About stem cells and Cancer Do stem cells have an apoptosis mechanism and , if they do could this be used to repair the  cell self-destruction pathways in a cancer cell?

No but they can be used as part of a gene therapy to induce cellular death in cancer.

TRAIL-secreting mesenchymal stem cells promote apoptosis in heat-shock-treated liver cancer cells and inhibit tumor growth in nude mice

  Liver cancer is one of the top six leading causes of cancer-related death. Radiofrequency ablation (RFA) is an important means of treating liver cancer. Residual cancer after RFA is the most frequent cause of recurrence in cases of liver cancer. The main difference between residual cancer cells and ordinary liver cancer cells is that residual cancer cells experience heat shock. The secretable form of trimeric human tumor necrosis factor-related apoptosis-inducing ligand (stTRAIL) induces apoptosis in a variety of human cancers but not in normal tissues. It has shown potent cancer-selective killing activity and has drawn considerable attention as a possible cancer therapy. In the present work, the therapeutic potential of this stTRAIL-based gene therapy was evaluated in hepatocellular carcinoma subjected to RFA. Rat bone marrow mesenchymal stem cells (BM-MSCs) were isolated and transduced with a lentiviral vector encoding stTRAIL (stTRAIL-MSCs, T-MSCs). Cells treated with heat treatment at 43 °C for 45 min served as simulated residual cancer cells. After treatment with T-MSCs, apoptosis in heat-shock-treated liver cancer cells increased significantly, and caspase-3 was upregulated. When T-MSCs were subcutaneously injected into nude mice, they localized to the tumors and inhibited tumor growth, significantly increasing survival. Collectively, the results of the present study indicate that BM-MSC can provide a steady source of stTRAIL and may be suitable for use in the prevention of the recurrence of hepatocellular carcinoma after RFA with secretable trimeric TRAIL.


How does loss of the electrochemical gradient result in heat production? As far as I understand, uncoupling of the flow of protons and ATP-synthase  provides a bypass for protons between the outer and the inner membrane of mitochondria so that the protons don't have to go through the ATP-synthase on their way to the matrix. I see how it results in loss of electrochemical gradient. But why is heat produced?

ALiceD's comment is perfectly true. (Though in real cases, the short circuiting is seldom absolute as there is usually some finite resistance in the short circuiting wire.)

You can understand this in two ways.

Intuitively, the uncoupling provides a channel for the hydrogen ions to move across the membrane in the direction of their electrochemical gradient without having to do any work. Therefore, the energy it gains by traversing a potential difference, can be thought of as being converted to kinetic energy, i.e. the hydrogen ions are accelerated by the potential difference which causes them to gain speed and hence move at a higher speed than the average in the final compartment. This will cause increased collisions (and more energetic) with the surrounding molecules, slightly increasing their kinetic energy too, which will ultimately increase the average kinetic energy, the measure of which is called temperature. If it was coupled, the hydrogen ions would not have gained the kinetic energy, as the energy they gain by traversing the potential difference would have been used to do work in the ATP synthase machinery.

Rigorously, you can show this using some chemical thermodynamics which includes using $\Delta G$ functions, $\mu$ functions and some related thermodynamic variables. Let me know if you want that explanation.(though I stand the risk of having lost the touch to the mathematical aspect of thermodynamics)

PS:- While the thermodynamic explanation also accounts for the increase in temperature due to obliterated concentration gradient, it is difficult to explain with the former model. You can think of this, as the neutralising of the concentration gradient changes the number of collisions per unit volume (and time), and hence also contributes to the observed temperature change.


If someone with "XO" is one of the identical twins with the other twin as male, then what would the sex chromosome of the other twin be? A more complete question: If someone with sex chromosome of XO is one of the monozygotic twins with the other twin as phenotypically male, then what would the sex chromosome of the other twin be?

I had heard that both XXY and XY is possible. Is it true?

"XO" (an unpaired X chromosome) is characteristic of Turner syndrome.  The Wikipedia article https://en.wikipedia.org/wiki/Turner_syndrome provides a typical image - a woman with a fairly distinctive broadness of the neck.  The phenotype is described as female, though of course gender identity can be unpredictable for anyone.

For the other monozygotic twin to be phenotypically male, the most likely explanation is a Y chromosome - a Y chromosome that was lost in all or many of the cells of the XO woman.

A set of monozygotic twins with one XXY and one XO would be very surprising - in other words, with the twins differing by two chromosomes - would be very surprising.  But nothing is truly impossible in biology.  And ... this may be such a reference, but I didn't look at the full text to make sure: https://www.ncbi.nlm.nih.gov/pubmed/27315788


Does GABA enhance or inhibit negative effects of glutamate? A study on NCBI studied the correlation between a depressive mood and chronic pain. I researched this because today I noticed unusual emotional volatility as a result of 2 days of acute back pain combined with acute muscle soreness (DOMS).
I am certain that the pain and difficulty sleeping (although I slept in on both days), and challenges with finding a sleeping position without pain, and continuous pain on most moving, standing, and sitting, that this has caused some emotional volatility on a physiological level. (Psychological effects as a direct result of temporary chemical changes in the body/brain due to acute pain; not due to neural pathways causing depression, of which I do not have, and I am a joyful person normally).
This question is not about alleviating pain, as it will go away on its own soon. The back is getting near healed by end of week and the sore muscles which have DOMS due to intense workout will also resolve on its own in a few days to a week.
Rather, my question is specifically concerning a particular phrase which I am unclear about:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

I am unclear if this is stating that GABA reduces the effects of glutamate or if it enhances the effects.
There is no clear answer to my full [temporary] issue, since the study itself states that neither the corresponding pathophysiological mechanisms of chronic pain and depression nor their mutual correlation has been identified, so there is no pathophysiological scientific answer to the chemical workings, so I can only speculate.
The end result is I wanted to discover whether increasing or lowering GABA could have any effect on my mood as a result of my pain in the short term, which is easily experimented rather safely by either taking GABA or taking a supplement that inhibits GABA. It could have no beneficial effect - no problem. It's worth a try though. I've taken GABA before BTW.
To reiterate the particular question: With regards to the statement:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

Does this imply that GABA enhances or reduces glutamatergic activity?
Note:
I think it's saying that GABA creates glutamatergic activity which inhibits the neuroexcitatory effects of glutamate. That is, taking GABA would decrease effects of glutamate. Let me know if this is correct or not.

Glutamate causes an EPSP (Excitatory Post Synaptic Potential,) thereby making the neuron less negative depolarize) and closer to voltage required to cause an Action Potential (AP)  and thus fire.  GABA causes an IPSP (Inhibitory Post Synaptic Potential) making the neuron more negative (hyperpolarize) and further away from the voltage required to fire and cause an AP.  GABA & Glutamate receptors  are generally on different neurons that synapse with other interneurons & oppose each other, although neither one is generally the end neurotransmitter of the locus,  nor the only neurotransmitter of the neuron, so basically act as neuromodulators on the post-synaptic neuron. Glutamatergic receptors generally affect Sodium Channels &  GABA-ergic neurons generally  affect Chloride Channels. In theory, inhibiting an inhibitory neuron would be the equivalent of exciting an excitatory neuron, but since they primarily affect  post-synaptic neurons, the effect is cumulative, so the post-synaptic interneuron is basically adding up all the EPSPs & IPSPs to get a RMP (Resting Membrane Potential) & some additional stimulus must occur to get the neuron to fire (AP)


Are thunder and lightning necessary for any organisms? Comparatively irregular events such as forest fires are necessary for some plants to grow (see here).

But do any plant or animal species have similar dependence on thunder and/or lightning?

Lightning results in nitrogen fixation (Draphco et al., 1967; Hill et al., 1980). It is one of the main abiotic nitrogen fixation mechanisms. As you would know very well, nitrogen fixation is important for all organisms.


What does "PDPN+ cells" means? Are they podoplanin positive cells (cells that tested positive for podoplanin)?

"...though it has been shown that podoplanin (PDPN+) cells analogous to mouse FRCs are found in human secondary lymphoid organs..." (https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2005046)

"Although rare, the few SFTPB+ observed in HLOs resemble AECII cells seen in the adult human lung, and PDPN+ cells resembled the elongated AECI cells in the human lung" "Few PDPN+ cells also showed elongated, squamous morphology seen in the adult lung." (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4370217/).

Thank you.

In this context, that nomenclature means "cells which express PDPN"


what these suffixes mean,-coel,-blast,-cyst? in the connective tissue (Bones) we have 3 types  osteoblast, osteocoel,osteocyst what are they and why they differ.

You can easily search this on the web.

Osteoblasts are the immature cells of bone which are responsible for the production and mineralization of bone matrix.

Osteocytes are the mature cells of bone found in open spaces in bone called lacunae. The functions of osteocytes includes maintenance of bone and  calcium homeostasis.

Osteoclasts are responsible for removal of bone.

Source : Tortora and Derrickson


Does learning increase the number of neurons in the brain? I am attempting to understand neurogenesis related to learning. Does learning increase the number of neurons in the human brain? What would be some good scientific publications to read?

Short answer
Training increases white and gray matter densities in the brain. This may reflect increases in neuronal cell counts especially in the hippocampus. In the cortex, however, such observed changes are probably more reflective of other processes, such as synaptogenesis.

Background
Gray matter is generally viewed as being the neuronal cell bodies, while white matter corresponds to myelinated fiber tracts. Changes in both can be reflective of changes in cellular content, but changes in gray matter are generally more directly related to changes in cell numbers, which you are after.

A striking example of the effects of learning on the brain is observed in subjects that start to learn to juggle. These people have been shown to have increased gray matter density in the occipito-parietal regions (the visual motion areas). These changes are apparent after as little as 7 days of training. Such experience-dependent changes are also observed in white matter. Occipito-parietal regions are involved in visuo-motor coordination, reaching and grasping. There have been a host of other studies that showed similar changes in the brain. For example, taxi drivers were shown to have increased hippocampal volumes.

There is good evidence for adult neurogenesis occurring with learning in the hippocampus. Adult neurogenesis also produces thousands of new granule cells in the dentate gyrus every month, but this is a relatively small increase in total number of hippocampal neurons. Furthermore, although there have been reports of neurogenesis in the mammalian adult neocortex, this is controversial.
Thus, neurogenesis is likely a minor factor in MRI changes, particularly those found outside the hippocampus.

Instead, other factors such as increase in glial cell numbers, synaptogenesis, changes in dendritic structures, axonal sprouting and re-routing and even vascular changes may underly the observed changes in imaging studies.

Note: there is a host of imaging studies available on effects of learning on structural changes in the brain. The referenced review article cites many.

Reference
- Zatorre et al., Nature Neurosci (2012); 15: 528–36


Hybrid seed production requires a male sterile parent. Why? Hybridization is the process of crossing two plant species or varieties. In this case, two varieties of plants. In plant breeding, crossing is a very useful technique to improve the features of the offspring. For example, if a maize corn variety has lost yield over the years, it can be crossed to a variety with a higher yield and the offspring will also have a higher yield.
In order to cross these two varieties, the male needs to be sterile. Why is that? I don't understand how the process works and I cannot find the reason anywhere. The answer should be pretty basic, and I think I am missing something that everybody assumes I should know.

To get a hybrid you need pollen from a different plant. Corn is likely to self-pollinate if some action is not taken to prevent it. I don't know of sterile males plants - in the US corn belt the self-pollination is prevented by detasseling. Many young people get summer jobs detasseling (cutting off the tassels) for seed corn.


Brain capacity of Cro-magnon man vs Modern man Cranial capacity of Cromagnon man was about 1650cc whereas average cranial capacity in modern human is 1450cc.

My question is, why during the course of evolution, a reduction in cranial capacity is seen ?

Some of the possible explanations are summarized in Selection for smaller brains in Holocene human evolution. It's a blog post (but from a well-regarded anthropologist and heavily referenced), but I'll excerpt a few quotes here:

  Less well known is that the terminal Pleistocene and Holocene (ca. 30,000 years ago to present) witnessed a substantial decline in endocranial volume ... This decrease of approximately 240 ml in 10,000 years is nearly 36 times the rate of increase during the previous 800,000 years.  ...

He considered one possible explanation, that the smaller brain size is due to smaller stature, and determined that it's not likely:

  Here, I apply a quantitative genetic model to test the hypothesis that Holocene evolution of brain size may be explained by reductions in body size. ... The net change in endocranial volume, roughly 130 ml from the terminal Pleistocene to late Holocene skeletal sample would predict a reduction in stature of 13 cm, if the brain size had changed only because of correlated changes in stature. That degree of stature reduction is not biologically impossible although it would be extreme. ... The evidence suggests substantial reductions in brain size in some recent human populations, more than can be explained by correlated changes in body size.

He then lists six possible alternate explanations, which are not mutually exclusive:

Chance.
Plasticity.
Climate.
Nutrition.
Function.
Development.

He spends some time discussing each but concludes that at the present time the cause can't be definitely determined.

Here's his conclusion:

  The available skeletal samples show a reduction in endocranial volume or vault dimensions ... This reduction cannot be explained as an allometric consequence of reductions of body mass or stature in these populations. The large population numbers in these Holocene populations, particularly in post-agricultural Europe and China, rule out genetic drift as an explanation for smaller endocranial volume. ... Therefore, smaller endocranial volume was correlated with higher fitness during the recent evolution of these populations. Several hypotheses may explain the reduction of brain size in Holocene populations, and further work will be necessary to uncover the developmental and functional consequences of smaller brains.


Why do these earthworms stay between the road lines? This article shows pictures of earthworms during floods in Texas. The worms ball up, supposedly in order to survive the floods.

Photo Credit: Texas Parks And Wildlife Department

Can anyone explain the phenomenon a little? I can't seem to find anything about this online. I know that earthworms surface when it rains for oxygen, but it seems weird that they meet in the middle of the street.

The first question: what the worms do on the ground during the flood? One of the answers to this question is -

"It gives them an opportunity to move greater distances across the soil surface than they could do through soil," said Dr. Lowe. "They cannot do this when it is dry because of their moisture requirements."

The second question: why they form ball after moving to the ground. There are two answers to this question:

First, as a part of surviving mechanism to prevent drying. As you can see, they cannot come back to the soil across the asphalt, thus they form balls and wait the weather to improve.

Second reason to form the balls - communication:

"The earthworms use touch to communicate and influence each other's behaviour, according to research published in the journal Ethology.
By doing so the worms collectively decide to travel in the same direction as part of a single herd."


How are human rotaviruses generally transmitted? I know rotaviruses are double stranded RNA viruses and i am wondering if the human transmission is similar to the modes of veterinary transmission.

Faecal-oral transmission. Ref from https://en.wikipedia.org/wiki/Rotavirus


What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like? What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?

Colour (darkness of green, redness)
Waxiness
Veins

I'm guessing that soil ph, nutrients, and other factors play a part. Vacciniums seem to have very specific needs, and as far as I know, assessing the leaves is one of the best ways to determine plant health.

Vaccinium species are ericaceous plants (acid soil loving) so they will not do well in alkaline soils, and/or being watered with hard water. In fact they have a narrow optimum pH range 4.8 - 5.2 (Source http://www.westernfarmpress.com/management/blueberry-iron-chlorosis-has-multiple-causes)

The pH of the soil will effect the plants ability to access the minerals in needs from the soil, and mineral deficiencies will indeed show themselves in the leaves first.

Here is a photo of a healthy Highbush Blueberry leaves


Genetic linkage greater than 50 centimorgans Classically, the linkage between two loci can be measured in centimorgans (cM), which represents the percent chance that these two loci will recombine an odd number of times (generating a recombinant genotype).

Due to independent assortment, markers on different chromosomes are expected to recombine 50% of the time. As I understand, if one conducts a classic experiment and counts various progeny, then deduces the apparent linkage, values of 50 cM or more are interpreted as "impossible to determine whether on separate chromosomes or just recombines very often". See (source), with grammar corrected:

  The final point that we need to make regards the maximum distance that we can measure. Because of the way in which the calculations are performed, we can never have more (than) 50% recombinant gametes. Therefore the (maximum) distance that two genes can be apart and still measure that distance is just less (than) 50 cM. If two genes are greater than 50 cM apart, then we can not determine if they reside on the same chromosome or are on different chromosomes.

Wikipedia gives an analytical solution and also remarks that (d is physical distance):

  The probability of recombination is approximately d/100 for small values of d and approaches 50% as d goes to infinity.

However, what happens if the linkage is greater than 50 cM? It seems like classical experiments aside, such a situation is possible in reality.

For instance, yeast chromosome IV is 1530 kb long, and averages 0.31 cM/kbp. Let's take two genes on Chr.IV:

DNF2 is at about +631 kb.
TOM1 is at about +1370 kb.

The physical distance between these is about 734 kb. According to the cM/kbp value, the centimorgan distance is $734\text{ kb} \cdot 0.31\text{ cM}/\text{kb} = 228 \text{ cM}$ . How to interpret this 228?

If I mate a haploid yeast which is DNF2 TOM1 with another which is dnf2 tom1 (lowercase indicating minor allele rather than deletion), then sporulate them, what is the chance of getting spores with DNF2 tom1 or dnf2 TOM1 genotypes?

I realize that the cM/kbp value is only a simplification and that in practice linkage is a more complex phenomenon. Nevertheless, it seems plausible that several crossover events can happen on Chr.IV since it is so big. This includes the possibility of 1, 3, 5 and more crossovers which would create a hybrid (assuming they all happen between these two loci), as well as the possibility of 2, 4, etc crossovers which would create a non-hybrid spore (at least as far as our chosen markers are concerned).

Understanding the statistics we use when talking about recombination rate is an important question that is unfortunately too often dismissed in an intro course to evolutionary biology or population genetics and that is misunderstood by many. I have a partial understanding of it but hopefully, I'll manage to write a decent answer.
#Short answer
A recombination rate and a genetic distance (in centiMorgan) are two different things. While the recombination rate is bounded between 0 and 0.5, the genetic distance is bounded between 0 and infinity. There is a one-to-one function from the genetic distance to the recombination rate. For small recombination rate, the recombination rate and the genetic distance take very similar values but for greater values, the recombination rate is much lower than the genetic distance.
#Long answer
There is a tiny bit of math below. These equations are mainly for curiosity as one can understand the answer without understanding the maths behind it.
Definitions of $r$ and $M$
You are getting confused between two different statistics

The rate of recombination $r$ between two loci
$r$ is the probability for two loci to remain in the same gamete after recombination occurred. This probability cannot be greater than 0.5 ($0 \le r \le 0.5$).
The distance in Morgans $M$ (or more commonly in centiMorgans) between two loci. $M$ is the expected number of cross-over that occurs between the two loci.

Morgans and centiMorgans
You will note that I talk in Morgans rather than centiMorgans, which is not typical in the literature, but it helps at conveying the intuition of what it means. If $150$ centiMorgans $=$ $1.5$ Morgans. For two loci distant by 1.5 Morgans, the expected number of cross-over between the two loci is 1.5 (by definition). Below are some more explanations on these two definitions with some drawing :)
Case study with loci A and B
While $M$ and $r$ are closely related, they are not exactly the same thing. Consider the following sequence with the loci A and B
---[A]------------------[B]---

Let's assumed the two loci are very far apart and $M=2$. The probability of having exactly $k$ crossovers is therefore given by a Poisson distribution with rate $M=2$
$$P(k) = \frac{e^{-M}M^k}{k!}$$
Let's say for a given case that $k=1$ (a single cross-over occurred). This cross over is represented by a "/" below
---[A]-------------/----[B]---

Here clearly the two sequences at loci A and B will be separated. Let's say now that $k=2$ (two cross-over occurred).
---[A]---/-----/--------[B]---

Here, even if crossovers have occurred, the two sequences at loci A and B will remain together. Only the sequence in between the two cross-overs will come from the homologous chromosome.
Relationship between $r$ and $M$ - in words
You might see it coming from the previous section. The probability $r$ of these two loci A and B to be separated via recombination is the probability of an odd number of recombination events to occur between them (knowing that $M$ is the expected number of cross-overs).
Relationship between $r$ and $M$ - in equation
Let's calculate first the probability $p_{even}$ that an even number of cross-overs occur. This probability is just
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!}$$
, where I just added the constant $2$ before $k$ at both the numerator and denominator. With some algebra and trig, one can show that
$$p_{even} = \sum_{k = 0}^{\infty}{e^{-M}M^{2k} \over (2k)!} =
e^{-M}\sum_{k = 0}^{\infty}{M^{2k} \over (2k)!} = $$
$$e^{-M} \: cosh(M) = e^{-M}\left ( \frac{e^{M} + e^{-M}}{2}\right ) =
{1 + e^{-2M}\over 2} $$

As, $r = p_{odd} = 1 - p_{even}$,
$$r = 1 - {1 + e^{-2M}\over 2} = {1 - e^{-2M}\over 2}$$
Here we go! We have our relationship between $r$ and $M$! Let's graph it
#Relationship between $r$ and $M$ - on a graph
I just graphed the above equation in Mathematica (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 5}])

Here is the same graph but zoomed on lower values of $r$ and $M$ (Plot[y = (1 - Exp[-2 M ])/2, {M, 0, 0.1}])

We clearly see from the graph that for low values of $M$, as $M$ increases $r$ increase quasi linearly ($M≈r$). For greater values of $M$, $r$ still increases but slower and slower until reaching an asymptote / plateau at $\frac{1}{2}$. $r$ is indeed bounded between 0 (when $M=0$) and $\frac{1}{2}$ (when $M=\infty$).
Note, the fact that the sum of probabilities of every even $k$ in a Poisson distribution is always lower or equal to 0.5 is an interesting math fact in itself!


Why spider's web don't burn when electricity touches it? I saw and spider on it's web at an electrical cable and thinked: If the web is made of proteins, why dont burn.

Sorry, the photo is dark because is night in Ecuador

Spider silk can conduct electricity. Some spiders use this material property of conductivity to capture prey. https://www.ncbi.nlm.nih.gov/pubmed/24323174

So I'm going on the assumption that both electrical lines spanning the web are bare and that they are live, i.e. carrying current. I will also assume that these lines are carrying the same current.

With electricity, it might help to think of the analogy of a waterfall. Water at the top of a waterfall has potential energy, which is converted to kinetic energy when it goes over the waterfall. The water accelerates towards the earth as it falls. There is a height or "gradient" between the top of the waterfall and its bottom, which allows water to accelerate from the top towards the bottom of the fall.

Electrons in electricity work in much the same way. Between two points along a conductor, you need a voltage gradient to establish an electric field, which moves electrons in a particular direction — just as the waterfall creates a gradient of high ground to low ground that enables water to flow.

If you have two wires (both conductors) running at the same voltage, and if you connect them with another conductor, like a spider's web, electrons will not run through the web because there is no voltage differential that creates an electric field that drives the flow of electrons between that connection. https://en.wikipedia.org/wiki/Electric_potential

Here, the web and spider are likely unhurt, because the two lines do not provide a voltage difference needed to have electrons move across the silk, like water would flow over a waterfall.

If the spider web was grounded — if its web were instead connected from one of the electrical wires to the earth — electricity would likely run through the web and, potentially, burn the web (and the spider). But from your photograph, it looks like the web is connected to both wires that ℗r assumption) are at the same voltage.

This is the same principle that allows electricians to work on maintaining electrical pylons without shutting down the power grid. https://en.wikipedia.org/wiki/Live-line_working

They work in such a way as to maintain the same voltage as the lines they are working on. If they were grounded — if they held a copper wire, say, that was plugged into the earth — or if there was anything conductive that the electrician was connected to that established a dangerous voltage gradient, and if they started working on live electrical lines, they would get fried. Same with the spider, if the web was grounded in a similar way.

Further, if the two wires were running at different voltages, then electricity could conduct through the spider web and cause some damage.

This answer relies on a lot of assumptions from the photograph. Feel free to clarify if those assumptions would change the parameters of the question and my answer.


Why are two-winged animals much more common than four-winged? In flying vertebrates, almost all have only two wings (with the exception of Microraptor and its close relatives). This makes some sense because you need some way to walk also, and a wing isn't very good as a leg, hence why bats are so bad at walking. Of course, bats do demonstrate that being able to walk well is not necessary to be a successful clade.

As far as insects are concerned this might seem like an odd question, since most insects technically have four wings. But among the four largest insect orders (which together make up a sizeable majority of insects), Coleoptera, Lepidoptera, Diptera, and Hymenoptera, all of them functionally have two wings. In Diptera and Coleoptera, only one pair of wings is used to fly. In Hymenoptera and Lepidoptera the two pairs are attached and don't move indepedently.

So my question is, why is two-winged flight so much more common than four-winged? If two-wingedness is advantageous, why do other insects retain four-winged flight (most notably Odonata)?

Note you are talking about two very distinct conditions

In vertebrates, 4 "wings" only evolves once in vertebrates (in early birds) and only one set function as wings the others "wings" are control surfaces for low speed stability, they generate insignificant amounts of lift. for large animals like vertebrates you can't fit two sets of functional wings on the same animal. Large wings need a lot of space to flap and you would need to make the torso longer to give enough room for a second set of flapping wings, which would add a lot of weight and defeat the benefits.

In Insects four wings is the default, the groups with two wings got them by transforming one set of wings into something else useful. Wing covers in beetles ,which protect wings from damage, and Halteres in flies which act as a sort of sensory organ to determine position. Two wings are more common numerically becasue those two groups are extremely successful. Basically if you have two of something but one will also work and evolution can turn the other set into something useful then you have a chance to lose one set of that thing. Two wings are more common numerically becasue those two groups are extremely successful. By turning four wings into two those groups ended up with more abilities than their four winged relatives, becasue they did not just lose the wings they turned them into something else.

In insects wings actually evolved from gill covers, insects could have had six wings, why the first set never evolved would be an interesting question. It may be due how HOX genes are expressed in insect segments.

Source


Vigorous shaking for HFR interrupted mating I am trying to reproduce E. coli interrupted mating using an HFR strain, and I read that the cultures should be vigorously shaken  at times to interrupt the DNA transfer from the F+(HFR) donors to the F- cells.

How vigorously(I'm OK with a qualitative answer) should I shake the culture for optimal results?

I remember doing this experiment many years ago in an undergraduate practical where we used vigorous vortexing of culture samples in glass tubes to achieve interruption and separation.

According to Griffiths AJF, Gelbart WM, Miller JH, et al. Modern Genetic Analysis. Bacterial Conjugation:

  ... sampling is accomplished by using a kitchen blender to separate
  the joined cells, resulting in interrupted conjugation.


Difference between Trophic and Tactic movements What is the difference between Trophic (eg. Chemotrophic) and Tactic (eg. Chemotactic) movements?

In Bryophytes, Anthrezoids are attracted towards Archegonia. This is Chemotactic movement. In Spermatophytes, Pollen tube moves towards Ovule. This is due to Chemotrophic movement.

This is was taught in our school today. But to me, in both cases the male part is attracted to female part using certain chemicles. So what is the difference between them? Broadly speaking, what is the difference between Tactic and Trophic movements?

I think that you got a bit confused about terminology. In fact Chemotrophic is an organism that obtain energy by organic or inorganic molecules.
In your case I think that you want to know the difference between Chemotropism and Chemotaxis.
Chemotropism

Chemo-tropism is the growth of organisms (or parts of an organism, including individual cells) such as bacteria and plants, navigated by chemical stimulus from outside of the organism or organisms part [...]
An example of chemo-tropic movement can be seen during the growth of the pollen tube, where growth is always towards the ovules.

Chemotaxis

Chemotaxis (from chemo- + taxis) is the movement of an organism in response to a chemical stimulus.Somatic cells, bacteria, and other single-cell or multicellular organisms direct their movements according to certain chemicals in their environment. This is important for bacteria to find food (e.g., glucose) by swimming toward the highest concentration of food molecules, or to flee from poisons (e.g., phenol). In multicellular organisms, chemotaxis is critical to early development (e.g., movement of sperm towards the egg during fertilization) and subsequent phases of development (e.g., migration of neurons or lymphocytes) as well as in normal function.

Hence, to sum up (Chemo)taxis is the physical movement of a cell (or an organism) in response to a (chemical) stimulus, as done by the Antherozoids that are attracted towards Archegonia.  However (Chemo)tropism is the growth on organism toward a (chemical) signal, like done by Spermatophytes where pollen tube moves (so it growths) towards the Ovule.
Hope this explanation help you to clarify.


Where can I find a list of common enzyme cofactors and/or co-enzymes? Where can I find a list of enzyme cofactors and/or co-enzymes, ordered by how common they are?

For example, $O_2$, $H_2O$, $ATP$, $ADP$, $NAD$, should be ranked in the first places, because they participate in most reactions.

Check this out. This resource lists organic cofactors and the associated enzymes.
See the wikipedia page also.

Many metals also serve as prosthetic groups in enzymes. They include- Magnesium, Manganese, Iron, Cobalt, Nickel, Copper, Zinc, Molybdenum.

FeS clusters are also an important part in many important enzymes in mitochondria and plastids.


Parameters that determines the thermal stability of DNA Why a DNA with a high GC content more stable than one with a less GC content? Is it because of the three hydrogen bonds in GC base pair which is one more than a AT base pair or is it because of the more stable base stacking of GC base pairs?
In my book it is given that it is due to the hydrogen bonds but in a research article I found it is saying that base stacking solely determines thermal stability. enter link description here

Although taken in isolation GC bonds should be more stable than AT bonds, due to their higher binding energy (three hydrogen bodns versus two), it is the stacking energy that is considered the stabilizing factor of the DNA:

We find that temperature and salt dependences of the stacking term
fully determine the temperature and the salt dependence of DNA
stability parameters. For all temperatures and salt concentrations
employed in present study, base-stacking is the main stabilizing
factor in the DNA double helix. A•T pairing is always destabilizing
and G•C pairing contributes almost no stabilization. Base-stacking
interaction dominates not only in the duplex overall stability but
also significantly contributes into the dependence of the duplex
stability on its sequence.

The reason for that is that one can have the same number of pairs under many different configurations of strands, which means high entropy and instability, unless there are stacking interactions. This is why most models of DNA and RNA helices are based on adding the stacking energies, although there are some additional contributions, particularly in the case of RNA - initiation energy, energies associated to the inner loops, etc.


Nomenclature of genes and proteins With respect to this paper:

Identification of Host Proteins Required
for HIV Infection Through a Functional
Genomic Screen

In the abstract, I found names such as Rab6 and Vps35 and TNPO3. So Rab6 and Vps35 are proteins and TNPO3 is a gene? So the strings written in full caps are the genes and those strings whose just first letter is capital and the rest of the letters are small is a protein?

Genes, conventionally, are always written in italic (e.g. SHH) which is not the case for proteins (in the former example SHH). That should allow you to tell apart gene and protein symbols (SHH vs SHH).

The capitalization of gene/protein names is a bit more in the grey area. Usually one will use capitalized gene and protein symbols for human and primates (e.g. SHH and SHH) and use non-capitalized symbols for mice and rat genes (e.g. Shh but still SHH for the protein). This is dependent on the organism and journals usually have specific guidelines on how to exactly write gene and protein symbols.

In your case the article refers to Rab6, Vps53 (not 35) and TNPO3 as proteins, if not clearly stated differently, such as the Rab6 siRNA, not only in the abstract alone but over the entire article. They use italic names for genes as shown in one of the sentence:

  ... and 48 hours later staining for p24, produced from the HIV gag gene...

Just as a footnote, full gene names (e.g. the sonic hedgehog gene) are not italicized.


Effect of histidine on the binding affinity of HisP I was asked the following question by my teacher:

  A gene regulatory protein called HisP regulates the enzymes for
  histidine biosynthesis in the bacterium E. Coli.  HisP is a protein
  whoes activity is modulated by histidine.  Upon binding histidine,
  HisP alters its conformation, dramatically changing its affinity for
  the regulatory sequences in the promoters of the genes for the
  histidine biosynthetic enzymes.

  If HisP function sas a transcriptional repressor, would you expect
  that HisP would bind more tightly or less tightly to regulatory
  sequences when histidine is abundant? Why?

My own attempt at a solution:

Less tightly.  If histidine is abundant, HisP's job is to stop the histadine pathway as a "repressor."  If HisP binds less tightly to promotors, the pathway should not produce as much histadine.

Still if you change your question as (If histidine is abundant, HisP's job is to stop the histidine pathway as a "repressor." If HisP binds less tightly to promotors, the pathway should not produce as much histidine.)
Then it should be under another assumption that what is the effect of HisP binding promoter of enzyme's gene. Is it suppressing the transcription or amplifying the transcription.
If it suppresses transcription then answer is more tightly, if it amplifies the transcription then answer is less tightly. I suggest you put this clearly in your answer, as the question is not quest accurate.

I guess your answer might be wrong.
The question should be under another assumption that how does this protein HisP regulate histidine biosynthesis. positiver or negative feedback regulation.
Generally, amino acids synthesis is regulated by negative feedback loops so that cells could control the amount of amino acids they want. In this case, the answer should be more tightly. As it functions as a repressor then it should bind promoter more tightly so that to repress the transcription more which then generate less histidine synthesis enzyme. (I believe this is what your teacher want you to answer)
In the other case, biosystems sometimes have the positive feedback regulation so that they can amplify the sensitivity to the environment noise or generate bistability (phenotypic switching). In that case, the protein bind promoter less tightly in order to generate more histidine.


What could cause individual false positives in ELISAs, while the rest of the plate looks fine? I run indirect ELISAs for COVID antibodies. That's my whole job right now as a research technician. I coat the plates with a pure RBD, then detect antibodies in serum. Recently it's come to light that I've run plates with false positives. Running those same serum samples again gives VERY different (negative) results. If entire plates were giving false positives we could figure out what mistakes I'm making, but for the most part the duplicates look good, the standard is good, the dilutions are good... The person who wrote this protocol hasn't included a negative control because there have been occasions during the development of the protocol where pooled serum from 2018 or earlier was used as a negative, but those pooled serum controls were somehow consistently more positive than that of several confirmed, post-recovery COVID patients. Obviously that lack of negative control has predictably come back to bite us.
Originally we thought it was a plate washer malfunction, but it turns out these smatterings of false positives predates the plate washer acting up.
The short of the long is that some of my plates have very clear, obvious negatives, some borderline positives, and some clear, obvious positives. The issue is that some of those positives are false positives and neither I nor my supervisor can for the life of us figure out why.
Ideas would be awesome. ELISAs are my entire job right now, and the PI is understandably not thrilled with me.
Additional details:
Plates are washed by an automatic plate washer after the incubation of sample dilutions, and after the incubation of the secondary antibody/HRP. The plates are blocked before sample addition with a fractionated bovine serum/gelatin/tween20 blocking buffer. Dilutions are made in that same blocking buffer, and the secondary antibody is also diluted in blocking buffer. We're using Immulon 4HBX plates. The plates are developed with ABTS in McIlvain's plus H2o2.
Ask my anything else that might help figure this out. I'll answer what I can.

Is your detection or secondary antibody aggregating? I've done extensive clinical ELISA development in the past and when this problem inevitably crops up for these assays the most likely culprits in order were:

Plate washer acting funny
Antibody aggregates binding nonspecifically to the plate
Inefficient blocking reagent/not enough time spent blocking
Person running the samples is mixing things up

Even if your false positives predate the platewasher malfunction, you could still have a leaky/clogged dispensing nozzle. Try rotating the plate 180 between wash steps or hand-washing and see if that helps.
For aggregated secondary/detection ab, give them a brief spin and pipette off the top, and for blocking increase volume/time.


What is the name of this flower? This is from Bangladesh though I am not sure it's native here

Google image search gave me answer as "Plumeria"


Is plaque formed even if you do not eat anything? Some people report that their gum and dental health improves when they are fasting. Many forums contain crazy amounts of misinformation and claims which are unsupported by serious scientific research, so many people attribute various effects of fasting to their body being "purged of toxins" and all sorts of other nonsense.

I have noticed one of these effects on myself when I'm fasting - my teeth get somewhat sticky in the evening. The same effect is reported by many people on the aforementioned forums. On normal days when eating food, this does not happen.

It's pretty certain it's not some sticky toxins being excreted by the teeth. So what is it? I strongly suspect that it's just normal plaque, which would otherwise be abraded by chewing on food. But I always assumed that plaque is formed by food remains in the mouth, so it leads me to the question:

Is plaque formed even when one does not eat any food?

Citations of scientific literature are welcome.

But I always assumed that plaque is formed by food remains in the mouth

It's not surprising that you'd have this assumption. The clinical term, dental plaque, refers to soft deposits on the teeth. While is often described to the lay public in connection to eating (without brushing), it is not food, or the remains of food, it is a biofilm. Biofilms are complex masses of bacterial colonies in a gel-like matrix produced by those same colonies. The matrix typically, helps the colonies adhere to some surface and protects them from external threats.
Good supporting electronic references of what, exactly, a dental biofilm is and how it impacts the health of your mouth and body are behind a paywall, but you may be able to access them at your local public or school library. Socransky and Haffajee have a good review in Periodontology. You can find it on Pubmed (behind a paywall).
As you suspected, not eating does not prevent plaque formation, but it is not because your teeth are excreting sticky toxins. Your mouth is full of bacteria, most of which lives peacefully without causing any problems. They're the ones that make the plaque, and they will make it whether you eat or don't. Whether or not those bacteria are more likely to cause problems (e.g., cavities and gum disease) if you fast is a question for future research.
There is some evidence that the bacterial composition in the mouse gut changes when they fast, and that obesity is associated with periodontal disease in humans. There is some interesting evidence in support of effects of intermittent fasting that would make it reasonable to ask a research question about the impact on dental caries and periodontal disease, but that evidence isn't enough to support fasting as a treatment for any disease.
tl;dr
Plaque is (caused by) bacteria, not food. It's produced whether you eat or not. Fasting is certainly not an approved treatment for periodontal disease or cavities, and I'm not aware of any direct evidence supporting it.


Classes of Graphs used in Biology I am a student of Mathematics.Since I found no better place to ask my question I post it here.

I was looking for some classes of graphs which are used in biology.

I came across this particular class of graphs called kite graphs whose link can be found here https://rpubs.com/thoughtfulbloke/kitegraph.

I found it interesting because graphs are mathematical objects and finding them useful in biology is naturally very interesting.

I also find research papers in Mathematics involving kite graphs.

My question is what are some classes of graphs like the kite graphs which are used in biology.
Where can I find them?

In case someone helps,I will be grateful to them.

I don't think there is a single "class of graph" that isn't used in biology.

In biology (just like in any other natural science), we have all kind of data types;

non-ordinal variables
boolean
ordinal categorical
numeric
tree data
other types of network data
pure functions (from statistical or theoretical models)
pictures
sounds
etc..

We make all kind of graphs out of these data;

scater plot
points or lines with eventually error bars
bar graphs with eventually error bars
kites
boxplot
images (colored shaped kind of things; e.g. density maps)
phase diagrams
multidimensional graphs
pie charts
function graphs
Venn diagrams
existential graphs
flow diagrams (incl. alluvial diagrams, spankey diagrams, ...)
trees
matching trees
other types of networks
schematic representations
pictures
spectrograms
videos
interactive graphs
etc...

One can really display any kind of data / information in anyway (s)he wants to.

Kite graphs are just simple graphs to compare frequencies variation along a continuous variable and among a categorical (ordinal or not) variable. It isn't the most common types of graphs but we see them. As a matter of fact, in a paper of mine that is currently under revision the figure 1 is a kite graph (with nested non-ordinal categorical variables).

Just look at random papers to find graphs. Go on google.scholar.com and search for any biology subject and you'll find papers with graphs.


Can chromosomal crossover undo itself? If I have alleles AB on one chromosome and ab on another, and if A and B are far from each other (and also a and b), then there is a lot of chromosomal crossovers happening. If I crossover 7 times, will I end up with the same chromosomes as if I cross over once?

Good thinking. Yes, it is theoretically possible. It is often modelled like this. Have a look at this answer for the maths.

Note however, that to my understanding (and I might be wrong) there is typically either 0 or 1 crossover per pair of chromosomes as cross-over is directly related to the way homologous chromosomes bind together during prophase I of the meiosis by the synapsis. My confusion lies in the fact that, I think, there are sometimes (often?) several synapsis per chromosome pair. Hopefully, someone else will be able to clarify this for us.

As a consequence, the genome-wide recombination rate in humans is almost exactly 23 in humans (Wang et al., 2012). So in practice, such mulitple crossover would very rarely (if ever) happen.


How different can the Tm be between 2 primers? I have a forward primer with Tm 85 degree Celcius. I cannot change this primer. But I have two options for the reverse primer. One with Tm 65 degree Celcius (Annealing at 65 degree Celcius) and another with 72 degree Celcius (Annealing at 72 degree Celcius).
First of all, will either of the primers work for me?
If so, which pair would be better?

The default parameter provided by "primer-blast" is 3 degree (max difference between the melting temperatures of the pairs) .
that said I think it really depends on the application. in case of cloning (in my experience) you can allow wider ranges of delta Tm between primers (in this case I used to use the average Tm of the two primers as annealing temperature). you accept to have a bad efficiency but eventually you can pull out your insert from the gel and clone it in a vector for a prep.


Will the heart keep beating if it's separated from the body? The heart is a vital organ in our body, as it drives blood circulation. I was wondering if a heart keeps beating if it is separated from the body? If yes, then why?

Short version
The heart  has the ability to beat independently of the brain as long as it has oxygen. The heart will eventually stop beating as all bodily systems begin to stop working shortly after brain death. Remember the heart can beat, but your diaphragm and lungs wont. hence the cardiac muscles undergo asphyxiation and die off. However, immediately after death, there is enough oxygenated blood in the body to keep thing moving for a while

Long version
There is a simple explanation why.

As you know every muscle in the body has to receive stimuli from the neuromuscular junctions (and subsequently the nervous system) in order to contract.

The heart is a bit different in that it is not regulated by the brain, but the regulatory mechanisms lie within the heart itself. The heart conductive system contains a special group of cells called the pace maker cells (SA node) that fire at regular intervals and cause the heart to beat.

  Each heart beat is triggered by an electrical pacemaker - a group of cells in the heart that have the ability to generate electrical activity. They cause electrical impulses to spread over the heart and make it contract.
  The largest natural pacemaker of the heart is called the sinoatrial or SA node and is found in the right atrium. From it, specialised groups of cells that carry the electrical charge lead off to the rest of the heart.

(Taken from here)

The brain regulates the rate of the heart beat sure, but it does not send the signals that cause the heart to beat in itself.

In short, even after disconnection, the SA node still sends the impulse down the AV node and purkinje fibres that spread out across the cardiac musculature and cause them to contract, causing the heart to beat. This will continue for a while till they run out of energy and stop.

You can read more about it here:Wiki


How can (or did) Deinococcus radiodurans continue to evolve after developing resistance to mutation? Deinococcus radiodurans has a remarkable ability to resist damage to its DNA due to radiation, dehydration or (to my knowledge) any other source. It keeps multiple copies of its genome and has a repair mechanism as well.

My question is: how could this thing evolve to be so sophisticated at preventing the processes behind evolution? It seems that a mechanism to prevent errors would also prevent changes, so that as soon as the organism got OK at preventing changes it wouldn't be able to evolve to get better at it. Were genes for these processes borrowed from other extremophiles? Is the assumption that it was in such extreme environments that the damaging influences were keeping up with the repair mechanisms? That's my guess, but I'd love to hear from others with more knowledge of evolutionary processes.

According to the "Functional adaptation" section of this webpage, Deinococcus radiodurans uses repair proteins to stitch up DNA after radiation damage. Meaning, after a burst of radiation, the DNA will be in pieces and the repair proteins put it back together. It seems like this mechanism would not come into play during other forms of DNA mutation that happen during replication, such as point mutations or inversions.


Is the occurrence of a particular enzyme in a given subcellular location a random phenomenon? Enzymes occur in different subcellular locations. Some are specific to a given subcellular location, whereas others are heterogeneously distributed. What evolutionary decisions influence the occurence of enzymes in particular compartments?. Are the locations species-specific?

There are various methods for targetting proteins to subcellular organelles or membrane locations. In general they depend on ‘tagging’ or ‘signal’ sequences in the proteins. Such tags or signals are recognized by specialized proteins that are able to conduct the protein through the membrane barrier to the particular location.

The individual processes for different target locations vary, so I do not think it appropriate to provide details here. You can read a summary of them in this Wikipedia article. For more extensive treatment you can look at the relevant chapters in Lodish et al.  or in Alberts et al. on-line (old edition).

(Please consider donating to Wikipedia, if you use it.)


How long does antibiotic-dosed LB maintain good selection? Various people in our lab will prepare a liter or so of LB, add kanamycin to 25-37 mg/L for selection, and store it at 4 °C for minipreps or other small cultures (where dosing straight LB with a 1000X stock is troublesome).  Some think using it after more than a week is dubious, but we routinely use kan plates that are 1-2 months old with no ill effect.

How long can LB with antibiotic such as kanamycin, chloramphenicol, or ampicillin be stored at 4 °C and maintain selection?

This Bitesize Bio article is very informative on this issue.  The 1970 study they cite found negligible reduction in the the efficacy of non-beta-lactam antibiotics (kanamycin, chloramphenicol) over spans of 4 weeks or 60 days.  Ampicillin loses about 10% activity at 4 weeks.

In my lab, we only take care not to use LB/Amp plates that are older then 4 weeks, for LB/Km, we store them at 4 °C for more then a month, sealed in a plastic bag.


Are free-nuclear division and endomitosis the same? As far as I understood it, both are cases of karyokinesis, not followed by cytokinesis.

No. If you google the terms you'll get a lot of sites with definitions. For example:

Nuclear division
Definition
noun
The process by which a nucleus divides, resulting in the segregation of the genome to opposite poles of a dividing cell.

source: http://www.biology-online.org/dictionary/Nuclear_division
Edit:
or

free nuclear division    mitotic division of nuclei without accompanying cytokinesis, i.e. nuclei divide in a common cytoplasm, the cells walls only forming around each later

source: http://ecflora.cavehill.uwi.edu/bio_courses/bl14apl/Gloss.htm
versus

endomitosis
mitosis taking place without dissolution of the nuclear membrane, and not followed by cytoplasmic division, resulting in doubling of the number of chromosomes within the nucleus.

source: http://medical-dictionary.thefreedictionary.com/endomitosis
or a bit more revealing:

Duplicated chromosomes produced by endomitosis exist as discrete units
in a single polyploid nucleus or may be packaged into separate nuclei,
depending on the phase at which mitosis is aborted

source: http://en.wikipedia.org/wiki/Endoreduplication
So as you see by definition nuclear division is part of a bigger process (cell division), and accoriding to the first source karyokinesis is a synonim for nuclear division (karyo = nucleus kinesis = moving, both come form greek language).
Edit:
If you check the definition above, you can see that free-nuclear division is a mitosis without cytokinesis, thus chromosome separation still occurs.
In endomitosis the can end up with a polyploid nucleus, in contrast to the other two aforementioned mechanism where no polyploidy occurs.


Do gene expression levels necessarily correspond to levels of protein activation? I have seen a lot of research into molecular mechanisms of diseases/phenotypes use measures of RNA as a 'proxy' for the level of protein available in the cell. Is this actually valid?

My problem with the assumption that RNA levels correlate with that of the active product (i.e. the protein) is that a lot of post translational regulation occurs, including co-factor binding and phosphorylation, to name but 2. Does anyone know of any studies that have looked into the correlation between RNA levels and protein levels, and separately into the correlations between RNA levels and active protein?

It makes sense to me that RNA would correlate with protein certainly, but whether this relates to the proteins active function is what I wonder - i.e. there could be a pool that is replenished as and when the protein levels drop, but the proteins are only actually active for short periods in response to specific stimuli. So, does anyone know of any studies that have looked into the correlation between RNA levels and protein levels, and separately into the correlations between RNA levels and active protein?

Update (04.07.12)

I have not accepted any answers as yet because none address my question about levels of protein activation, but I concede to Daniel's excellent point that proteins are not all activated in the same way; some are constantly active, some require phosphorylation (multiple sites?), some binding partners... etc! So a study looking at 'global' activation is not yet possible. Yet I was hoping that someone may have read some specific examples.

I today found an unpublished review by Nancy Kendrick of 10 studies that have looked at the correlation between mRNA and protein abundance - still not relating to activation. However she finishes the paper as follows;

  The conclusion from the ten examples listed above seems inescapable:  mRNA levels cannot be
  used as surrogates for corresponding protein levels without verification.

If this is her conclusion about protein levels, then any correlation between protein activation and mRNA abundance seems unlikely (as a rule. Some protein levels do correlate with the RNA - see the paper).

I am still interested in any answers that give any information about specific examples of protein activation and mRNA levels - it seems highly unlikely there are no such studies, but I have been as yet unable to find any!

It has been well established that mRNA abundance serves as a poor proxy for protein abundance in most cases. This paper on yeast and this paper on cancer both establish this, although using older techniques (SAGE and microarrays, respectively), while this more recent review discusses the topic in light of more recent technologies (e.g. RNA-seq).

Perhaps the difficulty with exploring the correlation between mRNA levels and levels of active, mature proteins is that we still know so little about so many proteins and and what makes them active and mature versus inactive, premature, etc. Not all proteins need post-translational modifications to be active, but some do. Currently, this is investigated on a very detailed protein-by-protein basis (as far as I know), so gathering enough data for a large-scale study could take a long time. On the other hand, there are a variety of (increasingly affordable) high-throughput methods for measuring the abundance of thousands of RNA species simultaneously. I think people are using mRNA levels to estimate expression not because it's the most biologically cogent course of action, but rather because it is much easier, more affordable, and more high-throughput (which is all the rage these days).


Blast output - program to count the number of hits I have to use the old version of Blast (not Blast+) to compare DNA sequences and I have to know the number of all hits. They are not given in the header and I have to know them for many many of blast outputs and its nearly impossible to count them (or to export them in excel). I think I probably have to write a 'Perl Script' and I did my best but I am not familiar with programming and it is not working. Furthermore I had a look on the internet and they are always comparing it to BIO Search. I have e code, which for me looks pretty good,but it also done a comparison with BIO Search, what I don't need/want.

use strict;
use warnings;
use Bio::SearchIO;

Usage information

die "Usage: $0 <BLAST-report-file> <number-of-top-hits> <output-file>\n", if (@ARGV != 3);

my ($infile,$numHits,$outfile) = @ARGV;
    print "Parsing the BLAST result ...";
    my $in = Bio::SearchIO->new(-format => 'blast', -file => $infile);
    open (OUT,">$outfile") or die "Cannot open $outfile: $!";

# print the header info for tab-deliminated columns
print OUT "query_name\tquery_length\taccession_number\tlength\tdescription\tE value\tbit score\tframe\tquery_start\t";
print OUT "query_end\thit_start\thit_end\tpositives\tidentical\n";

# extraction of information for each result recursively
while ( my $result = $in->next_result ) {
    # the name of the query sequence
    print OUT $result->query_name . "\t";

        # the length of the query sequence
        print OUT $result->query_length;

        # output "no hits found" if there is no hits
        if ( $result->num_hits == 0 ) {
      print OUT "\tNo hits found\n";
         } else {
      my $count = 0;

                # process each hit recursively
        while (my $hit = $result->next_hit) {
            print OUT "\t" if ($count > 0);
                            # get the accession numbers of the hits
       print OUT "\t" . $hit->accession . "\t";
                        # get the lengths of the hit sequences
                        print OUT $hit->length . "\t";
                            # get the description of the hit sequences
       print OUT $hit->description . "\t";
                        # get the E value of the hit
            print OUT $hit->significance . "\t";
                            #get the bit score of the hit
       print OUT $hit->bits . "\t";

                        my $hspcount = 0;

                        # process the top HSP for the top hit
            while (my $hsp = $hit->next_hsp) {
                            print OUT "\t\t\t\t\t\t\t", if ($hspcount > 0);
                             # get the frame of the query sequence
        print OUT $hsp->query->frame . "\t";
                                # get the start and the end of the query sequence in the alignment
                print OUT $hsp->start('query') . "\t" . $hsp->end('query'). "\t";
                                # get the start and the end of the hit sequence in the alignment
                print OUT $hsp->start('hit') . "\t" . $hsp->end('hit') . "\t";
                                # get the similarity value
                printf OUT "%.1f" , ($hsp->frac_conserved * 100);
        print OUT "%\t";
                                    # get the identity value
        printf OUT "%.1f" , ($hsp->frac_identical * 100);
                    print OUT "%\n";
                                $hspcount++;
                            }
       $count++;

                        # flow control for the number of hits needed
            last if ($count == $numHits);
        }
        }
}
close OUT;
print " DONE!!!\n";

May someone help me, please. I need a program, which first tells me the header and then the number of hits. I am a little bit desperate and would be so happy if someone can help me. That would be so nice. Greetings Tina

This script, named blast2table.pl is from the code accompanying the Blast book by Korf & Yandell (there is a 3rd author whom I haven't met).

#!/usr/bin/perl -w
use strict;
use Getopt::Std;
use vars qw($opt_p $opt_b $opt_e $opt_m $opt_n);
    getopts('p:b:e:m:n:');
    my $PERCENT = $opt_p ? $opt_p : 0;
my $BITS    = $opt_b ? $opt_b : 0;
    my $EXPECT  = $opt_e ? $opt_e : 1e30;
my $START   = $opt_m ? $opt_m : 0;
    my $END     = $opt_n ? $opt_n : 1e30;

my ($Query, $Sbjct);
my $HSP = "";
    while (<>) {
        if    (/^Query=\s+(\S+)/) {outputHSP(); $Query = $1}
        elsif (/^>(\S+)/)         {outputHSP(); $Sbjct = $1}
        elsif (/^ Score = /) {
            outputHSP();
            my @stat = ($_);
            while (<>) {
                last unless /\S/;
                push @stat, $_
            }
            my $stats = join("", @stat);
            my ($bits) = $stats =~ /(\d\S+) bits/;
            my ($expect) = $stats =~ /Expect\S* = ([\d\.\+\-e]+)/;
       $expect = "1$expect" if $expect =~ /^e/;
            my ($match, $total, $percent) = $stats =~ /Identities = (\d+)\/(\d+) \((\d+)%\)/;
            my $mismatch = $total - $match;

        $HSP = {bits => $bits,
                    expect => $expect,
                    mismatch => $mismatch,
                    percent => $percent,
                    q_begin => 0,
                    q_end => 0,
                    q_align => 0,
                    s_begin => 0,
                    s_end => 0,
                    s_align => ""};
        }
        elsif (/^Query:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{q_begin}  = $1 unless $HSP->{q_begin};
            $HSP->{q_end}    = $3;
            $HSP->{q_align} .= $2;
        }
        elsif (/^Sbjct:\s+(\d+)\s+(\S+)\s+(\d+)/) {
            $HSP->{s_begin}  = $1 unless $HSP->{s_begin};
            $HSP->{s_end}    = $3;
            $HSP->{s_align} .= $2;
    }
}
outputHSP();

sub outputHSP {
    return unless $HSP;
        return if $HSP->{percent}  < $PERCENT;
        return if $HSP->{bits}     < $BITS;
        return if $HSP->{expect}   > $EXPECT;
        return if ($HSP->{q_begin} < $START or $HSP->{q_end} < $START);
        return if ($HSP->{q_begin} > $END   or $HSP->{q_end} > $END);
        foreach my $field ('percent', 'q_align', 'mismatch', 's_align', 'q_begin', 'q_end', 's_begin', 's_end', 'expect', 'bits'){
        print "$field not defined\n" if not defined $HSP->{$field};
        }
        print join("\t", $Query, $Sbjct, $HSP->{percent}, length($HSP->{q_align}), $HSP->{mismatch}, countGaps($HSP->{q_align}) + countGaps($HSP->{s_align}), $HSP->{q_begin}, $HSP->{q_end}, $HSP->{s_begin}, $HSP->{s_end}, $HSP->{expect}, $HSP->{bits}), "\n";
    $HSP = "";
}

sub countGaps {
    my ($string) = @_;
        my $count = 0;
    while ($string =~ /\-+/g) {$count++}
        return $count;
}


Is Mutation Theory still "valid" for complex organisms? I'm afraid like most people I suffer from having learned "A History of Evolution" in school, rather than cutting to the chase and learning the actual "up to date" version of the subject. (Imagine if programming classes did the same thing and you were forced to learn FORTRAN and BASIC before learning JavaScript) So please help me fill in some gaps:

From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.

It is possible to introduce new genetic changes through mutations. When asexually reproducing organisms receive a mutation, they pass that mutation on to their offspring. Mutations are somewhat rare, and beneficial mutations even less so, but happen frequently enough to make a dent over a long period of time.

The problem I don't understand is with larger organisms, aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents*? At the very low probability of a beneficial mutation occurring in a single cell of a male's leg, not only is it unlikely he would benefit by this mutation, but even if the male reproduced, this mutation wouldn't be passed on, and would die with the male.

Are mutations viable methods to introduce new variations in more "complex" organisms that reproduce sexually? Or is there another theory or system that bridges Natural Selection and Mutation Theory in larger organisms?

Change in genetic variance

  From what I have been taught, Natural Selection (or even Artificial Selection) is great for panning favorable genes from a species and bringing them to the fore, however, it does not introduce new genetic changes.

Yes, you are pretty much right. In a given population, directional selection will ultimately reduce genetic variance (Natural Selection selects for a few variants letting the other variants disappear and therefore diminishing the genetic variance) while mutations bring variance back to the population on which further selection can occur.

To go slightly further (but without developing this part too much): Genetic drift decrease genetic variance (on average). Balancing selection (such as negative frequency-dependent selection or spatially heterogeneous selection for examples) help to retain variation (but never create more variation) in comparison to what genetic drift alone would do. Different kind of spatial population structure also affect patterns of genetic variation. The important point to understand is that in an isolated population, mutation is the only process that can create new variants.

Mutations in multicellular organisms - Somatic vs. Germaline mutations

You seem to call complex organism what we usually call multicellular organisms. You are very right that some mutations might be passed on while others won't.

As you said, a mutation occurring in the left leg will never be found in your gametes. We call such mutations that can't be passed on somatic mutations. On the other hand, mutations that can be passed on are called germline mutations. Of course, in unicellular individuals, all mutations are germline mutations.

  [..] aren't those already rare mutations only passed onto offspring if they occur in the short-lived sperm or egg cells of one of the parents

Germline mutations are not only mutations that occur in the eggs or the spermatozoids (egg and spermatozoids are called gametes). Germline mutations are any mutation within the lineage of the gametes. For example, a mutation that occurs during mitosis during the morula phase on the right cell is also a germline mutation. A mutation that occurs in the testis during the division of a cell type Ad spermatogomium to give rise to another type Ad spermatogomium and a type Ap spermatogomium is also a germline mutation (see figure at the bottom of this answer and see the Age-specific mutation rate section). There are therefore tons of divisions during which germline mutations can occur in big multicellular organisms, while (germline) mutations can occur during only the single cellular division in unicellular organisms.

How many new mutations do humans passed on to their offsprings?

Generally speaking, the germline mutation rate per nucleotide is around $10^{-8} \text{or } 10^{-9}$ but don't consider this value too much as the per nucleotide mutation rate varies a lot between species and especially between different genomic regions. FYI, the haploid human genome (just to consider an example) consists of about 3 billion ($3\cdot 10^9$) base pairs.

The number of new mutations per offspring in humans is a Poisson distribution with mean and variance of about 100 mutations (this estimate might be quite inaccurate). This is maybe more mutations that you may have expected.

Age-specific mutation rate

There are typically a lot of cellular divisions happening in the testes in order to produce the very important number of spermatozoids a male produces in his lifetime (See figure at the bottom of this answer and see spermatogonium). Mutations also occur during those divisions and therefore we observe a correlation between the age of the father and the number of new mutations transmitted to the offspring. Hong et al. (2012) suggest using the following formula. The number of new mutations transmitted to the offspring by the father in humans is equal to $25 + 2(g-20)$, where $g$ is the age of the father. Of course, this is just a formula that matches quite well the observations but has no theoretical meaning. This formula applies only to males that are older than 20 years old.

Drake's rule

Empirical observations show that the higher is the number of base pairs $n$, the lower is the per-base-pair mutation rate $\mu$. This correlation between $n$ and $\mu$ is roughly linear with a slope of about 1. In other words, the genome-wide mutation rate $U = \mu \cdot n$ is more or less constant in all species. This correlation is referred to as Drake's rule and again, it is a rough approximation of a more complex reality.

Sexual reproduction vs Asexual reproduction

I am not exactly sure why you are talking about sexual reproduction in your post. Note that the mutation rate during meiosis (a process that occurs during sexual reproduction) is much higher than the mutation during mitosis.

Mutational effects

The mutation effect is the effect of a given new germline mutation. Of course, not all mutations have the same effect and there is, therefore, a distribution of mutational effects. Most recent studies (often mutation accumulation experiments) tend to show that a highly skewed gamma distribution (the negative exponential distribution is a special case of the gamma distribution) is a good fit to model the distribution of mutational effects of either beneficial or deleterious mutations. So the whole distribution of mutational effects is estimated to be best modeled by a gamma distribution for the beneficial mutations and a reversed gamma distribution for the deleterious mutations put side by side (where the density probability of having a perfectly neutral mutation is at the intersection of the two gamma distributions). The exact parameters for those distributions are likely to vary depending on the species but most likely depending on the exact stretch of DNA under consideration. Different papers offer different estimates (the work of P. Keightley on the subject is particularly influential). You might want to have a look at this answer for a summary of empirical data on mutational effects... The two gamma distributions need to be rescaled to make sure that the whole thing sums up to one and I don't know of any paper that suggest actual parameters for this rescaling.

Probability of fixation

Fixation is the event of a given allele (=variant of a gene) to reach a frequency of 1 in the population. In other, one allele is fixed, whenever at the locus (=genomic region of arbitrary size) under consideration is not polymorphic anymore in the population. The probability of fixation of a given mutation is a very important statistic. Let's call $s$ the mutation effect (if $s>0$, the mutation is beneficial). The probability of fixation of a neutral mutation given the population size is $P(s=0 | N) = \frac{1}{2N}$ (assuming a diplontic life-cycle) as it can be demonstrated from Coalescent theory, Wright-Fisher model of genetic drift or Moran (birth-death) model. The probability of fixation of a beneficial mutation is higher, while the probability of fixation of a deleterious mutation is lower. Those probabilities can be estimated with different techniques that use different assumptions: Haldane's technic (assuming that the number of offspring follows a Poisson distribution), Kimura's technic (using diffusion equations), Birth-death models, etc... Some methods assume small values of $s$, some others assume that $2Ns >> 1$, etc..

Number of new mutations in the population and rate of neutral substitution

If the genome-wide mutation rate for neutral mutations is $U_n$ and the population size is $N$, then there is a Poisson distribution of the number of new mutations at each generation with mean and variance $2 \cdot U_n \cdot N$ (assuming a diplontic life-cycle). Because each one of these mutations has a probability $\frac{1}{2N}$ to get fixed, the rate of neutral substitution in this population is $\frac{1}{2N}\cdot 2 U_n N = U_n$. Therefore, the rate of neutral substitution is a function of the genome-wide neutral mutation rate only. This classic result is used in estimating time since the last divergence between sister lineages (molecular clock)

Did you say Mutation Theory?

I have never heard of Mutation Theory. I am pretty sure Mutation Theory is NOT an existing concept (but the question is clear).

Spermatogonium figure


Indestructible Super Shrimp How are shrimp and other animals able to not be crushed by the 1000x greater pressure at the bottom on the Mariana trench?

Wiki says the trench is home to "large living creatures such as a sole or flounder about 30 cm (1 ft) long, and shrimp"

I understand natural selection, but what features has evolution "selected" that enable soft flesh and bones to not be instantly crushed like our own skulls would be at that depth?

Aquatic animals brethe the water around them and this equalizes their body pressure with that of the surrounding environment.

This is how you can still find say a piece of pottery or a watch from a shipwreck... They are filled with water and don't experience the pressure.

Such pressures do affect humans because we breathe air and so we can't adapt to pressures underwater and we need a shell that allows the ship environment to be tolerable for humans beyond a couple of hundred feet or so.

I think the change of pressure would also affect fish or other animals If they dropped in depth too quickly.


What is the very hard sphere inside the eye of many common fish made of and how is it called? Inside the eye of many common fish, like tuna, scad, snapper, actually probably all fish I have eaten, is a small sphere made of some very tough substance. This sphere is even hard to crush with teeth, and seems to be made of homogeneous material. That is after the fish is cooked, not sure how it is uncooked. It is immersed inside a quite soft, almost liquid substance inside the eyeball.
Is that the lens, or is the whole soft semi-liquid tissue the lens?
What substance is the small tough sphere made of? I imagine some type of proteins, but what type of proteins exactly?

From what you describe, it seems the hard sphere is the lens and the semi-liquid substance is the vitreous humour. Like the lens of other vertebrates, the fish lens is made of lens fibres—cells rich in proteins called crystallins.
For more on the anatomy of fish eyes, you could read this page and watch this dissection video.


Counter Staining with Safranin After Gram Staining,
We use counter staining to find out that is there any gram(-) bacteria present on the prepared slide.

My question is-

What component in the cell wall of gram(-) bacteria is responsible for the retention of Safranin dye?
Like the Techoic Acid is responsible for the retention of CVI complex in gram (+) bacteria.

As I have just studied the staining process,any additional useful information is appreciated.

Thanks!

Safranin is retained, very much like Crystal violet, by the peptidoglycans in the cell wall. However, the main difference is the thickness of the peptidoglycan layers in Gram positive and Gram negative bacteria.

Gram positive bacteria, due to their thicker peptidoglycan layer, have a higher affinity to and retention rate of crystal violet. On the other hand, Gram negative bacteria, due to a thinner peptidoglycan layer cannot retain crystal violet as well and are more likely to retain safranin.


What prevents the human intestine from 'exploding' as a consequence of bacteria growth? Usually bacteria grow by dividing and they can do that very fast. So after a couple of hours or days you have many bacteria in your intestines.
And we keep feeding them by eating. In some way you would expect that the growth of bacteria has been so overwhelmed that after a week our intestines would 'explode'.

Of course this doesn't happen, but what factors protects our intestines from bacteria overgrowth?

Bacteria can't create mass, even when they divide. During division, you go from one "big" bacterium to two "little" bacteria, which then have to accumulate nutrients and grow bigger before they can divide again.

When nutrients are plentiful, this can happen rapidly, and you do see exponential growth. But the exponential growth phase is only valid when there is an excess of food in the environment. Bacterial growth curves follow a typical lag/log/stationary/death profile. The log (exponential) phase only applies when nutrients are in excess. Whenever some nutrient becomes limiting (because it's already incorporated into another bacterium, for example) the bacteria switch to stationary phase growth, and reduce replication or stop it completely.

So you would never get an "explosion" of intestinal bacteria - the bacterial mass is strictly limited to the amount of mass (food) input into the system. Once that's all (or mostly) converted, the bacteria will stop growing and start dying.

If you kept accumulating mass in your intestine, you're correct that eventually it would "explode". However, most people regularly (pun intended) eliminate excess intestinal contents. (Which, as bpedit mentions in their answer, contains a high proportion of bacterial cells.) This limits the total mass contained in the intestine, and keeps it from "exploding".


S. pyogenes' skin infection diagnostics S. pyogenes is "flesh-eating" bacteria.
It results from life-theatening myonecrosis caused by this organism.
S. pyogenes avoids phagocytosis (mediated primarily by capsule, M and M-like proteins, C5a peptidase), adhere to and invade host cells (M protein, lipoteichoic, F protein), and produce toxins (streptococcal pyrogenic exotoxins, steptolysin S, streptolsin O, streptokinase, DNases).

Suppurative diseases: pharyngitis, soft-tissue infections.

Erysipelas: localised skin infection with pain, inflammation, lymph node enlargement and systemic symptoms.

Cellulitis: infection of the skin that involves the subcutaneous tissues.

Necrotising fasciitis: deep infection of skin that involves destruction of muscle and fat layers.

I think these are most its skin infections. But what about its diagnostics?

I think take biopsy from living tissue, not from necrotic.
If pus, then probably from it.
I think we can do Gram staining, recognise gram-positive cocci like in a string
Then, we can do hydrogen peroxide test - if no bubbles, then suspicion to S. pyogenes, since catalase negative.
The do optochin test which is positive for S. pyogenes.

What is the correct procedure for doing skin infection diagnostics for group A streptococci?

S. pyogenes cultured on Blood Agar should show beta-hemolysis. B-hemolytic colonies can be further identified as S. pyogenes by the results of negative catalase (hydrogen peroxide) test, positive L-pyrrolidonyl arylamidase (PYR) reaction (1) and sensitivity to Bacitracin (2). See https://www.inkling.com/read/medical-microbiology-murray-rosenthal-pfaller-7th/chapter-19/streptococcus-pyogenes

PCR may also be used: http://www.sciencedirect.com/science/article/pii/S0923250805000215


A question regarding evolution I'm not a biologist so bear with me. I know that the DNA molecule carries extremely large amounts of information. If the process of evolution is driven by completely random process .I think about it as the complex interactions between environment and random genetic mutations that leads to natural selection.
I've two questions:

What's the probability of evolution of intelligent human beings within this scenario? I've heard that the probability of spontaneous generation of a good protein molecule should be nil in our universe: is this correct ?

If the process of evolution is driven by completely random process...

It's not.  The evolution of "better" protein (and other) molecules happens because of selection, a very non-random process.  The repeated selection of better molecules, and then of the variants of the better molecules, repeated many times, will lead to "good" molecules (in the sense that they work better for their producers).


Staying underwater: would mutual rebreathing help? If two people want to stay underwater for as long as possible, could they last longer if they exchange breaths in turns (ie: through a simple tube or mouth-to-mouth) than if they simply hold their breaths alone?

Would there be any dangers in doing this somewhat regularly?

Theoretically:
I'm going to assume that in your scenario, both individuals took a deep breath of regular air before submerging themselves, as this changes quite a lot (you'll see why in a second). Regular air on Earth as you probably know is made up of 78% Nitrogen, 21% Oxygen, and other trace elements like CO2 and ArgonColumbia University. What we care about is oxygen, as this is what our body can't function without.

The air we exhale is approximately 14-16% oxygen [2], which is a significant decrease, but is still very breathable. If we choose 15% as the exhaled percentage and 21% as the inhaled percentage, the percentage decrease is approximately 29%. Thus, with each breath taken by the other individual the amount of oxygen in the shared air decreases drastically. Another problem is the dilemma of CO2, which is exhaled at a 5% percentage increase. I would imagine the two people wouldn't make it more than a minute before the oxygen level in the shared air is too little to be absorbed and the CO2 makes them both lightheaded to the point where they faint and forget about the tube altogether.

If both individuals had breathed in pure 100% oxygen it would delay their impending deaths but it wouldn't prevent it. I love doing this sort of stuff and could calculate the difference in time between both before the air is unbreathable but...

Practically:
It wouldn't work. It may sound like something that would work but think about it this way: the very first breath one of them takes it literally sucking the air out of the other's lungs. No matter how much one tries to synchronize breathing in and out with the other -  based on lung size, lung volume, diaphragm surface area and many other factors - one's breathing in simply cannot equal the other's breathing out. One of them would eventually breathe in too much, leaving the other choking and gasping for air, leading to a tug-of-war of air, that unless they resurface will lead to both of them drowning.

[2]:
P.S.Dhami; G.Chopra; H.N. Shrivastava (2015). A Textbook of Biology. Jalandhar, Punjab: Pradeep Publications. pp. V/101.


Why aren't green eyes more prevalent? Why aren't green eyes more prevalent, given that the green allele is dominant over the blue one?

My understanding is that human eye colour is determined by two genes:

1) HERC2, with alleles Bx, BB or xx,
2) gey, with alleles GG, Gb or bb,

where

B means brown
x means not brown (this is less confusing than using b for blue here, because having no B allele in HERC2 doesn't necessarily give someone blue eyes; their eyes will be either blue or green depending on the gey gene)
G means green
b means blue.

Capital letters stand for alleles that are dominant; lower case, ones that are recessive.

So the 'algorithm' goes:

1) look at HERC2; if it's anything other than xx, you've got BROWN eyes
2) if HERC2 is xx, look at gey; if it's anything other than bb, you've got GREEN eyes
3) still here? then you've got BLUE eyes

My question is this: why is it that green eyes are so rare if the green allele is dominant over the blue one? When a blue-eyed person and a green-eyed person interbreed, their offspring will either be equally likely to have green eyes as blue (if the green-eyed parent is Gb) or always have green (if that parent is GG).

But many more people have blue eyes than green eyes, despite blue being recessive to green.

The obvious answer is that people with blue eyes (xx bb) and people with green eyes (other xx-ers) have tended to avoid breeding with each other to a large extent. Is any other explanation in the ring? Perhaps the greens are catching up?

A gene being dominant does not necessarily imply the gene is also common.

An easy counterexample is Huntington's disease. The gene is dominant, and only one mutant allele of huntingtin would result in development of the disease. However, the allele prevalence of the mutant is low in the general population.

In the absence of a selective advantage of green eyes over blue eyes, the two alleles of the gey gene should remain in genetic equilibrium, and therefore the number of people with green eyes will not increase. In fact, a similar misunderstanding applies to the disappearance of blondes/redheads. In both cases, the allele frequencies will remain unchanged in the absence of selection pressure.

The initial imbalance in the allele frequency could be due to many reasons. Population bottlenecks, genetic drift, and historical selection pressure could all be valid answers.


Does an increase in cancer cell traction forces increase metastasis of the cancer cells? I am not very familiar with biology, but I have read some articles about cell traction forces lately, where the cells are cancer cells. I found this very interesting, so I thought it might be nice to read about the relationship between cell traction forces and metastasis for cancer cells. I thought that an increase in cancer cell traction force should indicate that there would be more metastasis. I have looked at two references, but one of the articles says that increasing the cell traction force increases metastasis [Kraning-Rush et al. (2012)], while the other says the opposite [Indra et al. (2011)]. Both are experimental articles.

My question is therefore:

Is it correct that most often, an increase in cancer cell traction forces would increase metastasis, or should it most often decrease metastasis?

You have pointed out in your question that two different research groups have differing conclusions about your question.  The answer is not known which is why they are studying it.

Their differing results probably turn on how cell traction force is defined and the experimental system used to measure it.  It may not even be consistently ture - for example metastasis via the lymphatic system may be mediated by different properties than metastasis through the bloodstream or local tissue invasion.


Why can't neurons undergo cell division? Many cells in the human body can divide and reproduce, making healing possible. Neurons, however, cannot reproduce, which makes diseases affecting the brain particularly crippling. Why can't neurons divide - that is, what makes them different from "normal" cells? Are there any ways to artificially stimulate neuron cell division?

Morphological point of view

Neurons cannot divide because they lack centrioles.

  Because centrioles function in cell division, the fact that neurons lack these organelles is consistent with the amitotic nature of the cell [1].

Functional point of view

New cells in the nervous system wouldn't do any good. The whole nervous system is based on interneuronal connections, so adding an extra neuron would mess up these connections and alter both the functionality and the "stored" information.

  Each nerve cell has a specific place in our nervous system. Its job is all about taking a signal from one specific place to another one. Adding new nerve cells would mess up these very specific connections in a very complex system [2].

References:

SEER Training. NERVE TISSUE. Available from http://training.seer.cancer.gov/anatomy/nervous/tissue.html
UCSB Science Line. Available from http://scienceline.ucsb.edu/getkey.php?key=1710


Species identification: 2.5mm (3/32" or 1.5/8") brownish ant in highrise apartment Can anyone please identify this ant?

In case it helps, 3 attempts of using Ortho Ant Bgon Max gel and bait has not helped.  They 2 were administered 2 weeks apart.  Apparently, it's basically borax and sugar water.

A respondent at this DIY Stack Exchange page referred me to "Ant Identification Keys" section at this site.  It seems that it may be a 2-node Big-Headed Ant, but it's hard to be sure.

Photos:

Update:

Location: Ottawa, Ontario (Canada); latitude 45 degrees north. It's an urban centre, and my highrise is by a main city street, but also with a creek on one side. I first noticed the ants in the kitchen in July, at the height of our summer heat, or perhaps at the tail end of it. I'm rent a 1-bedroom apartment on the 9th floor, facing the creek side and the major street.

Of possible relevance: The neighbour on my kitchen side says that he has never seen an ant. My unit is quite clean, with the only exception that I generate so little garbage that I change it infrequently. I spray inside with alcohol several times a day so that I'm not ravishing the environment by changing bags frequently. Most of the content are fruit/veggy peels/cuttings (no meats/fats or starch), and mostly oranges, which ants apparently hate. I've recently sprayed and wiped down the garbage in order to not use it until I've solved my ant problem.

Since paying close attention, I notice the ants on the floor and upper cupboards, whereas I only saw them before when they crossed the counter. Back then, I thought the ants were attracted to water from a leak that I found under the kitchen sink, or the dampened particle board due to water seeping from the rim of the sink. The latter would suggest carpenter ants, which like sweet things, like the borax/sugar mix that my store-bought baits were apparently based on.  However, the 2.5mm size of my foraging ants are much smaller than the 6-25mm described by this local federal government site.  My ants' 3/32" is also much smaller than the 6/32"+ C. sayi carpenter ant described here.

The leak has been repaired for about 2 months, and I've taken care to wipe up around the sink. No apparent relief from the ants, and the bait is mostly untouched. I'm wondering if the ants may be coming from elsewhere.  Upon reflection, however, I do recall seeing what might bhe the calling card of carpenter ants for years -- fine wood chips under some of the bottom hinges of the cabinet and cupboard doors in the kitchen.  It literally took years for them to accumulate to the point of noticability.  Maybe carpenter ants been visiting for years, and only this summer decided to move in.

According to the pest control expert, the ants are likely pharaoh ants.  It matches the description on the Wikipedia page in all respects:

Colour
Size
Pervasiveness in indoor environments throughout the world

He is treating the problem in my unit and a neighbour's unit using Maxforce Quantum.  It could take some time :( .

This is not conducive to a fitness regime of pushups, situps, leg lifts, and side planks (all on the ground, of course).  It doesn't help that my apartment largely has wall-to-wall carpeting coloured with a brown and white texture.  Spraying down the vicinity with vinegar is unlikely to help, as the ants have clearly demonstrated a lack of repulsion from vinegar droplets.