Can Fluoride be absorbed into the blood from within the mouth without swallowing? I'm having a discussion with somebody regarding Fluoride usage. I told him that even if he doesn't like the idea of ingesting it, brushing and spitting it out will do you no harm. He then said this:

You have missed the point of ingestion massively! Brushing with fluoridated paste is NOT fine.
The mouth, with its gum entry and under tongue glands are the PERFECT entry point to the blood, without even swallowing? What do you think oil pulling is all about? Fluoride passes those barriers as easy as the shit that resides in your blood can!"

Now I call BS on this, but I'd just like an expert opinion with cited sources if possible. Can Fluoride be absorbed purely by the mouth without ingestion?

Although I'm having a hard time finding a source that provides specific information on fluoride in toothpaste, this review explains that fluoride is most readily absorbed through intestinal epithelia and that fluoride absorption through other tissues, such as oral epithelia, depends strongly on other chemical properties of fluoride-containing compounds: their

  "reactivity and structure, solubility, and ability to release fluoride
  ions."

This suggests that you would need additional information concerning the overall toothpaste formula.

This review shows the rates at which fluoride ions are released from various toothpaste formulations. Figures 2 and 3 show that the highest discharge rate is roughly 1.7ppm and the lowest was just under 0.5ppm, both occurring after a 24hr period. The authors note in the discussion that these measurements are likely higher than what would occur in the mouth, since they had to use deionized water for their experiments, in which fluoride is more soluble than in saliva.

Wikipedia lists fluoride toxicity levels as being between 0.5 and 1.0mg/L. Fluoride's molar mass is 18.9984 g/mol and this calculator shows that 0.5mg/L of fluoride translates to about 0.5ppm. While at first this makes the above results sound a dire, it's important to note that toothpaste remains on your teeth for far less than 24hrs and to remember that less fluoride is released into saliva than into deionized water.

Wish I could find better results on how much fluoride might be released during a typical toothbrushing session, but I'm inferring from the linked review that it would be small enough to not merit a health concern.

I emailed a dentist friend for more info and will update this post as I hear back from him.

As for the comment about glands, it's important to understand that the glands found in the mouth are secretory glands, which means that they are optimized for discharging fluids and not for accepting them.

--Update--

My dentist friend wrote back, confirming that no significant fluoride absorption occurs through the gums. From him:

  the only significant absorption would be through swallowing fluoride.
  Any that was just in the mouth would not be well absorbed...
  that is why we do the high dose swish and spit treatments is to avoid
  fluorosis but deliver sufficient fluoride to the teeth.

In short, it looks like the answer to your question is: no, fluoride is not significantly absorbed into the blood from within the mouth without swallowing.

Sorry I'm a lil late at finding this but thought I'd share two studies I found proving 'absorption of fluoride through the oral mucosa of rats'
https://doi.org/10.1016/0003-9969(68)90140-4
https://doi.org/10.1016/0003-9969(78)90219-4
*the second link is a study on radioactive fluoride.


Why sleep? No, actually, why wake? I was just reading the sleep threads, and I wondered, why is the body so constructed so that sleep is necessary? (Is it just a design error?) But then, how do things come to be awake at all? How did this happen? Yes, I can see the advantages, but how did it happen? What is "awake"? Are single-cell animals awake?

The question I want to ask is, how did things progress from just sitting around ingesting and growing, like plants, to being something more? Is it more? What do "wakers" have that the rest don't?

Sorry, I'm not a biologist, this may be a foolish question, or in the wrong place.

Based on various comments, I've expanded this answer. Though long, I cannot cover the depth of the topic of sleep but I tried to address the issues asked in the original question while broadly highlighting various aspects about sleep research. I welcome any suggestions for improvement.

What is sleep?

To know what it means to be awake, you must know what it means to be in a state of sleep. These are two alternative states for animals that sleep.

Finding a concise scientific definition of sleep is difficult, probably because sleep is a very complex process. For example, Diekelmann and Born (2010) state that,

  Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory...

and later

  Sleep is characterized by the cyclic occurrence of rapid eye movement (REM) sleep and non-REM sleep, which includes slow wave sleep (SWS, stages 3 and 4) and lighter sleep stages 1 and 2....

Most attempts to explain what sleep is include the four stages of sleep along with REM (rapid eye movement sleep). The stages are nicely explained by this National Institutes of Heath website on Brain Basics: Understanding Sleep. Each stage of sleep can be identified by specific types of brain waves, shown below (image from here).

Notice that the first wave pattern is characteristic of being awake.  The wave patterns change as an individual becomes drowsy and then falls asleep. While asleep, the brain cycles through the different stages, each with its characteristic brain waves.  Associated with these stages are changes in metabolic activity and physical capabilities. For example, the Brain Basics site notes that we become less responsive to external stimuli and metabolic activity slows. During REM, breathing becomes rapid and we can't move the muscles in our arms or legs. Similar states are found in other invertebrate and vertebrate organisms, which suggests that these are common indicators of sleep or a sleep-like state. Some examples of these states are given in the citations and links below.

Defining "awake" seems just as difficult as defining "asleep" but once again neural activity seems to be key indicator. As shown in the figure above, being awake has characteristic wave patterns in the brain that are distinct from the wave patterns associated with sleep. In addition, none of the physiological/physical states associated with sleep stages are present when you are awake.

In both cases, asleep and awake, the indicators seem to be based on characteristic neurological activities in the brain or, in the case of some invertebrtes, the organized nervous system.  This interpretation is important when considering whether organisms without any type of nervous system is capable of sleep or the alternate state: awake.  More on this at the end.

Why sleep?

Science magazine, in the 125th anniversary issue, made a list of 125 big questions that remain to be answered by scientists. One of those questions was "Why do we sleep?" The role of sleep remains elusive but many ideas have been put forth about the role of and the evolution of sleep. The leading idea seems to be memory consolidation. This article by Kavanau (1997) reviews ideas about the function of sleep and why it evolved.  He suggests that sleep and memory evolved as as ways to improve or maintain effective connections among the nerve cells in the brain. Some circuits are used frequently, such as those used to process sensory information like vision. Other circuits are used less frequency, such as circuits that can be used to store memories. Sleep may allow those infrequently used circuits to be activated and used without causing conflict with the circuits used during "restful waking." In other words, sleep may allow the lesser used circuits to be exercised, which can help to consolidate memories. So, at least one function of sleep may be to help maintain efficiency in how information is moved around the brain by maintaining the brain circuitry.  See also this review by Siegel (2005) and the previously mentioned article by Diekelmann and Born (2010).

This Scitable article has a nice overview of the importance of sleep for humans, as does the Brain Basics site.

What organisms sleep or have sleep-like activity?

Sleep has been well-studied in vertebrates, from fishes (Marshall 1972) to mammals (Pace-Schott and Hobson 2002). However, not all vertebrates necessarily sleep (Kavanau 1998). For example, continuously swimming fishes like some sharks and blind cave fishes may not sleep. These are just three references of many about sleep in vertebrates.

Sleep and sleep-like activity has not been as well studied in inertebrates. As noted in this thread, there is evidence for sleep in at least some insects. Cephalopods like octopuses show signs of sleep (Mather 2008). Caenorhabditis elegans, a nematode worm and model biological system, shows sleep-like states tht are similar to mammals and fruit flies (Raizen et al. 2008). The most basal organism that shows evidence of sleep-like patterns is a jellyfish called Chironex fleckeri (Kavanau 2006). Cnidarians like jellyfishes are the basal (most "simple") group of organisms with an organized nervous system. Interestingly, C. fleckeri process a lot of visual information obtained through their 24 eyes. Twelve of the eyes are simple, light-receiving structures but 8 of the eyes are camera-like, meaning they have a lens.  Kavanau (2006) argued that sleep (up to 15 hours) in this jellyfish allows time for its simple nervous system to process the visual information obtained while it is awake. The presence of sleep-like activity in jellyfish and nematode worms suggest that sleep is an evolutionarily ancient phenomenon.

This Wikipedia page on sleep in non-humans overviews evidence for sleep in vertebrates and invertebrates. It's not clear whether androids sleep or what they dream about if they do sleep.$^1$

Do single-celled organisms sleep?

This is (to me) a tricky question. Sleep is associated with specific types of neural activity in the brain or nervous system. In addition, sleep-like neural activity has been found in diversity of organisms with some type of nervous system, and seems evolutionarily old. I therefore think that any organism that has some form of organized neural center (brain, brain-like organ or centralized nervous system) has the potential to show some type of sleep-like patterns.

In contrast, organisms lacking any type organized nervous system would not be capable of sleep, at least as currently defined. If they do not sleep, then they also cannot be awake because being "awake" seems to be recognized as neural activity not typical of sleep.  Therefore, it seems to me that single celled organisms like bacteria and paramecium are neither sleeping nor awake.  Plants are neither sleeping nor awake. They are metabolically active but they are neither asleep nor awake because they do not have any type of neural activity.

I'm not a sleep researcher (but sometimes I am a sleepy one) nor am I a neurophysiologist. I just walked through my train of thought. I welcome contrary views along with the supporting science.

Literature Cited

Diekelmann, S. and J. Born. 2006. The memory function of sleep. Nature Reviews Neuroscience 11: 114-126.

Kavanau, J.L. 1997. Origin and evolution of sleep: Roles of vision and endothermy. Brain Research Bulletin 42: 245-264.

Kavanau, J.L. 1998. Vertebrates that never sleep: Implications for sleep's basic function.

Kavanau, J.L. 2006. Is sleep's 'supreme mystery' unraveling? An evolutionary analysis of sleep encounters no mystery; nr does life's earliest sleep, recently discovered in jellyfish. Medical Hypotheses 66: 3-9.

Marshall, N.B. 1972. Sleep in fishes. Proceedings of the Royal Society of Medicine (abstract).

Mather, J.A. 2008. Cephalopod consciousness: Behavioral evidence. Consciousness and cognition 17: 37-48.

Pace-Schott, E.F. and J.A. Hobson. 2002. The neurobiology of sleep: Genetics, cellular physiology and subcortical networks. Nature Reviews Neuroscience 3: 591-605.

Raizen, D.M. et al. 2008. Lethargus is a Caenorhabditis elegans sleep-like state. Nature 451: 561-572.

Siegel, J.M. 2005. Clues to the functions of mammalian sleep. Nature 437: 1264-1271.

Footnote

I could not resist.

All organisms (except viruses?) need some kind of nutrition to survive and reproductive activities for the species to survive. As humans don't do these while asleep in a first approximation I would consider those life phases as sleep when these do not happen. In this sense clostridium bacteria could be considered asleep when in their endospore states, a sunflower seed could also be considered asleep as it is inactive.


What is a pA(2) value? I saw this article http://www.ncbi.nlm.nih.gov/pubmed/16710314 and it mentioned pA(2) values and I had no idea what they were. What are they? What do they mean?

If possible it'd be just dandy if you could cite some journal articles/books/other reliable sources for me to dig up.

Digging around a bit, I found a few resources:

Design and models for estimating antagonist potency (pA2, Kd and IC50) following the detection of antagonism observed in the presence of intrinsic activity.

and PHARMACODINAMIC on page 30, describes pA2 as:

  indicates affinity of antagonist for receptors

(as Alan Boyd just commented on)

Below are responses generated using the isolated guinea-pig ileum preparation to determine a pA2 value for a sample of the cholinergic antagonist homatropine.
Responses are expressed in millimetres +/- SDM (n =4). Plot the data and then determine by Schild analysis the pA2 value and Schild slope. What conclusions can you draw; does the experiment/data fulfil the criteria for a valid Schild analysis?

Acetylcholine      ACH Alone    ACH +Homotropine       ACH +Homotropine   ACH +Homotrop
Concentration                     3x10^-9 M              1x10^8M            3x10^-8M
[Molar]

3 x 10^-9            3+/-1
6 x 10^-9            8+/-3            Not Response
3 x 10^-8            28+/-6             10+/-4             No response
6 x 10^-8            38+/-8             21+/-9           5+/-2                                                    No response
3 x 10^-7            55+/-5             43+/-7                27+/-9             10+/-4
6 x 10^-7            56+/-5             52+/-3              38+/-7             20+/-7
3 x 10^-6              -                55+/-4              53+/-6             43+/-6
6 x 10^-6              -                   -                56+/-2             54+/-5


Why didn't humans evolve to reproduce identical twins all the time? According to the selfish gene theory, it seems like because identical twins sometimes get produced, a mutation to a gene that says, "if you have an identical twin, be fully altruistic towards them" would get selected for when ever it happens to arise in an identical twin. After humans evolve to be fully altruistic towards identical twins, wouldn't a mutation to a gene that makes a woman more likely to produce identical twins also be selected for because if it happens to appear in a a child who has a non-identical sibling, that gene might be discontinued from reproduction by the partial selfishness of the sibling but if it appears in an identical twin, the other identical twin will preserve that gene with their altruism.

What you describe could have happened under the right conditions. However, there are a few things you haven't considered.

Because humans are especially altricial, always having twins would double the cost of children on parents.
The benefit of sexual reproduction is immune diversity. So a population like this could be far more vulnerable to disease.

So as far as this thought experiment goes, genes can't be too selfish or they dramatically reduce their own fitness. It's something worth simulating computationally to see what happens.

References

Sexual reproduction as an adaptation to resist parasites (a review)

If we produced identical twins all the time then we'd completely lose genetic diversity which would, I assume, overwhelmingly compromise our adaptive capabilities. Don't forget, those identical twins then need to reproduce with other identical twins of others families. Moreover, and this is the more obvious explanation, as a consequence deleterious recessive disorders would rapidly increase in rate.

For more, see
https://en.wikipedia.org/wiki/Inbreeding_depression
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109585

You might also like to study frequency dependent selection for why it is sometimes advantageous to have identical twins, albeit at a low rate.


Is it possible to consume O2 via a pill form to inhibit the need to breathe? Just wondering if it would be theoretically possible to consume oxygen via O2 pills, in the effort of being able to hold one's breath without limit.

Totally just curious.

The problem is volume and surface area for gas exchange.  The volume in a pill is puny compared to the amounts you pull in and out breathing.

But could you use something other than the lung for gas exchange?  The colon has a lot of surface area and the small intestine even more.  Maybe if you flooded your gut with an oxygenated fluid like that liquid fluorocarbon the mice breathe, or even oxygen saturated water you could get some of that out via your intestinal villi.  Dragonfly larvae do something like that, performing gas exchange with their rectums.  You would need to exchange the liquid at least as fast as you breathe, getting all the depleted liquid out and new oxygenated liquid in.

Some of those high colonic machines work like that, as I understand: fast in and fast out.  People might not notice you were holding your breath because they were distracted by the churning machine with the hose up your trouser leg.  Maybe you could pass out cards or wear a T-shirt explaining what was going on because you would still have to breathe to talk and that would ruin it.  If you do this would you please post video and link it up here?  Thanks.


Why are restriction sites palindromic in nature? Any restriction site given in any fragment of DNA or vector molecule is a palindrome. eg restriction site for the endonuclease EcoRI is

5'...GAATTC...3'
3'...CTTAAG...5'

Clearly, this is a palindromic sequence. Why is that?

Not all restriction sites are palindromes : https://en.wikipedia.org/wiki/List_of_restriction_enzyme_cutting_sites:_E%E2%80%93F#Whole_list_navigation

EcoRI: GAATTC (note that this is not 'palindromic' in the usual sense (e.g.'anna', GAATTC read backwards actually gives CTTAAG), but only if given the G-C A-T binding)

The double strand of DNA is composed of one strand in direction 5'-3' and another into the other direction (3'-5'). Restriction enzymes tend to be homodimers, thus would bind to both sides of the double strand, expecting the same recognition sequence. But as one strand runs into the other direction, the strands need to be palindromic to form a double strand.

So that these enzymes can recognize the sequence on the both strands. It's the mechanism bacteria have evovled to degrade the only double stranded RNA and not single stranded.


Can tardigrades survive being eaten? Compared to a tardigrade, the cockroach seems fragile.

But can tardigrades survive the acidic environment of being eaten by most animals?

In there natural state no, tartigrade have absolutely no way to survive the acidic content of stomachs and are fragile.

In their cryptobiosed form (extremely resilient form) there has been no research to determine if they could survive extremely acid environnements. The things that we know they can survive is:

Temperature
Pressure
Dehydration
Radiation
The outer space environnement
Toxins

However, very few organisms possess mechanisms to tolerate highly acid environnement since acid affect cell membranes by "attacking" mainly the proteins and lipids. These organisms have evolved these traits because they live in acidic environnements, tartigrades on the other side don't.

Another point to add is, entering cryptobiosed form takes time, if the tartigrade would be eaten in it's natural form, it wouldn't have the time to cryptobiose and thus it would die.

Tartigrades

I hope this gives you some useful information

That depends on how long it takes for the tardigrade to get from point A, your mouth, to point B, your rectum. Provided you aren't extremely allergic to tardigrades or eat something poisonous or die while digesting the tardigrade. Also provided you had unlimited time with the tardigrade in an area of your digestive system that does digest things, not point A or B, eventually the tardigrade will succumb to your body's attempts to kill/digest it.


Why can't we propose a solid theory regarding origin of life? What  information is greatly lacking which does not allow us to propose a  solid theory for origin of life ?

First of all, we do have some solid theories to explain the origin of life. That said, the main thing missing in order to be able to accept one of these theories with a decent amount of certainty is the ability to run a planetary scale experiment for a few billion years.

The theories are fine, the problem is that we cannot really test them. In order to test a theory that describes the origin of life, we will have to recreate the original conditions (think of a test tube the size of the Earth) and then pump energy into the system and watch what happens over the next few billions of years. This is not really feasible, for obvious reasons. I really doubt you will be able to get funding for an experiment that will run that long.

The reason for no single, solid origin of life (OOL) theory is that there are
many and none of them explain or resolve the overall or the detailed issues of OOL, encompassing wide differential and even conflicting approaches, e.g., reproduction vs metabolism, and RNA vs DNA. Further, all are using naturalistic processes, requiring validation by the laws of physics and experimentation. While there are numerous theories, they are either geochemically irrelevant or outside the laws of physics. Whether RNA world, panspermia, hydrothermal vents, small warm ponds, all embrace various levels of chemical evolution for the initial, intermediate and ultimate biochemical assembly of increasingly more complicated levels of organic elements considered vital to OOL. No viable processes have been found to naturalistically create life.

Increasingly, wild speculation of geochemical conditions and trivialization of biochemical assembly, metabolism and reproduction are being proposed. The intractable problems that apply to naturalistic theories begins with the fact that chemical evolution of non-living compounds produces no viable pathway to increased complexity, that is, there are no cosmic evolutionary processes capable of the complex structure, design, order and operation of biochemical systems required for even the simplest organism.

The universal challenges that must be fully resolved in all theories include:
1. The homochirality essential in nucleotide amino acids,
2. The homopolymerization of the DNA side chains,
3. The nucleotide coding using information design,
4. The cell membrane formation essential encapsulation.
5. The chicken and egg issue of proteins and complex structures.

These are affected by requirements for colocation. coincidence, contamination mitigation and concentrations that are absolutely precise.

Finally, lab experiments must accurately reflect geochemically relevant conditions and not overly manipulated by experimenters, which would simulate intelligent design but produce questionable results.

The number of sources that could be listed is extensive. A simple search internet of the main descriptive words would provide detailed definition and additional detail. Regarding the 5 universal challenges: 1. homochirality relates to the right/left handedness of the amino acids since they are not symmetric. DNA amino acids must be 100% left handed or DNA will not work. One of the challenges to get comprehensive sourcing is due to the reluctance of present biological entities to fully acknowledge the delineated intractable issues.


Why doesn't nitrogen diffuse into blood? In school, I have learnt that the deoxygenated blood brought in to the Alveoli by Pulmonary Arteries contains Carbon Dioxide. And that Carbon Dioxide present in the blood diffuses into the Alveoli and squeezed out with the help of Diaphragm.

Then, why doesn't the Nitrogen present in the Alveoli gets diffused to the blood? My guess was that the blood vessels don't allow anything other than CO2 and O2 to pass through.

But I recently saw a video on KhanAcademy where Sal said that some amount of Nitrogen does get mixed with blood. Is Sal right? If yes, then why doesn't the whole Nitrogen present in the Alveoli gets diffused from there (where it is present in high concentration) to blood (where it is present in low concentration)?

To summarize,

Why doesn't the inhaled-Nitrogen present in the Alveoli diffuses into the blood present in Pulmonary Veins, similar to how CO2 present in blood gets diffused out to the Alveoli?

I like it that nitrogen came to your mind ;)

I guess in school they didn't tell you about the nitrogen at all, for the matter of simplification, because it is of no function in the body and the $O_{2}$ and $CO_{2}$ are the important gasses for biological function of breathing.

However, all of these small gas molecules are very small and generally the biological membrane is very permeable to them. That's why the cell cannot decide to let $O_{2}$ and $CO_{2}$ in and $N_{2}$ not as you suggest.

(However, the cell is able to control the permeability of these gases to some content, based on the level of cholesterol in its membrane$^1$)

The process of gas exchange is generally passive. In alveolar membrane the gas flows from the site of its higher concentration (in case of gases we talk rather about partial pressure) to the site of lower concentration. The speed of this process depends mostly on the difference in partial pressures and if you let the blood "interact" with the air in alveoles for long enough, partial pressure of all small gas molecules would come almost to equilibrium. (This happens under physiological conditions for all of the three mentioned gases)

Khan academy is right too actually. This is because as $N_{2}$ isn't either produced or consumed in the body, its partial pressure in the venous blood is similar to that in the alveolar air, and there is no force to cause its movement between these two compartments in general.

In the table you can see, that the partial pressure of nitrogen in the blood is the same as in the alveolar gas.

Picture source

Nitrogen is not a metabolic gas, its partial pressure is very high. No compound of blood can react with Nitrogen hence its diffusion is not possible.
its diffusion is only possible when a person is suddenly lifted from depth of ocean, such diffusion causes bubbles in blood vessels leading to death due to disease called KESHAN
THIS IS WHY WARNINGS ARE GIVEN PRIOR TO SCUBE DIVING


When is it better for a gene to cause a biased sex ratio? Because genes are selfish and want to maximise their transmission from generation to generation, if they can distort a population's sex ratio, isn't it always in their interest to cause a biased sex ratio? Or are there cases when distorting the sex ratio isn't in their interest because they decrease the overall fitness at the higher level, i.e., incur too much damage in the individual/population? Their main priority is still to subsist in a population before spreading, right?
Thanks in advance :)

Well first if a gene is not on a a sex chromosome there is little advantage in changing the sex ratio. This is why most of the ultra-selfish genes we know about are on sex chromosomes. A gene is not helping itself spread if makes more Male offspring unless one of two things is true, it is on the Y chromosome or there is already a bias making male offspring more successful. the latter actually helps keep populations rex ratios stable since if there are more of one sex generally having offspring of the other sex is an advantage.
The most impactful sex ratio altering genes we know about result in selfish sweeps where populations can collapse as they take over and eventually prevent mating entirely. but up until that final generations with no mates the gene in question has an advantage, evolution does not care about the survival of the species or population, if a gene can improve its own ability to spread at the cost of the population then so be it. fitness at higher levels is basically irrelevant. A gene is perfectly capable of spreading by favoring itself and driving the species/population extinct. In many ways run away sexual selection is this in a nut shell, detrimental to the individual and population but beneficial to the gene.

First of all, we have to define what is meant by distorting the sex-ratio.
1) Changes to the sex-ratio as defined by the principles of the underlying Sex-determination system, can be seen as extremely unlikely:
In most species, sex is determined by inheritance of sex chromosomes, which based on meiosis results in a 50:50 sex-ratio. In this system, sex is determined by the presence or exact count of the sex-chromosomes (dependent on the species). Once this sex-system is established, I would personally see it as "frozen" and very unlikely to ever change. Other sex-determination systems are based on temperature and other environmental factors, and you can safely assume that evolution of their sex-ratios is based on advantages in the spread of the responsible genes. (Either through higher transmission rates within each population, or through a higher survival of the populations as a whole.)
2) Distortion of the perceived sex-ratio within the XY sex-determination system via TRD:
Transmission ratio distortion (TRD) occurs when one of the two alleles from either parent is preferentially transmitted to the offspring. This leads to a statistical departure from the Mendelian law of inheritance, which states that each of the two parental alleles is transmitted to offspring with a probability of 0.5. A number of mechanisms are thought to induce TRD such as meiotic drive, embryo lethality, and gametic competition. Importantly, such mechanisms only affect the sex-ratio, if the corresponding selfish gene sits on a sex-chromosome.
In this context, it is important to distinguish between true meiotic drives and killer meiotic drivers, as can be read in this review-paper. Killer meiotic drives often use complex [poison|antidote] systems, in which a tightly joined pair of a killer and an antidote gene together cause lethality in (haploid) gametes lacking the antidote containing chromosome after meiosis, while the poison is still present.
In general, drive alleles are predicted to be transient and evolutionarily labile. The transmission advantage enjoyed by drivers can allow them to become fixed in a population. After fixation, all individuals will be homozygous for the driver and exhibit no drive phenotype. However, if it affects a sex-chromosome, it could cause a bizarre state: On the x-chromosome, the mechanism would create a disadvantage in propagation due to the lack of male off-springs. On the y-chromosome, it might theoretically eradicate the whole population. By the way, such systems are considered for mosquito control.
Importantly, I would also like to address the gene R2D2 is an example of the true meiotic (see original publication), which is a “selfish” genetic element that exploits asymmetric female meiotic cell division to promote its preferential inclusion in ova (while the other female haploid cells die). However, against the suggestion of a commenter, this gene is NOT able to cause a distortion of sex ratio in mice, as females are homologous in X chromosomes; the ova always contains an x-chromosome.
So I will answer your question regarding selfish-genes, if it "isn't  always in their interest to cause a biased sex ratio" with a clear NO! Distortion of the sex-ratio is an extremely rare event that can result in strong disadvantages for the responsible gene, causing its own distinction.


Why don't macaws get selenium poisoning from brazil nuts Google research has indicated macaws love or eat a lot of Brazil nut. These are highly toxic to humans in somewhat small quantities due to their selenium content.

Given the mass difference between a human and macaw, lets say 80kg and 2kg, if toxicity for humans 'starts' around 900micrograms or ~9 nuts, maths would indicate toxicity for a macaw might be around 20% of a nut?

These figures are all based on google and the margin of error I expect is quite large, nonetheless it seems quite disparate if a macaw could consume even a single nut a day on average, without consequence?

One explaination is that macaws (Ara sp.) eat clay and other food item which absorb the toxins. Here is the full answer from Wikipedia:

  Like all macaws and most parrots seeds and fruit are the major part of the diet of the genus Ara. The particular species and range of diet varies from species to species. Unlike many birds macaws are seed predators not seed dispersers, and use their immensely strong beaks to open even the hardest shells. Their diet overlaps with that of some monkey species; in one study of green-winged macaws in Venezuela they shared many of the same trees as bearded sakis, although in some cases they ate the seeds at an earlier stage of ripeness than the sakis, when they contained more poison. Macaws, like other parrots, may consume clay to absorb toxic compounds produced by some poison...but with further research we now at last know it is just to eat life saving sodium that is missing. As well, the toxic compounds of some foods may be neutralized by compounds, such as tannins, found in other foods consumed at the same time...but we have found that it is untrue and really just to gain access to sodium missing otherwise in their diet because of the area they live in.

Source: Wikipedia - Ara (genus)


Values of the blood tests pancreatic amylase and lipase Anyone know what is considered slightly elevated, moderately elevated and strongly elevated values of pancreatic amylase and lipase?

Many different laboratories in my country divide between these categories for interpretation, but they don't specify which values qualify for each category.

Hope this is the right place for this kind of question.

Thanks in advance.

It is not necessary a fixed value. I think it depends on the doctor that interprets it. For e.g if amylase's normal value is 70, and laboratoy value is 80, i would say it is slightly elevated. A value of 300 is strongly elevated.


Bed bug or booklouse? I found this creature climbing on the lower part of a wall inside apartment. Can you distinguish if it's a bed bug nymph or a booklouse? Sorry the photo quality isn't great, because it's so small (2 mm). Thanks in advance!

After looking it up, I can, with some confidence, confirm that this is a book louse in the larval stage, as seen in this picture:
https://bpca.org.uk/write/MediaUploads/Pages/A-Z/Booklice/booklice-1.jpg
I hope this answers your question!


Does the given pedigree show a Y-linked dominant trait? I think that since every generation has males affected only, the trait must be Y-linked. Also, since every generation expresses the trait, I think it should be dominant. However, the answer key says that the answer is autosomal dominant. Could someone please clarify this and give a tip on how to recognise the difference?

You're right that this could just as well be Y-linked dominant (althought that is pretty rare due to the small size of the chromosome).

The only reason pointing more towards autosomal dominant is the mention of "extra fingers and toes". Most cases of polydactyly are inherited in an autosomal dominant way.

Does seem like an unfair question, though, since (at least in theory) there's more than one possible answer.

Ok so this is how I solve a pedigree:

This clearly shows that the disease is autosomal dominant. But there is one problem.

An autosomal dominant pedigree has the following features:
1. Appears in both sexes with equal frequency.
2. Both sexes transmit the trait to the offspring.
3. Doesn’t skip generations.
4. When one parent (heterozygous) is affected, and the other parent is unaffected, there is a 50% chance of the offspring getting affected. (You can refer to the cross I’ve drawn below your picture)

The pedigree in the question satisfies all 3 points except the last one. If there are 6 offsprings, at least 2 of them should be affected (if not 3), but there is only one, and that too a male.

Since only the male is affected in all generations, you’re right in thinking it’s Y linked. In my opinion, it can be Y linked dominant, since that’s very rare. And your question specifies that the trait is rare. It could DEFINITELY be autosomal dominant, had there been more affected offsprings in the third generation.


What nutrients can humans absorb in the mouth? For instance, I realise being able to absorb simple sugars in the mouth is pivotal in the rapid action of oral glucose gel. Thus I was wondering what nutrients in general can be absorbed directly within the mouth, and at what speed?

Quite a bit can be absorbed through the mouth. Most commonly, starches are broken down to maltose (two glucose molecules formed by a condensation reaction) and are easily absorbed by the bloodstream.

A lot of other factors balance into this, ie pH, lipid solubility, and molecular weight. Generally, if a substance is easily dissolved in saliva, it can be administered buccally or sublingually because the only remaining step is the diffusion into the subepithelial capillaries. In regards to speed, anything properly absorbed via buccal or sublingual administration goes to work much faster than a standard oral medication, and with a higher availability in the bloodstream. You are taking first pass metabolism and enzyme breakdown in the stomach out of the equation by diffusing the drug directly into the bloodstream.

There is quite a laundry list of medications that can be administered transbucally or sublingually, just a few of these:
Nitroglycerin
Acetylsalicylic acid (aspirin)
Glucose gel (as you mentioned)
Fentanyl (a narcotic painkiller)
buprenorphine (for opioid dependency)
Benzodiazepines (alprazolam, clonazepam)

Many vitamins are absorbed in mouth. Even spraying vitamins will help you overcome vitamin deficiency.
Even some drugs can be absorbed directly into mouth.


Use of progesterone in preventing ovulation? I have heard that progesterone in contraceptive pills or interuterine devices have been known to prevent ovulation. How is this possible since the LH and FSH are only affected by oestrogen not progesterone (am i wrong?)  Also,  my textbook says hormonal intrauterine devices contain progesterone to lessen uterine lining but doesnt the uterine get maintained by progesterone ?

Edit : I have yet to receive a satisfactory answer... Help anyone?

When progesterone alone is used as a contraceptive it is assumed that the oestrogen level is endogenously maintained by the follicular cells.

Yes mainly oestrogen and only little does progesterone inhibits LH or FSH secretion.

LH surge is the principle stimulator of ovulation.

  However,experimental work has suggested that immediately before the LH surge occurs, there is probably a sudden depression of estrogen...and this might be ...that leads to LH surge
  [source: Textbook of medical physiology A South Asian Edition- Guyton & Hall]

If progesterone or progesterone-oestrogen combinations be given before ovulation then feed back inhibition of LH surge occurs.This would lead to contraception by anovulation.

Progesterone is only known to proliferate the endometrial lining.

However, administration of progesterone or oestrogen -progesterone combinations after ovulatory phase helps to achieve high concentration of these hormones ,much before the normal time required to attain peak levels due to endogenous secretions alone.

This helps to depress the FSH -LH secretion by feedback inhibition very quickly causing involution of the corpus luteum and early shedding of the endometrium termed as breakthrough bleeding

REFERENCE:

reference site
Textbook of Medical Physiology A South Asian Edition-Guyton & Hall

This might and must be known to you that progesterone is known as the pregnancy hormones as it maintains the endometrial lining to Slough off  the  baby along with the corpus luteum (strata functionalis) and thus maintaining the pregnancy   and as far as the contraceptive pills and IUDs' are concerned they contain PROGESTIN i.e synthetic progesterone which inhibits LH production and hence anovulation  which is a type of we can say contraception  (prevention ) from pregnancy ;)÷


Reward pathway sequence of events So I've been reading a lot of papers on the reward pathway. But since I'm not schooled in any relevant knowledge I'm having trouble grasping the chain of events. Most papers detail just bits and pieces, but not the full sequence of events.

I'm trying to grasp how the error prediction signal works.

This is my guess so far:

Players:

  Photosensitice cell A
  Light processing neuron B
  Dopamine neuron C
  Motorneuron D

Event:

  Light strikes A
  A triggers B
  B spikes after N triggers.
  B triggers C
  C spikes after N triggers.
  C keeps repeadetly spiking for as long as its internally coded reward size/duration expectation.
  D receives predecition triggers spikes causing action.
  Reward comes, neural connections are strengthened.
  If reward doesnt come in predicted time connection degrades.

Am I correct in this deduction or way off?

How does the actual reward get communicated? By dopamine release in blood?
By the same neurons that coded the reward prediction? If so, how do those exact neurons get triggered to release reward?

Essentially that's what I remember, but there can be a lot more steps between A and C, i.e. more pathways interacting in different systems to produce an associative memory. Pavlov's dogs is the classic example:

1: Pavlov rings bell, dogs hear bell

2: Pavlov feeds dogs, (dogs rewarded)

3: Repeat 1 and 2 for a few days.

4: Ring bell, dogs will salivate and expect food, even if no food is on the way.

So, in the skull, the dogs are making a link between hearing a bell and a reward.

Dopamine is released at dopaminergic synapses, the limbic system is probably the best understood part of the memory/reward system, particularly the mesolimbic pathway for reward.

Neurons get triggered by presynaptic neurotransmitters, some require convergence of signals to reach threshold and trigger an action potential. Connections are strengthened by long-term potentiation, which has been argued to be the basis for memories, but that's a massive topic I'm not qualified to discuss.

I haven't heard of the "error prediction signal" before, might be a new discovery/thinking that I'm a bit behind on.


What animal / bird can be heard in this evening sound recording from Western Washington, USA? We heard this animal outside in Western Washington (Port Townsend area) during the late evening. I think it is a bird, but it honestly sounds sort of like some creepy woman singing or something. The audio is linked below. The sound (in the audio) was repeated for a long time at random intervals averaging probably every ten seconds.

https://clyp.it/tzybty1w

Anyone know for certain?

I asked the same question on another forum here: http://www.birdforum.net/showthread.php?p=3454684.

It looks like another possibility is a barred owl. It also sounds somewhat similar.

It could be the Sri Lankan spot-bellied eagle-owl lost in America.
Link = [https://www.google.com/search?q=spot-bellied+eagle-owl&oq=spot-bellied+eagle-owl&aqs=chrome..69i57j46j0i22i30l7.931j0j7&sourceid=chrome&ie=UTF-8][1]


Polymerase Chain Reaction Questions First question is about why we use primers in PCR. It requires two reasons. I know only one reason though. It is so that DNA polymerase can attach to primer and make a copy of nucleotide from there. But i don't know what is the other reason.
Another question is about why the primer bonds to 3' end of the DNA you want to copy. and explained why. I really have no clue for this one. Plzz help.

We use primers in PCR because we are mimicing natural processes. DNA polymerase cannot act without primers. It needs primers to start it's work. Binding of molecules happen by chance, so the more there are of your primer, the more likely it is that it would bind to any given string of complementary DNA. DNA replication occurs in the five prime to three prime direction because phosphate doesn't allow the reverse reaction.

Beside helping Taq to add dntps to the growing strand
Primers minimize the risk of mishybirdization as they are designed specifically for a specific region of DNA


Fuel from photosynthesis I was reading how plants make use of sunlight, CO2 and some other stuff to make energy. So why can't we create artificially engineered bio solar panels which will take sunlight, C02, water and other things and give us energy (maybe electricity or heat etc). So basically instead of solar panels which are made of silicon or something we can have bio panels made of organic materials. Then we need to supply it with water and it will convert sunlight into electricity.

I googled this on the internet and I don't find anything relevant in this regard. So I am assuming there must be a very good reason we are not trying to do this. I want to know if there is any research going on in this regard and if not why this idea is not feasible.

What you are suggesting is an organic photosynthesizer,but that's not necessary when you already have plants that have genetically adapted for millions of years just to be suitable for this very purpose.
 Of course,artifical photosynthesis already exists,essentially using the same process;photons,chloroplasts,calvin cycle,photosystems 1 & 2,etc.It utilizes the general concept with photoelectrochemistry,so basically just replacing the organic tools with artificial photoelectric cells,which also uses h20 and light.What you are asking is why we have not developed genetically engineered organic matter to produce higher efficiency.As a matter of fact,GMO plant's already exist with immunity,though I have not heard of GMO that catalyzes photosynthetic reactions,and best not,because genetic engineering is still at it's best a new field that is too complex,for example,the general GMO is to incorporate the bacterial enzyme cas9 to cleave away specified DNA to alter an organism's genome,such as inhibiting receptors to cannabinoids,or to fight pests with substances that are not harmful to humans,etc.But it has consequences,such as permanence of that edited genome,so if the organism/plant reproduces,the progeny would also exhibit the same GMO properties.
 Photosynthesis is a complicated series of reactions that uses complicated enzymes and such.For example,the enzyme rubisco that changes co2 to energy rich molecules such as glucose,from highly unstable phosphoglycerates.Artifical photosynthesis is quite new,but it also uses the same fuel;co2,h20,and light,not sure if it uses biological nutrients like soil,but the process also uses Nicotinamide adenine dinucleotide phosphate,or NADP+.It is used for anabolic reactions,so it builds up molecules,vice versa are catabolic reactions,which is when enyzmes break down lipids and molecules in metabolism.Albeit I do not know for sure if this molecule has the same purpose in artifical photosynthesis,but for general photosythesis,yes.NADP+ also absorbs electrons for independent and dependent reactions to generate ATP and NADPH,etc.
 I hope this simplifies some things.CONCLUSION:we do have artifical photosynthesis,but gmoed photosynthesis may be harmful to a plant's heredity if we damaged it's genome,causing potential harm.
  Artifical is quite similar to organic,so I guess you say they are biopanels,using h20,co2,and light.


Why are ducks more cautious than pigeons? In my city park there are mostly two types of bird:

Mallard ducks
Rock doves (pigeons)

When I feed pigeons, they approach me very closely. Sometimes they peck the food that fell on my feet. If I hold my hand with food in the air some pigeons will land on my hand and eat.

In the same park there are Mallards, who are always very cautious and they try to maintain about 1-1.5 meters distance from me. They also run away when they see some rapid movement of mine.

Why are ducks more cautious? Why are pigeons more careless?

A possible reason is that pigeons in a city live there year around, while urban ducks often migrate, or their populations are refreshed by new "recruits" from wild populations ; so pigeons have more opportunity to adapt to being close to people.  Another possible reason is that pigeons are more agile than ducks on land and are more able to escape if you decide to grab one for dinner.

This could be due to the fact that mallards are wild animals, whereas, although they may appear to be, ferral pigeons/rock doves, are not. They are, as the name suggests, ferral. Meaning they were once domesticated and then their ancestors were set free and left to breed out in the wild. Therefore they may still have some ingrained trust in humans whereas mallards would not.
Edit: sorry I'm new here and didn't know that it was necessary to add sources.
https://books.google.co.uk/books?hl=en&lr=&id=whScRZEmRl4C&oi=fnd&pg=PA3&dq=info:Xm_-vES8Sv0J:scholar.google.com/&ots=eWsLsAP-9I&sig=5j0XfJ8vaEMTTEL6djwXOq4409c&redir_esc=y#v=onepage&q&f=false
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=why+pigeons+are+feral+and+not+wild&btnG=#d=gs_qabs&u=%23p%3DtgCc_1AYDyIJ


How many molecules of ATP are actually produced in aerobic respiration? I have been through the process of aerobic respiration a few times in different text books and almost every book quotes a different value for the number of ATP molecules produced. The consensus seems to be 30–32, but why is there disagreement and why aren’t the numbers exact?

The possible reasons I can think of are:

Phosphorylation of ADP is not directly coupled to redox reactions.
The number of ATP molecules produced depends on the shuttle used to transport electrons from the NADH in the cytosol to the mitochondria, i.e.  whether it’s FADH2 which enters the ETC or NADH. (I have a silly question on that, but I need confirmation, does the electron carrier chosen depend on availability?)
The proton-motive force can be used to drive other cellular processes other than the production of ADP? (I'm guessing.)

Are these suggestions correct, or is there some other explanation?

The discrepancy between 30 and 32 molecules of ATP quoted in the question may well arise from the two possible ways in which the reducing equivalents of the two molecules of NADH generated in glycolysis may be shuttled across the inner mitochondrial membrane into the mitochondrion (suggestion 2).

If one assumes that the malate-aspartate shuttle is used, then NADH is transported into the mitochondrion as such, and the yield of ATP is the same as for those molecules of NADH generated in the mitochondrion — 2.5 ATP per NADH from the most generally accepted measurement.

However, if one assumes the glycerol phosphate shuttle is used then the reducing equivalents are transferred from NADH to FADH2, from which only 1.5 molecules ATP is produced per molecule.

In summary, using the malate–aspartate shuttle a total of 5 molecules of ATP (2 x 2.5) will be produced from the two molecules of glycolytic NADH, whereas using the glycerol phosphate shuttle there will be only 3 molecules of ATP (2 x 2.5). This gives a difference of 2 molecules of ATP, which would cover the range in the question.

As the relative proportions of the two shuttles varies between tissues, a range of values is actually possible.

You are totally spot on with #1. ADP phosphorylation pump is driven by the proton gradient and ADP availability, while the the electron transport chain slows when it becomes too hard to pump protons.
Furthermore, other processes (mostly channels) may use up a proton from the gradient.

The different electron carriers have store different amounts of energy (NADH is more energetic than FADH) and differ in the uncatalysed energy required to release the electron pair, hence why there is not a one size fits all.
NADPH vs. NADH is a special case as NADPH is anabolic (builds), while NADH is catabolic (the electron pair is used for energy generation) and the enzymes in the cell keep it so that NAD+ levels are higher than NADH, and NADPH higher than NADP+. The passing of a pair from NADH to NADPH (a membrane bound transhydrogenase) actually utilises a proton off the gradient to drive it.


An online tree of life with extinct species present? There are awesome online phylogenetic trees such as OneZoom.

But they all only list living species.

I want to see dinosaurs between birds and crocodiles.

I wanna see that humans are reptiliomorphs and eupelycosaurs.

species.wikimedia.org seems to contain this info, but it's not presented in a navigable tree structure.

The tree of life project is your best bet, its not 100% complete but it is more complete than any other project I have ever seen, and unlike most actually includes many if not most extinct taxa. http://tolweb.org/tree/phylogeny.html
It also includes citation and brief descriptions of links and groups to make it easier. Some extinct lineages suffer from unresolved phylogenies but many of those are in constant flux or are actually unresolved in the fine scale so I can't blame them, especially considering they were originally based entirely on genetics, and is updated constantly.

Had this same question, and after a lot of digging, came up with this http://lifemap.univ-lyon1.fr/explore.html
Very cool tool!!


What are the consequences of inbreeding? Inbreeding increases the risk of getting two identical recessive genes, alleles, that cause a disease which wouldn't have been activated with mixed genes. That's how I understand it anyway. But I sometimes read and hear that inbreeding among humans also causes decreased intelligence, especially emotional and social intelligence. Is there any support for such claims, and if so how does that work?

You are right. Inbreeding strongly increases overall homozygosity which subjects inbred individuals to diseases caused by rare recessive alleles. In non-inbred individuals the chance is quite low to receive those because many deleterious variants (and in fact, most segregating alleles we can observe) are recessive. Most often, but depending on the dominance coefficient, these 'hide' in healthy heterozygous carriers and when very closely related individuals breed (with a lot of variants that are identical by descent) there is a high chance that some of the 'hidden' deleterious variants are passed to the offspring.

You have to be aware that there are in fact two conceptually different processes that can be both be referred to as inbreeding but are also somewhat continuously linked (see below):

Mating systems that allow offspring between actually related individuals (measured by the degree of relatedness), what in humans often is referred to as incest or consanguinity.
Populations with very low effective population size $N_e$ generally exhibit higher relatedness due to lack of genetic diversity (excess of homozygous sites). Therefore, populations with low $N_e$ are referred to as inbred even if no actually related individuals are mating.

There is some evidence that inbreeding in the first sense is linked to cognitive abilities in humans:

Bashi (1977) investigated the effect of offspring having first-cousin (i.e. between children of siblings) and double first-cousin (i.e. between children of siblings and unrelated siblings, sharing as much variants as half-siblings but with more recombination events) parents while (at least somewhat) correcting for socioeconomic effects. He found an inbreeding depression with respect to cognition that could

  result either from the general increase in homozygosity [...] or from decrease in performance resulting from homozygosity for specific recessive alleles (highlighted by me). The higher variance of the double cousin group in some of the tests favours the second interpretation.

Woodley (2012) presents evidence for slightly lower IQs caused by inbreeding, however, he also mentions that the effect is way smaller than socioeconomic effects:

  Consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.

Fareed and Afzal (2014) investigated verbal IQ, performance IQ, and full-scale IQ and found that all of these IQ parameters are significantly lower in inbred children compared to non-inbred children - actually the difference increases significantly with the degree of relatedness. They conclude that there is

  evidence for inbreeding depression on cognitive abilities among children.

Please keep in mind that, for for sociological/ethical reasons, this is highly controversial, especially when the two concepts above are intermixed - human populations underwent differential and variably strong periods of low $N_e$, i.e. were subject to stronger or weaker inbreeding in the second sense. When reading the citation of Bashi (1977) above carefully, you will notice that he takes good care not to intermix those. Inbreeding in the first sense leaves large runs of homozygosity (ROH, blocks without heterozygous sites, i.e. a clustered and local lack of variation) whereas inbreeding in the second sense increases homozygosity in the genome less selectively. Therefore, the distribution of homozygous sites can be used to infer whether inbreeding is recent (first sense) or old (second sense) (see for example McQuillan et al. (2008) - here you see that both concepts form a continuum: where do you set the cutoff between recent and old? what is an appropriate threshold size for ROH? ...). Regardless, Bashi's findings indicate that effects of inbreeding are caused by recent inbreeding as he presents evidence that his results are rather driven by specific deleterious recessive variants than overall excess homozygosity. Finally, even though the study by Fareed and Afzal (2014) shows rather large effects of recent inbreeding in IQ measures, the results from Woodley (2012) show that one needs to be really careful to separate genetic from environmental components as his study suggests that the latter contribute more to the observed decrease in IQ.

My understanding, NOT based on any study, it purifies the gene 'pool' since mutation derived alleles variation will be lost thru' generations just like we don't have much of our grand grand's 'unique' allele.

This is bad as it happens in farms, when an decease that infects one, could eliminates all the populations, to be exact, barring a few left.

In the ever changing environment as in evolutions, singular gene pool will be hit with extinction even thought it might prosper if and only if the same good old 'environment' persists.  Environment here includes everything in the ecosystems.


How are neural pathways discovered? I have seen the spinal cord and it's a white, soft, slippery cylinder that has a small diameter (about 25-30 milimeters). It absolutely doesn't have a macroscopocally reticular texture that would allow us to track down individual pathways. Same goes for the brain, it's also not macroscopically reticular and yet we know a lot of connections inside the brain.

So what's the technique used to discover these neural pathways and the information about in which parts of the pathway are synapses located?

Example of what we know is here under the "Major neural pathways" title.

There are are few ways this can be done.

One important example, is case of Phineas Cage who's accident lead to severe brain damage. This changed his behavior, which allowed scientist to connect physiology with behavior. Namely, left frontal lobe damage caused change in personality, without significant change in other important behaviors such as memory.

Same way we can look on naturally occurred brain damage via modern imaging techniques (X-ray, CT, MRI, fMRI) and connect those to behavioral abnormalities.

We can also learn about neural substrate of behavior by experimenting in the lab: by looking at effects of tissue damage. Basically, you ask "what happens if we damage this part of the brain". This way we can figure out parts of brain that regulate different parts of sleep by dissecting animal's brain stem in different regions.

Another option is to "look" at brain while it functions and detect important active regions. Here you can use any number of techniques: fMRI, EEG, direct electrode probing of brain regions, or in animals optical calcium imaging. Point is that in these experiments you ask (or make) your subjects to perform behavior X and see how and where that behavior activates neurons.


Identifying a weird Texas tree I recently saw this tree in Texas, with many bees on it. I think it attracts   bees. However it didn't have any specific smell, so I don't know why there were so many bees (they were bee for sure). I tried to identify the leaves but couldn't. Dear experts: could you please identify this tree?

That looks like a live oak covered with oak galls


Can exercise strengthen tendons and ligaments? Is is possible to strengthen tendons using exercise to prevent injury, for example preventing shoulder dislocation?

yes..It takes approximately 10 weeks of regular resistance exercise to strengthen your tendons, and it takes longer for them to thicken. You can expect up to 20 percent increase in strength and thickness of your ligaments and tendons with regular training.


Do bald people not grow hair, or does their hair simply fall out immediately? This image is not directly related but it made me wonder if there was a relationship between the nature of the hair follicle and baldness, namely that the follicle cannot 'hold' the continuously growing hair, and it constantly falls out in. I wonder if this is the case or if the hair literally just does not grow out from the follicle at all.

I'm no expert on the whole matter, but I know that at least when it comes to male pattern baldness, it is caused by a hormone called dihydrotestosterone. As those men with the right (or wrong genes, however you choose to look at it) age, this hormone causes the hairs to progressively lighten and thin up until the hair stops growing altogether. The hair follicle dies out basically.


Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence? I was reading this(1) and it led me back to ask a very basic question (I'm not a neuroscientist).  All the way back to undergrad anthropology and neuroscience courses I remember being taught the general rule of relative intelligence was that one looked at the ratio of the brain mass over the total mass of the animal (or the estimations therein from let's say fossils).

I know a lot of the interesting neuroscience research going on these days does looks into bird brains, particularly within Corvidae.  It would seem that birds are often much more efficient in the abilities they seem to show with considerably less brain mass.  I do realize that birds often weigh very little as well, so perhaps the ratio is preserved?

I also realize that within birds, they see better ratios in more intelligent birds.  But what about the comparison from mammals to birds?

Dinosaurs are often predicted to not be intelligent because of the enormous body size and small cavities for a brain.  Now I realize that some dinosaurs were actually quite tiny, but this is just an example.

Given birds' close genetic link to dinosaurs, could it simply be that they were just doing more with less?  The mammalian brain is a huge caloric burden, so perhaps this would show an efficiency that could be selected for?

Thus as the title suggests, my main question:

Is the ratio of brain mass to body mass still considered to be a valid indication of intelligence of a species in modern (current) neuroscience?  Certainly there are exceptions, but is it still considered the rule of thumb?

EDIT: I also wanted to point out the first article(2) I started to read after formulating the question.  It made me question the usefulness of encephalization in addressing this issue at all, but I don't/didn't feel adequately trained to evaluate the conclusions of the meta study.

Again, this still leaves us comparing within primates, which still leaves me feeling that Corvidae have some really impressive efficiency going on with their overall brain mass.  Which then leads to hope that some dinosaurs could be at least equally intelligent, if not more so (noted that this is complete conjecture).

(1) Front Hum Neurosci. 2013 Jun 6;7:245. doi:10.3389/fnhum.2013.00245. Print 2013.

(2) Brain Behav Evol. 2007;70(2):115-24. Epub 2007 May 18.

I don't know about brain mass to body size, but ratio of neocortex to brain volume is correlated with primate evolution (Figure 3, here). If you subscribe to the view that humans and more closely related primates are more intelligent than more distantly related primates, then that is an important correlate.
I think the issue with this question is that we're still having trouble defining intelligence.

Considering that as humans had larger brains in prehistoric times, then no, brain size doesn't mean more intelligent.
I aren't well versed into this subject, so I don't particularly know if they could learn better than us, but there are speculations of why their brains were larger than ours.
The most primitive humans, had to deal with a lot of predators, and unnatural things in their environment. Mist of them contained a vast amount of knowledge of what is "bad" or "good", and that was a requirement if they wanted to survive in that period.
As we settled down, and our natural predators became our food, such needs became less and less important.
Maybe they were actually smarter than us.


What's the (or some of the) minimum(s) amount of atmospheric carbon dioxide needed by plants? We currently have a problem of increasing $\ce{CO2}$ in the atmosphere.  But assuming we find a way to carbon sink it, what is the minimum $\ce{CO2}$ we need to leave in the atmosphere to provide a source for plants to photosynthesize?  I'm assuming this may vary per plant, and that we could choke plants so they're less productive - but at some point they will starve to death if we remove too much $\ce{CO2}$.

Where does this point lie?

Approximations, or a specific data point (say for one plant, or one type of plant) would be an adequate place to start.

Current atmosphere composition is $\pu{0.035\%}$ carbon dioxide.  In the past it has been higher (has it ever been lower?), which in theory has resulted in higher plant growth - but I've seen some contradictory statements about higher Carbon Dioxide.

(related: What is the effect of a pure-oxygen environment on a plant?)

The values provided in the other answer are actually related to the minimum values experienced by land plants in the past, not the theoretical minimum possible concentration of CO2 capable of maintaining plant life.

According to Gerhart and Ward (2010):

  During the Last Glacial Maximum (LGM; 18 000–20 000 yr ago) and previous
  glacial periods, atmospheric [CO2] dropped to 180–190 ppm, which is among the
  lowest concentrations that occurred during the evolution of land plants.

Thus, what is the theoretical minimum possible concentration of CO2 capable of maintaining plant life?

According to the same paper (Gerhart and Ward, 2010), there has been several experimental studies focusing in low concentration of CO2:

  In the mid-1990s, a later phase of technology was introduced at the Grassland, Soil, and Water Research Laboratory (USDA-Agricultural Research Service) that involves an outdoor tunnel system, whereby plants are grown across a continuum of modern to low [CO2] (Mayeux et al., 1993; Fig. 3b,c). During the day, air of known [CO2] is pumped into one end of the tunnel where plants experience relatively high [CO2]. Plants near the end of the tunnel, on the other hand, experience low [CO2] (similar to glacial values) as a result of photosynthetic removal of CO2 from air as it moves progressively through the tunnel. At night, airflow is reversed while plants are solely respiring, and this serves to equalize [CO2] throughout the tunnel.

Despite those studies not focusing explicitly on what's the minimum possible concentration, we can still draw some conclusions based on them. For instance, in Fig.4 (ibidem):

As you can see, those vertical lines represent the minimum concentration experienced in the past. However, we still observe CO2 assimilation (photosynthesis) below those values. Unfortunately we cannot simply get the value where the line touches the x axis, because those values are intracellular CO2 concentration.

That being said, the answer depends on other concept: CO2 compensation point. For a C3 plant, carbon dioxide compensation point is around 50ppm (Tolbert, Benker and Beck, 1995).

Thus, we can say that, as a rough estimate, the value you want lies between 50ppm and 170ppm (probably closer to 170ppm than to 50ppm).

Of course, that minimum possible value depends on several factors, as the species of the plant, the type of photosynthesis (C3, C4, CAM), temperature, humidity etc.

Sources:

Gerhart, L. and Ward, J. (2010). Plant responses to low [CO2] of the past. New Phytologist, 188(3), pp.674-695.
Tolbert, N., Benker, C. and Beck, E. (1995). The oxygen and carbon dioxide compensation points of C3 plants: possible role in regulating atmospheric oxygen. Proceedings of the National Academy of Sciences, 92(24), pp.11230-11233.

Minimum  concentration in PPM to support plant life varies from 185 ppm to 225 ppm. We are at 433 ppm at the moment. Prior to this Ice Age cycle that started about 3 1/2 million years ago the PPM Norm was between 900 and 1120 ppm. For reference if anybody is interested in knowing where we are at prior to man cause global warming we were at 240 to 250 ppm.  Yeah when I discovered with the plant life minimum was and then where we were at it scared the shit out of me too I.


Is this flying bug swarm termites? Found in New York city, approx 7mm Just saw a giant swarm of these fly out in between pavers and a door sill from a small crack in the ground here in New York City.  There seemed to be hundreds of them swarming out very quickly.  They are about ant-sized.  Are they termites?
Here are photos:

Yes it looks to be Reticulitermes flavipes aka the Eastern Subterranean Termite.


Do the individual claws of a bear have names? The question seems pretty self-explanatory (if perhaps a little odd). Anatomical names or colloquial names are both appreciated, especially the latter if they exist.

I would be surprised if they do!

Bears have 5 clearly visible toes per paw. You could just name the claws based on the fingers it is on (thumb, index, middle, ring, pinky).


What does it mean to have different "metabolism"? We hear talk of different body types, and that it is more difficult for certain people to lose weight than others. On the other hand, when my physician recommends that I lose weight, they say that it is really just as simple as "calories in, calories out". How can we reconcile these two?

Perhaps the "calories out" portion is different for different people? I.e. some people burn more calories than others do, doing the same activities, but their hunger level does not compensate for this?

Apologies if this is off-topic

There are differences in metabolism, and the "calories in" part is the one which differs more than the "calories out" part.

People do lose different amount of calories for the same action, but for mostly mechanical reasons. If a 50 kg person walks up a mountain at 3 km/h, and a 100 kg person walks up the same mountain at the same speed, the 100 kg person will expend more energy, because they did more work. And then there are slight differences in how we do our movement - some people's gait is more efficient than others', and uses less energy. But this is not really interesting for the explanation of having it easy/hard to lose weight.

The point is that the amount of food we intake is determined by our hunger, and our hunger is determined by hormones. Then, the amount of fat we store is also determined by hormones. If your body "thinks" you should be putting on weight, and you go on a calorie-reduced diet, it won't just start complementing the missing energy from the fat stored in your adipose tissue. Rather, it will continue diverting some of your food intake to make more fat storage, all the while rationing the energy available for other activities: making you feel tired so you don't move much, shutting down some luxurious, energy-hungry processes in the brain, mostly the ones associated with higher mental functioning, and making you feel hungry and cold so you will be more motivated to seek out food and eat. The hormones which regulate these processes are many, most of them are poorly understood, some are probably not yet discovered (orexin, one of the main hunger regulating compounds, was only discovered sometime in the last 5 years I think), and we really don't have a complete picture of everything that is involved. It is a complex mesh of finely balanced homeostatic systems which interact with each other and the environment.

The people who say that it is as simple as "calories in, calories out" are right. They are right in the sense that, if you just observe a human being and measure their energy household, you will be able to document the amounts of energy consumed, expended and stored, and the energy consumed will equal the energy consumed plus the energy stored.

But to derive from this that we are talking about a passive overflow system and, if we reduce intake, storage is also reduced, is a big leap of faith and has been proven wrong again and again. Living systems are actively reacting to any influences from outside, by mechanisms much more intricate than simple mechanic rules. Mechanics tells us that if I push you, you will fall over; experience tells us that if I push you, you will brace yourself so you don't fall over, and then try to stop me from pushing you by using words, force, or whatever else you have at your disposal. Our physiological systems are the same way. They like the situation they have chosen to be in as much as you like standing upright. If somebody comes from outside and tries to forcibly change their status quo, they do whatever they can to 1) resist and retain the status quo, and 2) stop the outside force if possible.

As for the difference in metabolism: the hormone systems of different people are differently "tuned". For example, eating pure glucose causes insulin production to spike, and excess insulin causes glucose to be removed from the bloodstream, plus a handful of other effects. But the size of the insulin spike is different in different people. Also, the extent to which cells react to elevated insulin is different. When the reaction becomes dangerously weak at even high insulin levels, we say that it's a pathological variation, and call it "metabolic syndrome". If goes really towards zero, it's called diabetes type two. And this is an example about just one of the hormones connected to metabolism and the distribution and use of energy in the body.

On a simpler level, there is no difference in metabolism where physical energy calculation is concerned. Expending one molecule of ATP will let the same number of Na+ ions to move the same distance along a nerve dendrite, across humans. But this level is not really interesting when it comes to gaining or losing weight.

Some people burn more calories than others, in the default mode.

Just sitting in a chair, I warm the seat much more than some other members of my family.  That heat has to come from somewhere.

That's a different metabolism.

But, that's not something you can order and install.  It's not a pill.  Your doctor is right to focus on what you can control, and that's intake - along with your activity level; or outgo.  (But most people are unwilling to actually do the work to change their activity level to a higher one, which is why doctors don't even try anymore - patients just lie, and then doctors have to try to catch them at it, and nobody's got time for that).

What you eat may also impact the number of calories that stick.  Not everything you eat gets digested, some passes through.  And digestion itself burns calories.  Things that are harder to digest take more energy, and leave less surplus behind.
Easy things are... easier to digest and get all the calories from.

In addition, thinner people lose weight easier.  Not fair, right?  That's life.

It may have something to do with your microfauna, but that's not well studied.  And, we're not even sure if you can permanently change those populations.

http://www.mayoclinic.org/healthy-living/weight-loss/in-depth/metabolism/art-20046508

  The warming of the seat is anecdotal speculation.

So you're arguing that heat happens magically, and doesn't require caloric input? Do tell us more, I can't wait to hear about it.

  And why should thinner people loose weight easier?

If I had a handy cite, I'd give it to you.  Yeah, yeah, Abraham Lincoln said don't believe everything you read on the internutz

  You say "Not well studied" - It is important to cite some material that is studied in your answer.

http://www.nytimes.com/2013/09/06/health/gut-bacteria-from-thin-humans-can-slim-mice-down.html?pagewanted=1&nl=todaysheadlines&emc=edit_th_20130906&_r=2&pagewanted=all&

  And what are 'those populations'?

Populations of microfauna

  It is more of a comment as it stands. Earn 9 more reputation and you can comment anywhere.

Thanks for the upvote, to help me comment - oh wait.


Is the lac operon repressed in the presence of both glucose and lactose? In the presence of both sugars (glucose and lactose) will there be repression of the lac operon completely?

I know that more glucose means less cAMP --> less CAP --> less positive regulation, and thus less lac operon, but does that mean there will be repression of the lac operon?

According to Molecular biology of the gene by James Watson, in presence of both glucose and lactose, the lac operon has a basal level of transcription. However, when only lactose is present, the operon has an activated level of transcription, due to the CAP mechanism.


Why don't rats have a gallbladder, unlike other rodents? It has long been known that rats do not have a gallbladder, though other species including humans, monkeys, cows, reptiles, dogs and mice, all have a gallbladder.

In this paper from almost 100 years ago, scientists were studying what differences the presence or absence of a gallbladder gives the composition of bile. The authors found (what we now appreciate very well) that bile from mice who have a gallbladder was much more concentrated than rat bile - i.e. one of the functions of the gallbladder is to concentrate bile.

I know this is a very speculative question, but is it known whether having or lacking a gallbladder confers some sort of evolutionary or biologic advantage (or disadvantage)?

There are many different theories on this aspect of evolution, some of them are proved and others are just conjectures. Materials and research in this particular aspect is very few. Here I tried to provide an answer in reference to the particular animal you mentioned, i.e. rat.

Rats don't have a gallbladder possibly due to the following reasons -

The concentrating power of bile in rat's liver is high, so the main function of bile concentration by gallbladder is unnecessay in them. This is probably the most supported theory regarding this.
Rats frequently take their food so they require a continuous supply of bile. This eliminates the necessity of bile storage.
Harbivore animals relatively lack fat in their food. This reduces the need of large amount of bile salts in the intestine.

References -

https://theparadigmshiftgroup.com/animals-no-gallbladder/
Zoology textbooks
http://www.sciencedirect.com/science/article/pii/S0375090613000323?np=y

It's probably due to the fact that rats have an usually "harder do digest" diet. A gallbladder means a source of extra bile at the time of digestion. As you said mice have one but smaller, possibly rats used to have one of the same size, but as they adapted to urban live, bigger ones became advantageous.


White water bird with black 'hat' The white bird in this picture, swimming between the ducks, was seen in Beijing, China, in januari 2017. It was cold: the water seen in the picture is liquid, but not far from this, the water was frozen. We also saw it standing on the ice.

It has an orange beak with what seems to be a small black spot at its end. It also has black as the top of its head. We did not find a similar bird when searching ducks, goose or even swans. What species is this?

It is a domestic form of mallard. They are bigger, often white or mostly white. Try to google image domestic mallard and you will see the phenotypic variety that domestication has created.

Note the irregular and not symmetrical shape of the "hat" and read the description below from the biggest research center on birds of the world.

Extracted from:
http://www.birds.cornell.edu/crows/domducks.htm

  (...)lots of white is often involved, including all-white breeds like the popular Pekin Duck (...) Usually these white spots are not symmetrical across both sides, and that asymmetry should tip you off to think domestic influence.

It may be a duck or maybe a swan lets not forget that new species are born every year or decade and so on thanks to 2 different reasons or factors.
1. animal crossbreeding.
2. a change in their DNA.
but for this case I am guessing is more the 2 one and this may happen for many reasons perhaps this kind of gene was actually existant the whole time although it wasn't dominant as such it took many generations to appear, perhaps a change in the environnement had been a cause of a mutation. As such this creature may be a in the first factor a hybrid or in the second one a mutant.(https://www.wired.com/2009/11/speciation-in-action/)


Enzymatic error rate I am aware that each enzyme generate a certain amount of misproducts.
This is well documented, for example, for the DNA polymerase.

I am interested in enzyme involved in biochemical processes, so for example methytransferase, oxidoreductase, carboxylase and so on.
I have been looking for any reference that could report the error rate or the amount of misproduct for any of these enzymes, but I was not successful.

Does anyone know a reference reporting the error rate, or any other information about the misproduct generate by these enzymes?

EDIT

I will try to clarify a bit better my question.
Let's assume that we are considering an enzyme that add a methyl group to a molecule, we can choose propionic acid for example.
In theory the correct product would derive from the addition of a methyl to the C3.
For the biochemistry study we know that the activation energy is decreased by an enzyme for example by orienting the molecules in the right way to react with the second molecule.
Therefore, if the enzyme in question will not be able to orient the molecule in the right way there is a certain probability that there will be a mis-product.
For example the methyl group could be added to the C2 and not the C3. Now. the probability for this process is quite low, but it cannot be excluded from happening.
My question is, if there is anything known about this type of error rates in the different type of enzymes.

I hope this make things a bit more clear

EDIT 2

Lets consider the imagine below that was taken from here

In B you can see the interaction of the active site of the enzyme with a substrate (for the example it does not matter if it is the real substrate or an inhibitor). I would say that among al possible interaction that this active site can make with substrates there are some much more likely than others. An hypothetical chart could be created considering the free energy of the complex enzyme-substrate, higher the free energy lower the stability.
Therefore among all possible enzyme-substrate combination we will have just few possibilities that have a low free energy. In the first place we will find the "correct" substrate, then we will find eventual competitors and other molecules that have similar chemical features as the substrate. Even though with low probability these interaction, enzyme-competitors, will happen.
This might led to the formation of "unwanted product" that I refereed to in my question as "misproduct".

I am interested in reading some paper that are considering thie phenomenon and also quantify its rate. I am also curious if this phenomenon can happen with different rates in different enzymes.

First it is important to define what actually an error is. What you call misproduct is actually a right product for a different substrate. The enzyme has a low specificity; but you won't say hexokinase is error prone because it has wide substrate specificity. The question is — is specificity critical?

Coming to the example of DNA polymerase, you should note that DNA polymerase only adds a nucleotide to the DNA strand. Here the template DNA strand acts like a co-enzyme and it is the template DNA that provides specificity to the reaction. In this case the specificity is really critical and there are mechanisms that help in ensuring that.

Other enzymes also make errors and the probability of making errors depends on different parameters. Take the example of restriction enzymes that are supposed to cut at a specific site. When this specificity is lost we say that the enzyme is showing a "star activity" i.e. non-specific cleavage. This depends on different parameters such as buffer composition, enzyme concentration etc.

In general specificity is provided because of high affinity of binding towards one molecule compared to the other. These binding reactions are second order — a high affinity substrate will bind to the enzyme even at a low concentration, however if you increase the concentration of the low affinity substrate or the enzyme, then at some point the rate of binding may be significant enough to create a "wrong" product.

Sometimes there are cases where the enzyme can bind to a wrong substrate but cannot create a product. This is the typical case of a competitive inhibitor. It is also possible that a certain molecule is good at binding but the conversion rate is slower.

To conclude, these kinds of "errors" happen with many enzymes but it is very critical in case of DNA polymerization. You can get information on star activity of restriction enzymes (just google it).

Since chemical reactions are governed by quantum physics, there is a whole lot of products that can come out of mixing together several multi-atom molecules. And all of those will have non-zero probability of occurrence. But this probability is extremely low at normal temperatures, so you don't see those products.

Enzymes lower activation energy and so increase chance of reaction, but only for certain substances and products (spatial position of reagents can influence outcome). In case of DNA replication, when wrong nucleotide is inserted, it happens because enzyme/template nucleotide complex has not enough specificity. All 4 nucleotides have rather high chance of participating in the reaction (but errors are still on order of $10^{-6}$ and lower).


Why should evolution not be equated with progress? My science textbook says this:

  Evolution should not be equated with progress. In fact, there is no real 'progress' in the idea of evolution. Evolution is simply the generation of diversity and the shaping of the diversity by environmental factors. The only progressive trend in evolution seems to be that more and more complex body designs have emerged over time. However, again it is not as if older designs are inefficient! So many of the older and simpler designs still survive [..] In other words, human beings are not the pinnacle of evolution, but simply yet another species in the teeming spectrum of life.

I am not sure if I agree with this; after all, humans do seem to be more advanced than dogs. Many people have asked me why I thought this was true, so here is my answer: Today, humans could wipe out dogs from Earth if they wanted, but you can hardly imagine  a scenario in which dogs would do the same to humans.

What am I missing here?

I'm glad you've asked the question as it is a common layman misunderstanding.

Dog vs Human

Your example comparing humans and dogs is actually very central to the logical flaw that yields many to equate evolution with progress.

There are several issues when you say

  humans do seem to be more advanced than dogs

Humans are not more evolved than dogs

Humans, dogs, jellyfish, oak tree, fungi, bacteria, .... we have all evolved during about 3.5 billion years. None of the extant lineages is more evolved than any other at least in terms of the number of years of evolution. Note, however, that what matters most when considering evolutionary time is the number of generations. Humans having a rather long generation time, it tends to make fewer generations. In this regard, one could expect a dog to have been through more generations than humans and could eventually be called more evolved but even there it is not that easy. See also Are we “more evolved” than present-day bacteria?

You are a human, be aware of your biases

As @Jamesqf rightly said in the comments, you did not feel like considering the dog's extraordinary sense of smell, better hearing, higher jumps, stronger jaws or protective fur. Not to mention, dogs can typically raise way more offsprings than humans can. Not to become personal but my 8 months old, 9 kg Cocker Spaniel runs 300 meters at the same time Usain Bolt runs 200 meters! You seem to have only considered things that make you human such as opposable thumbs and high cognitive abilities. Coming to cognitive abilities you will note that a puppy learns by association faster than a baby human. Dogs just plateau much quicker than humans.
Make sure that you understand that high cognitive abilities are not a goal or a direction of evolution. While it is hard to measure the evolution of intelligence for both a question of definition and question of measurement tools, it is very very likely that many lineages (incl. eventually the Homo lineage) have evolved toward reducing intelligence at some point (see this post).
You say humans could wipe out dogs from Earth however again it feels very human (and awkwardly combative and hostile) to consider the ability to kill as a measure of progress.

The illusion of considering two variables

You consider a correlation between two variables 1) how evolved a lineage is and 2) how advanced a lineage is. (As discussed in the first point, there is actually no variance in how evolved lineages are if we consider evolutionary time). You are determining those that are more evolved by how "advanced" you visualize the lineage. Your explanatory and response variables are therefore the same and you do not explain anything by saying 'humans are both more advanced and more evolved than dogs so evolution should equate progress'

Definition of progress

A big issue in your question is the definition of progress. For example, if you define progress as an increase of mean fitness (the concept of fitness in biology has nothing to do with bodybuilding, see here) over time, then yes evolution is in part to be equated with progress as increase in mean fitness over time is exactly what natural selection is doing (see the so-called Fundamental Theorem of Natural Selection).

Evolution ≠ Natural Selection

So, let's assume we define progress as an increase in mean fitness over time. As stated in the previous section, this is exactly what natural selection is doing. So, instead of saying Evolution should not be equated with progress, one could say Natural selection is to be equated with progress (as a reminder this assumes a very specific definition of progress)

You will note that I replace the term evolution with natural selection. It is often unclear to laymen but these two terms, while related, are different.

Evolution is a change of allele (loosely speaking, an allele is a variant of a gene) frequency over time. There are a number of mechanisms that can cause evolution, one of which is natural selection (which itself is caused by a fitness differential associated with genetic variance). But there is way more to evolution than just natural selection. Genetic drift, mutations, migration and other demographic elements are all important factors causing the evolution of populations.

You should have a look at Understanding Evolution by UC Berkeley. It is a very introductory online course on evolutionary biology that will teach you about the basic forces that cause evolution.

There is no real progress behind the idea of evolution.
Evolution is simply the generation of diversity and shaping of diversity by environmental selection.
The only progressive trend in evolution seems to be that more and more complex body designs has emerged over time. It doesn't means that the older designs are inefficient.
However, one of the simplest form of life (Bacteria) can even survive in harsh conditions such as hot springs or ice of Antarctica.
Therefore, Human beings aren't the pinnacle of evolution, but simply yet another species in teeming spectrum of evolving life.

SOURCE: NCERT Class 10 science textbook


Evolutionary advantage of F plasmid in bacterial conjugation Hi I would like to ask a question on bacterial DNA exchange, namely conjugation via F plasmid. It seems to me that all the F plasmid codes for is the sex pilus. What is the evolutionary advantage of the F plasmid? Does it code for anti-biotic resistance as well? Or enhances binary fission for reproductive success? Also, if conjugation transfers duplicated F plasmid from a F+ cell to an F- cell, why aren't all bacteria cells (that are capable of being F+/-) already F+? Is there a mechanism that somehow degrades your F plasmid?

Thank you in advance! I couldn't find the answers anywhere online.

F plasmids allow for the genetic exchange of material between cells, it's the closest thing to sex for most bacteria. Parts of the F plasmid are homologous to the chromosome of E. coli (mainly the transposons present on the plasmid) and through homologous recombination they can pick up bits of the chromosome. A lot of studies have been done where bacteria acquire traits such as galactose or lactose utilisation through these genetic exchange. They therefore allow fitness enhancing DNA to spread quickly through a population or species barriers [Ref].

Antibiotic resistance is not carried on F plasmids but there are many conjugative plasmids that do carry resistance genes (R plasmids). The F plasmid does carry a toxin/antitoxin system (ccdB/ccdA) [Ref]. If the cell loses the plasmid it will not be able to replicate its DNA because the toxin protein is very stable while the anti-toxin is rapidly degraded. So besides the evolutionary advantage there is also the possibility that it is simply 'selfish DNA' (see Richard Dawkins the Selfish Gene for details on this).

There are certain circumstances under which the F plasmid does not transfer such as low temperature so it is possible for a bacterium to lose the F plasmid and not get it back by conjugation. Maintaining a relatively 'useless' piece of DNA does have its metabolic cost so loss might confer a growth advantage.

Seems like the F plasmid would be more of a burden than anything.  Perhaps its just a selfish epitope.  Seems comparable to a parasite.  Maybe its a disadvantage to the individual, but an advantage to the bacterial strain due to recombinants generated through transfer of chromosome in Hfr cells.


Want to know about a creature which bite me I am Sachin from MP India. Few minutes back I have gotten bite by a creature. What is its name? Is it harmful if I got bitten by it? Feeling little pain there.

That is an insect, in the order Zygentoma. These are harmless, and do not bite. If you were bitten by something, it was not this?


What jellyfish is this? I saw this jellyfish at Brighton Beach, Victoria, Australia. I have searched jellyfish images but there is nothing similar. It is round with a diameter of approximately 80cm and the blue part looks like hundreds of thin tassels.

Looks like Pseudorhiza haeckeli. Based on cross motif, and long tail. Grows over a metre across. There is a photo at https://www.abc.net.au/science/photos/2012/01/11/3406019.htm?xml=3406019.mediarss.xml#bigpicturepos
but dont copy it here - copyright.