain_reaction
Also, if you have the choice between intercalating agents and fluorescent probes, go with fluorescence. Intercalating agents are hazardous.
Hope that helps.
Edit Adapted from comments -
We don't have access to a real time pcr intrusment sadly. All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/…. Are there ways to work with the intensity of the bands I get to be " more reliable"? – Ro Siv
Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.
If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.
If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'
I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat. Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf
Question: If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? rsb.info.nih.gov/ij I think its GUI interface is alot more workable for me.
Response: From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.
Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.


How do I identify the different stages of meiosis under microscope? This is a question I'm troubled with as my exams are knocking at the door. I need help so I decided to post this here.

Here's what I know and understand about meiotic stages:

Specimen: Grasshopper (Gesonula punctifrons) testis whose 2n= 23

Note: The character in bold and italics is the identifying feature of the concerned stage.

Prophase:

Leptotene

The uncondensed chromosomes are visible as a cloud of thin threads.
Each chromosome consist of two chromatids which are not visible.
The single darkly stained X chromosome is found at the periphery of the nucleus.
Late in this stage the chromosomes attach themselves by telomeres to the inner membrane of the nuclear envelope forming a bouquet.
Nuceolus and nuclear membrane are present.(not visible under compound
microscope)

Zygotene

The uncondensed chromosomes are visible as a cloud of threads.
Homologous chromosomes undergo synapsis  forming bivalent.
The single darkly stained X chromosome is present slightly off the periphery of the nucleus.
Nucleolus and nuclear membrane are present.(not visible)

Pachytene

The chromosomes show some degree of condensation.
The sister chromatids separate to form tetrad a structure with four chromatids.
Crossing over between non sister chromatids of homologous chromosomes occur leading to formation of X shaped chiasmata.
Nucleolus and nuclear membrane are present.(not visible)

Diplotene

The chromosomes are thick and darkly stained.
The chromosomes are wooly in appearance.
The paired chromosomes separate from each other except for the chiasmata.
Nucleolus and nuclear membrane begin to diappear.(can't be detected)

Diakinesis

The chromosomes are thick and darkly stained.
Terminalisation of chiasmata initiates.
The bivalents appear rod, diamond or oval shaped.
The nucleus and nuclear membrane disappear completely.

Metaphase-I

The chromosomes are thick and darkly stained.
Presence of twelve chromosomal elements (11 tetrad + X chromosome).
The chromosomes are aligned at the equitorial plate.
Terminalisation of chiasmata completes.

Anaphase-I

Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are T or V shaped.
Each chromosome is in dyad state.
The centromere is undivided.

Metaphase-II

There is 11-12 dyads present.
The chromosomes are thick and darkly stained.
The dyads are arranged in circle or flower like fashion.
The chromosomes are rod like

Anaphase-II

The sister chromatids of a dyad separate due to splitting of centromere.
Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are rod like

Here's an image which has nearly all the stages except telophase.Can someone label the stages?

Here's what I feel about them:

Finally am I correct? How do I identify them correctly? Could you site some authentic references?

ID characteristics that can help you recognize diplotene  better:

diplotene :
the only difference between this phase and Diakinesis is that The centrosomes reach the poles.

you can see the photos of diplotene and diakinesis here :

http://www1.biologie.uni-hamburg.de/b-online/e09/meiosea.htm

(a) polyploid nutri-tive cells with many heteropicnotic chromatin bodies; (b) leptotene-zygotene; (c) pachytene; (d) diffuse stage; (e) di-plotene; (f) diakinesis; (g) metaphase I; (h, i) anaphase I; (j) telophase I;. (k) metaphase II; (l) anaphase II; (m) telophase II; (n) round spermatids; (o) elongating spermatids; (p) head of sper-matozoas. Big arrows indicate sex chromosomes, small arrows point to nucleoli and arrowheads indicate m-chromosomes

You can see all the phases clear and perfectly separated here :

http://biology.about.com/od/meiosis/ss/meiosisstep.htm#step1

by the way , try to adjust microscope as best as you can & don't put much  oil immersion .


Why the name coined for MARKUP LANGUAGE for SBML? I'm get the confusion about  SYSTEM BIOLOGY filed.  SBML is refer to as SYSTEM BIOLOGY MARKUP LANGUAGE why we should called as MARKUP LANGUAGE? In HTML,XML and other field Mark up language mean particular function is declare into the Angular bracket like <H1> for Heading Tag this is displayed on the browser. Markup Language was actually developed for Wep application.

In other words, MarkUp language only displayed what we want., not display the simple mathematical function. Like, I need add function 1 + 1 which is display on the browser Markup language is not add, which is done by the CGI programming Like PERL,PYTHON, javascript.

So, in SBML(System Biology MarkUp language) Tools are not only display the what we want it? and It is not run on the browser? So why we called it is MarkUp Language?

SBML follows in the same vein as XML, in that it provides a standardized and flexible method for structuring information. XML and its ilk aren't just for making web pages, they're for sending structured datasets between systems and programs (in fact, XML is a fairly common configuration format). Why? Because the structure makes parsing simple (well, simple-ish).

BTW, markup languages were not invented for the web, HTML was far from the first one. The origin of markup languages is typesetting and in fact one of the most common uses these days is still in writing papers (ask a local math/physics/CS person what he/she uses to write papers and the answer will be Latex...a markup language).

Edit: BTW, this really has nothing to do with biology and you could have at least read the wikipedia page on what a markup language is.


What happens when we stretch? From the wikipedia page on stretching:

  Stretching is a form of physical exercise in which a specific muscle or tendon (or muscle group) is deliberately flexed or stretched in order to improve the muscle's felt elasticity and achieve comfortable muscle tone.

How is this improvement of elasticity achieved, at the physiological level?

Searching around on this topic brings a lot of articles about the types of stretches (e.g. again, wikipedia) and what are their benefits and disadvantages.
But how do they differ at the biological level?

Short answer: Due to habituation. You do something enough number of times, then that event ceases to be something new, and your body adapts to it.

In this case, you train your body to accept more risks allowing greater lengthening, before it begins to internally signal the muscles that an injury is incoming.

Read below for the slightly longer version:

  The stretching of a muscle fiber begins with the sarcomere, the basic unit of contraction in the muscle fiber. As the sarcomere contracts, the area of overlap between the thick and thin myofilaments increases. As it stretches, this area of overlap decreases, allowing the muscle fiber to elongate. Once the muscle fiber is at its maximum resting length (all the sarcomeres are fully stretched), additional stretching places force on the surrounding connective tissue.

  There are two kinds of muscle fibers: intrafusal muscle fibers and extrafusal muscle fibers. Extrafusil fibers are the ones that contain myofibrils. Intrafusal fibers are also called muscle spindles and lie parallel to the extrafusal fibers and are the primary proprioceptors in the muscle.

  When the muscle is stretched, so is the muscle spindle. The muscle spindle records the change in length (and how fast) and sends signals to the spine which convey this information. This triggers the stretch reflex (also called the myotatic reflex) which attempts to resist the change in muscle length by causing the stretched muscle to contract. The more sudden the change in muscle length, the stronger the muscle contractions will be (plyometric, or "jump", training is based on this fact). This basic function of the muscle spindle helps to maintain muscle tone and to protect the body from injury.

  One of the reasons for holding a stretch for a prolonged period of time is that as you hold the muscle in a stretched position, the muscle spindle habituates (becomes accustomed to the new length) and reduces its signaling. Gradually, you can train your stretch receptors to allow greater lengthening of the muscles.

You can read more about it (including the role of the lengthening reaction by the gogli tendon organs) here: http://people.bath.ac.uk/masrjb/Stretch/stretching_2.html#SEC13

It has also been published in a short section in this paper. I am sure you can follow the reference chain if you need to.

Smith, Craig A. "The warm-up procedure: to stretch or not to stretch. A brief review." Journal of Orthopaedic & Sports Physical Therapy 19.1 (1994): 12-17.