Can defibrillation be done with a car battery? Can successful defibrillation be done with a car battery? Is it POSSIBLE for this to work?

Let's say you are stuck on a very remote place and something happens to someone...

Moreover, can you jump start someone's heart using the battery of a car and the jumper cables, keeping in mind that:

in order to start a stopped heart you need electrical current applied in a short period, like 20 ms, and at a relatively high tension (200v) and small intensity?
car battery provides low tension current (12v) at a relative high intensity (70-80A) and the period cannot be 20 ms, but around 200-300 ms giving the fact that humans are not able to react that fast.

In general, no.

Car batteries are designed to provide a large amount of amperage, to turn the starter with a high amount of torque via an electric motor.  Generally this is done at 12 or 24 volts.

The current recommendations for a defibrillator requires 200V, and a very small amount of amperage.  This is one of three settings in a standard defib procedure.  The second setting is 300V, and the final is 360V.  The point of defibrillation is not to provide power to the heart, it is to disrupt the heart's built-in electrical (biological) circuitry, such that the heart can go to rest (not beating).

Many cardiac events involve the heart beating in an uncoordinated manner, such that many or all of the muscle fibers in the heart beat in a manner that doesn't provide the squeezing action on the chambers to push the blood forwards.  Defibrillation seeks to correct such an uncoordinated beating by resetting the heart to rest, after which it will hopefully start beating again in a coordinated manner.

In short, attaching a car battery is more likely to cook the heart (if it even gets that deep) because it is providing too much power, and it is unlikely to disrupt the heart's electrical field because it is too low of a voltage.  With this in mind, one could theoretically attach enough electrical transformation equipment to a car battery to use it as a power source for defibrillation.  But there are other issues with such an idea.

Car batteries are not designed for the usage that would mesh well with a defibrillation machine.  Car batteries are designed to be recharged.  Your car battery basically drains pretty heavily upon starting a car, and then the alternator recharges it by harvesting mechanical power from the engine during your trip.  This heavy drain / heavy charge cycling is hard on batteries, and car batteries have been specifically designed to endure in such a scenario.

A defibrillator machine has a different use scenario.  Basically it sits idle for long periods of time, and when it does require charging, it gets electricity from a wall socket, at higher voltage (and generally lower amperage).  This means it tends to charge more slowly, which in general means longer battery life.  Also the battery is built differently, to hold charge better at the expense of not being recharged as quickly.

In short, a car battery is really the wrong tool for the job.


Number of different clones of B lymphocytes My professor told us that there are about a million different B cells based on their surface receptor.

I have read that we have about 30000 genes in all. Since receptors are proteins how do these 30000 genes make such a large number of receptors?
I read about something called alternative splicing. Is this the mechanism behind this?

Alternate spicing of mRNA is a real phenomenon, but it's not the source of immune cell receptor diversity.  The DNA of immune cells is rearranged in a slightly random manner, to make a receptor with a random sequence in the variable portion of the receptor.  As Armatus already said, the process is VDJ recombination.  Here is a link to a textbook on NCBI

https://www.ncbi.nlm.nih.gov/books/NBK27113/


What does pseudo-irreversible mean? In this publication (PDF) I encountered the following word:

  Binding of rupatadine to histamine H1 receptors isolated from the
  guinea-pig cerebellum and lung was demonstrated by inhibition of
  3H-mepyramine binding; equilibrium inhibition constant (affinity) [Ki]
  values were 26–256 nM in the various experiments. Binding was
  time-dependent and pseudo-irreversible. Rupatadine was ~7.5 and
  10-times more potent than the structurally-related anti-histamines
  loratadine and fexofenadine. H1 receptor occupation by rupatadine in
  guinea-pig cerebellum and lung after oral (PO) dosing was relatively
  rapid (with maximum binding evident at 2–4 hours post-dose) and
  dose-dependent; low or no binding was seen at 48 hours post-dose.

In this context, what does pseudo-irreversible mean? Since it goes on to say the binding had dissipated within 48 hours, it seems to mean persistent or long-lived. Is that correct or does it have a more specific meaning in biology?

it seems to mean persistent or long-lived. Is that correct...?

Yes, it's correct, but how persistent the effect is is related to the rate of dissociation or rate of turnover of the receptor. It is relative, so to speak; relative to the effect of non-irreversible receptor binding.

Irreversible inhibition of, say, a cell surface receptor means that a drug (agonist/antagonist) binds permanently to the target receptor, usually by binding covalently; the chemical reaction is not reversible. This isn't synonymous with a permanent effect on a cell or organism; that depends on turnover of the receptor. A "faulty" receptor may be replaced quite quickly or not; it depends of the cell and the receptor.

Pseudo-irreversible means that the drug acts in a manner similar to  irreversibly bound agonists/antagonists, but there is no covalent bond formed; if a drug/molecule which has a sufficiently high affinity for the receptor is introduced (in a sufficiently high quantity), the new molecule will replace that which was strongly bound before (the pseudo-irreversibly bound drug.)

Some of these types of reactions have been studied more than others. One  example of this can be seen with h5-HT7 receptors, which are subject to pseudo-irreversible inactivation by risperidone and 9-OH-risperidone.

Clozapine and other competitive antagonists reactivate risperidone-inactivated h5-HT7 receptors: radioligand binding and functional evidence for GPCR homodimer protomer interactions


What kind of bug is this one? We are trying to figure out what kind of bug this is? It appears to have larvae on its back it is not dust and debris.

This is a kind of neuroptera larva https://www.google.com/search?q=neuroptera+larva.

The smooth jaws discard an antlion https://en.wikipedia.org/wiki/Antlion.

Is more like a chyrsopidae https://www.google.com/search?tbm=isch&q=neuroptera+larva&chips=q:neuroptera+larvae,g_1:chrysopidae:qWI0Ngq4zAQ%3D. They like to camouflage with debris found around them.


Hormones - biotic or abiotic Are hormones biotic or abiotic? I have tried reading different articles, and  I've found that it is both, but can that be true?

Hormones occur inside organisms as signaling factors, and arise from biological activities, the development or homeostasis of the organism.

Thus, they are considered neither biotic nor abiotic factors in ecology.

(Terrible analogy warning!) It's a bit like asking whether the wheel of a car is petrol- or diesel-based. It makes no sense!

Here's a helpful, comprehensive website.

Biotic (living) factors are living organisms in an ecosystem, that must share common resources or compete in a habitat one way or another. Abiotic (non-living) factors are things like temperature, wind, salinity, etc. that affect individuals or the community of an ecosystem.

As you can see, hormones are just one of many components of a living organism. They aren't living themselves. It's a silly question to ask, as I hope you can see now.


Green insects on gooseberry plants I have green insects that eat the leaves of my gooseberry plants:

Location: Toronto, Ontario.
The insects seem to only eat the leaves of the plants (not the fruit).
They have been present since mid-May, and I expect that they'll be present until mid-June, based on past experience.
They do not have spots.

What is the name of this insect?

The species name of this insect is the gooseberry saw fly. There are three related species, I think this is the pale spotted gooseberry sawfly because it has a pale green head. They usually have black dots as well, but this might develop when the larvae grow. At least, this is what I observed once in my garden.


Do ant colonies prioritize survival of particular members above others? In some (perhaps small) human communities people may starve because they have no income. This could be interpreted as a consequence of them not participating in the community, hence they don't get any income and are left to their fate of starvation. Also, we can imagine that important members of the community are less likely to starve, as they are given priority treatment (e.g. a royal family will less likely starve to death during a given famine).

Do ants in a given colony allow members to starve when they don't serve the colony, even if there is no scarcity of food?
Secondly, do ants follow a chain of importance and are members of least importance allowed to starve first in times of shortage?

I couldn't find any information about ants starving in times of plenty, most likely since it's difficult to determine whether an ant colony is "letting" certain members starve or whether the ants have just died for whatever reason. To your second question, though, yes! This paper, The Effect of Colony Size and Starvation on Food Flow in the Fire Ant by Howard and Tschinkel, shows the effects of different lengths of starvation on the passing of radioactive food through different sized ant colonies. First, the queen:

  Generally, queens received radioactive food earlier in starved colonies than in well-fed ones

Starved foraging ants distributed food more quickly than forager ants who had not been starved:

And interestingly, in large colonies, larger worker ants were more likely to receive food (radioactivity) than smaller ants. Very cool paper.


All or nothing phenomena We know that an action potential is produced by an active cell membrane when the stimulus reaches a certain threshold. When it does, an action potential fires, and when it doesn't, nothing happens.

There are dozens of videos online painstakingly illustrating this point, using examples going from plumbing to pebbles falling down a paper towel.

But this is such a simple idea. There doesn't need to be analogies. When I push a button, something moves, when I don't push it, nothing moves.

But what is the fundamental principle behind this? What biochemical device causes this all or nothing phenomena?

The fundamental principle behind this is a "sensor" or the excitation-contraction coupling, regardless where you are.
Let's consider the striated muscle and the cardiac muscle.

The function of excitation-contraction coupling in skeletal muscle is as voltage sensor to tell the SR, "We have got an action potential; release Ca2+ for contraction".
This is a contrast to a heart muscle which works like a Ca2+ channel (i.e. Ca2+ is flowing in cardiac muscle continuously).
Similarly, xcitation-contraction coupling in cardiac muscle translates the action potential into the production of tension.
There are individual steps in this process of cardiac muscle:

The cardiac action potential is initiated in the myocardial cell membrane, and the depolarization spreads to the interior of the cell via the T tubules.
Recall that a unique feature of the cardiac action potential is its plateau (phase 2), which results from an increase in Ca and an inward Ca2+ current in which Ca2+ flows through L-type Ca2+ channels (dihydropyridine receptors) from extracellular fluid (ECF) to intracellular fluid (ICF).

Entry of Ca2+ into the myocardial cell produces an increase in intracellular Ca2+ concentration.
This increase in intracellular Ca2+ concentration is not sufficient alone to initiate contraction, but it triggers the release of more Ca2+ from stores in the sarcoplasmic reticulum through Ca2+ release channels (ryanodine receptors).
This process is called Ca2+- induced Ca2+ release, and the Ca2+ that enters during the plateau of the action potential is called the trigger Ca2+.
Two factors determine how much Ca2+ is released from the sarcoplasmic reticulum in this step: the amount of Ca2+ previously stored and the size of the inward Ca2+ current during the plateau of the action potential.

and 4. Ca2+ release from the sarcoplasmic reticulum causes the intracellular Ca2+ concentration to increase even further.
Ca2+ now binds to troponin C, tropomyosin is moved out of the way, and the interaction of actin and myosin can occur.
Actin and myosin bind, cross-bridges form and then break, the thin and thick filaments move past each other, and tension is produced.
Cross-bridge cycling continues as long as intracellular Ca2+ concentration is high enough to occupy the Ca2+-binding sites on troponin C.

A critically important concept is that the magnitude of the tension developed by myocardial cells is proportional to the intracellular Ca2+ concentration.
Therefore, it is reasonable that hormones, neurotransmitters, and drugs that alter the inward Ca2+ current during the action potential plateau or that alter sarcoplasmic reticulum Ca2+ stores would be expected to change the amount of tension produced by myocardial cells.

I like this figure about the topic in summarising stimuli in the smooth muscle:

In heart

In the gastrointestinal tract, we have then again special cells, Cajal cells, that work as "pacemakers" of the GI tract.
Myenteric Interstitial cells of Cajal [ICC-MY] serve as a pacemaker which creates the bioelectrical slow wave potential that leads to contraction of the smooth muscle.
This activity differs along the length of the system

3 per minute in the stomach
11-12 per minute in the duodenum
9-10 per minute in the ileum
3-4 per minute in the colon

You can see them as to work analogously through the "all-or-none" principle.

Sources

Costanzo, Physiology
Pocock, Physiology
My notes during during years 2011-2014 (in three Physiology courses and research)


evolution or chance? I was reading my chemistry textbook, when in the chapter on 'solutions', i came across a problem, which calculated the amount of oxygen that can be dissolved in 1cc of water at STP. Then they commented, "this amount is just perfect for aquatic and marine life. Had this been lesser, life in the oceans might not exist at all.' This raised the following question in my mind:

1)aquatic species of flora and fauna evolved over time to adapt to this concentration of dissolved oxygen, and their biological processes were also fine tuned based on the environmental conditions.

2)It really was fate that the dissolved quantity was just enough to support marine life, as the textbook said.

Which of the two is the actual scenario? My personal pick happened to be 1), but I have no proof of it. Can someone explain?

Oh my. Do the authors provide any support for this claim? More importantly: what is their affiliation with creationist organizations? Well, back to science.

First, a note about your question. It might seem that you have sketched out two scenarios, but for the biologist, they are equivalent. We know two things: life exists, and life adapts. Yes, the specific circumstances on Earth have made life possible, and subsequently, life has adapted and fine-tuned itself to those circumstances.

Now to answer your question.
I really like the visual representation of the Life Timeline on Wikipedia. 4.1 billion years ago, earliest life appeared on Earth. At that time, all oxygen on the Earth's surface was bound in chemicals like CO2, iron oxide, etc. We are unsure whether the earliest life-forms originiated in the ocean, but we know they ended up there one time or another. The absence of athmosphetic and water-dissolved oxygen of course meant those first life-forms were anaerobes (lived without oxygen). In fact, oxygen was extremely poisonous for our teragrandparents. (We are the ~ 10^12th generation of life.)

So, aquatic life has existed without oxygen, and still exists, whether the solvabily of oxygen is 'perfect' or not.

Another fun fact debunking your chemistry authors statement: water oxygen saturation doesn't reach 100% at all times (linked article provides lots of great information about dissolved oxygen and life, by the way). Lots of life-forms requiring oxygen hence live in a world where the solvability of oxygen is even more than perfect. Furthermore, life exists (but doesn't thrive) in low-oxygen conditions (e.g. pubmed:9510533).


Why is translation so much faster in prokaryotes than eukaryotes? Prokaryotes perform transcription and translation much faster than eukaryotes. If memory serves, a single 70S prokaryotic ribosome can incorporate around 20 amino acids per second, whereas the 80S eukaryotic counterpart is much slower, at around 2 amino acids per second. Is the reason for this known? The only possibility I can think of is that prokaryotic mRNAs are often polycistronic, whereas eukaryotic mRNAs are not and tend to involve co-translational protein folding. Slower translation may be able to improve folding accuracy. Other than that, I can't think of any reason the 80S ribosome would be physically slower than the 70S ribosome. It's not like DNA replication where accuracy is exceedingly more important in multicellular organisms than in fast-replicating unicellular prokaryotes.

Unless the poster can cite more recent papers to support the assertion regarding a difference in rates of prokaryotic and eukaryotic protein synthesis, I would say that this is incorrect.

Lacroute and Stent (1968) reported a rate of 15 amino acids per sec for β-galactosidase in Escherichia coli, whereas Knopf and Lamfrom (1965) reported a rate of 7 amino acids per sec for globin chains in rabbit reticulocytes. This does not appear much different to me, especially as a recent study by Li et al. (2014) showed that the rate of protein synthesis varies with the complexity of the assembly (if any) into which a protein is incorporated.


Is it possible to have raw ngs data to practice I'm looking for raw human ngs data to practice in bioinformatics. Better if it is from different machines (illumina, roche, pacsbio, etc). Panels, exomes and genomes.
Anyone knows something?

At least PacBio do provide some example datasets on their DevNet resource. You should be able to get a lot of different Illumina data from the public data in BaseSpace. I am not sure where to look for official samples from Roche 454, but I wouldn't bother too much as it is discontinued anyway. Rather go for MinIon or IonTorrent data, if you want more.


What is the result of modifying the reagents in the Sanger method? If one of the dideoxynucleotides is omitted while using the Sanger method how would that affect the chain termination method of DNA sequencing?

If by one of the dideoxynucleotides, you mean one of ddATP, ddCTP, ddGTP, or ddTTP was omitted from the process, then the sequencing would only be able to terminate for the other three dideoxynucleotides. And you would not be able to get the full sequence, and only nucleotides of whatever three you had.

The function of ddNTPs (the dideoxnucleotides) is to stop the elongation of DNA and to subsequently be read by either fluorescence or radioactivity.

Source: https://en.wikipedia.org/wiki/Sanger_sequencing


Difference In Telomeres Between A Thale Cress Plant And A Methuselah Tree From what I have read and understood telomeres cap off how many times a cell can divide before it can no longer divide and that is what causes aging.

A thale cress plant apparently has a life cycle of 6 weeks before it dies, while the Methuselah tree has set the record at over 4,800+ years.

What is the difference between these two plants regarding their telomeres?
Is the cell division rate different between both plants instead of a telomeres difference?
If given ideal conditions what could the potential life-span of a Methuselah tree be?

Btw you don't have to answer all these. Just curious and looking for some insight into why the stark difference between both plants' aging.

Telomeres do not "cause" ageing as such - although you are right that they limit the number of times a somatic cell can divide.

Each time a cell divides the chromosomes are replicated in an imperfect way, and as such a small amount of DNA is lost from the end of the chromosome during each round of cell division. Telomeres are just extensions to the chromosomes, so that the DNA that is lost is not important. When a cell runs out of telomeres it ceases to divide.

However it is a big generalization to say that telomere length is therefore correlated with lifespan. For instance a recent study has shown that mice have telomeres 5-10x the length of humans, but live 30x shorter (1).

Inter-species differences in lifespan

Whilst I am no expert on these 2 plants, it is quite an obvious thing to say that organisms age at different rates. Mice, for instance, live 3 years in a protective environment, whereas humans can live 30x that. The difference is down to the life strategies acquired by natural selection: it is more advantageous for a mouse to develop very fast to reproductive maturity and have as many offspring as possible, because there is a very high mortality rate for mice. Conversely for humans, in takes more than a decade for us to reach reproductive maturity! Our "rate" of development/ageing is lower, which is completely related to our reproductive strategies.

I imagine that a very similar story is true for plants - for some it will be advantageous for them to "live fast, die young", whereas for others the best strategy might be to take a long time creating less, but more robust, offspring.

At the molecular level

I have answered a related question previously (Do trees age on a microscopic level?) which might be of interest to you.

In short, the phenotype of ageing is associated with irreparable damage at the molecular level - be it to DNA, organelles, protein aggregations... you name it! Organisms that have a higher metabolic rate, such as mice, accumulate this damage faster. This gives them the benefit of being able to reproduce much earlier, at the cost of reduced overall lifespan.

Plants age slightly differently, but at the genetic level much the same repair pathways are conserved throughout the kingdoms of life, with some alterations of course - for instance plants seem almost completely immune to cancer (2)!

As I argue in the linked to question above, plants have a potentially indefinite replicative potential, as every cell has the capability of regenerating its telomeres, because plants do not have a conserved germ line as animals do - any cutting from a plant has the potential to create an entirely new plant. This varies from plant to plant of course, and plants are still susceptible to damage, they just have modified/adapted repair pathways to cope with their specific lifestyle.

You ask whether it is the telomeres or the "rate" that differs between the plants - the answer is almost certainly a combination of both, amongst the other myriad of factors that influence lifespan!

Refs

Colado, et al, 2013. Telomere dynamics in mice and humans. Seminars in hematology [PubMed]
Doonan & Sablowski, 2010. Walls around tumours - why plants do not develop cancer. Nature reviews cancer [DOI]


ID request - larvae on potato plants Several of these were on my potato plants in Washington state, USA. This one about 7mm in length, some were a bit larger. They were moving in an inchworm-like fashion, but only by touch - I don't think they have eyes.

This specimen was photographed after placing in isopropyl alcohol, which changed the color (it was almost white while alive) and the shape somewhat.

One notorious pest of potato plants are cutworms. Unfortunately due to the the discoloration of the species I am not able to identify for sure which species of cutworm it is.
Cutworms attack a wide host of plants (more info here). According to that same website, the main ways to avoid the damage these larvae can cause are to:

Remove all plant residue from soil after harvest or at least two weeks before planting...

... plastic or foil collars fitted around plant stems to cover the bottom 3 inches above the soil line and extending a couple of inches into the soil can prevent larvae severing plants; hand-pick larvae after dark; spread diatomaceous earth around the base of the plants (this creates a sharp barrier that will cut the insects if they try and crawl over it); apply appropriate insecticides to infested areas of garden or field if not growing organically

These larvae come from a large variety of insects so don't associate them too quickly with one insect or another (many websites associate them with moths but that is not always necessarily accurate).
Here's a source that elaborates a bit more on how to treat them plus another source for how to use pesticides in a garden safely (if no other option is convenient).


What is the name of cell structures that have an adaptation to increase their surface area? Epithelial cells that line the small intestine have an adaptation to increase their surface area - what is the name of these structures? And why would the small intestine require a large surface area?

The small intestine requires a high surface area in order to increase the rate of absorption of digested food.


Why is beta actin commonly used as a control in Western blots? It is about the western blot question. The paper:http://www.sciencedirect.com/science/article/pii/S1931312813001145.
In the western blot experiment in this paper, they use beta actin as control. And also I saw other research paper also use beta actin as control. So why is beta actin used, not other gene? is it because it expressed in all different kinds of cells?

β-actin belongs to a class of genes called housekeeping genes. Their proteins typically perform functions that are required across essentially all cell types (for example, β-actin is part of the cytoskeleton's microfilaments), and are supposed * to be not affected by experimental conditions. In Western blotting, they are run as a "loading control" to show that very similar amounts of protein were loaded in each lane. This is absolutely essential in some experimental systems where it may not be possible to always collect the exact same number of cells for each sample, such as when working with primary cells, tissue samples, or systems where you may be altering protein synthesis, cell size/number, or apoptosis.

There are many different loading controls to choose from, and some may be dictated by the cell/tissue type you are examining — for example, when working with stem cells, you may want to show that your experimental conditions didn't induce differentiation in the cells, so a pluripotency marker like Oct-4A or Sox2 may be chosen. In other cases, you may be examining fractionated lysates (a membrane preparation, just the nuclei, mitochondria, only the soluble fraction, etc.) and so may choose Na/K ATPase, Histone H3, COX IV, or GAPDH, respectively.

The choice of loading control can also be influenced by the size(s) of the protein(s) you are analyzing, as investigators frequently either strip Western blots and reprobe them with the loading control, or run two different species and detect with different colored secondary antibodies when performing fluorescent Westerns. In either case, you want your loading control to be a different size than your original targets.

Finally, all of this is assuming that the researcher has already attempted to load equal amounts of total protein per lane by using any one of a variety of methods for quantitating protein concentration. These include Bradford, Lowry, and BCA type assays, which may or may not be detergent compatible, staining the membrane after transfer with dyes such as Ponceau S, SYPRO Ruby, or India ink, or staining the gel with Coomassie or other proprietary Western-compatible stains.

*In reality, some scientists are becoming more and more aware that many experiments actually do affect a number of "housekeeping" genes, but when most see variations by, for example, Western blot or qPCR, they often choose a different loading control to use.


What is the difference between hilum of the lung and root of the lung? In my book they describe root of the lung like this:
In the region of vertebrae TV to TVII, the mediastinal pleura refects off the mediastinum as a tubular, sleeve-like covering for structures (i.e., airway, vessels, nerves, lym-phatics) that pass between the lung and mediastinum. This sleeve-like covering, and the structures it contains, forms the root of the lung.

And hilum of the lung like this:
The root joins the medial surface of the lung at an area referred to as the hilum of the lung. Here, the mediastinal pleura is continuous with the visceral pleura.

I dont see the difference between Root and hilum.
Can somebody please help me out?

Short answer: Hilum is an area(has only 2 dimensions) where as root is a body( has 3 dimensions).

  The root of lung is a short broad pedicle connecting the medial surface of the lung with the mediastinum. It consists of structures entering and leaving the lung at hilum. The root of lung is surrounded by a tubular sheath derived from the mediastinal pleura.

and

  The hilum is the area on the mediastinal surface of the lung through which structures enter or leave the lung.

Source: pg no 239

Consider the following image( edited by myself):

If the cylinder is root of lung then lateral opening(blue) is hilum.

The region bounded( within the limits of pleural membrane) by those two planes is root of lung and the area bounded by the lateral plane is hilum.


What's the difference between growing cells in culture and cloning them? The wikipedia page on Hela cells refers to George Gey being able "to isolate one specific cell, multiply it, and start a cell line." Later it says, "In 1955 HeLa cells were the first human cells successfully cloned."

What's the difference between multiplying the cells and cloning them? How is multiplying not cloning?

Clones are genetically identical daughter cells from one parent cell. So when you start you culture from one cell, all new cells are clones of this cell.
The first three cells (red, green and blue) undergo clonal expansion.

If you multiply cells in cell culture you usually start with thousands of cells, as this can be seen in the second part of the figure. These cells are not genetically identical, as they individually collect mutations. So the daughter cells of each "starter cell" (a lot of them) in the mixture are technically clones, but the whole culture is not seen as clones. See also the Wikipedia on this topic.


What if our whole body is made up of cancer cells? Today I learnt in my biology class that cancer cells are immortal.  That left me wondering what if our whole body is made up of cancer cells?  Will that make us immortal? Is it possible or why is it not possible?

No.

One aspect of cancer cells is that they no longer follow their programming, ie they stop doing all the work that a normal cell in that particular part of your body would do.

The next aspect is that cancer cells keep growing even when they are told to stop, even when there is no more space to grow.

Cancer cells also tend to destroy surrounding extracellular matrix in the quest for more nutrient. SO stuff like bone get deformed or just broken down leaving holes.

So if your entire body were made of cancer cells... well it would fall apart as cell stop doing their assigned job in the body, start growing without care and break down existing structure for better access to more nutrients.

What you want are immortal cells that still do their job.. stem cells.


Polar bodies in females What is the fate of first and second polar bodies formed during the menstrual cycle in human females?

Do they degenerate?

Does any other mammal also produce polar bodies?

According to this article polar bodies sometimes apoptose but sometimes are "capable of developing into complex, highly organized structures, or even enabling parthenogenesis". Despite their fate being far less than the oocyte.

It also states they're present not only in other animals, but also some plants.

"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo. These apparent “oddities” reveal the diverse mechanisms used during reproductive development and may even allude to the origins of meiotic strategies."

It looks like polar bodies are very important in humans, but not other organisms:

"Polar bodies may, however, give rise to human embryoids if fertilized and twins may even result when one spermatozoa fertilizes the ovum and a second sperm fertilizes its sister polar body (Bieber et al., 1981). No twin pairs resulting from fertilization of the second (haploid) polar body have been reported (Machin, 2009), but clearly polar bodies have cellular and developmental potentials beyond apoptosis, even in humans."

"But in many other organisms, polar bodies are not dispensable. They are not simply waste bins for three-quarters of the genetic material produced during oogenesis, and they do not disappear following meiosis."


Identification of a spider from my basement It's a little over 1" long including legs, and I found it in my basement in Pennsylvania. My guess is a funnel weaver, which would be nice since then I can free it (right?) from the tin can it's currently sitting in.

Thanks!

I think it's a common wolf spider, which closely resemble funnel weavers. It's almost a toss-up. I can't tell from the resolution of your photograph, but funnel weavers have spiny legs whereas the wolf spider has smooth legs and has a bit more of a difference in the comparative size of the abdomen to thorax.

Wolf spider (coloration varies) vs. funnel weaver (in this case, a barn dweller)

Another distinctive feature of the wolf spider are the two especially large eyes (The Tenegra domestica's eye arrangement is different) which gives the wolf spider such great eyesight. If the legs are smooth, and you shine a light on your spider and see two eyes shine back at you (called eyeshine), I think you have your answer.

  Wolf spiders can be found in a wide range of habitats both coastal and inland. These include shrublands, woodland, wet coastal forest, alpine meadows, suburban gardens, and homes.


What is an in-frame activating fusion? In [1] it is written that:

  Whole-genome and RNA sequencing identified recurrent in-frame activating FGFR3–TACC3 fusions

What is a recurrent in-frame activating fusion?

[1]   Cancer Genome Atlas Research Network, “Comprehensive molecular characterization of urothelial bladder carcinoma.,” Nature, vol. 507, no. 7492, pp. 315–322, Mar. 2014.

This is explained in the linked article.

  We found several recurrent translocations of likely pathogenic significance, including an intra-chromosomal translocation on chromosome 4 involving FGFR3 and TACC3 (n=3). The breakpoints were in intron 16 (2 cases) or exon 17 (1 case) of FGFR3 and intron 10 of TACC3 (confirmed by DNA sequencing and RNA-seq). All three lead to fusion mRNA products whose predicted proteins include the N-terminal 758 amino acids of FGFR3 fused with the C-terminal 191 amino acids of TACC3 (Fig. 2a). Based on the structure of the FGFR3-TACC3 fusion protein, we predict that it can auto-dimerize, leading to constitutive activation of the kinase domain of FGFR3. FGFR3-TACC3 fusion, which was recently described in both glioblastoma21 and bladder cancer7,8, represents a promising therapeutic target.

FGFR3 is a member of the fibroblast growth factor receptor family. It is a transmembrane kinase that is normally activated upon ligand binding which triggers dimerisation. TACC3 is a protein that can dimerise through a coiled-coil domain.

The FGFR3-TACC3 gene fusion that is generated by the reported intra-chromosomal translocations thus generates a version of the receptor that is predicted to be constitutively active because it can dimerise in the absence of the growth factor.

Recurrent means occurring frequently.


Can the sensory neuron network and the motor neuron network be considered separate networks? I am reading up on the nervous system using wikipedia and trying to interpret one infographic on this page:

I've always thought of the human nervous system as a singular network of neurons. This diagram however makes a distinction between 'Motor neurons' and 'Sensory neurons'.

Can the sensory neuron network and the motor neuron network be considered seperate networks?

Indirectly they will definitely be interconnected (because of impulse-response relations), but physically, are they connected or disconnected?

Or are there more?

It is very well possible that I am missing some knowledge to make this question make sense.

The sensory and motor pathways can indeed be considered separately both in concept and physically. Of course the nervous systems is a single network of neurons, but that doesn't stop it from having separate components.

One can indeed often simplify neural pathways as "IN (sensory) ===> (black box with decision-making magic) ===> OUT (motor)"

Reflexes

Reflex arcs are a great way of demonstrating this separation because they do not involve the more complicated integration of the brain. Let's take the knee-bend (patellar) reflex as an example: https://en.wikipedia.org/wiki/Patellar_reflex

The diagram is correct in concept but let me add the anatomical detail to illustrate how sensory and motor pathways are separate, yet connected: When the reflex is triggered, the signal travels up from the sensory neuron ends located under the knee cap (these are dendrites) to the sensory neuron's body in the spinal chord. The sensory cell relays the signal via its axon, which then synapses with a motor neuron's body also in the spinal chord. The motor neuron then sends a motor impulse via its axon back down to the leg, where it triggers muscle contraction.

Physically, in this case there will be a separation also in nerves (at least if I may trust Wikipedia for now), where the sensory reflex neurons' dendrites travel from the leg to the spinal chord through an afferent nerve and the motor neurons' axons travel in the reverse direction through an efferent nerve. The only physical and conceptual connection between the sensory pathway and the motor pathway is the synapse between the sensory and the motor neurons in the spinal chord.

More complex sensorimotor pathways might include interneurons or integration with various circuits in the brain, but it is usually possible to define discreet separate parts of the pathway, one sensory and one motor, with the only connection being those interneurons.

Sensory and motor separation in the CNS

The central nervous system (CNS, which includes the brain and the spinal chord) is actually surprisingly organised in this regard, with quite strict separation of motor and sensory pathway components. For example, the cortex of the brain has distinct regions which contain sensory neurons for evaluation of various types of peripheral skin sensation. Separate from these are regions which contain motor neurons for movement of skeletal (voluntary-control) muscle. The interaction of these is of course more complex given that it involves skin sensation and conscious decision making in regards to movement.

Likewise, the spinal chord is structured into sensory and motor regions. In summary, the spinal chord consists of: 1) cell bodies (motor, sensory, inter; grey in the picture), 2) ascending axons (blue), 3) descending axons (red). Similar to nerves, axons going up or down the spinal chord are bundled into "tracts". Sensory axons are never bundled with motor axons, making it possible to create a map of the spinal chord in cross-section.

The tracts' names might be a bit confusing at first, but on second look are actually pretty self-explanatory. They usually contain where the axons come from and where they are going in order to synapse with other neurons. E.g. the spinocerebellar tract is formed of axons coming from the spine and going to the cerebellum. Given that the cerebellum is near the brain and the spine is further down, this is obviously an ascending tract - and ascending tracts are always sensory (because sensory information never needs to be carried downwards due to the brain being at the top).

Where it gets blurry

The sensory/motor separation isn't always as clear as I've described above. In fact, nerves (bundles of axons anywhere in the body outside of the CNS) will usually contain both sensory and motor pipelines. In particular, the cranial nerves (12 of the most important nerves) all include sensory and motor components for the respective part of the body that they manage. E.g. the facial nerve contains both the sensory connections for parts of the tongue and the motor connections that control facial muscles.

Another more complex example is pain sensation, where interneurons in the spinal chord can feed back onto sensory neurons and inhibit their signals, or axons can inhibit those packed in the same nerve bundle simply due to electrical effects.


What determines the fate of a cell with respect to differentiation? I have been reading about Townes and Holtfreter's work in 1955, in which cells are dissociated from a blastocyst in an alkaline solution then mixed together and spontaneously reaggregates based on type, so epidermal cells around the outside and neural plate cells in the middle.

I understand enough about cell adhesion to understand why the cells will seem to attract cells of their own type, but would like to know how they can initially detect what to become and where they are needed in a specialised form, without something acting like a brain telling them what to become and where to go.

If the selection from the available types is random, as I suspect, what happens to blastocysts with too much epidermal tissue or vice versa? I'm struggling to imagine how organisms like this can develop without something taking the lead and actively coordinating what goes where.

Cell differentiation, cell fate and cell mapping is an interplay of accessible evolutionary strategies/programmes and responses to dynamic environmental cues such as specialized hormones (e.g. morphogens) and physical parameters and constraints. That is putting it very broadly. It is a complex issue, if L. Wolpert's PLOS assays are any indication. I compiled a few links to get you started.

Specifically, reappraising the topic of your cited classical experiment are R.Moore et al:

  The classical cell sorting experiments undertaken by Townes and
  Holtfreter described the intrinsic propensity of dissociated embryonic
  cells to self-organize and reconcile into their original embryonic
  germ layers with characteristic histotypic positioning. Steinberg
  presented the differential adhesion hypothesis to explain these
  patterning phenomena.....

(Source: Robert Moore, Kathy Q. Cai, Diogo O. Escudero, Xiang-Xi Xu, Cell Adhesive Affinity Does Not Dictate Primitive Endoderm Segregation and Positioning During Murine Embryoid Body Formation, Genesis. 2009 September; 47(9): 579–589)

Regarding: ...without something taking the lead and actively coordinating...

On a hunch that you are not talking about complexity, attractors and polarity, I would like to share a few words. You may completely disregard them if you'd like.

My personal experience (from my country) is that few biologists delve into "that" branch of EvoDevo, because a profound understanding involves calculus, modeling and a knack for theoretical biology. Yet, afaik few struggled comprehending the evolutionary logic of making an organism based on Albert's book chapters alone.

See:

Reaction–diffusion system
Cell fate determination
Fate mapping
Asymmetric cell division
Pattern formation
Alberts Molecular Biology of the Cell describes this very well (can be accessed online for free)

I personally recommend G.Müller's authored/coauthored papers:

(open access)
http://homepage.univie.ac.at/gerhard.mueller/publications-papers.html

Disclaimer: I am not specialized in the field of EvoDevo or Theoretical Biology.
Views expressed here are my own.


SNR for good MRI imaging Resolution of MRI can be improved if FOV is reduced keeping other factors constant, but this reduces voxel volume, which in turn reduces SNR. How much SNR is enough for good imaging?

[Old question, but...]

There is an old adage in MRI:  High signal to noise, high resolution, short scan time... choose 2.

The question of "How much SNR is enough?" can't be answered without talking about specifics, primarily, what is the scan going to be used for?

For example, a typical MS diagnostic scan doesn't really need to be too high a resolution or signal to noise as typically the lesions are large and hyperintense.  BUT with higher field scanners one is able to see smaller and smaller lesions.

If one is doing quantitative work off of an MRI scan, then it will depend on the type of quantification, algorithm etc.

So, in some ways the question is very broad and it depends, significantly, on a lot of other factors.

Doing some Google Scholar / Pubmed searches for SNR and MRI might help with specific areas you are interested in (e.g., https://scholar.google.com/scholar?hl=en&as_sdt=0%2C9&q=minimum+signal+to+noise+ratio+in+magnetic+resonance+imaging&btnG=)


Why do some trees have a life span, while some don't? I have heard that there is no limit on the growth of trees, but then why do some trees, such as boxelders and poplars, tend to live shorter than redwoods, for example? Some advertisements for improved lombardy poplars state that their trees have an extended life span, up to 75 years? The trees with shorter life spans seem to weaken at a certain age, and then contract diseases more easily.

The answer to this could be that there are many factors contributing to the length of the life of tree species.

Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.

For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.

As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees

Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!

Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.

If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.

This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.

Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F7709949_Analysis_of_telomere_length_and_telomerase_activity_in_tree_species_of_various_life-spans_and_with_age_in_the_bristlecone_pine_Pinus_longaeva%2Ffile%2F9c96052bcf0a51be49.pdf&ei=zzrCU9OcMIjV0QXmt4CwCQ&usg=AFQjCNH7853fvZ8yneznSfIQQPsxtIDQag&sig2=-PELK5RCQlAGTvQODoyZ2A&bvm=bv.70810081,d.d2k

we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.

http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).

Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.

That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!

This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506

What some companies may have done is   try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!

I hope I answered you question adequately!


How to isolate two plasmids from E. Coli strand? I have an E. coli cell line I use to express a protein using a two plasmid system. One confers AmpR and one KanR.

For mutagenesis I would like to separate the plasmids to increase efficiency of the mutagenic PCR reaction. I was able to cure the cells of the KanR plasmid because it is low copy whereas the AmpR is high copy so I could easily grow the cells in ampicillin only and I ended up with only the AmpR plasmid. However I was unable to do the same to isolate the KanR plasmid.

My next idea was to run the plasmids through a gel and do an extraction. Since I didn't do a digest it was very hard to differentiate the bands and I ended up getting a negligible yield. I believe the plasmids were simply smeared through the gel due to tertiary structures.

My final hope is to perform a digest on the plasmids using a restriction enzyme that cuts each plasmid once. My concern is that I will not be able to get the stoichiometry correct due to the plasmids both being simulatenously present in vastly different concentrations.

Does anyone have any tips on how else I could isolate the plasmids? Or maybe does anyone have experience running a digest on plasmids with unknown concentrations? I really need help doing this. The mutagenesis project has been going on for months and this isn't even a molecular biology lab... so it's detracting time from main research goals!

A retransformation should get you a pure plasmid. Transform the plasmid mix into empty E.coli (don't use too much DNA), plate on Kan / Amp depending on what you need. The probability that one cell took up both plasmids is extremely low, and you could check with colony PCR just to be sure.

Otherwise: ask around, there must be (old) stocks of the single plasmids around, or glycerol stocks of E.coli containing only one of the plasmids.

Third option: take a look at your mutagenesis method. For your needs there might be techniques around that'll work on a mixture of plasmids. If you just need one variant or a single site saturation library you could use Quikchange for example. I don't see a reason why this wouldn't work on a mix of plasmids.


Is it possible to have a mechanism to use carbon dioxide as a source of oxygen in human body? Is it possible to seperate O2 from CO2 and use it for energy In Human? Why Plants and not Humans can do it?

Most energy in humans is generated by reducing O2 to water and CO2, using something like sugar or fat. Converting CO2 into oxygen would require energy, not generate it.

Plants do have mechanisms to convert CO2 into oxygen, but they use light as an extra energy input to push this energy-costing process.


About sandwich ELISA In sandwich ELISA the Fc region of primary antibody bind to the polystyrene coated well. But what are the specific interactions (like 'hydrophobic interaction' or 'van der waals force') happen between well and Fc region?

This page from Cole-Parmer includes everything you could possibly want to know about the adsorption of biomolecules to polystyrene. To summarize:

binding is neither covalent nor ionic, but
it is generally mediated by non-specific intermolecular van der Waals interactions, which generally are about 100X weaker than ionic or covalent bonds
the exception is some hydrogen bonds, which can be 10X stronger than the other types

  Intermolecular attraction forces are based on intramolecular electric polarities of which two types can be distinguished: alternating polarities (AP) and stationary polarities (SP), i.e. dipoles.

these interactions can be both hydrophobic and hydrophilic, depending on the surface chemistry of the polystyrene

If you're interested in the specific chemistry of everything, feel free to read the entire thing, it's quite detailed.

I would to note one thing from your question. In the absence of a specific binding partner like Protein A, antibodies bind to polystyrene completely non-specifically, meaning that not only does the Fc region bind, but Fab as well, including the CDRs (antigen binding domains). An ELISA depends on the fact that not all antibody molecules bind this way, so many or a majority of them have their antigen binding sites available to capture their target.


What are differences between formation of embryonic disc in chick and mammal embryo? Exam question which got lowest average points in my university: 1/5 average.
No markscheme available so my attempt below.

I assume that embryonic disk prefers to germ disk such that Formation prefers to only to the 3rd developmental week because of the Wikipedia fact.
I also went through the points during 2nd week of development and did not notice major differences. So let's consider only the 3rd week:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord
Location of the epiblast cell target and the development of the primitive streak
The bilaminar membranes
Evolution of the mesoblast
The intraembryonic coelom
Induction of the neural plate – neurulation

The following differences are based mostly on Gilbert's Developmental Biology 9e -book.

Other Differences which seems to at least start at the 3rd week of development

Chick meroblastic cleavage, human holoblastic. TODO do not know how that causes differences yet during the 3rd week.
Chick has yolk, human not so human placenta development and implantation. Chick dependent on yolk nutrients, human not.
Human embryo gets mother nutrients through placenta.
Chorion formation and finally from it the fetal portion of the placenta.
Chorion also includes the uterine cells to form the maternal of the placenta, the decidua.
The decidua will come rich in the blood vessels that will provide oxygen & nutrients to the embryo.
Human oviduct expansion to the uterus.
Chick embryo externally developing from the mother, human not. Chick egg is telocithal with a small disc of cytoplasm: blastodisc - sitting atop a large yolk. The yolk, eggs of birds undergo discoidal meroblastic cleavage. Cleavage occurs only in the blastodisc which is about 2-3 mm in diameters & is located at the animal pole of the egg. The first cleavage furrow appears centrally in the blastodisc; other cleavages follow to create a single-layered blastoderm.
The cleavages do not extend into the yolk, cytoplasm, so the early-cleavage cells are continuous with one another & with the yolk at their bases.
One chick hypoblast streak, human multiple. Chick must have some control mechanism.

What are the differences between formation of embryonic disc in chick and mammal embryo?

Embryonic disc forms on top of yolk during cleavage on chicken embryo, while between amniotic sac and yolk sac inside blastocyst after implantation on human embryo.

Some further processes take place on and in the embryonic disc: specifically these here during the week 3.

Embryonic disc formation includes still during the 3rd week of development:

Formation of the primitive streak
Genesis of the germ layers
Genesis of the notochord

Formation of the primitive streak: The process of primary neurulation appears to be similar in chick and mammalian. The embryonic disc becomes oval and then pear-shaped, the wider end being directed forward. Near the narrow, posterior end, the primitive streak makes its appearance and extends along the middle of the disc for about one-half of its length from migrated ectoderm cells.

Genesis of the notochord: “The notochord extends beneath the neural tube from the base of the head into the tail.” - As the mesoderm develops between the ectoderm and endoderm it is separated into lateral halves by the neural tube and notochord.

Figure 2: Neurulation. NB the use of neural groove is correct. Notochord is below neural groove. - Genesis of germ layers here: from a flat thing to a developed one.

Figure 3: Genesis of notochord and primitive streak. Yolk-sac surrounds notochord and primitive streak.


How similar are Circulating Tumor Cells and Cancer Stem Cells? Circulating Tumor Cells (CTCs) are linked with metastasis and their presence can be used to indicate the onset of metastatic cancer. Likewise, the Cancer Stem Cell (CSC) hypothesis suggests that tumorigenic stem cells are the source of cancer. However, microscopy experiments and cytometry have suggested that the morphology of CTCs and CSCs are quite different. Essentially, we have not been able to find Circulating Cancer Stem Cells (asides Myeloma since they are circulating anyways).

My question is how similar are these cells? If they are different, is relapse caused by the CSCs from the primary tumor or CTCs in metasises that have become CSC-like?

There are several competing models of metastasis, and this question does go right to the differences between them.

The primary thing to remember about CSCs is that all evidence suggests that they are a tiny, tiny subset of tumor cells.

CTCs, meanwhile, consist of whichever cells manage to acquire the right combination of motility, invasiveness, and resistance to anoikis (apoptosis caused by lack of attachment to neighboring cells or extracellular matrix).

So, one possible explanation is that CTCs are drawn from the whole population of tumor cells, and that CSCs therefore make up a very small, nigh-undetectable subset of CTCs-- but that this is the subset that ends up founding the distant metastases while the rest of the CTCs get cleaned up by the immune system or lie dormant in the target tissue. You could call this the stochastic model: CSCs form some small, randomly determined fraction of the CTCs, but they preferentially survive and found secondary tumors.

Another model posits that the cells undergo substantial changes in phenotype driven by responses to their microenvironment. CSCs, like normal stem cells, presumably require a pretty specific niche to maintain their stemness. CTCs, meanwhile, acquire their invasiveness and anoikis-resistance in response to conditions in the tumor, such as hypoxia. So, another possiblity is that, in response to stimulus from the microenvironment, a cell with the potential to be a CSC undergoes some phenotypic changes and becomes a CTC. It circulates for a while, finds a target tissue, extravasates, invades the target microenvironment, then starts re-setting up the microenvironmental niche to re-establish its stem-like properties. Call this the dynamic hypothesis: it's a single potential CSC the whole time, but it looks like a CTC while it's circulating and like a CSC only in its niche.


Multiple sequence alignment - how to align everything to 1 gene sequence? I'm having trouble aligning 3 sequences together - the total gene (~2500bp) and the forward and reverse sequences that are ~1000bp in length. Now I'm using Clustal X2, but the problem is that the program does complete alignment, which is useless for me right now.  Could anyone recommend or suggest any parameters or methods on how to align more that 2 sequences together, but that each sequence is aligned to the first one (the total gene)?
Thanks!

Your question is not very clear, but I think what you are trying to do is align sequencing results to a reference gene sequence.

Your total gene sequence spans ~2500 bp. It sounds like you have a forward sequence at the start of gene, reading only about 1000 bp and the reverse strand reading in 1000 bp from the end (if this is Sanger sequencing, you likely only have 800-900 bp of accurate base reads by the way). Therefore, you have a gap of about 500 bp in the middle of your gene of interest.

There are (at least) two ways to do the alignment, and I would suggest the manual method if you are trying to verify gene sequencing.

Manual Method:

In a word processing document, paste in your gene-of-interest (or the recombinant gene you are trying to make), as well as the base reads from the forward strand, and the reverse complementof your reverse strand. Make sure you remove any whitespace like line breaks and spaces as this will disrupt the rest of the process.
Manually select a small portion of your forward read (20-30 bp for example) and search for the same "phrase" in your gene-of-interest. If you find it, highlight it in both the sequence it came from and the gene-of-interest so that you know you have already matched them.
Carry on with adjacent bases for the forward strand. Repeat for the reverse complement of the reverse strand.

Semi-Automated Method:

Go to NCBI Blast, and under the heading Basic Blast, click "nucleotide blast".
Check "Align 2 or more sequences."
Enter your Query Sequence as your 1000 bp sequences, entered in FASTA format. FASTA format will allow you to enter multiple sequences, but if you just enter one at a time, that will work perfectly well. Results will only display one at a time anyway.

For example:

> sequence name here
ATCGATCGATCGATCGATCGATCG....

Enter your gene of interest as your Subject Sequence. Format does not matter here, but for consistency, I use FASTA format.
Keep "Highly similar sequences (megablast)" selected. You shouldn't need to play with these parameters, they just change how the alignment method penalizes alignments for gaps and mismatches.
Hit BLAST.
Interpret your results. I've included an example of BLAST results below.

At the top of this window is a schematic, showing exactly how much of the the query sequence aligns with the subject sequence. The longer the line, the more bases align. Similarly, the closer the colour of the line is to right of the scale (e.g., red), then the more continuous the segment is indicating a longer, continuous alignment.

Below the graphic is a table of results. Briefly, the table highlights all possible alignments that the BLAST algorithm has found, including how much coverage there was, confidence of the alignment and length of alignment coverage.

Below the results table, are the detailed results which were summarized in the table. This detailed report shows you exactly which bases align or mismatch, or any gaps. The top line is the subject sequence; the bottom is the query sequence. The other thing to keep in mind here is the Strand line. In this case, it says "Plus/Plus, meaning that the aligned sequences were the forward sense, or plus strand, of each of subject and query sequence, respectively. If you entered a reverse complement sequence instead (such as the reverse sequencing results) then this would change to "Plus/Minus".

From here, you will still need to manually line these results up to your gene of interest to determine exactly which portion of the gene is missing sequence coverage, as well as any mutations that may have cropped up in the cloning process.


Cancer history on environment-cancer relationship I am interested to know how environment-cancer relationship knowledge has developed.
I know that all began when Muller first proved that mutation could be induced via ionizing radiation, X rays in the case, and hypothesized for the first time the role that this could have on carcinogenesis. Do you know further data and the main or most significant events that leaded from that point until the current state of the art? (like when smoking and cancer were proved related)

(all factors enhancing risk would be included in the query, as human behavioral aspects (such as diet), work environment...)

Actually, "soot wart" was identified by Percival Pott in 1775. It is the first reported occupational cancer (it is a squamous cell carcinoma of the skin of the scrotum). It was shown in 1922 that an active ingredient of coal soot was a carcinogen. I'm not sure of an expansive, technical text on environmental cancers, but you may want to check out
"The Emperor of All Maladies: A Biography of Cancer" which covers the origins of man's understanding of cancer starting with the ancient Greeks, progressing to mention Percival Pott, and then moving on to modern day science and medicine. This book won the Pulitzer in nonfiction a few years ago and is well worth your time.


What is this hummingbird-like insect? I just saw this insect collecting polen from bougainvillea blossoms on the Greek island of Skyros, in the Aegean sea. For future reference, this is in the middle of August and the sighting was at around 17:00.

I posted all 4 photos I took since the rude little thing didn't have the decency to sit still to let me get a clear shot. I'd say it was about 2cm long, certainly no more than 3.

Hummingbird hawk-moth (Macroglossum stellatarum). For what it's worth, there are also a variety of sphinx moths around the world.

Here's a photo from the linked Wikipedia page. As you can see, it looks very much like the one in yours:


How does the zygote divide much faster than other cells? Normally a cell has a mechanism that controls its division. As far as I know, it checks surface area and stuff like that to decide to go for mitosis or not.

However, this is not the case for a zygote. A zygote, after around ~14 days starts to divide rapidly and forms the blastula. What mechanism controlls this "rapid division"?
Why can zygote divide rapidly when it has not reached a high surface area or doesn't have enough mitogens to induce the cell division? Does the zygotes mini-cells have a cell cycle like other cells but they are really fast? Or do they just copy the DNA and divide rightaway?

And when I first saw the video of this stage, I was surprised. The DNA is a one long molecule; how fast do those replicators work?

A zygote generally has a lot of nutrients, essential biomolecules like RNA and proteins and cytoplasmic organelles for rapid division. So the cell does not grow and divide but rather undergoes "cleavage" (there is no G1 phase of cell cycle). However, it still undergoes DNA replication. And yes, DNA replication is fast because it is initiated at once from several parts (origins of replication) of the long DNA (it still takes a few hours† ).

 † See:

Confusion about the duration of different phases of the cell cycle such as G1, G2 & S
Time spent in phases of cell cycle


Why bacteria produce light? After seeing this video I am curious to know why the free living bacteria produce light. What advantage will they have ? Or is it just an "unintentional" result of one of their pathways ?

Go for the  link below, you will find an article on "How do marine bacteria produce light, why are they luminescent, and can we employ bacterial bioluminescence in aquatic biotechnology?"

www.biology-online.org/articles/marine_bacteria_produce_light/abstract.html

From this article :

  The question remains whether quorum sensing regulation of bacterial
  luminescence is a kind of a ‘social behaviour’ in which cells
  ‘predict’ the possibility of increased mutagenesis where conditions
  allow for efficient metabolism leading to extensive bacterial growth.
  Such conditions may cause the appearance of large quantities of
  metabolites, including mutagenic agents. Thus, one could speculate
  that enhanced light emission at a high cell density may ensure more
  efficient DNA repair in response to potentially increased
  concentrations of mutagens. Alternatively, quorum sensing may be
  needed for another role of bacterial bioluminescence, besides
  stimulation of photoreactivation.


Why is warm water comfortable, but warm air uncomfortable? I friend of mine tried floating, where you lay in a bath kept at body temperature (98.6 degrees F).  He said after a while you don't feel the water at all.

This made me wonder why being in warm water (bathtub, spa, etc) is comforting, but a hot weather feels miserable.  Can someone explain the difference?

You constantly generate heat from metabolism.  The ability of this heat to be transferred to your surroundings from your skin is tremendously different in air vs. water. This is known as thermal conductivity.

The ability of water to remove heat from your skin is roughly 24 times that of air. See list of materials and their thermal conductivity rates here

In water of close to body temp, you can still bleed off heat to water. Your ability to do so in air that is close to body temperature is greatly reduced, so much so that in order to keep up, you sweat and increase the cooling ability through the evaporation of that sweat at temperatures well below 98.6F.


How to perform a DNA structural alignment in pymol How can I "fit" two DNA structures having different nucleotide sequences in PyMol?

I would like to use the structure of a DNA-binding protein in PDB (1h9t), which is bound to DNA in the PDB file, and fit a longer DNA built in silico with a 3D dart (haddock.science.uu.nl/dna/dna.php).

Aligning in PyMol
PDB ID 1h9t contains a structure of both a DNA and a protein. It starts as one object.
Before we perform an alignment, we need to separate your DNA from the protein.

Show sequence (click the S at the bottom right).

Highlight all the "residues" from the chains X and Y (these chains contain each strand of your DNA) in the sequence bar at the top.

Use the GUI to extract selection to new object (it's a faff doing this by terminal I find).

Rename new object (automatically named obj01 probably) to DNA1, or whatever you prefer.

Load your new, unaligned piece of DNA (I used fetch 1BNA).

Pymol uses the CEalign algorithm to align structures in 3D space. You can call it using the following command:
cealign DNA1, 1BNA, object=aln

Output:

Another 3D alignment software I really like is the Dali server.
Haddock
Haddock doesn't care if two molecules are aligned pre-analysis assuming you are submitting each DNA separately alongside a protein for binding analysis. This is because it tries a huge variety of orientations. Here is a list of things that you do need to do to your pdb before submitting to HADDOCK


Substrates of cytochemical reactions in this immunostaining Expression of extracellular protein Laminin 9 alpha-4 chain in human skeletal muscle.
Indirect immunostaining with HRP immunostain marker. Ob.x40.

I have unsuccessfully searched NCBI -database, JSTOR and other major Biology databases for an answer. This suggests to me that I do not understand what is going on.

1. What are the substrates of above cytochemical reactions for the given immunostaining above?

I need to give a simpler question where I apparently know the reaction exactly, since it is possible that people cannot answer the above question.

Mitochondria in Hep-2 cell line cells. Cytochemical test for mitochondria specific enzyme NAHD dehydrogenase. Ob.x40.

2. What is the substrate of the cytochemical reaction?

My answer:

The reaction of NADH dehydrogenase is:

  NADH + H+ + CoQ → NAD+ + CoQH2

Substrate: CoQ

It's hard to understand the question, but in any immunocytochemical staining such as the above, you have two different types of reactions:

the antibody binding to the target (in this case, some laminin)
the peroxidase-based colorimetric reaction with DAB. DAB (3,3'-diaminobenzidine tetrahydrochloride) is oxidized in the presence of hydrogen peroxide to form a brown precipitate, which becomes the stain.

The fact that is an indirect immunostaining implies that you have a non-conjugated primary antibody against laminin and a secondary antibody against the Fc part of immunoglobulins of the species in which the first antibody was raised. This secondary antibody will be conjugated with HRP (horseradish peroxidase, the enzyme responsible of generating the peroxides that will oxidize the DAB).

For a more complete reference of immunocytochemical stainings, you can read: http://www.ihcworld.com/_books/Dako_Handbook.pdf


How do parasitic fungi sense optimal fruiting conditions from inside the host? Question is pretty straight forward. Are there generally any chemical cues?

In model fungi, the G protein coupled receptor Gpr1 is known to sense sugars and upregulate a cAMP linked PKA pathway, while in pathogenic strains, it senses Methionine. This probably is the environmental cue that sets off fruiting. There is a recently published extensive review too: Heterotrimeric G protein signaling in filamentous fungi

Reference

Li, Liande, Sara J. Wright, Svetlana Krystofova, Gyungsoon Park, and Katherine A. Borkovich. “Heterotrimeric G Protein Signaling in Filamentous Fungi.” Annual Review of Microbiology 61, no. 1 (October 2007): 423–452.


Plasmid: Empty Backbone? When searching for a plasmid on Addgene what does it mean if it is said to be an "empty backbone"? Why would one want an empty backbone?

If you look on a very basic plasmid map, you usually see three different features: An origin of replication (often abbreviated ori or origin) which is necessary for the replication of the plasmid, a resistance gene (not necessary but useful to select for) and and multi cloning site (abbreviated MCS) which contains a number of unique restriction enzyme recognition sites, see the figure (from here):

In molecular biology plasmids are used to overexpress proteins in bacteria (or other cells) which are of any interest. To do this, you bring in the coding information for this gene into the plasmid using the MCS. Here you can cut the plasmid controlled (only open the ring on one site) and insert DNA of interest. An empty plasmid in this context means that it can readily used for cloning purposes as it does not contain any foreign DNA.


Large plasmid ligation: do I need alkaline phosphatase? I have a doubt about a protocol I'm using for a ligation of a very large plasmid (15kbp circa) with an insert: after digestion with a single-cut enzyme (sticky ends), the protocol passes directly to the purification of the plasmid without making any alkaline phosphatase. My doubt is during the ligation, the plasmid will self-ligated without accepting the insert?. Am I mistaken or the protocol is incorrect?

A plasmid vector will always be prone to recircularisation when a single restriction enzyme has been used, but recombinant plasmids will also be formed during the ligation. Alkaline phosphatase treatment can be used as you describe; you can also  simply make sure that the insert fragment is present in high molar excess and be prepared to work harder at the end to find the recombinant plasmids. Neither approach is correct or incorrect, they both have their limitations.

Of course the best approach is to avoid this type of cloning altogether.

Added later

Incidentally, the wording of your question suggests that you think you may have more of a problem because the plasmid vector is a little larger than usual. Not so! Circularisation is favoured because the two ends are tethered so the effective concentration of each is high with respect to the other. As the plasmid gets bigger the tether is longer and the tethering effect will be less.


Flower/Plant Identification Could anyone please identify this flower/plant found on the semi-shaded banks of a river in East Ireland? It was located near Japanese Knotweed and looks quite similar to this.

That is Himalayan balsam (Impatiens glandulifera).

  Tall, stems often reddish. Lvs opposite or in threes, with small red teeth. Fls large, pale to dark pink-purple, with short bent spur; July-Oct. Bare places, especially by streams.

The Wild Flowers of Britain and Northern Europe. Fitter, Fitter, Blamey. 1974. Collins, London.


Can someone help me with this Pedigree Analysis? $\text{So... here is the given pedigree chart:}$

  My question is ... whether this is an autosomal or a X-linked recessive trait.

The book I was following gave me this info:

My Attempt:

Looking at the chart ... it all comes down to either X-linked recessive or Autosomal recessive.

According to Rule 1. under these conditions:

If it appears with equal frequency in both Males and Females -- Autosomal
Otherwise , if more male than female -- X-linked

  But my teacher said ... "its not always so"

So.... I tried with both once (brute force method ... going through all possibilities) and I could not understand which one...

It seems both are correct (which obviously is not possible)

So can anyone please help me with this problem!?

Thanks!

With the currently given information both autosomal and X-linked recessive is possible:

(WARNING extremely sloppy Paint editing ahead)

This is a possible scenario for an autosomal recessive trait:

And this is one for a X-linked trait:

Ideally you would extend the chart until you encounter a scenario where an affected female has healthy male offspring (which indicates an autosomal trait).


Are Na+/K+ active pumps and K+/Na+ "Leak" channels same as given in the figure? Na+/K+ channels maintain the resting potential with other sodium and potassium channels. Then what are these "Leak" channels? are they the same Na+/K+ pump in a special condition? If so, what is it?

Source of Image: Guyton and Hall- Textbook of Medical Physiology

Below is the structure of a Na+/K+ ATPase, i.e., the sodium/potassium pump shown on the left in your figure:

(image from here)

Compare to the structure of a potassium leak channel (the type of channel depicted on the right in your question):

(see this publication; image from here)

It's clear they are quite different beasts, without much similarity at all besides both being membrane proteins with several transmembrane domains, which is a characteristic they share with countless other proteins with an incredibly wide range of functions.

The only similarity the pictures from your textbook are meant to convey is that they are both membrane-bound proteins and that they accommodate Na+ and K+; besides that, they are completely different. The figure clearly shows a different mechanism of transport, and the remaining similarity is just from the very abstract way that they are represented.


Sex determination in Drosphila Ive been taught that its based on genic balancing.
But I recently saw this question that has caused me some doubt.

I thought it would be the 1st option but unfortunately they said it to be the 3rd.
But in the answer key, they mention the same line of that of the 1st option.
Ive only been taught genic balance in a general sense .I solved by finding the ratio of no. of X chrom. to no. of autosomes. It would help if someone could give me some clarity.

I think the first possible answer is wrong because maybe by "set" they mean the total number of autosomes. Where as in the figure below it states that the autosome is only responsible for a repressor(Dpn), and that in normal conditions (in pairs i assume) they product equal amounts for females and males.

If the chromosome 2 was not in a proper pair, then I assume the dosage of the Dpn repressor would be off.

The gene dosage is with the activators produced also, sis-a, and sis-b. So I guess in females they produce twice as much activator for the Sxl protein, which later on allows for the repression of male genes and activation of female genes.


Corrupted chromosome will be in any cell of body if zygote was corrupted? For example, zygote had abnormal number of chromosome (45, 47, 48 etc) or corrupted chromosome. And fetus was born. Then it means that in any cell of newborn's body there will be the same not normal or corrupted amount of chromosome?

The terms 'corrupted chromosome' and 'corrupted zygote' are very unusual and quite loaded. Mutations occur all the time (of the order of 1-10 mutations per individual per generation in humans, Drake et al. 1998) and it is unclear how big a mutation needs to be so that you talk about "corruption".

But in any case, yes, the egg will copy itself via mitosis to create the whole body. As such any mutation (whether a small substitution or a chromosomal duplication) present in the egg will be transmitted to all the daughter cells and will therefore be found in the entire body. Note that many of the changes in chromosome numbers lead to unviable zygotes and the baby never develop fully.

Note that during mitosis, sister chromatids are being separated and therefore the number of chromosome copy should not matter much in the general case.


Physiological reason why leaves got twisted when treated with indole acetic acid I want to know the physiological reasons of why the leaves of my study plant got twisted when treated for 10 days with spray of indole acetic acid. I want to treat seeds with IAA, and I'm thinking about testing what will happen when I treat the leaves.

Here is a picture of what the plant looks like:

thanks

Disclaimer: Not my area of research

Since IAA (auxins) can induce growth, partially acting through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), it seems likely that the explanation to your result is differential growth/elongation rates on the upper and lower side of the leaves. This could result from uneven spraying, e.g. by spraying the leaves from the top. Faster growth on the top part of the leaf would lead to downward twisting, which seems to be what is happening most of the time.

You could test if this is the case by doing a simple experiment where you carefully apply IAA with a brush on both sides of the leaves for some plants, while others are sprayed. If uneven application is the cause you should see twisting when spraying but not when applying with a brush.

However, auxin is toxic to plants at high concentrations, so you also need to consider the concentration you are using.


Is there a consensus on the CaMV 35S minimal promoter sequence? We have an algal enhancer element and a transcription factor that probably binds it. Basal expression of the enhancer element or full promoter driving luciferase in tobacco protoplast was extremely low. I heard this could be overcome by fusing it to a minimal 35S promoter fragment but I can't seem to find a clear sequence for this minimal promoter.The best I could find was on the cambia website where they say it is -90 http://www.cambia.org/daisy/promoters/242/g1/250/264.html

1) Does anybody have experience with increasing the expression of enhancer elements like this?
2) And what sequence did you use for this?

In case anybody ever has the same question: I found the answer in this paper by Ow et al. 1987 (fig1)
http://www.pnas.org/content/84/14/4870.full.pdf

Just to clarify, I did not want to boost expression of the enhancer element in my algae, it needed boosting in tobacco protoplasts/leaves.


Are humans the only animal that requires "clean water"? I've seen a number of animals - dogs, cats, squirrels, ducks and geese, etc drink from puddles, some of them were muddy, others had green flora growing under water. Same goes for lakes and rivers. A human would not drink that. Do animals experience gastrointestinal discomfort or can they die from drinking water like that?

At the same time I hear about the problem of "clean water" in 3rd world countries and how diarrhea is the #1 killer of children under 5.

Are humans the only animals that require a certain purity of their drinking water? Why is it that a dog can drink from a puddle, but a human is likely to get sick from doing the same? Do baby animals get sick from drinking "dirty" water?

I wouldn't say that a human is "likely" to get sick by drinking from a puddle, I'd say "at some risk". It isn't desperately dangerous, although don't take that as a recommendation. There are many infections you can get from water (bacterial, viral, amoebal, and I presume fungal). You don't want to risk them, but probably won't actually encounter them in that puddle in your garden you see your dog drinking from. If the water is stagnant then the list of things in it that might hurt you is longer than if it's flowing. If you can avoid the mud, and anything that's been standing long enough to grow algae, fresh rainwater is a pretty good bet as these things go.

The same is true of other species, but the risk per drink is lower, since they drink it more and develop resistance to more of the things on the list. Humans are no different. For example some areas tend to have Hepatitis A in the tap water. The local population is immune after they've been infected once, and most childhood infections cause no symptoms, so it's not a problem for the locals. But to an unvaccinated visitor, the water's not safe. Hep A normally won't kill you, but is still well worth avoiding since it will make you sick for several weeks.

So basically, humans drink clean water because we can, not because we absolutely need to.

The lifespan of humans living "in the wild" (that is, populations prior to or independent of human agriculture) is pretty well agreed to be rather less than that of typical modern lifestyles. Water-borne disease is only one of many things responsible for that. The expected lifespan of a person used to purified water and so on, dropped into "the wild", is even lower again.

The "clean-water" problem in developing countries is primarily one of high population, relative to what the same area could possibly support in the absence of agriculture and other technology. The biggest risk of water-borne disease comes from contamination by human waste (although there are other sources, for example rats can contaminate water with Weil's disease). A small group of humans living in a large area doesn't have to worry about human contamination, they just drink upstream of where they defecate. This strategy doesn't help much once the population is dense enough that someone else is doing the same thing 20 metres away from you.

And of course, human agriculture also supports a much higher rat population than would otherwise be present (they're omnivores too, so they'll eat pretty much any food humans do). I suspect most human disease can be blamed on agriculture one way or another: if not on the animals then on the close-quarters living. If the population of humans was closer to what it was in the palaeolithic (a few thousand or tens of thousands of people in Europe), and was used to drinking from natural sources, then the water would be mostly (not entirely) safe.

So it's not so much that humans need perfectly clean water, it's that humans have figured out how to live in populations so large that we tend to make all the nearby water particularly dirty. Other species aren't completely unaffected by this, but they are less affected because our waste is specifically contaminating the water with diseases that affect us.


Bacterial Cell Problem A microbiologist has discovered what she thinks are two new types of algae. The first cell
(Organism 1) appears cubic and is approximately 1.5 μm long, 1.5 μm wide and 1.5 μm deep.

The second (Organism 2) is rectangular and 2 μm wide by 5 μm long by 2μm deep.

a.  What is the surface area/volume ratio of each organism?

b.  Which organism will find it more difficult to interact with surrounding environment (receive nutrients, excrete metabolites etc.)?

c.  How will this organism cope with the reduced capacity to interact with environment?

In respects to question A.

V of Rectangular organism= (V = L x W x D)

Surface Area= (L x W)

Im assuming these simple rules still apply to organisms concerning minuscule measurements.

Im assuming for question B., that the molecule with the smaller dimensions will have the most difficult time interacting with its environment, due to the fact that it has a smaller perimeter with less channels & ports.
I am completely lost for problem C.

Any insight Would be awesome. Thanks all !

B. Higher surface to volume ratio allows better interface with environment.

C. To increase surface area the cell can form processes such as microvilli.


How efficiently does the human body convert the energy stored in fat into kinetic energy? I read that one gram fat contains 9 kcal energy. There are many tables around claiming that x type of exercise for t duration burns roughly E kcal energy. I'd like to estimate how much weight one will lose by following a certain training plan based on these two values. I don't know whether I need to calculate with the heat loss too, or not. Most of these tables don't tell anything about the method they used to estimate the E values. I could workaround this problem by ignoring efficiency, but I can do that only if it is relative close to 100%. As far as I know fat goes through beta-oxidation and the citric acid cycle. After that ATP is used to move the muscles. It is hard to find anything about how efficient this process is.

this depends on largely how you define it, what we normally measure is efficiency including how much energy is used on metabolic upkeep and heating the body in addition to muscle output. we use oxygen consumption to know exactly how many calories we have "burned" when doing this.  In this study we get between 18-26% efficiency, thats calories ingested to work done. Most of the loss is in converting to ATP (~60% loss) and how much ATP we "waste" heating the body. Note efficiency drops quite a lot when you switch to anaerobic exercise.

keep in mind however the body will not start out burning fat, it has glycogen reserves it will start using first.


Number of dopaminergic neurons in VTA Do you know an authoritative source for the approximate number of dopaminergc cells in the ventral tegmental area (VTA)?
Ideally I would like to know this for mice, rats, as well as humans, but one species alone would be a nice start. I have looked for this via google scholar and pubmed, but found nothing.

Approximately, 250000-440000 neurons in Humans (Rice et al., 2016).

  The substantia nigra/ventral tegmental area (SN/VTA) complex is a
  heterogeneous collection of dopaminergic cell groups that extends from
  diencephalic to mesencephalic territories in many vertebrates,
  including rodents, non-human primates, and humans (Puelles and Verney
  1998; see as reviews Smits et al. 2006; Smidt and Burbach 2007; Smits
  et al. 2013). The SN/VTA contains the largest number of dopaminergic
  neurons in the brain (see as reviews van Domburg and ten Donkelaar
  1991; Haber and Fudge 1997; Nieuwenhuys et al. 2008), with average
  estimates ranging in most studies from approximately 250,000 –
  440,000 dopaminergic neurons within the complex (Bogerts et al.
  1983; Hirsch et al. 1988; van Domburg and ten Donkelaar 1991; Damier
  et al. 1999a; Kubis et al. 2000).


Could fingerprints potentially be changed using a gene gun? Not to confuse with your "DNA fingerprint"  I've read surgery is readily used to not just remove but even to change people's prints through employing very small grafts between opposing hands.

About 5 years ago a Chinese group identified SMARCAD1 as a key player in the development of fingerprints. this was  discovered by generating gene expression profiles of people with a very rare condition called adermatoglyphia. These people have  no finger prints.

A gene gun, which uses micropartical bombardment is a technique that propels microscopic particles of heavy metals, coated with the gene of interest, "deep" into tissues.

If you were to alter the genetics of the epidermal stem cells, you could potentially permanently change the tissue that arises from those stem cells. Could this in principle work if over expression of SMARCAD1 resulted in remodeling of the prints or has other more important genes been shown since to be involved?

Do any model organisms have fingerprints, or a version thereof?

I know I'm fishing here, lots of questions. I thought it was an interesting topic and wanted to see what people here had to say.

Chimpanzees have fingerprints.  Next all you have to do is find the homologue of SMARCAD1 and let the animal testing begin!  But actually I doubt it will work.  This website goes into some depth and links some additional sources that show fingerprints are developed in the womb and are fully set by 6 months of gestation.

It seems likely that SMARCAD1 may have to do with having fingerprints or not, but not likely that it has anything to do with their composition.  It would be difficult for one gene to have enough variation to provide 6 billion variations in output.  You could hypothesize that it's a combinatorial output from other genes as well, but the studies linked above focus more on environmental interaction as the cause of variation.

I would guess that the patterns are set and no amount of gene therapy is going to change your fingerprints.  The simplest experiment would be to knockout the above gene in an adult for some period of time and see if the fingerprints fade.


Immune reaction to "new" protein I read in Bruce Alberts Molecular Biology of the cell :

  Normal mice,for example, cannot make an immune response against one of their own protein components of the complement system called C5.
  Mutant mice, however, lack the gene encoding C5(but are otherwise
  genetically identical to the normal mice) can make a strong immune
  response to this blood protein when immunized with it. Natural
  immunological tolerance for a particular self molecule persists only
  for as long the molecule remains present in the body. If a self
  molecule such as C5 is removed, an animal gains the ability to respond
  to it after a few weeks or months. Thus, the immune system is
  genetically capable of responding to self molecules but learns not to
  do so.

So, why does an immune reaction not happen when a new protein is introduced to patients lacking it ? For example if you give clotting factor to hemophilic patient.

You are absolutely right in that there will be immune reaction against proteins that are not naturally present in the body.

However, hemophilia is not caused by complete lack of protein. It is due to loss of function of the clotting factors due to mutations. The proteins are still present, but they do not have the ability to bind and/or activation of their catalytic function. So, there will be no immune activity against exogenous clotting factors given to hemophiliac patients.


Actual definition of cardiac output Is cardiac output the amount of blood pumped by both ventricles in 1 minute or only by the left ventricle in 1 minute?

Cardiac output is the amount of blood pumped only by the left ventricle, per minute.


Use of amino-acid sequences versus use of nucleotide sequences in phylogenetic analysis Reading a  paper about gene evolution, I see that they do phylogenetic analysis for bacteria using protein sequences. They take the method from another paper.

I can suspect that amino-acid sequences are more stable than nucleotide sequences, to the presence of synonymous substitutions.... but, is this stability required between closely related species? doesn't it make the analysis less powerful? does it make it more reliable? In other words, what's the advantage of using amino-acid sequences versus using nucleotide sequences for phylogenetic analysis?

In general, many sequence alignment programs can use multiple substitution models, distinguishing between nucleotides, amino acids, and codons. A protein sequence has functional information that is not directly visible in the nucleotide sequence.

The papers you link deal with horizontal gene transfer, where a gene is passed to more distant  organism. Different species have different codon usage biases, i.e. the translation efficiency is different for different codons. On one hand, this means that HGT is more likely to occur between species of similar codon usage. On the other hand, "codon usage of horizontally transferred genes approaches the host usage over time." Thus, on the nucleotide level, the phylogenetic signal will get lost due to the evolutionary pressure on translation efficiency, while on the protein level, there will be more conservation.


How to monitor the use of Nootropics? How do you monitor the use of nootropics?

What is a good process to measure both: side-effects and any improvements.
Where can I find resources with scientific and tested data of short and long term usage of various Nootropics? (I'm using google as well)

Thank you!

The process of measuring the effect of nootropics would be the same as for any other drug: Do a double blinded placebo study and the follow the parameters you hope to influence. For example do "brain tests" if you want to test for enhanced brain function. If there is any function of your drug in the body, you will see a difference between the treatment and the control group. You could start by reading the Wikipedia article about Nootropics which is quite exhausting and also has quite a lot of references and go on with these two papers "Does taking vitamin, mineral and fatty acid supplements prevent cognitive decline? A systematic review of randomized controlled trials." and "Cognition enhancers between treating and doping the mind."