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Which animal species are known not to murder (a targeted attack leading to death) members of their own species?
Is there any evidence to suggest that some animal species do not murder  (a targeted attack leading to death) members of their own species? If so, which are the relevant species?

I think it might help to give a little bit more context - is this purely idle curiosity (in which case the answers will be all over the place) or do you have some particular goal ... ?

I asked this question from a general interest, as a view on murder (and the lack of it) from an ethological perspective.

Here are a few suggestions:

Any coral
Any sponge
Blue mussels
Sheep
Dugong
brown-headed cowbird
Blue whale
Common earwigs
Plasmodium falciparum (causing malaria)

If by the use of the term "evidence", you are expecting a peer-review paper that discuss the matter, I am afraid you wont find any as it is not really a question of interest to researchers. If you can prove wrong any of the above suggestions I will be happy to remove it (and eventually add some others).

Thank you very much for your answer. Would you think it would be possible to create some kind of a preliminary classification, as to categorize species into particular reasons which may cause the inability to, or non-occurence of, killing their own?

I suppose you would based the distinction based on whether a behavioural change might change the ability to kill an individual from the same species. You might quickly get into semantic issues esp. with species that have no brain. Also you would quickly run into the issue of guess work as you can't test the ability of a blue whale to kill another one because you cannot play out with blue whale behaviour as you want (and that would be way too expensive anyway).

As your follow-up question is a guesswork type of question, you might have better luck on WorldBuilding.SE but I am not quite sure what their rules are.

Did you mean the plasmodium parasite when you meant malaria?

Yes, that's what I meant. I edited to Plasmodium falciparum. I was looking for something deadly which does not kill members of its own species. There might be more obvious ("more true") examples.

@Remi.b Pandas do exhibit aggressively dangerous behaviour, therefore it's likely that some pandas have killed eachother. Cf. e.g. https://www.washingtonpost.com/opinions/five-myths-about-pandas/2015/08/28/d4a96b1c-4bfe-11e5-bfb9-9736d04fc8e4_story.html: Indeed, they do harm one another, particularly when males are establishing dominance or competing for females. Males in China’s Qinling Mountains are often observed with torn ears and bite wounds from tussling with other males. And in 2007, the first captive-born male reintroduced into the wild died after an apparent fight with other pandas.

@Remi.b I assume that the same counts for sheep? I am not inclined to think that, even regarding domesticated sheeps, the features which would normally account for dangerous damage during aggression have been bred out by domestication?

@Remi.b Regarding the questions surrounding "semantic issues" which you raise, I assume it's best to define killing as murdering due to a targeted attack. I have adapted my question accordingly.

@Remi.b The brown-headed cowbird is also known to be aggressive and kill other birds (cf. e.g. http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1188&context=usgsnpwrc). Why can we be sure that this doesn't sometimes happen to members of its own species?

It is a fundamental concept of the philosophy of knowledge, you can't ever be sure that something is not happening. I just know there are not territorial and I don't think they fight for access to mate.


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Why does a broad-leaved evergreen (Mahonia aquifolium) has red leaves?
To my knowledge, oregon grape (Mahonia aquifolium) is purportedly an evergreen shrub? Deciduous broadleaf plants lose their leaves in autumn usually and before that as the leaves die they oxidize and turn shades of yellow and red as carotenoids and anthocyanins are expressed.
For what reason does M. aquifolium turns red in the fall given that they DON'T drop their leaves? Does it somehow benefit the plant? Is it because oregon grape's ancestor used to drop leaves?

I don't know about Mahonia aquifolium, however, an "evergreen" plant does not mean the leaves will  stay green forever. Normally, all leaves of all kinds of plants, get old ("senescent"), take retirement from metabolic functions, store only waste products; and new leaves take the major metabolic functions. Now; a Typical Deciduous plant sheds all the senescent leaves on a Particular Season of the Year, whereas, a so-called "Evergreen" plant, typically, does not shade all the leaves at a particular season. Rather, they shade some leaves throughout year without bias to a season.

btw, write questions in more clear way. focus the topic you are asking about. You could also use separate paragraph or points. Also, avoid using short-scientific name from the beginning. Because, Separate, unrelated species, starting with same letter for genus, and with same "specific epithet" (of course they belong to different "species", but the "specific epithet" is same); may exist. You can use the short-name only-after you've once mentioned the full name. You need-NOT to memorize this as a rule, rather, can do it from common sense.

Tag edit suggest:  appropriate tags are botany, plant-physiology, ECOLOGY, and biochemistry. Molecular biology is not primarily  an appropriate tag (for me at least), because molecular biology is focused on the biochemistry of gene-expression mechanism. Adaptation-advantages, though discussed both in EVOLUTION and ECOLOGY, the present-day ECOLOGY seems more appropriate here, for limited number of tag-fields.

The photo input continues while the enzymatic reactions decline with failing temperatures which would mean the thylacoid pH will get out of hand. Anthocyanin shading the light harvesting centers is one means to prevent this. Yellow xanthophylls (yellow) is another but accomplishes the same end differently. It's about reducing PS2 activity, IMHO.

@user17343 I edited your post to try to improve the format. Feel free to roll back if you don't like the edit. +1 btw

Thanks to all the helpful answers!! I'm a little put off by the condescension on here, particularly in the scientific topics. It's an app, not a journal. We're coming to YOU for YOUR expertise, so talking down to people about their grammar or use of Latin here seems exceeding condescending and priggish.  Either way I appreciate all the input and time spent

Not directed at you @Remi.b

@JaguarDomingo I just had suggested you that how you could write the question so that more people could easily realize its content. I did not shown any condescension (& I'm not a  moderator).

@JaguarDomingo It is sometimes hard not to be considered pedantic when you are trying to (1) explain things and (2) improve the quality of posts so that it gets more view and motivate people to answer the question. As you agreed, we all appreciated AlwaysConfused's contribution to this post.

So, this 'condescension' label is directed at me?

No @JimYoung, I meant Always Confused --they've dogged other posts of mine with useless grammar suggestions and no actual answers or ideas. Yours was the most useful comment offered.

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What's this insect (Oregon, USA)?
Any ideas? This was taken in July on the beach of Bandon, OR, in the USA.

Your picture most likely shows Lichnanthe rathvoni of the family Glaphyridae.

The older answer is almost certainly not correct in any of its guesses; all of the possibilities listed are Palaearctic (see the sites https://fr.wikipedia.org/wiki/Epicometis_hirta, https://en.wikipedia.org/wiki/Tropinota_squalida, and http://www.coleo-net.de/coleo/texte/oxythyrea.htm for confirmation; the first and third will need translating for those not fluent in French and German, respectively).
Referring to Part V of M. H. Hatch, The Beetles of the Pacific Northwest (1971) (which covers the states of Idaho, Oregon, and Washington, and the province of British Columbia, in their entirety, and the western part of the state of Montana), and assuming the subfamily Cetoniinae is correct, I had thought this was Trichiotinus assimilis Kirby; there are inconsistencies between this photo and those provided by bugguide.net (see http://bugguide.net/node/view/22486); specifically, the elytra here are well-separated apically, and the coloration is quite different.  A review of Volume 2 of American Beetles showed me my error: the insect is a member of the family Glaphyridae (formerly a subfamily of Scarabaeidae), and the genus Lichnanthe; returning to Hatch, 1971 shows only L. rathvoni LeConte from the covered area; photos of that species in bugguide.net (see  http://bugguide.net/node/view/115846) show some variation in markings from the photo here (which is to be expected), but are structurally fairly close.
The genus Lichnanthe was most recently revised in the following paper:
Carlson, David C..  1980.  Taxonomic revision of Lichnanthe Burmeister (Coleoptera: Scarabaeidae).  Coleopterists Bulletin, 34(2):177-208.
which is available through JSTOR (a subscription, one-time payment, or access through a university will be needed).

This question already has an accepted answer. Given that your answer suggests the question refers to a different species than the one in the accepted answer, you should provide further evidence to why you think your answer is the correct one (at least a picture and a contrasting discussion what features match your ID but not the suggested one), otherwise your answer will probably be down-voted. Thanks!

In addition to my comment under the previous answer, see figure 103.34 (page 69) in the reference I cite there (the elytral markings differ from those in the photograph, but those can vary from one individual to another).  Figures 101.34 and 104.34 illustrate two of the other three Pacific Northwest genera (and the genus that is missing is most frequently encountered with ants).

After considerable delay I finally obtained a copy of Carlson 1980; that work reinforces the identification given above (the new species named by Carlson were not found in Oregon at the time of description).

Awesome, I already up-voted after your last edits, so my +1 still holds. :-)

I'm pretty sure it is in the Cetoniinae (flower beetle) family. Off-hand I would put it in the genus, Tropinota. It may be a subspecies or relative of Tropinota squalida or Tropinosa hirta. But it could also be closer to the genus Oxythrea.

The two (three? I'm assuming that either "Tropinota" or "Tropinosa" is a misspelling) genera given here do not appear in Arnett, et al., 2002, American Beetles volume 2 (pages 67 to 71).

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Effect of paracetamol or any antipyretic tablets
We all consume a paracetamol or any antipyretic tablet when we have cold or flu. And these tablets just reduce the body temperature. So my question is, when we have an infection and due to that infection we get fever, so unknowingly if we consume antipyretic tablets it will reduce the body temperature, so that means during that condition reduction of body temperature is harmful for our body as the infectious agent can make copies of it, as the body temperature is decreasing.

http://biology.stackexchange.com/questions/7627/how-does-paracetamol-interfere-with-immune-system?rq=1   also, http://biology.stackexchange.com/questions/7541/if-fever-is-a-natural-immune-defense-why-do-people-take-drugs-to-lower-it?noredirect=1&lq=1

The OP is possibly asking, "if fever is a natural protection process, then why fever-reducing (with a medicine or anything else) doesn't  promote the growth of the pathogen?"

This is a controversial topic. I co-authored a paper that drew on this research to make conclusions about population-level effects. The only situations I can recall where antipyretics have been shown to be clinically beneficial is in severe cases where inflammation itself is causing neurological damage (e.g., acute brain injuries); results for e.g. infectious diseases are ambiguous. In our paper, we summarized previous research on the costs and benefits of fever suppression as follows (our summary may be slightly biased in the direction of "fever suppression is bad" ...)

Previous investigations of the effects of fever suppression have focused on the clinical benefits and costs to the individual [8,9]. The adaptive value of fever [10–13] is well known to immunologists; for example, Janeway's Immunobiology [14, p. 110] notes that ‘At higher temperatures, bacterial and viral replication is less efficient, whereas the adaptive immune response operates more efficiently’. Others argue that the adaptive value of fever arises instead from activation and coordination of the immune response [12]. By contrast, a common view in the medical community, as expressed for example in Harrison's Principles of Internal Medicine, is that the ‘treatment of fever and its symptoms does no harm and does not slow the resolution of common viral and bacterial infections’ [15, p. 107] ...

References from this section:

Mackowiak PA. 2000 Physiological rationale for suppression of fever. Clin. Infect. Dis. 31, S185–S189. (doi:10.1086/317511)
Eyers S, Weatherall M, Shirtcliffe P, Perrin K, Beasley R. 2010 The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analyis. J. R. Soc. Med. 103, 403–411. (doi:10.1258/jrsm.2010.090441)
Kluger MJ. 1991 The adaptive value of fever. In Fever: basic mechanisms and management (ed. Mackowiak PA), pp. 105–124. New York, NY: Raven Press Ltd.
Hasday JD, Fairchild KD, Shanholtz C. 2000 The role of fever in the infected host. Microbes Infect. 2, 1891–1904. (doi:10.1016/S1286-4579(00)01337-X)
Blatteis CM. 2003 Fever: pathological or physiological, injurious or beneficial? J. Thermal Biol. 28, 1–13. (doi:10.1016/S0306-4565(02)00034-7)
Simon HB. 2003 Hyperthermia, fever, and fever of undetermined origin. In Infectious diseases: the clinician‘s guide to diagnosis, treatment, and prevention. (ed. Dale DC). New York, NY: WebMD Professional Publishing.
Murphy KM. 2011 Janeway‘s immunobiology, 8th edn. New York, NY: Garland Science.
Dinarello CA, Porat R. 2008 In Harrison's principles of internal medicine (eds Fauci AS, Kasper DL, Longo DL, Braunwald E, Hauser SL, Jameson JL, Loscalzo J), 17th edn, p. 2958. New York, NY: McGraw-Hill.

Both @ashafix and @benbolker have given a pretty nice answer, I just wanted to add some more points to it. First of all, it wouldn't be correct to say that these tablets just reduce the body temperature as in that case, intaking antipyretics would be the same as drinking a glass of cold water in fever which, generally, shows the same effect as you mention in the question.
Paracetamol does reduce body's temperature. Though its exact mechanism is unknown, a theory from here[1] suggests that:

The COX family of enzymes are responsible for the metabolism of arachidonic acid to prostaglandin H2, an unstable molecule that is, in turn, converted to numerous other pro-inflammatory compounds. Classical anti-inflammatories such as the NSAIDs block this step. Only when appropriately oxidised is the COX enzyme highly active. Paracetamol reduces the oxidised form of the COX enzyme, preventing it from forming pro-inflammatory chemicals. This leads to a reduced amount of prostaglandin E2 in the CNS, thus lowering the hypothalamic set-point in the thermoregulatory centre.

But, it also does other jobs like this[1]:

An article in Nature Communications from researchers in London, UK and Lund, Sweden in November 2011 has found a hint to the analgesic mechanism of paracetamol, being that the metabolites of paracetamol e.g. NAPQI, act on TRPA1-receptors in the spinal cord to suppress the signal transduction from the superficial layers of the dorsal horn, to alleviate pain.
This conclusion has been contested in a new hypothesis paper on how paracetamol might act. The author concedes that NAPQI is the active metabolite but that this reactive compound should react not only with the thiol in TRPA1 but also with any other suitably available nucleophile that it happens to encounter. It is suggested that thiol groups in cysteine proteases, e.g. the proteases that take part in the processing of procytokines, such as those generating IL-1β and IL-6, might be the targets giving rise to overall analgesic effects.

Coming back to your main point i.e. when paracetamol reduces the body temperature (which it does), how is it helpful for the body to fight infections. Refer to this answer[2]:

So when your body begins to fight an infection you get a fever (which can make the environment uncomfortably hot/cold) and the tissues around your joints swell (which makes movement and relaxation uncomfortable). NSAIDs like Ibuprofen reduce those symptoms, making the duration of the infection more bearable. They do not reduce the length of the infection by any measure (and might increase it, though the research is not particularly conclusive), but can make the day go by better if you've used up all your sick days or have a child to take care of.
Basically, people take NSAIDs to reduce fevers for the same reason most take any over-the-counter pain medications. To make life a little easier in the meantime.

A direct answer is given here[3]:

While quality research has been lacking, there's some evidence that shows reducing a fever actually hinders recovery from infections, the cause of most fevers in the community, Young says...Also, if you take paracetamol to lower a fever, it may make you feel better because it also acts as a painkiller. (Whether lowering a fever in itself makes you feel better isn't clear.)...But when you're critically ill, some evidence suggests treating a fever might make it less likely you'll survive.

References:
1.https://en.wikipedia.org/wiki/Paracetamol
2.If fever is a natural immune defense, why do people take drugs to lower it?
3.http://www.abc.net.au/health/talkinghealth/factbuster/stories/2012/07/31/3557498.htm

According to this study paracetamol/acetaminophen does not have any effect on the influenza virus.

Regular paracetamol had no effect on viral shedding, temperature or clinical symptoms in patients with PCR‐confirmed influenza. There
  remains an insufficient evidence base for paracetamol use in influenza
  infection.

Your statement "And these tablets just reduce the body temperature." might be an oversimplification. The mechanism of action of paracetamol is still a mystery but it is an analgesic which explains its use during viral infections.


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Why is RAS undruggable?

Why can't mutated RAS get inactivated by GTPase?
Why don't we have any inhibitors for RAS-GTP binding?
Why is RAS undruggable?
How can mutated RAS be inactivated?

I had been researching on the topic and had a lot of doubts in the regard. Please provide me direction, as to where can I find answers to the questions and continue the research "how can mutated RAS be inactivated?"

This is not one, but four questions and all of them are quite complex - actually these are the key question to treating a lot of cancers. Can you please narrow it down?

Do you have a reference for question 3? Why do you think RAS is undruggable?

www.nature.com/nrd/journal/v13/n11/full/nrd4389.html


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Evolving a smaller brain
In Kurt Vonnegut's novel Galapagos, a certain mammal species, due to drastic and peculiar environmental changes, evolves (among other features) a smaller and smaller brain.
Has this ever happened? Are we aware of any species whose ancestors had remarkably bigger brains?

Could these be an example of island dwarfism affecting a human-like species?

Brain size vs intelligence
Of course brain size and intelligence are two very different things. Sure these two characteristics are correlated (assuming we manage to define intelligence in any intelligible way). The sperm whale has a brain that is 8 times larger than the human brain for example and the Brown thrasher (small bird) can learn thousands of songs while other birds can memorize the location of thousands of seeds. So really size is not the only thing that matters.
You might want to read about brain-to-body mass ratio and the encephalzation quotient.
Evolution toward smaller brain size
I am pretty sure such examples should exist but it might be hard to come up with good citation on the subject because

It is hard to tell other than through fossil record how big was the brain of a certain ancestor
It is quite a specific question

Someone might well come up with good answers. Of course, most examples of evolution toward smaller size (such as through insular isolation as pointed out by @user137) will result is reduction in brain size however, I am not sure these example would satisfy your needs/curiosity.
Evidence of metabolic cost of brains
In the meantime, I would like to point to a few among many evidences that brain comes at a fitness cost (that might be compensated by benefits of learning and other "brain abilities"). Those evidence mainly comes from experimental evolution in labs but some comes from comparative genomics as well. In short:
Brain consumes a lot of energy (Magistretti 2013). There are evidences in Drosophila (Mery and Kawecki 2003), birds (in this review I think: Nowcki et al. 2001) and guppy (Kotrshal et al. 2013) that evolution of learning abilities comes at an important metabolic cost. Johnston (1982), and more recently Snell-Rood et al. (2009) made reviews on the cost and benefits of learning abilities that you might want to have a look at.

Thank you, I'll read the resources you linked. Just one thing: the key word in my question is drastic: I'm not looking for a little reduction in brain size, but to a great one, so much that it almost certainly must involve a reduction in intelligence.

@giorgian I expanded the first part a little bit just to give an indirect justification of the importance of this part ;)

The acanthonus armatus is famous for its small brain. As a deep-sea fish it is required by its environment to consume very little energy, and so it is at least plausible that this is an adaptation to its environment. It's hard to compare it to the fossil record because brain size is usually estimated by the size of the cranial cavity, but a. armatus has a fairly ordinary cranial cavity .It is very nearly empty, with the small brain filling only a small fraction (dwarfed by the semicircular canals). The authors of the paper linked above weighed a number of brains, the largest of which was 48.7 mg in a 180 g fish.


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Does apoptosis occur more at a particular time of day?
I am interested to know if apoptosis (programmed cell death) occurs more frequently during daytime or nighttime hours, e.g. if apoptosis is associated with a circadian rhythm.
A simple search turned up a couple of articles:
Diurnal variations in the expression of radiation-induced apoptosis
The Circadian Clock Controls Sunburn Apoptosis and Erythema in Mouse Skin
However, I'm not sure how to interpret these and would appreciate the help of a biologist. I don't have a very good idea of the limitations of our investigative tools, or indeed whether my question is well-formed. Thank you!

Your question is quite well-formed, however all I can say so far is: I don't know. Maybe it is known, however I could not find any information on this in the literature. In general, little is known about the crosstalk between circadian rhythms and apoptosis. It is known that circadian rhythms regulate DNA damage repair, so I would assume that the same is true for other maintenance functions such as apoptosis of redundant or damaged cells.
I don't know which research tools are available to you, but if you want to look at the effect of the clock on apoptosis signalling in a simplified setting, I would recommend synchronising the clock of culture cells with dexamethasone (you'll find a lot on that in the literature) and then using the apoptosis read-out of your choice on samples of these cells taken in regular intervals. I recommend taking samples every 4 h over the course of 24-48 h. You can make this less tedious by synchronising separate batches at different time points. As read-out for apoptosis I recommend Caspase-3 / -7 activity, ideally by Western Blot or an enzymatic activity assay using Ac-DEVD-AMC or something similar.
If you want to have a look at the effect in a more complex, physiological model, you will have to use mice.
I hope I could help you a little. Good luck!


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Boys born in excess - how can the nature draw from non-natural distributions?
The probability of a newborn baby to be a boy is not exactly 50% but a bit more. I have been given the explanation that it is because boys act more self-destructive during the early ages and so the distribution evens out during time. But how can the nature know beforehand that boys should be made in excess?
It would make sense that the nature followed natural distributions in its choices like uniform, gaussian, exponential etc. but this seems not to be the case. What are the motivations and mechanisms to deviate from natural distributions? Can you come up with another examples of such "non-natural behaviour" in nature?

Welcome to Biology.SE.
"Natural" vs "non-natural" Distribution
There is no such thing as a "natural probability distribution". Actually, biological system often produce distributions that does not match with commonly used distributions just because the assumptions yielding to these distribution are sometimes poorly met in nature. In other words, many biological variables meet more complicated distribution than the standard uniform, binomial, geometric, beta, exponential, and other distribution you know of.
Of course the gaussian distribution is kind of a special one that is often approximatively reproduced by biological system as a consequence of the central limit theorem.
Some distributions are more used than others but there exist an infinite number of definitions and anyone can construct one. Here is my distribution of the day. $P(x | y,z) =  C \frac{y^x - exp(-yz)}{x+z+y}$, where $C$ is a constant of integration to ensure $\int_{-\infty}^{\infty} C \frac{y^x - exp(-yz)}{x+z+y} = 1$. I will call this distribution the "remi.b distribution". I have no idea what kind or process it can model and nobody will probably ever use it but it is a legit distribution.
Developmental mechanism
You can read this post and that post about the developmental mechanism that yield to such bias sex-ratio at birth.
Evolutionary processes

how can the nature know beforehand that boys should be made in excess?

Organisms producing a bias sex-ratio are selected for as they increase the average fitness among their offspring. As such the population is selected toward creating such bias sex-ratio. Organism don't know, they just do.
In order to understand the evolution of sex-ratio a bit better, you should have a look at this post.


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How many cells of each cell type are there in C.elegans?
C.elegans is a very well studied organism. Of its approximately 1000 cells in the adult stage, how many of each cell type are there? The only information I could grab from the internet (wormatlas.org) is that there are about 300 neurons. What about the rest of the cells? An answer for other simple animals such as sponges, planaria, jellyfish etc., even in relative proportion of cells, would be accepted.
(I appreciate that this question is somewhat broad and unspecific: eg. are all neurons of the same type? (Yes) Are germ cells included? (No, because they vary) Please ignore such niceties.)
Edit: To clarify, the question asks for a breakdown of the cells along the lines of:
Neurons 300 cells, Epithelium 200 cells, etc., Total 1000 cells

I guess you didn't find this page, then? I'm not a worm biologist, so how did I find such information? I googled list of c elegans cell types. PLEASE do your own research before asking here.

@MattDMo You should make an answer out of the link you post. An answer as simple as There are about n types of cell (see here) would be enough.

The cell map of C.elegans is well known.

Sorry, did I ask "How many cell types are there in C.elegans?" No I did NOT want a list of cell types. PLEASE read the question carefully before answering.

-1 and VTC because this question is unclear (what exact do you define as a "cell type"?) and easily answerable yourself once you have a clear definition.

Thanks to @MattDMo comment...
There are about 17 cell types in hermaphrodites C. elegans (see here). However, it varies very much depending how you count. You might want to have a look at  Sulston and White (1988).

Actually http://www.wormatlas.org/celllistsulston.htm is probably closer to what OP is after, although the whole site is highly relevant.


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Confusion about the brain regions - temporal cortex, hippocampus and and white matter
I am a computer scientist working with brain data. I have some data from different brain regions, and the regions are called temporal cortex, parietal cortex, hippocampus and forebrain white matter. I want to show those regions on a brain image in a presentation.
The problem is, when I search the brain images online, I cannot find the regions my data mentions. The regions in the search results are usually called "lobe" rather than "cortex". And when I search for "forebrain white matter", the results are usually about "cerebral white matter". I am totally confused. Here are a few questions:

Are "cortex" and "lobe" the same thing? Or does cortex means gray matter while lobe contains both gray and white matter?
Does hippocampus contain gray and white matter? Or does it reside in the inner side of the temporal lobe, meaning it is in the white matter part of the temporal lobe?
Are "forebrain" and "cerebrum" the same thing?
Why is hippocampus considered part of the temporal lobe although it has the long side of it outside of the temporal lobe?

Lobes are zones (or portions) of cortex

most portion of hippocampus is grey matter. However wikipedia tells some portion of hippocampus, contains white matter. such as Alveus of hippocampus, Fimbria of hippocampus, Perforant path,Schaffer collateral. https://en.wikipedia.org/wiki/Hippocampus_anatomy table at bottom

Cortex, in general, means the outer part of an organ. The opposite of cortex is medulla.

Me too have confusion on Forebrain ("Procencephalon") and Cerebrum are same things or not?

"Lobe" refers to a section of the cerebral cortex, which is the outer part of the cerebrum. The cerebrum contains several structures, but the one that most people care about is the cerebral cortex, which is the 2-4 mm thick layer on the surface of the cerebrum. The cerebral cortex (or "cortex") is divided into several lobes, e.g. temporal lobe, occipital lobe. So, cortex and lobe are not the same thing, as the lobes subdivisions of the cortex as a whole. (See https://en.wikipedia.org/wiki/Cerebral_cortex)
The hippocampus is a region of the cortex in the temporal lobe. Therefore, it consists of gray matter. However, it is connected to several other structures by white matter (e.g. the fornix), and these structures are related to the hippocampus. (See https://en.wikipedia.org/wiki/Hippocampus#Anatomy)
Forebrain refers to the cerebrum as well as other structures, such as the thalamus and hypothalamus. The forebrain is defined as the telencephalon (which is basically the cerebrum) and the diencephalon (which contains the thalamus and hypothalamus). (See https://en.wikipedia.org/wiki/Forebrain and https://en.wikipedia.org/wiki/Diencephalon)
I don't know what you mean by the temporal cortex having "the long side of it outside the temporal lobe", but the temporal cortex and temporal lobe are basically the same thing.

Sorry, I had a typo in the 4th question. It should say "hippocampus". Corrected.

So, then, although "cortex" and "lobe" are different things, what my data means by "temporal cortex" is probably the same as "temporal lobe"?

I did not know temporal cortex consists of gray matter. So, temporal lobe thickness is 2-4 mm since it is part of the cortex. How about the gray matter thickness?

@user5054 the cerebral cortex is composed of the gray matter; so thickness would be the same. However, cortex is not equivalent to gray matter. In the spinal cord, the organization is reversed (outer part is white matter). The term, "gray matter", IMO has relatively little significance nowadays because we can see the anatomy of the brain at a much higher resolution. So, while the organization does matter, the terms - gray/white matter per se convey little information.


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Can anyone help identify which insect is this?
I know this may not be the right forum for insect identification, but I couldn't find any reliable source of information. Please bear with me

The insect was found on my front door, total length may be about 2 rice grains
You can see wings and slender legs behind the body
I live in India, if it matters.

I think @picapica is correct. According to this website, there are about 126 species in India, and you can narrow your search down by checking which genera & species occur in your biogeographic sub-region of India. If you happen to encounter Ephemeroptera again, and want a species-level determination, I would suggest you try to get a photo against a lighter background. The veins on the wings should be visible, as they are important for determination.

I think this is some species of mayfly (order Ephemeroptera). There are some 3000 species in the world so I can't be more precise than that. It looks very pale and it's got a bit of a strange posture, so I'm guessing it just emerged from it's larval skin (in that case the skin should be left behind close by).


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What is the difference between endomysium and sarcolemma
They both are lining of muscles so how can we differentiate these two? Please answer in simple terms.

What's an endomyceus? When I search google it says 'endomysium'. Am I still new in the field or is the spelling wrong?

Sorry,it is endomysium

If you try "endomysium" in Google, the very first result (wikipedia) is very clear: endomysium is a layer of connective tissue that surrounds the muscle cell, whose membrane is called sarcolemma.

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Check this other image too from google. A single muscle cell or fibre has been magnified to show the sarcolemma and other contents like eccentric/peripheral nuclei as well as sarcoplasm. It's not the best image but hope this is ok.

If you have more information to add to your answer, please use the edit link (between share and delete just below the text of your answer). Please do not create a new answer unless it is substantially different from the first. Finally, you must cite/link to the sources of all images you use in answers (and questions). It helps to provide context, may give additional sources of information, and is just scientific common sense - you always cite your sources.

Just to illustrate Gerardo's answer, this picture is provided. The endomysium as you see is a layer of connective tissue which surrounds the individual muscle fibres (cells) (in between one muscle cell and the next) but each muscle cell in particular is lined or covered by a plasma membrane called the sarcolemma.


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Pharmacological inhibition of Ras
I was reading this review and came by this:

Direct pharmacologic inhibition of RAS has been a major challenge.
  Interference with the nucleotide-binding pocket of the protein seems
  to be far more difficult than interfering with the analogous
  ATP-binding pocket in kinases. This is presumably due to the much
  higher (picomolar) affinity of RAS for GTP.

What is meant by affinity? How do inhibitors work (in this context)?
Kindly help me as to what does this mean, I am new to biochemistry.

It is a paid subscription, but still here is the link http://www.nature.com/nrd/journal/v13/n12/full/nrd4281.html

There is a section with a non-mathematical description of Receptor/ligand binding affinity in the Wikipedia entry for Ligand, and a numerical approach in Alberts et al. — especially Fig.3-44. The treatment of protein inhibitors in textbooks is usually done in relation to enzymes, which are more complex than other binding proteins. However the section on competitive inhibitors in Wikipedia, for example, is relevant to other proteins.

I have edited your title to make it appropriate to the specific question you have asked about inhibition of Ras (note conventional capitalization). This makes for better indexing, should others have a similar question later.

Protein binding interactions are usually referred to by how easily the binding partner can be displaced by something other than the preferred substrate. Usually, this is in reference to the concentration of the binding partner required such that the average occupancy of the protein (in this case RAS) to the binding partner is ~ 50%.
If the affinity protein for a given binding partner is in the picomolar range, that means that it binds so tightly that very very little substrate is needed to achieve 50% occupancy. In order to interfere with RAS's preference for GTP, you would have to design something that RAS likes to bind to with even greater preference that would be able to displace GTP. This has proven quite challenging.
Other kinases, whose affinity for their substrate is not nearly as high, have been easier to design molecules that displace their endogenous ligands and hence interfere with their function.
I know it is Wiki, but the activation/deactivation section of this Page provides some insight into how RAS binds GTP and turned on, how GAP functions to help RAS hydrolyze GTP->GDP, resulting in turning off RAS downstream signalling. RAS signalling is actually a balance between Guanine nucleotide exchange factors causing RAS to drop GDP for GTP (turning RAS on) and GTPase activating proteins mentioned above (GAP).
Mutated RAS in cancer often involves a coding change such that the ability to hydrolyze GTP->GDP is mitigated, thus leaving RAS in the ON state.
For your initial question of inhibitors (and more general). Cellular signalling involves the interaction of proteins with other proteins and/or signalling molecules and/or DNA/RNA. Very generically, inhibitors interfere with this interaction.
Example: Kinases add a phosphate group to another protein, that can among other things change the affinity of that protein for its binding partners, and thus set off a downstream signalling cascade. If kinase A phosphorylates protein 1, and you inhibit kinase A from doing this, you have inhibited downstream effects from protein 1's signalling cascade.
Take a look at this picture:  The two drugs in red interfere with downstream signalling cascades in B-cell receptor signalling by preventing endogenous binding/signalling events.


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What kind of fish is this?

What sort of fish is the big one in this picture? I saw it in an aquarium so I don't really know anything about its habitat.

Its a Giant Gourami, Osphronemus goramy.
The giant gourami (Osphronemus goramy) is a freshwater species  believed to be native to Southeast Asia, and has been introduced to other parts  of the world.
This species is commercially important as a food fish and an aquarium fish.

(Source: tropical-fish-keeping)
Reference: fishbase

Several smaller gouramis' are common in the aquarium trade ; this one maybe only as a special order. Interestingly one of the small ones is also called "giant" (about 4 in. long).


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Why can't the mutation for this simple pedigree be X-linked recessive?
http://ocw.mit.edu/courses/biology/7-012-introduction-to-biology-fall-2004/exams/finalprac.pdf
For question 7a on pages 10-11 of the above link, why can't the mutation be X-linked recessive?
The solution says "An autosome, because individual 6, a male, has 2 alleles." However, can't individual 6 just have a wild type X-chromosome if he inherited a Y-chromosome from his dad and a wild type X-chromosome from his mom? Also, if he is heterozygous for this trait, it also seems from the DNA fragment analysis that he expresses both alleles; how is this possible f the mutation is recessive?

think about what the genotypes and phenotypes of the third generation (i.e. individuals 5-8) have to be if it was a x-linked recessive gene...remember that x-linked recessives will be manifest in all males and only females who happen to get a recessive X chromosome from mom and dad

Say X is dominant and x has the recessive phenotype. Couldn't the layout be: XY (grandfather), Xx (grandmother), XX (1), xY (2), Xx (3), XY (4), Xx (5), XY (6), XY (7), xY (8)? Or is the reason why we know individual 6 has both the dominant and recessive alleles is because of the DNA fragment analysis- because there is a 1000 bp fragment and another sequence that was cut into 600 bp and 400 bp fragments?

This cannot be X-linked recessive because of the picture of the gel that has been shown.
If it were x-linked recessive, then person 6 would be completely clean from the gene mutation since he is male. If that were the case, he should only be showing two small bands at 600 bp and 400 bp since he has only one good X chromosome.
However, his gel column shows a 1,000 bp fragment, which means that one of his genes was not cut by the Nhe1 enzyme. This implies that that one gene is being vut (hence the 600 bp and 400 bp fragment) and one gene is uncut (hence the 1,000 bp fragment). Since person 6 has two genes, and males only have one X chromosome, this must be an autosomal disease.
This is also reinforced by person 5, who has the same column as person 6. Person 6 also shows an uncut and cut gene by Nhe1. Since their dad has the disease, and neither of the children have the disease, it must be recessive in nature.
Person 7 has two normal genes (hence the two thick bands at 600 bp and 400 bp) and person 8 has two recessive genes (hence the one thick band at 1,000 bp). Their parents must both have a recessive trait for this to happen.
Hope this helps! Let me know if anything is unclear


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Resources to study the cell as a "mechanism"
I am looking resources that effectively describe the cell as a mechanism. The cell might be irreducibly complex, but the individual components must necessarily have simple functions, locks, keys, switches, gears, membranes, and extruders. Is there any resource that exists that classifies the great many substances in the cell in this manner?

The basic cell biology textbook does explain different parts of the cell. Can you please clarify your question?

The cell is not "irreducibly complex" at all. What makes you think it is? As @WYSIWYG suggested, you should read up on the field of "Cell Biology".


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Is nucleoside-triphosphate delivery to RNA or DNA polymerase active or passive?
Are nucleoside triphosphates (NTPs) actively delivered to RNA polymerase (similarly dNTPs to DNA polymerase) through some active chaperoned process, or are they so abundant in the nucleus that they rely simply on stochastic diffusion?
Are there any relevant papers on this process?

You or someone else seems to have changed the question from dNTPs and DNA polymerase to NTPs and RNA polymerase. This negates the answer that @BlueFoxy went to the trouble of providing. In any case I'm still not clear what you are asking. Are you asking about how the precursors get from the cytoplasm, where they are thought to be synthesized, to the nucleus, or to the polymerase when already in the nucleus? If the later, why do you think the situation is any different from any other stochastic process involving enzymes and substrates?

The principles would be the same for NTP-RNAP and dNTP-DNAP so it doesn't really matter.

@WYSIWYG — Not necessarily, although the whole idea of chaperones for (d)NTPs seems absurd to me. I've changed the title slightly as I see the question has been edited to include this.

There have been significant edits to my question by moderators or others, and I'm not sure I understand the wording of my own question anymore. My question is literally just the colloquial "is there something in the nucleus actively delivering nucleic bases to polymerase to attach to new DNA strands, or does it just happen through random collisions/diffusion)

@MikeFlynn We just made the statement more scientifically accurate. Don't worry; we have not changed the meaning. If left to what it was, your question would have been considered unclear.

In PCR the same thing take place without any help of chaperones etc.

@Mike Flynn Delivering NTPs to be used by a polymerase expends energy from ATP ... therefore it is active transport. :)  (While that seems like an abuse of the definition, I'm not sure it is!)

The amount of dNTPs is so important and sensitive the level of dNTPs should be optimum  not lower or higher. Lower amounts lead to insufficiency  and higher amounts lead to increased mutation rates. Also, this optimum amount of dNTPs should last for a couple of minutes to supply dNTPs needed for replication. The delivery of dNTPs is due to molecular signalling & stochastic diffusion.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2847218/
"Eukaryotic cells contain a delicate balance of minute amounts of the four deoxyribonucleoside triphosphates (dNTPs), sufficient only for a few minutes of DNA replication. Both a deficiency and a surplus of a single dNTP may result in increased mutation rates"

http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.2010.01719.x/pdf
"Optimization of intracellular concentrations of dNTPs is critical for
the fidelity of DNA synthesis during DNA replication and repair
because levels that are too high or too low can easily lead to
increased rates of mutagenesis"

http://www.nature.com/ncb/journal/v14/n7/full/ncb2540.html
"Production of deoxyribonucleotide triphosphates (dNTPs) is essential for DNA synthesis during replication and repair, and abnormal or imbalanced dNTP levels increases mutation frequency. Pagano and colleagues now demonstrate that the SCF-cyclin F ubiquitin ligase controls dNTP production during the cell cycle and following genotoxic stress"

http://www.ncbi.nlm.nih.gov/pubmed/22234185
"alterations in dNTP pools are associated with increased mutagenesis, genomic instability and tumourigenesis"

To be clear, are you saying that nucleosides can arrive both by chaperones and diffusion?

@James chaperons have nothing to do with dNTPs delivery at least not directly . http://faculty.washington.edu/baneyx/Chaperones/Chaperones.html chaperons just control the folding and unfolding process of proteins by interacting with mediators .

You provide some good references on the regulation of dNTP synthesis, but you do NOT answer the question. I would up-vote your answer if you added a conclusion on the lines of "In none of these papers is there any suggestion that the dNTPs enter the nucleus and reach the DNA polymerase by any other mechanism than diffusion. Furthermore, with rare exceptions (e.g. exotic metal cofactors), chaperones are only involved in the delivery of proteins. In the absence of any published evidence it is reasonable to conclude chaperones are not involved."

Many processes in the cell, also processes involving compounds that have a lower abundance than the NTPs, rely on stochastic diffusion. Even the polymerase is not actively transported to the nucleic acid, it just diffuses until it finds a proper binding place.
Also, the energetics of active transport would not make sense. One of the NTPs is ATP, one of the major energy carriers in the cell. It would make little sense for the cell to actively transport ATP to the polymerase on the nucleic acid, because active transport needs energy, thus likely ATP or something similar itself. This would then have to diffuse to the transporter to keep it moving. It would be cheaper for the cell to just use that ATP directly, because you're relying on diffusion in both cases.
This is not even taking into account that 1 protein cannot actively move across the cell, even expending energy. Systems that do something like this are much more complex, such as myosin (moving along actin filaments).

One of the dNTPs is certainly NOT ATP, it is dATP. And chaperones do not necessarily require energy. I'm afraid it's your arguments that don't make sense, irrespective of the validity of your conclusion.

Chaperones aren't diffusing any faster without energy, and sorry for automatically typing dNTPs (although you could have just corrected this).

As regards dNTP and NTP, I think the question has been changed from one  originally about DNA and I didn't notice. I assume we are talking of chaperone proteins. I know of no chaperone proteins (or indeed any other protein) which uses the energy from hydrolysis of ATP to increase its diffusion in solution (rather than across a membrane, which is not relevant to the question). Do you? And what do you mean by 'active transport' needing energy? Are you thinking about active cation transport, which is irrelevant here?

Diffusion is free, if you want to actively create a concentration gradient (higher at one point than another) it's going to cost energy, no matter how you do it.

I know diffusion is free, but you seemed to be suggesting you could use "energy" to accelerate it. But who wants to create a concentration gradient? If the NTPs diffuse to the polymerase they will be removed by reaction, pulling more into the nucleus by mass action.

That's why chaperones are not used here, I'll try to clarify.

I know chaperones aren't used here. I was criticizing the arguments in your answer, not your conclusion. The only examples of chaperones for small molecules I know are for things like Nickel in urease. Otherwise, they are only used for proteins.


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Memory capacity of the human brain in bytes?
Is there an estimate out there for how much memory (in bytes) an average human brain can have? Is there a physical limit?

This is heavily subjective. For example, one way of thinking about this whats the longest series of numbers (limited to 0 or 1) that you can actually remember? It's probably not that long. Does that mean one has the brain capacity of a dozen or so bits? Or do you say that it takes petabytes of memory to simulate the synaptic connections in a rat brain and extrapolate from there? Have you already hit the physical limit (odds are you can't remember what you had for breakfast 5 Tuesdays ago)?

Memory is much more than "remembrance". The cells store countless information. Technically every single molecule of certain proteins can store at least a bit of memory. You cannot really measure cognitive memory in terms of bits and bytes.

Here's one fun way of thinking about it: Say that the brain stores information as a connection between two neurons, so a bit is simply whether there is a connection between two neurons. There are estimated to be about 100 billion (1e11) neurons in the brain, so that's  2^(1e11 choose 2) bits, which is some absurdly large number (way way more than the number of atoms in the universe).

Not sure what I was thinking in the last comment -- it would of course just be (1e11 choose 2) bits, which I guess is about half a zettabyte, which apparently is approximately the content of the entire www in 2009 (wikipedia).

This not a bad question I think. I agree that brain information storage is not easy to define, and probably it's not feasible to give a good estimate, but the brain does store information, and information can be measured in bits. Yes, you need to be a more specific on what you consider "information" in this context, and probably you need some type of "fuzzy" or probabilistic measure, like how much information a normal adult would be capable of recalling on average. But I wouldn't be surprised if there are some estimates of this, or at least attempts to estimate it.

There are quite a number of very similar questions over at [cogsci.se]. You can start here and use the Related list of questions on the right.


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Stability of DNA double helix conferred by base stacking
Our school textbook states that base pairs confer stability to the B-DNA double helix in two ways:
1) Hydrogen bonding between purines and pyrimidines of opposite strands.
2) "Stacking of one base-pair plane over the other"
It's the second point that I'm not able to understand. I did try looking it up on the internet, but I'm not able to find anything relevant in that regard.
So could someone please try explaining that second point to me?

When you carefully look at the structure of DNA helix, you will notice that consecutive bases are partially layered i.e. one base is "on-top" of the other base. Stacking is a chemical phenomenon in which the cloud of the pi-electrons in an aromatic molecule interact with that of the other. This interaction is non-covalent. Since the DNA nucleobases are aromatic molecules, they also exhibit stacking which stabilizes the structure of the DNA. A study by Yakovchuk et al. (2006) suggests that base stacking has higher contribution to DNA stability than base pairing. Sponer at al. (1997) found that there is no great difference between the stacking energies of B- and Z- forms of DNA helix.

In short, because of the pi bonds in aromatic rings, they're attracted to each other when stacked (or in several other conformations). Explaining is maybe better done by the Wikipedia page, but this is what you're looking for:
https://en.wikipedia.org/wiki/Stacking_%28chemistry%29
For a more in-depth look you could take a look at this article for example:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360284/


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Resistance to Antiseptics
I know that bacteria can become resistant to antibiotics.
Why do antiseptics like alcohols, PVP-I, still work on the strains of bacteria we have today? Shouldn't some bacteria have evolved to be resistant to them? I only hear about antibiotic resistance, so my assumption was that antiseptic resistance isn't a thing that happens.
What fundamentally differentiates antibiotics and antiseptics so that antiseptics are not resistance-prone?

For some classes of antiseptics the effect is more simple chemistry or even physics than biochemical toxicity. Ethanol will just denature proteins and dissolve the membrane, and the used concentration of ethanol is so high that no amount of efflux pumps is going to save the bacterium. Some other compounds work in a similar brute force way: QACs will break the membranes, hydrogen peroxide will just oxidize everything. For iodine (like in PVP-1) the mechanism is not really known, but probably it also just reacts with all kinds of things in/on the bacterial cell and kill them.
Antiseptic resistance could happen for some other antiseptics (or low concentrations of the compounds mentioned above). For some antibiotics, resistance is caused by the expression of efflux pumps that just pump out enough antibiotics so the cell survives. Bacteria could do the same for these antiseptics. The reason why it's not that much of an issue is that the application is rather different. Antibiotics are for inside use, antiseptics for topical use, you cannot just flood your whole body with 70% ethanol to kill all bacteria, but for a wound / something dirty this is just fine. This makes it much easier to avoid creating resistance.

Please define and link to QACs. I know what they are, but many others will not, as it is not a common abbreviation, except possibly to chemists and certain microbiologists, as well as those who work in manufacturing. Overall, your post would benefit by several additional citations supporting your claims.

However, even for brute force mechanisms, there is a huge spectrum of concentrations and conditions in which we apply alcohol, bleach... That is what confuses me. What is the threshold number of ethanol molecules a bacterium's membrane could stand? Aren't a temperature that kills a whole population and other that only kills one individual appart just by a continuous gradient?

Of course bacteria can evolve resistance against antiseptics. Usually antiseptics inflict direct damage to the cell rather than interfering in some biochemical pathway. Also, antiseptics are used in very high concentrations which usually leads to complete elimination of the microbes. Moreover, different antiseptic/disinfectant agents have different toxicity to different organisms; for example anaerobic bacteria are more sensitive to oxidizing agents like hydrogen peroxide and potassium permanganate.
There are bacteria (Deinococcus radiodurans) and fungi that are even tolerant to ionizing radiation like gamma rays.
There are other extremophiles too which thrive in extreme physical/chemical environments (extreme heat/pH/salinity/pressure etc).
For more information on antibiotics vs antiseptics see this post: Why is triclosan not considered an antibiotic?


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How can you band wheat chromosomes using Giemsa dye?
I am working with wheat chromosomes and trying to stain the chromosomes. However, during staining with Giemsa dye chromosomes appear totally dark. I'm not sure why this might be. Anyone have any ideas?

Plant Science Letters
February 1975, Vol.4(2):85–88, doi:10.1016/0304-4211(75)90252-7
C-banding in wheat evolutionary cytogenetics
G.Y. HadlaczkyA. Belea- first of the articles

The Wright or Giemsa-stains can be influenced by the pH of the rinsing solution after the incubation in the dye-solution. The lower the pH the more pink will be the result. The higher the pH the more blue will be the result. Usually Giemsa-stains are differentiated at an approximately neutral pH. (Weise buffer pH 7,2 or acidified water pH 6,5). To lower the pH you can add few drops of acetic acid. This will also enhance the speed of differentiation.
Giemsa-stains are also sensitive for too long rinsing in diluted ethanol. The color turns blue and more faint.
Also it might be the trypsin that can digest some region rich in C or G. It's not condensed so appears light but the other region is very condensed so the trypsin can't enter and digest this region, which appears dark or the opposite.

Check for C-banding or GTG-banding protocols online to understand the chromosomes. Treatment with mild acid or trypsin gives you various dark and light regions usually light regions begin AT rich regions

can you add some external sources/references to support your answer?


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Can hepatitis B also infect vaccinated persons?
If a person is vaccinated against hepatitis B: Is there any chance that he also gets the infection by physical contact? Is it a congenital disease or not (if the parent is hepatitis positive is the offspring is also affected or not)?

I have edited your question to make it better understandable, feel free to roll back the edit if it not appropriate.

It is possible but the chance is somewhat low - 10%.
You can check to be sure that the level of surface antibody in your blood is efficient by a simple blood test.
The Hepatitis B vaccine is very effective at preventing Hepatitis B virus infection. After receiving all three doses, Hepatitis B vaccine provides greater than 90% protection to infants, children, and adults immunized before being exposed to the virus.
In highly endemic areas, Hepatitis B is most commonly spread from mother to child at birth (perinatal transmission), or through horizontal transmission (exposure to infected blood), especially from an infected child to an uninfected child during the first 5 years of life.
Find more about this here:
http://www.who.int/mediacentre/factsheets/fs204/en/
You can find all about Hepatitis B vaccine on the CDC's website:
http://www.cdc.gov/vaccines/vpd-vac/hepb/public/index.html


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Atrial contraction in complete SA block
In a complete SA block when there's block of impulse from SA node to Atrial syncitium, The ventricles start pumping at AV nodal rhythm but how do the atria then contract?

It depends.
It's likely that another point starts setting the pace instead of the SA node. More infos about cardiac pacing on Wikipedia
Or maybe different points try to set the pace contemporary, without generating a valid contraction but only electrical activity (such as in atrial fibrillation/AF, a very common disease mostly in elders).
An electrocardiogram could answer the question for the specific patient. If there is completely no atrial activity you'll find no P waves (no atrial activity) or baseline continuous little waves (in case of AF because of the irregular atrial activity) and probably bradycardia (because the pacer in the AV node is slower than the SA node).

Could you add some sources, please?

Done (as much as I could)

Looks much better! :)

What happens if the atria doesn't contract at all? like you said, no P wave. how does that effect ventricular activity?

If no contraction and no eletrical activity by the atria there is less efficiency in blood pumping (but you have to consider that normal atria do a little work compared with ventricular work).

Moreover if there is no atrial pacing, as I said in the answer, the rythm is slower than the normal one, reducing cardiac output ( https://en.wikipedia.org/wiki/Cardiac_output ) and with less response to exercise.


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What species is this large bug? (South India)
I found this bug in South India. What species is it? The tiles in the picture are 5x5 centimeters each. The bug was moving relatively slowly and didn't seem to fear me much.

I tried asking it directly, but it kept claiming to be a feature.

The question has been correclty answered I think but out of curiosity: what do you mean by I tried asking it directly, but it kept claiming to be a feature.?

@Remi.b http://www.urbandictionary.com/define.php?term=It%27s%20not%20a%20bug%2C%20it%27s%20a%20feature

I suppose it's a whip scorpion.

Whip scorpion (order Uropygi, sometimes Thelyphonida), any of approximately 105 species of the arthropod class Arachnida that are similar in appearance to true scorpions except that the larger species have a whiplike telson, or tail, that serves as an organ of touch and has no stinger. The second pair of appendages, the pedipalps, are spiny pincers, and the third pair are long feelers.

It is most common in India and Japan to New Guinea.

In the new picture, why are the mouth-parts different from the specimen in my picture?

Sorry I made a wrong edit. It happened while rolling back an edit made by another member of the community. I've corrected it now,.


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When did animals begin to "parent"?
After having a fun conversation with a friend regarding parenting, I actually had the general question arise in my mind of when did parenting actually start to take place?
But, first, I think we need to define what I mean by "parenting".  Specifically, what I am talking about is when animals decided to give birth to their young and not abandon them to immediately fend for themselves.  Instead, parenting is taking care of, and protecting children for a period of time (even a brief one) until they are grown enough to take care of themselves.
Also, I think it's worth not counting the actions of a mother or father hovering over eggs of unhatched offspring until they hatch.  True, this is a form of parental watching but I'm more interested in the general timeframe of when parents started watching over the general actions and "shenanigans" of their offspring in order to protect them from harm and to give them a better chance of survival.

Which animals are you asking about specifically? There are quite a few species and the answer will be different for nearly all of them.

Any!  Although multiple species may have started this independently, which started it first.  Generally, I'm interested in the genesis of this behavior.

Parental care
What you call "parenting" is called "parental care" and "parental care" is any investment of the parent to improve the fitness of their offspring. Parental care can take many forms from niche building for the offspring to parental feeding passing by placing plenty of ressources in the egg.
Issue with the definition of parental care
Given the vastness and eventual lack of a strict enough definition of the concept of parental care, it will likely be difficult to really know what you would consider as being parental care. Below I am suggesting two possible cases. If you were expecting to another answer, you will need to provide a nice and strict definition of parental care.
Mutation rate
Under a very broad definition of parental care, one could argue that first examples of parental care would be found in very early organisms (bacteria/archae, eventually viruses) that would at some point (for a given lineage) reduce its mutation rate to ensure transmitting a good genome to its offspring cells.
Nutrients in eggs
If you feel unhappy with me using such a broad definition, you might want to consider the first examples of parental care as being the existence of anisogamy (see here), where females (by definition) produce large eggs filled with nutrients, proteins, mRNA and other things. I doubt we know what lineage first evolved but it could be an ascomycota eventually.


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How does the mutualism of figs and wasps exactly work?
I have just rudimentary knowledge about the mutualism of figs and wasps and would like to know how this works step by step.
Also how do humans use this mutualism? Do they support or hinder it at some points?

might help to define "mutualism" and add some links so that others can follow your question...it would definitely strengthen it

@Aspergirl89 Among different fig species some are monoecious (hermaphrodite) and some are gynodioecious (hermaphrodite and female flowers on separate plant). en.wikipedia.org/wiki/Ficus#Fig_fruit_and_reproduction_system. Thanks for knocking me, I didnot knew this

I've found something useful here : https://books.google.co.in/books?id=8_DfMSS9r9cC&lpg=PA185&ots=YfG6pVslTs&dq=Ficus%20benghalensis-%20Monoecious%2FGynodioecious%3F&pg=PA185#v=onepage&q=Ficus%20benghalensis-%20Monoecious/Gynodioecious?&f=false, on the google book Diversity and Evolutionary Biology of Tropical Flowers/ Peter K. Endress

@Aspergirl89 As the question stands, It is unlikely that you will get a satisfactory answer. I think it would help a lot, if you worked on your question instead of offering a bounty. Give more information what you already know about mutualism and then be more specific in what additional information you need.

@Thawn the bounty was started by me. However if I've a satisfactory answer even 30 yrs later; I'll post that.

Ficus sp. (various sorts of figs); have a close relation with a sort of Wasp's reproduction.
Tiny flowers of Ficus are enclosed inside a hollow, pear-shaped concave  special-type of inflorescence, also called hypanthodium (term commonly used in flower-stage) or Syconus(term commonly used for fruit stage) when flower stage sometimes c ( from outside it looks like a single fruit but it is not).
There is a very narrow entry-hole or orifice at the apical portion of the inflorescence.
Inside the inflorescence, there are  3 types of flowers.
1. Male flowers, 2. Female-flowers, and 3. 'Gall-flowers' those are assigned as female flowers but their 'style' is much shorter.
Male flowers located towards the orifice, whereas female and gall-flowers locates in deeper regions.
Blastophaga, a genus of wasp, brings in required pollen,  also called gall-wasp, lay eggs inside figs.
To do that, they enter inside the fig inflorescence, lay eggs on these dwarf 'gall flowers' using ovipositor.
The eggs develop larvae, which fed on some ovules, and form pupa.  When the pupa-stage develop into mature wasps, the try to crawl-out from the orifice, they brush against the male flowers.
This pollen-laden insect when enter in another fresh fg, it also pollinate that-fig.

Image URL : https://media1.britannica.com/eb-media/17/24017-004-98EF07A1.jpg .
Image Page-Source: https://www.britannica.com/animal/fig-wasp

Source: College Botany, Vol-1 / Gangulee, Das, Datta; New Central Book Agency.

P.S: I think my answer is NOT satisfactory enough
This question require more scientific details.
Widely known fact is, fig-wasps pollinate figs. But really there is a lack of detailed information like does the mother-insect die inside the fig and only the young insect go-out? or the mother insect come out from fig after laying eggs? if the larvae eat the ovules then isn't it harmful to the fig plant at any extent? How female-figs (in dimorphic members) are pollinated... does the wasp travels from one fig to another? When the young wasp come out from the fig it certainly take some months to reach maturation to lay eggs. Within that period does the pollens sticked in their body , and viable to germinate on stigma? There are many sorts of figs. Does all of them require wasps? Would figs survive without the wasps? --- What the question seeks, is, out of the popular children-book story; the Scientific-details behind figs and wasps. I assume the answer would not broader than reasonable; if someone knows their life-cycles and structures, I think it is possible to give very point-to-point answers within limited space.

I know that it is actually a "flower" - that's why it is sometimes poetically called secret garden.
What I want to know is: Does every plant has all kinds of figs (female, male etc.)?
The female figs are the figs humans eat. The hole is so small, that the wasp dies inside because it can just enter the fruit. What exactly happens inside? Does she lays eggs? Or does she just die?
And what about the male figs. Are they not edible because of the insects inside of them? Do they start to rot because of the insects?
How does the life of a female wasp looks like? And the life of a male one?

@Aspergirl89 Among different  fig species some are monoecious (hermaphrodite) and some are gynodioecious (hermaphrodite and female flowers on separate plant). https://en.wikipedia.org/wiki/Ficus#Fig_fruit_and_reproduction_system. Thanks for knocking me, I didnot knew this

You could elaborate these queries  in the original post. That would make your question more specific.


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Why are tree rings the same if rainfall is different from place to place?
I have looked at data from rain gauges and usually the rainfall levels are very different from place to even. Even in adjoining towns or townships the rainfall can exhibit much different patterns.
Nevertheless, all the trees in an area tend to show the same ring patterns. Why is this?

Those trees show tree rings, is not solely dependent on rainfall. They're dependent on their internal genetic program. Maybe also there are effect of daylight, temperature, etc.

Maybe not only  the exact-amount of rainfall, rather overall humidity and desiccation rate affect the process.

The rings are not only affected by time but also by location. So no, the patterns are not always the same depending where you are. Climate do affect the rings.
Typically a major factor affecting ring patterns is the seasonality. Depending on the number of rainy season, you might observe one or two rings per year.
If interested, here is an introduction to dendrochronology (from the University of Victoria).

I have a whole textbook on dendrochronology. It does not discuss this issue.

I must say I lack much citation and answer by what I remembered from my Bachelor degree. Citing wikipedia: , the variation of the tree-ring growths provides not only a match by year, it can also match location because the climate across a continent is not consistent. But please, wait for other users input before accepting the answer of someone who knows very little about dendrochronology.

What is your textbook by the way?

Fundamentals of Tree-Ring Research by James H. Speer


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What's the determinant of the male-biased birth sex ratio in humans?
Will the baby be male or female? If it was a random biological switch then, with a huge sample number, the sex ratio at birth would be exactly 50-50. But it isn't; the ratio is about 51-49 in favour of males. So how does this inequality arise?
Further to @Remib's comments. I was specifically thinking of the sex ratio in humans. Would it be true to say that the genetic determinant of the sex ratio would be exactly 50:50 M/F? If the disparity is environmental, then how does it work, and wouldn't an environmental effect be more variable than the 51:49% that we see?

Are you talking about humans only? Are you more interested into a mechanistic explanation or rather an evolutionary explanation?

If your interest goes beyond humans, then note that the sex-determination system varies (a lot) from species to species. The post Do males of all sexual species have Y chromosomes? gives an overview of this variation and while the answer does not specifically talk about the sex-ratio, I think you can easily make your way to the understanding of why the sex-ratio isn't always 50:50.

https://www.youtube.com/watch?v=3IaYhG11ckA This is a lovely video explaining it all. There are a ton of references down there in the description

There are a number of ways in which the true sex-ratio at birth (let's assume the 51:49 is well estimated and is the true ratio) could deviate from 50:50. This list is just an brief overview.

Sex, in humans, is determined by the sex chromosome present in the haploid sperm cell which fertilises the egg. If males produced more or less Y-bearing sperm than X-bearing sperm, then the birth sex ratio would be expected to deviate from 50:50. However, studies suggest that sperm production is not biased towards X or Y bearing in humans.
The probability of fertilisation may differ between X- and Y-bearing sperm. If Y-bearing sperm were more likely to succeed in fertilising the egg then there would be a male-bias in the birth sex ratio. I've seen it suggested that the small Y chromosome makes the sperm slightly smaller and therefore faster, but can't find those claims right now. Regardless, it appears that sex ratio at fertilisation is not sex-biased.
Bias in the birth sex ratio can come through sex-biases in the failure rate in fetuses. If female fetuses are more likely to miscarry than male fetuses, over the course of the gestation, then the sex ratio at birth will be male-biased. It appears that there is sex-bias in the failure rate of fetuses which can be male or female-biased throughout gestation, but the tendency is for female-biased failure rate during the second trimester to generate an overall male-bias birth sex ratio.

But would you really consider the 1.5% as a significant deviation? There are of course demographic differences which are in many cases affected by "cultural" practices. In many places the sex ratio is skewed toward male because of female infanticide (preference for a male child).

birth sex ratio won't be affected by infanticide - I've also not said that 1.5% is significant, I'm just operating under the assumption that the quoted statistic of 51:49 at birth in the question is correct and pointing out how it could be


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Do free computer programs exist that can simulate drug permeability in bacterial membranes?
I am currently trying to make derivatives of a molecule in hopes of making it more permeable to bacterial membranes. I wanted to know whether there are any bacterial membrane simulating programs where I can dock my molecule and see its predicted permeability. Preferably, I would like to use a free program that is known to be trustable/accurate.

I think it would be helpful if you could specify what type of molecules you are dealing with and what kind of derivatives you are thinking about. There is a nice answer below for peptides, but e.g. for hydrophobic molecules, the considerations will be completely different.

Also, gram positive, or gram negative bacteria?

I currently work alongside many biologists that are working on simulations of anti-microbial peptides in the membrane. These seem to have a similar mechanism to what you're aiming for — permeating the lipid bilayer.
Presumably you have already come to the conclusion that molecular dynamic simulations are probably a good shot for exploring what may happen at an atomistic and energetic level. Software does exist, but an accurate answer from a project like this may take months of work and time on an HPC cluster.
The only software recommended by PDB (trustworthy) explicitly for membrane systems is GROMACS (and it's free!). This has documentation on membrane simulation which I have used in the past. However you will need to be very careful in both designing the simulation and analyzing the output, and an expert guiding hand may be required.

Gromacs is very good. But it has a steep learning curve, which is to be expected from the complexity of the simulations.

@becko This is a good point, but I'd say one would struggle to find any aspect of scientific interrogation that doesn't have a steep learning curve!


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Mystery Plant ID
I found this odd rooty thing growing in one of the pots on my patio - any idea what it might be? I'm in Cape Town, South Africa, and it's the tail end of winter here.

Has this grown at all? If you have pictures of newer growth, it might help someone ID this plant...

Could it be a gymnosperm (cycad-group)? Just a bit visual similarity. Something else could be happen, such as a bulbous monocot.

This is possibly some species in the subfamily Scilloideae. (sometimes considered as separate family called Hyacinthaceae). This group of plants is a subfamily of bulbous plants within the family Asparagaceae.

Scilloideae are distributed mostly in Mediterranean climates, including South Africa

This subfamily contains many popular spring-flowering garden bulbs, so it would not be unlikely to see these growing up toward the very end of winter.
Drimiopsis maculata seems like a fair guess at the species (or closely related to the species in the question).

According to here, info pertaining to Drimiopsis maculata includes:

Distribution: widespread in eastern South Africa
Bulb description: Globose, fleshy, mostly exposed at the surface of the ground, about 2.5 cm in diameter and have large visible scales
Leaves: mottled, but typically lose color to become all green.

I'm hesitant to provide more info because I'm still not sure about this identification. Figured I'd throw it up to see if others could rabbit-hole their way to a better answer...

wow brilliant similarity.

@AlwaysConfused right?! except for the mottled leaves.... However, I assume since the spots fade in most specimens, they could possibly be absent altogether in specific cultivars? I looked into other species in this genus (and similar ledebouria) but didn't find anything that looked as similar to the OP's pic...


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Do low light levels during development affect the distribution of rods and cones in the retina?
I just can't seem to find any retinal development experiments that have been done using low light conditions. I am very interested in knowing if raising an animal in such conditions leads to a different distribution of rods and cones in the retina. Perhaps it would lead to a more uniform distribution that the skewed distribution that is normally found?
Any thoughts or pointers to resources would be appreciated!

I found a few studies in fish that showed constant light exposure changing rod density. First one in goldfish:
Raymond PA, Bassi CJ, Powers MK.
Lighting conditions and retinal development in goldfish: photoreceptor number and structure.
Invest Ophthalmol Vis Sci. 1988 Jan;29(1):27-36.
http://www.ncbi.nlm.nih.gov/pubmed/3335431

The retinas of 63 goldfish were examined after varying durations of exposure to one of three environmental lighting conditions beginning before hatching: constant light (340 lux), cyclic light (12 hr 320 lux, 12 hr dark) and constant dark. Up to 8 months, no effects of constant light or dark on photoreceptor numbers or structure were apparent. Densities of rod and cone nuclei were normal and all retinal layers appeared normal by light microscopy. Exposure to constant light for 12 months or longer resulted in a reduction in rod density by 37%. Cone numbers were unaffected by constant light, even with exposures of 3 yr, and rod and cone outer segments were normal in length at 11-20 months under all environmental conditions. Due to poor survival, only one animal was available for quantitative examination from the group reared in constant dark 12 months or longer. Photoreceptor size and number in this retina were similar to those in the constant light condition. The results suggest that the formation and maturation of rods and cones in goldfish retina is unaffected by rearing in constant light. However, long-term exposure (greater than or equal to 12 months) may disrupt maintenance of differentiated rods.

See also http://www.vision-in-cichlids.com/fenotypic_plasticity.htm where they say rod density changes in early retina development of Tilapia leucosticta.


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Cannibalizing behaviour in ants
Today I saw an ant question biology and was reminded of a picture I had clicked 2 years ago.
Here, you can see these black guys cannibalizing this other black guy.
To reiterate, these guys had their nest inside a tree. I had cornered one of them.
If I remember correctly the ant was walking fine and the only fault might have been that I lead the guy astray a bit (not further than the farthest guy in the colony) and near the colony I turned it on its back which lead to a lot of difficulty for getting up again (as any ant knows). I mean I waited maybe a few minutes but it just kept waving it's legs in the air.
So later on as soon as these other ants got sight of their lost friend when it was able to hobble back near the nest, they came over and just pulled him apart.
In the picture you can see the first guy just got to him and the others started aggregating as soon as this guy came over. Within five minutes some 10 or 15 ants were all over the place.
Which ant species is this?
Why did they murder/cannibalize a member of their own colony?
Is this a common behaviour among ants?

Interesting observation! From what I understand it can be very difficult to get the species from a photo like this (but I'm no expert, someone else might know better). Also, you're using "guy" and "him" in your text, but most likely these are female ants since all workers are female.

I did not mean male or female. I'll change everything to it. Tried to keep the post jovial

Yeah, I understood what you meant, I'm just being pedantic and ruining all the jovialness...

Potentially a nice question but you might run into problems as you're asking more than one thing - as you can see below, you already have an answer to the species-id part which is probably correct as far as it goes but it would be a shame to ignore the interesting behavioural parts. Since this has been answered now, you could consider editing this into a species-id question and paste the rest into a new behavioural question? Maybe? (I don't know, I'm fairly new to this).

Where did you found them? Which country?

India! new delhi!

Scientific name: Camponotus compressus
Common name: Common Indian black ant

Camponotus compressus tending soft scale insects growing on a stem

Source:

Common Indian black ant
Wikipedia

Cannibalism is common in social insects. It is a way through which they control the population of the colony and conserve nutrients. Members of Hymenotpera (this ant being one) are very quick to consume injured eggs, larvae and pupae. It has been experimentally observed that when a colony of Zootermopsis angusticollis(a species of termite) was kept on a diet full of cellulose i.e. deprived of protein, they attacked their own kind. But cannibalism dropped to zero when casein was introduced in their diet. So it is safe to  assume that these ants too engage in cannibalism for the same reason, proteins.
Reference: This book.

you say tending soft scale insects..Is there some sort of symbiotic relationship between these insects?


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How do sarcomeres coordinate contraction?

As can be seen from the figure

if myosins from both sides apply equal force then how does muscle contract? And also how do actins resist tearing?
Is there any kind of  coordination between different sarcomeres? How does they achieve it? I know that acetylcholine is released in response to action potential so does the release of acetylcholine controlled in each individual sarcomere?
Or simply there is an increase in the number of myosins as the distance of each sarcomere increases from the neuromuscular junction?

Can you focus your question more narrowly? Clearly, muscles do contract, so is the question just "how do sarcomeres coordinate contractions?"

I am waiting for a more physics oriented explanation but until that arrives, Think of all this as a rubber band. If you mark off sections on it to represent sarcomeres, then stretch it, each "sarcomere" will stretch. Then if you let go of one end of the rubber band, every "sarcomere" will contract, and the rubber band will contract toward the held end. When this happened, every "sarcomere" was being pulled in both directions, but the forces were all transferred from one to section another, because one end of the band was unable to move. On the whole, the band contracted towards the fixed end

For the second one, Nerves innervate the muscle and activate muscle fibres as a whole. A muscle fibre is a larger unit containing many myofibrils which are sarcomeres attached in series. Which of muscle fibres get excited is a different story. But when a muscle fibre gets excites, the impulse travels along its sarcolemma and when it reaches the the t-tubules leads to release of calcium from the cisternae. Because the contraction is finally mediated by calcium, the process is sychronized

I'm answering question 1, I think it'd be better to post these questions separately.
Consider action and reaction: myosins (thick) filament is experiencing force F towards Z line.

If the muscle is acting on something that is movable (e.g. you're pulling on a drawer which isn't locked), the force F towards Z line is greater than the force that maintains your thick filaments in place, and they'll slide towards Z line. The speed at which they slide is limited by the rate at which myosin heads can detach once they have performed power-stroke.
If the drawer is locked, then force F cannot overcome the external force. This force however is normally lower than the force required to tear actin or z-line, it is limited by two molecular factors: myosin will stall and not effectuate power stroke under too strong an opposing force, and myosin heads  will detach after some time and relax the tension they have built up. This is how you get the maximum force under clamped conditions.


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Picking up Plasmid DNA using Nanodrop, but not using Electrophoresis
I am currently trying to see if 2 bacteria contains plasmids or not. I had used promega plasmid extraction kit on the bacteria. I ran a gel electrophoresis (.8% gel) with the extract product, however its not showing the presents of any DNA. I also ran the product through Nanodrop (2000) and these where the concentrations I got:
1 : 6.5 ng/ul & 260/280 = 1.56
 2 : 49.4 ng/ul & 260/280: 1.96
Based on experience, I want to say #1 contains no plasmids, however #2 may have a small concentration of plasmids. Please give me your opinion on what to conclude. Also, if there is another test I can try to do to confirm plasmid presents or not, please let me know.

If your samples are contaminated with proteins (which can happen), then the resulting OD 260/280 gets higher and can falsely show some nucleic acids. If you run a few microliters on a gel and don't see anything, I would be suspicious. The concentration is sufficient to see something.

The amount of DNA is what matters when running the gel, not just the concentration. What volume of each sample did you run on the gel? Use the concentrations determined above to see how much DNA should have been there. If the hypothetical amount looks good, and you don't see anything on gel, I'd say there isn't any real DNA. As far as testing for presence of plasmid, you could try re-transfecting your suspicious sample into other bacteria, since you don't need many copies of the plasmid to get some good colonies.

This could be. I believe that the nano drop shows protein contamination. I am going to try to concentrate the plasmid DNA, and increase volume for gel. If I can not find plasmids, then I am going to assume that there are no proteins.

I don't know how much culture volume you used, but the amounts you have look more like a medium/high copy plasmid. I don't know if that's what you'd expect for a natural plasmid.
In addition to the other answer, it could also be sheared genomic DNA, cosmid (that would run too high on your gel to see), or maybe just nucleotides (if you messed up the prep in some way).
Another strategy to figure out if your strain has plasmids depends on what else you know about these strains. If you don't know that much: do 16S sequencing, it might be a known strain with known plasmids. If you already know it's a newly discovered strain: sequence the whole thing. Even with relatively low coverage the presence of plasmids will be quite clear. It's a bit more expensive than a plasmid prep + gel, but you'll also get a lot of other information about the organism.

Having a positive reading on the Nanodrop but no band on the gel can be due to a number of different issues (not exhaustive):

An incorrectly zeroed sample
Incomplete staining of the gel
Contamination of the sample
Human errors in loading of samples

You should try to exclude these possibilities by positive controls in order to find out the true reason behind the inconsistent results.

Depending on how you followed the protocol you could theoretical also have bacterial genomic DNA in your sample. If you follow the protocol strictly this should not happen, but if so, you would be able to measure the genomic DNA. In the agarose gel, however, it would usually be stuck around the top since it is too large to migrate.
Vortexing the sample before loading the column could cause this, for example (see Promega PureYield Manual).

Geo - if you could, please add some references/citations to your answer - I know at times it may be hard to reference something that may be common knowledge to you, but we appreciate it very much on this site. Thanks for your contribution!

I would recommend switching up your PCR cloning program. Often, even after purifying DNA and RNA in conjunction with great care PCR can be the bottle neck for Gel Electrophoresis, as well as ensuring the quality (depth, void of blunt edges, etc) of the agarose gel- 49 ng/ul is not enough for  progression. If all that still doesn't improve your case then it may be an issue with cultivating bacterica cultures -after purifying plasmids from bacterial clones vials should appear very cloudy (8-16 hrs was my go to time period), futhermore make sure to avoid light exposure on to the agarose gel as well as keeping it clean and submerged under cold PBS before inserting your buffered DNA (I used 10 microliters - but it tends to vary depending on the thickness of your gel) Also, when I would use a higher voltage during gel EP I would have a higher chance of having vertical streaking though it may be faster.
If nothing works... then I can only allude to possible human errors. Last thing! I hope you clean the nanodrop before you take count, having protein in your product can be a result of that. good luck! bacterica need love too!

Christopher - if you could, please add some references or external citations. We always appreciate it on this site. Thanks for your contributions!


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Is Infra Red light safe to use on your scalp?
I own an Anodyne Infrared therapy device which I use to treat ligament/tendon/muscular pains and it works nicely.

I see other infrared products used to combat hair loss (e.g. https://www.amazon.com/dp/B01B29PCUU), but I don't know the nuances of different infrared devices. Is it safe to use the device intended for the above uses on my scalp? I'd rather not purchase a separate infrared device for my scalp if I own the necessary technology already.

These are entirely different devices. First off, the Anodyne product is truly far-infrared, emitting at 890 nm (infrared is above ~650-700 nm). However, the hair loss product you linked is far-red/near-infrared, with laser diodes emitting at 650 nm (which is why it glows red). If you put the Anodyne product on your skull, you'd just heat up your brain, possibly burning any hair you have left. (Well, maybe not, but it sounds kind of funny.)
I would strongly suggest you don't try regrowing your hair using an instrument designed to relax your muscles. I will give you a recommendation - read the small print very carefully. The hair product is only recommended for a certain type of hair loss called Androgenetic Alopecia. Please consult with your doctor to determine if you actually have this condition, otherwise your investment of US$600-700 will be completely wasted.

Good to know. Thank you for the insight. Looking at this pic, I probably do have Androgenetic Alpoecia but like you say it's worth checking if this is true before I get my hopes up and spend effort (more burdensome than the money!).


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Wet weight measurements: Setting up cultures for measuring growth rate via wet weight
I have some isolates which I am trying to grow in some toxic leachate in order to measure their growth rate I also want to measure the growth rates of certain combinations of these bacteria.
I've tried a few ways to measure their growth rate in leachate (mostly turbidity), all of which have been unsuccessful. My supervisor has therefore recommended I try wet weight measurements.
I am a chemical engineering undergraduate, and I have never done wet weight measurements before, so please forgive my naivety!
My set up is as follows:

I have overnight cultures of the isolates which are being grown up
in leachate (themselves inoculated from agar plates) in falcon tubes
as an inoculum for my wet weight cultures.
I plan on having several (~20) 250ml conical flasks with leachate in them. I will innoculate these from my overnight cultures, so that different flasks contain different isolates
I want to take daily kinetic measurements in order to get the wet weight of the bacteria growing in leachate. This will be done over a period of 5 days.
I will take an aliquot each day for 5 days from the conical flasks, centrifuge in order to pellet the cells, then remove the supernatant and weigh the biomass.

So what I don't know are the specifics of how I might set this up.
I know that my isolates grow slowly in leachate, and therefore I will need a relatively large volume of liquid (around 5-10ml) in order to get a meaningful change in biomass.
So my queries are;

How many replicates is sensible for this sort of wet weight measurement? I know that they can be quite varied from replicate to replicate, but I have limited room in my incubator. I think 4 replicates might be too many, but I don't know the extent of the variability when it comes to wet weight measurements.
In 250ml conical flasks, what is the maximum volume of liquid I can put in them before there is not enough head-space remaining?
What volume of an inoculum would be sensible for this experiment? And if I am wanting to get a growth rate, then does it even matter? As I am only concerned with the rate of change of biomass over time and not the final amount.
I want to take large enough aliquots to demonstrate an increase in biomass, but obviously not too much that it begins to affect the culture growth. As this is destructive sampling, what volume of my culture can I afford to lose?
I have demonstrated that in a volume of 5ml of leachate, and given 72 hours, my isolates' biomass increases by approximately 8,000 μg - 10,000 μg. So by this logic, is it right to say for the daily measurements, aliquots might should be 15ml so that I can get meaninful readings?

I already know it is not feasible for me to do dry-weight measurements simply because of time and the system I'm working with.