text:
How is centriole number maintained during meiosis?
I've found a website (Pearson's BioCoach) that claims centrioles duplicate in Prophase II. Is this accurate? Does it depend on the species in question?
Looking at three textbook illustrations of meiosis, none of their illustrations are consistent. All depict the movement and number of centrioles through Telophase I the same way: centrioles replicate in S of Interphase, then do their thing through Meiosis I. We end up at Telophase I with 2 centrosomes, each with 2 centrioles. There is one centrosome at either pole of the cell.
After that, the diagrams are unclear:
One text (general biology) seems to indicate either centrioles or entire centrosomes replicate after Telophase I, because Prophase II is shows both cells with 2 centrosomes, each with 2 centrioles.
Another (basic genetics) illustrates 2 daughter cells of Meiosis I inherit one centrosome each following Telophase I. In Prophase I, the centrioles in this centrosome splits, with one centriole going to either pole. Cytokinesis after Meiosis II results in 4 daughter cells, each with one centriole.
A third (more thorough genetics) stops depicting centrioles after Telophase I, instead showing the spindles growing in an aster formation from an empty space, the space where there were 2 centrioles up until Telophase I.

Interesting question, I'm not sure that the answer is actually  entirely known. Here's some articles that may interest you: one, two

Indeed a nice one. The reality may not be exactly a duplicate, but varies in number - may be in terms of cancer. I am curious as well. You may take a look at this article as well.

It makes sense that it would have to be in Prophase II or in an interphase between the two meioses; the kinetochores need to be captured by the microtubules during Metaphase II. Campbell's Biology has that a stage in Prophase II is formation of Spindle and migration of chromosomes towards the metaphase II plate late in prophase II. If you look at an upper level textbook they will have a phase between telophase I and prophase II called Interkinesis. It is similar to Interphase in Mitosis, but without the duplication of chromosomes. So it is likely in interkinesis that centrioles double.

When a cell enters the cell cycle and passes through S phase, each centriole is duplicated. A "daughter" centriole grows out of the side of each parent ("mother") centriole. Thus centriole replication — like DNA replication (which is occurring at the same time) — is semiconservative.

Centrioles migrate to opposite poles at the end of meiosis and then the centrioles duplicate in the new cell and during the S phase. One centriole grows from the parent centriole. Therefore, like in DNA replication the centriole replication is semi-conservative.

You are correct about the replication being a result of a semiconservative mechanism, however the question is asking about the duplication between Meiosis I and II. There isn't a synthesis phase in this period. Consider adding a reference an incorporating your comment into the answer, as it is likely that most people are not aware that Centriole replication is via a semi conservative  mechanism.

A reference from my book -

Interkinesis or Intrameiotic Interphase
It is metabolic stage between
  telophase of meiosis I and prophase of meiosis II. Chromosome are
  elongated but chromatin reticulum is not formed. Protein and RNA
  synthesis may occur. Centrosome or centriole pairs undergo replication
  in animal cells. However,
  there is no DNA synthesis. It is important for bringing true haploidy
  (haploidy of DNA) in daughter cells.

From this site - https://openoregon.pressbooks.pub/mhccmajorsbio/chapter/meiosis-ii/
(search for centrosomes in that page)

The centrosomes that were duplicated during interkinesis move away
  from each other toward opposite poles, and new spindles are formed.


text:
Relationship between body size and damage done by electricity
We all know that if a person gets stunned by a 2000 volt stun gun, he/she may be knocked unconscious, but he/she is still alive and apparently no damage done on his/her body.
But what could happen if that 2000 volt is applied to a snail whose body is way smaller than that of a human being?
Will it create a lot of damage into the snail's body?
Or the same effect as that of humans.

Certainly it will be more. When a person gets stunned by a 2000 volt stun gun the electricity spreads into whole body. If the target is large the damage would decrease (as you see in humans it has no serious damage) but if the body is smaller, the damage will be greater.

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text:
Are low-intensity radio-waves carcinogenic?
A recent review article, Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation reached a surprising conclusion

our analysis demonstrates that low-intensity RFR [Radio Frequency Radiation] is an expressive oxidative agent for living cells with a high pathogenic potential and that the oxidative stress induced by RFR exposure should be recognized as one of the primary mechanisms of the biological activity of this kind of radiation.

They suggest the oxidative stress can cause cancer and non-cancer pathologies.
This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid? I would expect this to be front page news given the large number of studies reviewed.
Are low-intensity radio-waves carcinogenic?

I seriously doubt it, and there are a number of meta studies which support this. However, I will take a look at this study next week, when I have access to it.

A lot of processes generate oxidative stress: infection, digestion (metabolism), etc which are fairly common. The free radicals generated by ionizing radiations are different from the usual ROS.

This study has received next to no media coverage. With RFR impacting so many people it makes me wonder, is this study valid?

Well first of all, lets be clear: that is not a study.  Its a review article, basically a paper that summarizes a series of studies published.  The review itself isn't valid or invalid necessarily, it simply takes a series of papers (which may or may not be correct or relevant) and then summarizes them.
As for validity, that is a summary of a lot of obscure papers on mechanisms by which RF fields could interact with cells, rats or in a few cases plants.  Its hard to say if the conclusions are valid, but selecting a few papers at random, they are mostly very obscure journals and many report very specialized measurements that are far removed from demonstrating carcinogenic effects in humans.  Its difficult to draw conclusions that are relevant to human health from that, although it does seem plausible that low frequency fields could have a measureable effect on cells or even rats.

Are low-intensity radio-waves carcinogenic?

Assuming you mean in people, that is a hard question to answer, and not the right question given a review article that does not address effects in people.  A better place to look may be this review article:
Carcinogenicity of radiofrequency electromagnetic fields
published in The Lancet and addressing evidence of carcinogenicity in humans.  To summarize:

The Working Group concluded that there is “limited evidence in humans” for the carcinogenicity of RF-EMF, based on positive associations between glioma and acoustic neuroma and exposure to RF-EMF from wireless phones. A few members of the Working Group considered the current evidence in humans “inadequate”. In their opinion there was inconsistency between the two case-control studies and a lack of an exposure-response relationship in the INTERPHONE study results; no increase in rates of glioma or acoustic neuroma was seen in the Danish cohort study,4 and up to now, reported time trends in incidence rates of glioma have not shown a parallel to temporal trends in mobile phone use.
The Working Group reviewed more than 40 studies that assessed the carcinogenicity of RF-EMF in rodents, including seven 2-year cancer bioassays. Exposures included 2450 MHz RF-EMF and various RF-EMF that simulated emissions from mobile phones. None of the chronic bioassays showed an increased incidence of any tumour type in tissues or organs of animals exposed to RF-EMF for 2 years. An increased total number of malignant tumours was found in RF-EMF-exposed animals in one of the seven chronic bioassays. Increased cancer incidence in exposed animals was noted in two of 12 studies with tumour-prone animals12 and 13 and in one of 18 studies using initiation-promotion protocols.14 Four of six co-carcinogenesis studies showed increased cancer incidence after exposure to RF-EMF in combination with a known carcinogen; however, the predictive value of this type of study for human cancer is unknown. Overall, the Working Group concluded that there is “limited evidence” in experimental animals for the carcinogenicity of RF-EMF.

Note that cancers that people theorize to be associated with exposure to nonionizing EM fields tend to be extremely rare, meaning that studying them is very difficult.  This leads to a lot of uncertainty, because one must try to correlate very rare events with environmental effects. Therefore "limited evidence" does not mean "no", it just means that the effect is hard to measure and may or may not be significant given what we know.

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What is this worm like creature
What is it? It moves like a worm. The things on the body are some seeds.

It is found in Germany near Düsseldorf. It is 12:30 on 19.07.2024
It is 1cm long and 0.2 cm wide and high
The source is the trash can where more were found

You seem to indicate that it's half as thick as it is long, but the pictures tell a different story. Could you [edit] to clarify.

This bears resemblance to Calci worms (also known as Black Soldier Fly Worms).
https://kimmyfarm.com/en/black-soldier-fly/larvae
Hope this helps :)

It doesn't look like a Hermetia illucens maggot. A 1-cm black soldier fly would have a very characteristic appearance: dorso-ventrally compressed pigmented body with a pointed head. But it's certainly does look like a fly larva.

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Type of diffusion during depolarisation
How would you answer this question? Looks simple, but the emphasis on depolarisation confuses me.
During depolarisation sodium travels across the membrane by

facilitated diffusion;
osmosis;
active transport;
diffusion.

I didn't want to share my ideas so as not to enforce my way of thinking.
I answered 'diffusion' because during depolarisation the ion channels are open and sodium ions freely diffuse inside the neouron. That's why I think the word 'depolarisation' is important. However, the correct answer is apparently 'facilitated diffusion' since the question is about ions entering membrane and they do so through ion channels and hence via facilitated diffusion.
Is my reasoning also correct and does this question allow two interpretations?

Notice the prompt says "sodium travels across the membrane". Can you find a definition in your textbook for "facilitated diffusion"? What does it say?

It says 'Facilitated diffusion is a type of passive transport that uses specialized proteins, such as channel proteins and carrier proteins, to help molecules move across a cell membrane.' I understand that per definition the answer should be 'facilitated diffusion'. I'm just curious as to why the question mentions depolarisation at all.

When do the channels that facilitate movement of sodium across the membrane open?

They open when a membrane potential reaches a value of -55mV.

It's not quite as on/off or binary as a precise voltage "-55 mV"; the voltage-gated sodium channels have a higher probability of being open as the cell depolarizes; that is, as the voltage changes from rest (which, for a typical neuron might be around -75 to -60 mV) towards 0 mV.

From what I've read and seen, the voltage continues to change towards 0 mV only when ions are already going through the channel, not when they approach the channel, hence the confusion with the 'during depolarisation' in the question. Why should it be in the question if it could be substituted by 'Sodium ions enter the neuron membrane by..?'

"not when they approach the channel" doesn't make any sense - ions are always all around the channel, inside and out. They move through only when it's open. Sodium ions also move across the membrane in other ways, for example, the reason there is a lower concentration of sodium ions inside cells compared to outside in the first place is because of the sodium/potassium ion pump, which is a form of Active Transport. Your instructor/textbook writes "during depolarization" in there so you think about sodium channels moving through voltage- or ligand-gated ion channels.

Thank you every much for your time and expertise. Would it be correct to say that sodium ions travel through the channel via simple diffusion?

No, I would not say that. Simple diffusion would imply a channel isn't involved.

This multiple choice question is basically testing whether you understand your textbook's definitions of terms like "facilitated diffusion", and also that you understand that membranes influence how molecules/ions move, and that the mechanisms of movement across membranes depend on what exactly is moving. This is a central concept in biology necessary to understand how life works, because so much of life involves controlling and influencing what does and doesn't cross membranes.
As you mention in a comment:

Facilitated diffusion is a type of passive transport that uses specialized proteins, such as channel proteins and carrier proteins

You also mention:

during depolarisation the ion channels are open

The question prompt is (emphasis added):

During depolarisation sodium travels across the membrane by

The question is asking specifically about ions traveling across the membrane, you know that they move through ion channels in the membrane because you specifically mentioned ion channels, so the answer is clearly facilitated diffusion because it "uses specialized proteins, such as channel proteins". Plain "diffusion" would be used to describe something that moves across the membrane without needing to move through "specialized proteins, such as channel proteins and carrier proteins".

'Plain "diffusion" would be used to describe something that moves across the membrane without needing to move through "specialized proteins, such as channel proteins and carrier proteins".' This actually helps understanding the answer. Thank you very much.

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text:
Can anyone identify what is this?
I’m trying to see how can I identify this by similar characteristics but it doesn’t look like bacteria nor protozoo. This is a sample from standing water.
For the third image there is a dissected “caterpillar” which looks like part of lepidoptera family.
If someone knows what is this, let me know.
Thanks for helping!

Can you add some more information about it? Where did you find it (Region), where did you take the sample...

The teacher took the water sample and brought it to class. I only know that she said that the sample we were working on was standing water. Unfortunately, I can't express more information about it because she didn't mention the details.

The first two pictures show air bubbles trapped between the slide and coverslip. The dots are condensation droplets.
The 3rd photo shows a larva of some sort, possibly a beetle, but I have no expertise on that area.


text:
Confusing artifact in an electrically-stimulated compound action potential of the nerve
The condition is that the nerve has been pinched (essentially destroyed so no action potential gets conducted along the nerve) and then is being electrically stimulated to produce action potentials. Stimulus voltage is 60V.
I get this weird bump (like a decaying sine wave) in the compound action potential trace after the shock artifact instead of a flat line.
At stimulus voltages like 30V, I get the flat line like shown below.
What could be the explanation for this? Please help.

I think it's probably a stimulus artifact that's ringing through your equipment. Basically it's too strong of a stimulus relative to your setup. You might try a dummy setup e.g. saline with agar and try to replicate it.

Thank you Bryan. I will definitely try that. But do you have any suggestions for getting just a "normal" stimulus artifact at higher stimulus voltages? I was thinking it was something to do with the suction recording electrode that I have.

You might need electrodes with lower impedance/resistance, and/or a better ground. But you also might just be putting too much juice through your amplifier relative to the size of signals you record.


text:
What is the metabolic cost of regenerating oxidized nicotinamide adenine dinucleotide (NAD+)?
As I understand it, it can be difficult to compute the metabolic cost of regenerating the coenzyme oxidized nicotinamide adenine dinucleotide (NAD+). Is there a way to estimate it, for example, in terms of ATP consumed or something like that?

What do you mean by "metabolic cost"? That is a term used in physiology and exercise science relating to energy expenditure in movement. Please quote a source that provoked this question. If you refer to a specific reaction (eg pyruvate to lactate) one can find values of standard Gibbs Free Energy change, for, as you must be aware, no ATP is involved in that reaction. Or do you mean the notional loss in overall ATP generated from glucose compared with the aerobic process in which the pyuvate is oxidized to carbon dioxide and water? That depends a little on estimates of the yield in ox phos.


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

Yeah. Look at GEO and SRA.. You'll find tons of data.

You can also find it in the supplemental data sections of papers you're interested in.

yes, thank you. But there I found mostly trimmed and refined data. I'm looking for very raw data, meaning as the files exit from the sequencer. I want to practice with bioinformatics and so I need file as much raw as I can obtain.

Like fastq formatted files originating from the different technologies... on NCBI/EBI there are files, but their identifier is not the original from the machines.

This question was asked somewhere and nicely answered. You might find lot of examples of .bam files. see https://www.biostars.org/p/45320/

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


text:
Were Neandertals as Hairy as We Are?
What I mean to say regards facial and androgenic hairs.  There are many theories as to why some people have both kinds of hairs, while others have one or the same and others still have neither.  The best and most popular guess is that those hairs were secondary sexual organs, meaning that they just make the boys more attractive to the girls.
It's a well-known fact that hair provides insulation, and in the last ice age, Europe was dominated by a hominid built specifically to deal with the cold.  I am talking about, of course, the Neandertal.  Is there any evidence that the Neandertals, as a means of adaptations against the cold, were equipped with body hair?  If not, then would it be safe to speculate on such?

It is a good question (+1). You may want to have a look at this webpage for a quick summary of the discussion and different arguments about how hairy was H. neanderthalis. There are other threads online that explain more or less that there is no definitive answer but I failed to find a review in a peer-reviewed journal.

Just a detail about the form of the post: When you say There are many theories, (1) the correct term is "hypothesis", not "theory" and (2) you should link to a detailed explanation for hypothesis (or evidence if there is any in the post) that you talk about, especially when these aren't well known.


text:
The Mystery of The Cretaceous' Songbirds
Before Passeriformes perched on the branches of our trees and sang their sweet, inspirational tunes, there was Enantiornithes, the "Opposite Birds".  So far, we have discovered at least 80 species from five different families.  (However, some of those names come from just one bone, so the nomenclature may not be valid.)
The really odd thing is that despite their diversity, they had become extinct during the Mesozoic-Cenozoic extinction event 66 million years ago, even though their rivals, the forefliers of today's waterfowl, shorebirds, tube-noses, rails and ratites, did not.
The question is:  How come?  Was there any paleobiology saying that this particular order of birds was too specialized to withstand an impact winter?

This is a fine question, but I don't think you are going to find answers. Simply, we don't know enough about the physiology or life history of these birds to know. All we have are skeletons (and some feather impressions). Even if we did know all about their biology, we still wouldn't be able to say why they went extinct. The same question could be asked of any speciose, seemingly successful group that went extinct.

The short answer is that we will never know.
Luck can sometimes be a factor of who lives and who dies. But such an answer doesn't feel satisfactory given such a diverse group such as dinosaurs and other groups like Enantiornithes.

Together with hatchling specimens of the Mongolian Gobipteryx[35] and
Gobipipus,[36] these finds demonstrate that enantiornithean hatchlings
had the skeletal ossification, well-developed wing feathers, and large
brain which correlate with precocial or superprecocial patterns of
development in birds of today. In other words, enantiornitheans
probably hatched from the egg already well developed and ready to run,
forage, and possibly even fly at just a few days old.[34]
A 2006 study of Concornis bones showed a growth pattern different from
modern birds; although growth was rapid for a few weeks after
hatching, probably until fledging, this small species did not reach
adult size for a long time, probably several years.[37] Other studies
have all supported the view that growth to adult size was slow, as it
is in living precocial birds (as opposed to altricial birds, which are
known to reach adult size quickly).[26] Studies of the rate of bone
growth in a variety of enantiornitheans has shown that smaller species
tended to grow faster than larger ones, the opposite of the pattern
seen in more primitive species like Jeholornis and in non-avialan
dinosaurs.[38] Some analyses have interpreted the bone histology to
indicate that enantiornitheans may not have had fully avian
endothermy, instead having an intermediate metabolic rate.[39]
https://en.wikipedia.org/wiki/Enantiornithes

So we have this. Enantiornithes weren't completely bird like. They may have invested less energy in parental care. Perhaps taken longer to reach adulthood, longer to reach reproductive age. May not be as warm blooded as birds but not as cold blooded as a crocodile.  Maybe that is why they went extinct.
The Enantiornithes did not care much for their young, since they were born pretty much hardwired to be independent. This hard wiring probably worked find in a stable environment, allowing adult to spend more time and energy making more independent chicks. But in a hostile, changing world of post-impact, that was simply too much for a hard wired, semi-warm blooded chick. Especially one that took longer to reach reproductive age than most birds did. And birds by and large do invest in parental care of their offspring.
The answer is perhaps obvious if we could go back in time and observe the entire genera of Enantiornithes. But in the absence of a time machine and only fossils and estimated growth rates... we can only speculate.

All kinds of things effect survival of an impact, you don't just have a winter, the impact sets off every fault and volcano causing earthquakes, eruptions, tsunami, acid rain, and widespread forest fires. It's not really about who is killed by these events but which groups are best at recovering from it. And too much of that can be determined by things that don't leave evidence in fossils. Slowly reproducing and specialized organisms tend to go extinct but they are by no means the only things that go.


text:
These Mammals Had a Good Run, So What Happened?
One of the great mysteries of the mammals is that some of the longest-lasting just aren't with us today.  The list of these puzzling unfortunates is as follows:
Paleomerycidae

DURATION:
55.8 to 4.9 million years ago
Hyaenodonta

DURATION:
63.3 to 11.1 million years ago
Merycoidodontoidea

DURATION:  35 to 5 million years ago
Hyracodontidae

DURATION:  55.8 to 20 million years ago
Leptictidia

DURATION:  70 to 33 million years ago
Entelodontidae

DURATION:
37.2 to 16.3 million years ago
Amphiocyonidae

DURATION:
46.2 to 1.8 million years ago
Protoceratidae

DURATION:
46.2 to 4.9 million years ago
If all these numbers mean anything, it's that these groups had withstood millions of years of countless, various changes in their environments.  They had lived so long, yet despite their apparent flexibility, they tripped at the finish line.
The simple question is:  Why?

@JohnWDailey The questions is locked now, new comments are not possible any more. Please discuss this issue in the chat, the comments are not for extended discussion, so please stick to the rules.

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text:
When streaking microbes on a plate to test growth after uv exposure, does how I streak make a difference?
I've been working on what I think might be a special strain of E. coli, I've been streaking it on LB agar plate and exposing it to varied times of UVC via the germicidal hood.
I'm wondering if how I streak, as in too heavily, vs very lightly, or diluted culture, etc would make much effect in survival.
If I'm putting too much onto the plate, the e coli could be self-shielding, or some ecoli dying off, but the rest underneath being protected from the light.
I've done several generations of surviving colonies, I'm now comparing to wild type to see if my streaking method results in survival in both.
This test will also rule out if the lamp is failing and my surviving colonies are just the tougher ecoli compared to the growth on the control.
tldr
Should I lightly streak or dilute my culture to ensure all ecoli are being hit with the UVC?

What about using a suspension in liquid broth. Put it in a shaker, put it under UV light.

Wouldn't dilution be more quantifiable for replication purposes?

I work with e. coli myself though I do not know if your special strain has anything drastically different than my own so I'll just give advice that I've gotten from post docs and other PhDs on how to handle cultures.
(Note: This is methodology that I can't really find a "source" for so take with a grain of salt and change for your needs)
Typically when streaking I try to ensure that I make the streaks light enough so there aren't colonies within vicinity of each other. It's hard to really give a quantitative answer on how to do this so you will have to experiment on your own so your streaks aren't laden with massive amounts of colonies next to one another. It should look like consecutive "beads" on a string. This is generally what I try to accomplish with my colonies. Keep in mind I am focused on cloning plasmids so I'm not really concerned about experimenting on the e. coli themselves, just getting individual populations that do not have mixed variations of my plasmid. This is why having colonies with good separation is important for my particular project.
As for making sure they are all being affected by the UVC, I'm not entirely sure if having them to heavily grouped together would "shield" from UV. I feel as though UV can easily penetrate through e. coli colonies but I guess its not out of the question. Best bet is to keep your colonies well spread out, enough so you can pickup a single colony with a pipette tip and nothing else. This will make any genetic experiments you may want to do a lot easier as well. Which I think would be interesting if you are interested in the mutations occurring.
Is there something about your project that requires you to streak these out on agar plates? I saw comments suggest liquid broth. Maybe that's easier to do to make sure everything is exposed and then streak them out on a plate to see growth and/or test for mutations.


text:
Follow-up to The Red Queen by Matt Ridley?
I just finished reading The Red Queen: Sex and the evolution of human nature by Matt Ridley. Since this book is over 20 years old, I was wondering if more recent research made part of the book obsolete or inaccurate in some way. If so, would you have a recommendation for a recent book that would be a good complement to it?

Which part of the book? Which theory? I upvoted, but also vote to close because your question is unclear

Any part of the book, really. I was just wondering if any part of the book needed to be updated, I guess that would have been a clearer question.

This question is unfortunately too broad. Nobody is going to read the whole and search every single subject to see if there is need for updates.

My question was aimed at people who already know the book and the field. Maybe that's too narrow a target.

I haven't read the book, but in the context of parasite-host co-evolution, RQH-style thinking is very common.


text:
Devonian Fish Diversity--What Would it Have Looked Like?
For 70 million years, the oceans, lakes and rivers of the world teemed with seven groups of fish:

Placodermi

Acanthodii

Agnatha

Chondrichthyes

Sarcopterygii

Actinopterygii
Now two of those groups have been extinct for hundreds of millions of years, but they were still a pretty big deal back then.
So by using modern fish as analogies, which niche(s) did which group of fish occupy during the Devonian Period?

A fascinating question, I wish I had time to delve into it, but it seems I am not the only one unable to do it justice at the moment.


text:
Do evergreen trees have higher densities of stomata to compensate for retaining leaves?
According to literature (Walls-Thumma), evergreen trees have less stomata on their leaves (than deciduous trees) to limit water evaporation.
Does this mean they have less less stomata in total, or do they have stomata on the adaxial surface that compensates for the smaller amount of the abaxial surface (in comparison to deciduous trees?).
Thanks!


text:
why does brain produces noise?
when i look at a white wall i see little colored dots moving in circles filling my whole visual view, just like the static on a tv but then in color.
I thought everybody had this but recently i discovered it is not normal ?
furthermore i see something which looks like tiny cells, just like you look under a microscope and bright white dots which are moving from the top of my view to the bottom. it is always present but some days more than others.
when it i see it more it is sometime together with a high pitched noise for a few seconds or a weird in my head like you have a beer or 2.
I cannot remember a time in which I did not have this (now 24 years).
I would like to know why the brain produces this noise ? it is not helping me to "survive" so why does it do this ? and what parts of he brain are involved in this ?

@rg255 nope thats totally not it, thats why i asked it seperately

I think you mean muscae volitantes Unfortunately, I couldn't find anything for your first ("i see little colored dots moving in circles filling my whole visual view") and third ("it is sometime together with a high pitched noise for a few seconds") questions.

it explains what the "tiny cells" and "bright white dots" are. Note: "it is not helping me to "survive" so why does it do this" - not everything is adaptive.


text:
What is the advantage of using plant-derived antibacterials rather than bacteria-derived antibacterials?
So obviously we have a big problem with antibiotic resistance. Most of our antibiotics originate from bacteria themselves (or are synthetic variations on scaffolds which originate from bacteria). I have heard it asserted that using antibacterials derived from plants would lessen the problem.
One argument for the use of plants is that the bacteria from which we derive an antibiotic must themselves already be resistant to that antibiotic, meaning that the allele for resistance is already in the bacterial gene pool and when we exert a selection pressure by using the antibiotic, resistance will eventually appear among pathogenic species.
Another argument I have heard is that plants can provide a lot of structurally diverse metabolites from which we might discover new classes of antibacterials.
Is there anything else to this?
(I know I have answered my own question to an extent, but I am wondering whether there are any other good reasons to look to plants for the next generation of antibacterial drugs).
Thank you!

You're right that some antibiotics do originate from fungi e.g. penicillin, cephalosporin. But many antibiotics do come from bacteria (especially Streptomyces spp.) for example: chloramphenicol, erythromycin, kanamycin, streptomycin, tetracycline, vancomycin, gentamycin, rifampicin

Your first argument of use of plants isn't really valid.  Take streptomycin, which is derived from Streptomyces griseus.  If a person had an S. grisues infection, you wouldn't use streptomycin against it of course.  But if they get tuberculosis, you can use streptomycin without worrying the the TB will somehow transfer genetic information from S.g and gain it's "resistance".

I think you raise an interesting point, but I don't think anything is being ignored today as a potential source of antibiotics. Look at that 15th c. ox gall, copper, and this & that recipe to treat chalazions that is effective against MRSA.

@Nathan - If I'm not mistaken, horizontal gene transfer can result in exchange of genetic material between bacteria that are quite distantly related. I think it's possible that a Mycobacterium could acquire streptomycin resistance from Streptomyces.

@DIPEA Not to be cliche, but anything is possible.  But it seems rather unlikely that these two bacteria are going to transfer genetic material given their different native environments.  Also given that one produces a molecule specifically meant to kill, or at least, hamper the other.

@Nathan Here's a reference describing gene transfer between distantly related bacteria: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC284573/?page=1

@anongoodnurse you're probably right; I guess the search for new antibiotics has just broadened its horizons generally

@DIPEA - I think that knowing bacteria (and yeast) compete makes the ease of plating and measuring reaction to discs easy enough guesswork (wasn't penicillin discovered because of clear spots on a plate? I can't remember now.) Doing that with all known plants, though... that's a lot harder. Just my guess. But as I said, I think you raise an interesting and good point.

@anongoodnurse Yup, Alexander Fleming had contaminated Petri dishes and realized some fungi had a clear zone without bacteria around and said "That's funny" - true quote. And boom, pennicillin.

@DartFeld it wasn't quite "And boom, penicillin". More like  "And 12 years later, penicillin"

Bacterial isolates from ancient permafrost and isolated caves allow study of the resistome, or the collection of antibacterial resistance genes, in environments without exposure to modern antibiotics for medical and agricultural use. These samples have genes for resistance to antibiotics derived from a variety of sources, including fungal sources (penicillins, cephalosporins) and synthetic dyes (sulfonamides), as well as bacterial sources (macrolides, aminoglycosides, etc). This finding was surprising, but does help explain the rapid emergence of resistance in response to clinical use. The genes have been there all along.
The OP is correct that a great deal of our current armament of antibiotics were derived from bacterial products, but since fungal and wholly synthetic products don't solve the resistance problem, I don't believe plant products will either.


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Genotypes that are inherited linked
I am interested in whether it is possible to determine the proportions of individual genotypes of offspring from the phenotypes, and thereby the proportions of individual genotypes of gametes for two traits on a chromosome that are inherited linked (on the same chromosome).
If B represents color (B → purple, b → red) and P represents fruit shape (P → elongated, p → round), and the phenotypes are as follows:
1405 purple and elongated fruit,
95 purple and round fruit,
95 red and elongated fruit,
405 red and round fruit.
The red and round fruit traits are recessive, while purple and elongated fruit are dominant traits. We crossed two heterozygotes for both traits (i.e., we crossed an individual BbPp with BbPp) that are inherited linked. I am interested in the proportion of all genotypes in the offspring and the proportion of genotypes in the gametes.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

This is simple Mendelian inheritance. You should be able to draw a Punnett square for this.

is this from school? it reads like a test problem. See the homework policy for some suggestions.


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Why would villagers attack Orangutans?
I read today in the news that villagers in Borneo were attacking refugee Orangutans. Why would they do this?

In It’s Not Just Conflict That Motivates Killing of Orangutans by Davis et al. (2013), the authors identify number of conflict and non-conflict reasons reported in the study why orangutans were killed in a certain part of Indonesia:
Conflict reasons:

pest
fear/self-defence
paid or forced to kill
orangutans interrupted logging or forestry operations

Non-conflict reasons:

traditional medicine
food
to sell or keep young as pets
hobby/sport hunting
for other trade of animals or meat
killed accidentally or opportunistically while hunting other animals

The results from this survey are depicted in this graph:

Obviously in this case they were not attacked for food. The impression I got from the article makes me think it was probably motivated by people viewing them as pests or as a threat/danger. It is almost certainly more of a social reason than a biological reason. However, in the absence of specific evidence, it is probably not helpful to speculate why this occurred.


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What does it mean for a gametocyte to "reprogram" the genes inside of it?
I am aware that frequently clones have genetic defects not present in the donor organism, even though the two are genetically identical. The reason for this is that apparently the enclosing gametocyte "reprograms" the genes inside of itself and during the cloning process, this reprogramming is not completed because the novel DNA is in the host gametocyte for too brief a period. Here is a quote from an article on the subject:

In cloning, scientists slip a cell from an adult into an egg with its
  genetic material removed. The egg then reprograms the adult cell's
  genes so that they are ready to direct the development of an embryo,
  then a fetus, then a newborn that is genetically identical to the
  adult whose cell was used to start the process.

What do they mean by "reprogram" the cell's genes? How can a germ cell modify its own nucleus in a way that would not affect the base pair sequencing?

More detail please. Clones of what? And the source of your quotation.

https://en.m.wikipedia.org/wiki/Reprogramming


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How do rare mosquito borne diseases get transmitted if they are so rare?
I recently read a somewhat alarmist notice by the state board of health in NH who claimed that some man had tested positive for Jamestown Canyon virus, a rare disease even in its natural environment of Colorado. Supposedly the man has not travelled out of state.
So, I am wondering how it is possible for such a virus to be transmitted. My understanding is that a mosquito only bites twice then it breeds, so basically what has to happen is the first bite has to be on an infected human (or animal) and then the second bite on the victim. So, if this guy got Jamestown Canyon virus, then he must have been in mosquito range of some other infected creature of which we have no knowledge.
Now, unless there is some type of animal that is endemically infected with Jamestown Canyon virus which is transferable to humans, it would seem unlikely to me that there would be any source from which the man could have gotten the virus.
So, I am wondering what kind of plausible scenario would have made this disease transmission possible, assuming it really occurred?

Via Wikipedia:

The virus is transmitted in saliva to a vertebrate host when an infected mosquito takes a blood meal. It thus cycles between mosquito and vertebrate amplifier hosts, mainly white-tailed deer. In a study from Newfoundland, JCV was significantly associated with large mammals such as sheep, cattle and horses. In Michigan and Ontario moose and bison are believed to be the primary reservoir.[3]
The virus winters in mosquito eggs, which it reaches by transovarial transmission. The female mosquito lays eggs that carry the virus, and the offspring can transmit the virus to deer or ruminants and humans. Infected mosquitoes were found equally distributed throughout the state of Connecticut, irrespective of land use.[4]

So, the virus has a reservoir in (primarily) deer, an infected deer gets bitten by a female mosquito, the mosquito lays eggs with the virus, the resulting mosquitoes can spread the disease by biting another large animal or human.
The reservoir needs to be large enough to ensure the virus survives year over year, but there doesn't need to be any special mechanism for it to travel outside the predominant range; there have been cases in several states in the northeast, though rare.

References [3] and [4] are:
[3] Goff G, Whitney H, Drebot MA (2012). "Roles of host species, geographic separation, and isolation in the seroprevalence of Jamestown Canyon and snowshoe hare viruses in Newfoundland". Appl. Environ. Microbiol. 78 (18): 6734–40. doi:10.1128/AEM.01351-12. PMC 3426688. PMID 22798366.
[4] Andreadis TG, Anderson JF, Armstrong PM, Main AJ (2008). "Isolations of Jamestown Canyon virus (Bunyaviridae: Orthobunyavirus) from field-collected mosquitoes (Diptera: Culicidae) in Connecticut, USA: a ten-year analysis, 1997–2006". Vector Borne Zoonotic Dis. 8 (2): 175–88. doi:10.1089/vbz.2007.0169. PMID 18386967.


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How do bullfrogs eat?
I have a very small pond in my backyard and a bullfrog lives in it. I see him all the time, but I never see him eat anything. He either sits in the water with his head just above the water or he sits on a rock next to the pond.
He must be eating something, because he is getting bigger, but I never see him eating. Does he just eat late at night or early in the morning or something? How come I never see him eating?

Just because you did not happen to see it eating doesn't mean it is not eating. This is not even a controlled experiment. How much time have you spent in observing it?? You have been a member of this site long enough to know that questions like these are absurd. Moreover, it lacks adequate background (for instance, the species of frog).

I have discovered by further research that bullfrogs hunt primarily at night.
So, at night he is probably venturing into the lawn around the pond where there are various insects and smaller frogs, such as wood frogs, available to eat.


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Can we directly stimulate M cones in retina with current technology?
I wonder if we could try to see imaginary "supergreen" color by directly stimulating M cones. For this I suppose we'd need:

Non-destructively scan specific human's retina to locate exact positions of M cone cells.
Prepare a high-resolution image (on a retina-like display I guess), which would have light spots in some locations and dark in others, so that when the human we inspected looks at particular point of the image, these light spots were focused exactly on M cones.
Track the eye movements and adjust the image so that S and L cones avoided significant exposure to prevent misperception.

Is anything of this hard to implement with current technology, given typical human retina properties (M cones density, their apparent color etc.)?
If this is totally possible, has such an experiment already been performed?

You've probably seen the news reports by now, in which researchers targeted and stimulated individual cone cells in the eyes of volunteers: "The elementary representation of spatial and color vision in the human retina" Ramkumar Sabesan, et. al. (2016). This experiment is the first time that researchers have targeted and stimulated individual cone cells. The experiments mostly involved L- and M-Cones, though the published research noted the response obtained from S-Cones, too. The researchers used 543 nm laser light (25 nm bandwidth) and an optical tracking system similar to what astronomers use to correct atmospheric distortions. So, yes, the technology exists, but it looks like it is so new in this application that no one has performed other experiments with it, yet.

Technology is not advanced enough to achieve receptor-specific stimulation. Regarding your defined needs:
1) Identifying M cones: It is already challenging to distinguish cones from rods in the retina (Turpin et al, 2011), let alone identify the three classes of cones.
2) Your retinal-mosaic image would theoretically be possible, although very small pixels would be needed.
3) Eye tracking is doable, but not at this level of accuracy. Delays in the system will almost certainly result in transient activation of other receptors.

Regarding (1), there's a 2019 paper: Cone photoreceptor classification in the living human eye from photostimulation-induced phase dynamics


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How to identify Ag nanoparticles in a solution?
Doing an experiment involving the production of Silver nanoparticles using bacterial extracts. The issue is proving that they've been formed.
AgNO3 is added to the solution, and the reduction environment of the bacteria reduces into silver nanoparticles of various size, depending on many factors.
Color change can be seen, and a change in the UV-vis spec also, but beyond that, is there anything else that can be done?
The papers I'm basing this project off of have access to electron microscopes, I don't.
Is there any sort of biological assays that react to metallic silver? or maybe to Ag NPs?
Or anyone have any experience involving biologically producing nanoparticles?
I'll be asking in Chemistry as well for a possible chemical reaction of identify metallic silver.

This paper says that silver nanoparticles enhance the enzymatic reaction that happens in a normal ELISA assay. You should be able to observe a significative shift in UV absorbance comparing your bacteria to a control.
Otherwise, I'd think simply of lysing the bacteria and centrifugating the lysate. I'd expect the pellet to contain nanoparticles and to be somehow different (in color?) from a control pellet.


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Are seedless fruits considered life?
From school, I remember that for something to be considered life, it must be able to reproduce.  With the creation of seedless fruits (such as watermelon), would this be considered life as they don't have seeds so they can't reproduce?

Why wouldn't they be? They are part of a plant which are indisputably living in almost anyway that matters. Fertility is not a pre-requisite for life - just a common way to pass on genes to the next generation. I'm voting to close this question because it's not clear what your question is without a robust definition of life.

I'm voting to close this question as off-topic because it is a nice candidate for Philosophy.SE

What's life isnt a matter of Biology but Philosophy? Hmm.. for once thing, there are 4 tags labeled "life" in this SE, one of them with its own definition of life. And some of the definitions out there of "life" says "Life is a characteristic that distinguishes physical entities that do have biological processes" (hard to think that idea came from Philosophy and not Biology) and some of the definitions out there of Biology says "Biology is the natural science that involves the study of life and living organisms". How can you study life if you dont define what it is?

Definition of life
The definition of what is alive and what is not is not a matter of biology but a matter of philosophy. Most definitions are based on:

Physiology

Existence of a metabolism

Evolution

Ability to reproduce and have heritable traits

Ecology

Ability to respond to the environment

There are plenty of possible definitions of "life". Note also that behind the complexity of defining what is alive there is the issue of defining the unit (the individuality if you want) on which the concept of life applies.
Your definition of life
You suggest a quick and simple definition so let's consider it.

to be considered life, it must be able to reproduce

If you talk about the watermelon tree
If this is your definition, then Citrullus lanatus is definitely alive as it is able to reproduce (otherwise we would not be able to cultivate them).
If you talk about the watermelon fruit
Now you may ask is the fruit itself alive. Then, using your definition again, I suppose the answer is no because a given seedless watermelon will not be able to give birth to other seedless watermelons (even via the make-up of a watermelon tree).
Note that following the same logic one could argue that one's head is not alive either as one's head does not reproduce. Only your gonads do. Your dog might not be considered alive either. A castrato (singer) would not be alive either. A woman, after menopause, cannot reproduce either! Arguably, a cloud replicates or a fire replicates and could eventually be considered alive following your definition. So really, as you can see your simple definition hardly fit your intuition of what should be called alive.
My opinion on your definition
Personally, I am not a big fan of your definition but again it is nothing but a matter of preferences. I don't like that your definition is unclear because there are plenty of limit cases and because there are plenty of cases we would want to call alive that we can't anymore (like a woman after menopause for example!) Every definition of life would eave limit cases but with your definition, it really easy to find these limit cases.
Is this question about Biology?
No, it is not. It is a question of philosophy.
Other interesting post on Biology.Stack
You might want to have a look at why isn't a virus alive.

And if being able to reproduce is a criteria for being alive, then my dogs are not alive, since they've been neutered.  Since one of them is now shoving his head under my hand in order to get me to go out and play, I'd say they're quite definitely alive :-)

Thanks! I inspired from your example to add that to my answer.

Yes, they are considered life

Seedless fruits can develop in one of two ways: either the fruit develops without fertilization (parthenocarpy), or pollination triggers fruit development, but the ovules or embryos abort without producing mature seeds (stenospermocarpy). Seedless banana and watermelon fruits are produced on triploid plants, whose three sets of chromosomes make it very unlikely for meiosis to produce fertile gametes. This is because one of the three copies of each chromosome can't pair with another appropriate chromosome before separating into daughter cells, so these extra third copies end up randomly distributed between the two daughter cells from meiosis 1, resulting in the (usually) swiftly lethal aneuploidy condition. Such plants can arise by spontaneous mutation or by hybridization between diploid and tetraploid individuals of the same or different species. Some species, such as tomato,[4] pineapple, and cucumber, produce seedless fruit if not pollinated, but do produce seeded fruit if pollination occurs.

They fulfill all processes which are required for anything to be considered as life

Metabolism
Respiration
Sensitivity (responding to stimuli like gravity and sunlight)
Nutrition
Excretion (getting rid of CO2)
Growth
Reproduction
Homeostasis

Sources

http://www.scientificamerican.com/article/how-do-seedless-fruits-ar/
https://en.wikipedia.org/wiki/Parthenocarpy

Which definition of life are you using? Answering yes or no to this question suggests that there is such a thing as a scientific, objective definition of life, while there is none.

@Remi.b I am using the definition by the encyclopedia britannica, which states that there is a definition, at least to some extent, what makes things life

The vast majority of scientist disagree on a given definition and they all agree that any definition would leave limit cases. Wiki gives tens (or hundreds) of citations.

According to Wiki:
Life is a characteristic distinguishing physical entities having biological processes (such as signaling and self-sustaining processes) from those that do not, either because such functions have ceased (death), or because they lack such functions and are classified as inanimate.
If we consider, let say, infertile animal, it has signal system and that maintain homeostasis so we can definitely say that is life, but it's life.
I understand, that the question is about species, but if we can say, that
such plants can arise by spontaneous mutation or hybridization between diploid and tetraploid individuals of the same or different species, how can we deny mutations that occur in our life in a natural way and state that it is not life?
In my opinion, when someone says that something is not life, it's inanimate.
But that is out of the question, i guess.


text:
What's the mixture of carbon and haemoglobin called
I know of oxyhaemogloblin , the mixture of oxygen and haemoglobin  , but carbon and haemoglobin combination is what's confusing

Carbon and hemoglobin??? Hemoglobin is made of carbon and other elements; it doesn't transport it. Do you mean CO or CO2 perhaps?

Is there a name for it other than Deoxyhemoglobine?

I'm going to agree with the comment left by @anongoodnurse and assume you are looking for the terms that define CO2 + hemoglobin and CO + hemoglobin.
CO2 + hemoglobin = Carbaminohemoglobin
CO + hemoglobin = Carboxyhemoglobin


text:
Is the efferent arteriole a pathway for filtrate through the nephron ?
I am studying the urinary system. I have to identify what part of the nephron is not a pathway for filtrate. I believed the collecting duct is not a pathway for filtrate because once the filtrate enters this destination it is now referred to as urine, and no longer filtrate. I thought that inferred that it was not a pathway. However, the efferent may also be a strong answer because after glomerular filtration that small molecules that get filtered into the glomerular capsule are identified as filtrate. But the cell and proteins that do not get filtered are not, so not what are they referred to as non-filtered. However, later in the process of urine formation they become secreted back into the bloodstream through the peritubular network into the nephron at the distal convoluted tubule.


text:
What species is this "talking" bird?
This YouTube video shows a bird which appears to repeat some sounds (not speech though) after a human. Here're some cropped screenshots from the video:

What species is this bird? Can it actually mimic human speech, or are these sounds in the video its natural sounds?

A location would help narrow it down.

Unfortunately the only information I have is this video. I wasn't the one who filmed it, so I can't add much information aside from what is contained there.

It is a black-collared starling (Gracupica nigricollis).
According to the title of this other video, which is the same footage uploaded by another user and could be the original one, it has been recorded in Thailand, where the black-collared starling is common.
Also, from the same Wikipedia page:

In Thailand the collared starling is sometimes kept in captivity and taught to speak.


text:
What is this bird similar to a seagull but with a forked swift-like tail?
I observed these birds in Saint Petersburg, Russia this June, mainly in the evening when the sun was setting. They are similar to seagulls and often fly (presumably hunting) at the same location as the seagulls.
Easily noticeable differences from seagulls are:

Forked tail, like swifts have
Narrower wings, which seem longer
Higher-pitched short tweets, which never turn into "laughter". A sample (with car noise in background) can be heard here.

Here are some photos I could took. They are blurred and chromatically aberrated because it's hard to focus with a telephoto lens and such fast motion towards and away from me. I exposure-compensated them to make the colors visible, so the photos are a bit noisy. I hope they are useful for identification anyway.

It would be helpful if you could [edit] in data about size (e.g. by comparing them to the size of birds at the same hight that you can identify). At very least that would allow you to rule in or out the little tern, which is about 2/3 the size of the other reasonable candidates.

This is one of the numerous species of tern. They are common birds of the seashore and rivers world-wide. The characteristic forked tail and the black cap on the head is what gives it away.
It is hard to say for sure given the chromatic aberration altering the colours, but this is likely to be either from the genus Sterna (particularly the Arctic tern or the common tern), or possibly the little tern (Sternula hirundo).

Looks like an arctic tern. The translucent wing feathers are easier to see in this out-of-the-cam photo without exposure compensation.

@Ruslan Seems most likely given you were in northern Russia, and the others seem to be in more temperate ranges.

"Gull + a forked tail" = "tern". It's hard to tell from your pictures, but: Common tern: red bill with black tip. Arctic tern: red bill with no black tip.  Roseate tern (rare): black bill. Sandwich tern: black bill with yellow tip. Little tern (which is really small compared with the others): yellow bill with black tip: Most juvenile birds (of all species) have black or gray bills.


text:
What food has the highest calorie per unit price that you can buy and eat regularly?
What food has the highest calorie per unit price that you can buy and eat regularly? The food cannot give you any undesirable health effect due to the sole reason that you eat it regularly (say once daily).

This question is unclear. Calories aren't the same as nutrition; fat is the most calorie dense food. What do you want to know? The most nutritious food for the price? The price where? Or are you trying to gain weight? There are better ways to gain weight than eating cheap calories.

I'm looking for high calorie food, not the most nutritious, but the bottom line is you can eat it regular without causing any health concern....

I honestly do not understand why it would be opinion based (I am entirely amused by the absurdity of people calling a close of this question). At best you can say little research would have been able to provide answer to this question (I am not sure) and me, the author himself does not show enough effort on his own to answer. This question can be entirely answered scientifically, given enough data about price and calorie of food, as well as long-term nutritional and health study of food substances. What kind of reason is that to close a question (do you even think???)? What a shame.

The first part of the question can be answer by simplifying it a bit. Food can be divided into a few base categories
Carbohydrate (eg rice)
Fatty acids (ie fat, butter and oil)
Aminoacids (meat)
What is the cost of rice? It depends on the quality of rice you are willing to eat. Good quality US rice cost  about  = $530 Per Metric Ton. Low quality 100% broken rice cost USD 350 per ton
http://www.riceauthority.com/prices/
Cost of cheap fatty acid (palm old) = ~$650 per ton.
http://www.indexmundi.com/commodities/?commodity=palm-oil
Meat : well it is over $ 1000 USD per ton.
http://www.globalmeatnews.com/Industry-Markets/Meat-prices-to-remain-high-as-demand-increases
IN terms of energy per cost...
Rice 4 cal per g https://www.google.com/?gws_rd=ssl#q=calories+rice+per+gram
Oil 9 cal per gram https://www.google.com/?gws_rd=ssl#q=calories+oil++per+gram
So in terms of highest calorie per unit price, the winner goes to palm oil.
The second requirement.. is a bit difficult to answer.
Genetics can play a role. Specifically the innuit can have a diet were 50% of their calories is derived from fat, without suffering form cardiovascular problem and starvation from lack of carbohydrate (ie the brain only runs on glucose) https://en.wikipedia.org/wiki/Inuit_diet. How this is possible is debated. Idea include, high levels of animal glycogen in their diet where most meat is eaten raw, a miss calculation in anthropological studies on the amount of plant carbohydrate in Inuit diet, and genetic differences.
Traditional asian diets can have upto 70% of calories derived from carbohydrates.
https://hms.harvard.edu/news/lower-diabetes-risk-asian-diet
http://sampan.org/2015/05/follow-traditional-asian-diet-for-asian-american-and-pacific-islander-heritage-month/

Thx for your answer!!

The cheapest source of calories in the world is one that is contributing to global extinction and catastrophic climate change through the destruction of the rainforest (palm oil).  These definitely qualify as undesirable health effects.

Pick the fatty acid of your choice, any fat or oil has the highest calorie to weight than any other food. Most fats are fairly cheap, there is a reason fried foods are so fattening. As long as you are eating an otherwise healthy diet all the health risks associated with fats are from gaining weight.


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Have there been any study that document the evidence of the changing ratio of the biomass of different trophic levels?
You would expect a number such as the producers (photosynthetic) biomass to consumers + decomposers biomass ratio is a very important indicator for sustainability. It is also very probable that the ratio has been changed due to human activities (land clearance, animal agriculture etc.) which have resulted in the likes of climate change (which is in a sense just a problem of excessive mineralization (both industrial and biological) relative to immobilization by producers). Have there been any studies that try to calculate and monitor this number? I can't seem to find any.

Related: In a typical model ecosystem, what might the percentage of plants be to top predators and everything inbetween?

Related answer to References concerning the relative population sizes of predator and prey, specifically dealing with biomass scaling of predators and prey.


text:
Does the saliva of a person just recovered from an infectious disease help to cure another persons having the same disease?
I have always had this 'weird' thought (But could never quite test it...). Would the saliva of a just recovered person contains antibodies, or other immuno-boosting substances that can help fight off the same pathogen in another person? If yes, is the concentration (dose) of them in saliva enough to have any considerable effect directly (without any further artificial concentration or extraction done)?

Cross posting on Stack Exchange is discouraged.  I'm with you that knowledge is our real motivation here, and that sometimes this policy gets in the way... but there are many good reasons for this policy. Are you the same user as a25bedc5-3d09-41b8-82fb-ea6c353d75ae? I suggest you close one post and focus on the other.

It's unfortunate that Health SE is so quiet, I'd love to see it grow and encourage the Biology contributors to interact there as well.  Perhaps in that motivation, and given that your question is probably more on point there, you should close this question and try over there.  Then if your question receives poor response you can request to have it moved/reopened here?

@JeopardyTempest Yep, thats me in Health SE. I have no idea why my name is different on the two sites.. And yes, Health SE is too quiet.


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About the mechanism of coupled reaction/metabolism with ATP
I am not in the field of biochemistry so this may be a rookie question or misconception.
I heard occasionally about the energy "released" from ATP hydrolysis fueling (endergonic) biological reactions. I am concerned about how does the energy "released" actually "fuel" another reaction mechanistically. In chemistry and physics, you can say that the fact that energy is released is a sign that the process (ATP hydrolysis) is energetically favorable (more stable bonds are formed as some weaker ones are broken). Subsequently, when the released energy is heat for instance, this heat can be used to do (or "fuel") mechanical work (like in a car engine). This is intuitive to me but the same cannot be said with ATP hydrolysis. How does the release of energy from ATP-hydrolysis actually "fuel" other reactions? or is it a misuse?
Thank you so much.

This is a basic, although not simple, question which has been asked here before. It is best researched in a biochemistry text book rather than in an answer on this list. You will find a good account in Berg et al. of how the overall free energy change is regarded as determining whether a chemical conversion is thermodynamically favourable, and how an unfavourable reaction can be coupled to a favourable one.  After reading that, please repost here or on Chemistry for clarification.


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Can plasmodial slime molds be infected by virus?
According to the definition, plasmodial slime mold consist of a "single cell" with thousands of nuclei. How would such a unique type of cell response to viral infection (if any)? Google search yield nothing.

since all known cells are vulnerable to viruses I'm gonna guess yes. and slime molds are only "a single cell" in the same sense fungi are which also have multi-nucleated cells.

Why do you think having multiple nuclei would have an effect on viral infection? The motivation for your question is unclear to me.


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Why people have less hair than other primates?
Well as you can figure out, most primates such as monkeys, gorillas and chimpanzees, have all their body covered with fur. As we know they are evolutional "relatives" to us humans, but we dont have much hair(only on the head,on the armpits, on the groin, etc.). I would like to know why this "evolution" happened in a such brief era and why.

Why are "relatives" and "evolution" in quotes?

Because their DNA (and more specificly the monkeys DNA) isnt much similar with the human one. If u want you can edit my question.

You obviously haven't been to many beaches, especially Greek ones. There are many people out there that are quite hairy, with uninterrupted hair from the top of the head to the top of the feet. All mammals are covered with hair (the thickness varies, of course), even whales and dolphins. You also have another misconception, about DNA differences - the sequences of humans and monkeys are very similar, which is why we use them in medical studies for efficacy and toxicity. Finally, the last common ancestor between humans and great apes was ~7.5 million years ago, not a "brief era" at all.

@Orphee From the phrasing of your question and especially from your comment, it feels like you could make good use of a short and very introductory source of information about evolutionary biology such as Understanding Evolution by UC Berkeley for example.

@Remi.b I had read a small article about human and its evolution at dw.com, so these are only my knowledge.

Hence my recommendation. It is not a necessary a priori for asking question, not at all. But it would quickly increase your knowledge and your ability to ask further questions about evolution incl. human evolution.


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Legality of doing private or scholastic virology with human pathogens?
Is it ok for a student, say a graduate student in biochemistry, to do amateur virology using potential human pathogens?
For example, lets say the student gets a cold and tries to isolate the virus causing the cold. Is it ok for the student to do that in a school lab? How about a home lab?

I'm voting to close this question as off-topic because it pertains to law, not biology.

@canadianer Virology is part of biology.

Law isn’t though…

If you ask a question about the law, you need to state where you live. Alternatively, if you are in gaol, as your name implies, different rules will apply.

@canadianer This is not just about law, but safety as well, so I think it is better not to close this question.

tl;dr I think that doing this unofficially, at home, might be no big deal, but doing it in an institutionally supported lab (or any kind of institutional setting, e.g. if you wanted to publish a paper from the results) could involve lots of hassle and red tape.
I'm not a microbiologist, but ... technically I think this would fall under the category of BSL-2 - via Wikipedia:

Biosafety level 2 is suitable for work involving agents of moderate potential hazard to personnel and the environment.[9] This includes various microbes that cause mild disease to humans, or are difficult to contract via aerosol in a lab setting.[11] Examples include Hepatitis A, B, and C viruses, human immunodeficiency virus (HIV), pathogenic Escherichia coli, Staphylococcus aureus, Salmonella, Plasmodium falciparum, and Toxoplasma gondii.

BSL-2 requires (among others) access control for labs; special safety training for all lab personnel; use of containment equipment for procedures that may cause infectious aerosols or splashes ...
It may seem a little crazy to lump a common-cold-causing rhinovirus with HIV, but BSL-1 (the mildest level of infectious agent control) is restricted to

well-characterized agents which do not cause disease in healthy humans

(emphasis added). Note that even BSL-1 requires lab safety protocols beyond those for non-infectious agents.
A bit more internet searching on BSL classification for rhinoviruses (the typical cause of the common cold) suggests some variation: e.g.

Google search for "rhinovirus BSL" brings up a bunch of hits from the American Type Culture Collection (ATCC) for a variety of rhinovirus isolates that range from BSL-1 to BSL-2
the Public Health Agency of Canada classes rhinoviruses as BSL-2

Depends on. S/he already got that infection so it is not a big risk to get it again... BSL1 is ok I think.

It wouldn't be your/their decision, it would be the institutional biosafety office's decision. And it's not whether it causes disease in that particular person (e.g. even if you vaccinated everyone in the lab against a pathogen, you'd still have to obey BSL-2 protocols). (I agree that this set of experiments would be 99.999% safe, but the rules are still there.)

I agree that you have to obey BSL protocols if you are working with pathogens, but I think applying BSL-2 for a common cold virus would be a huge exaggeration. I guess the school lab has a supervisor, so s/he should ask that person whether working with common cold virus is allowed and if so which protocol should they follow.


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Why was the cackling goose split off as a distinct species from the Canada goose in 2004?
According to Wikipedia, in 2004 the American Ornithologists' Union made the cackling goose a new species, splitting it away from the Canada goose.  The British followed suit in 2005.
What was the basis for this split?  Why was a new species required here?  Were offspring of these two found to be consistently infertile, or was the change based on something else?

The accepted answer doesn't point out that you can get the answer straight from the AOU if you have access to a science library: they publish explanations of changes to the AOU Checklist in The Auk! The one involving Branta hutchinsii is from Banks et al. 2004; the exact text they use are:

pp. 59–60. Several genetic studies of geese, including recent work with mitochondrial DNA (van Wagner and Baker 1986, Shields and Wilson 1987, Quinn et al. 1991, Paxinos et al. 2002, Scribner et al. 2003) have verified previous suggestions based on differences in voice, nesting habits, habitat, and timing of migration, as well as in color and size (e.g. Brooks 1914, Aldrich 1946, Hellmayr and Conover 1948), that the forms treated as the single species Branta canadensis by all previous AOU Check-lists and most other works actually constitute at least two species, and further that each of the two species may be more closely related to another member of the genus than to each other. Thus, we divide B. canadensis by recognizing a set of smaller-bodied forms as the species B. hutchinsii, and rearrange our representatives of the genus in the sequence bernicla, leucopsis, hutchinsii, canadensis, sandvicensis. Additional analysis may result in further splitting.

So, yes, this is mainly because of mtDNA analysis and because of several studies between 1987 and 2003, as described in the other answer.

The "white-cheeked" geese have long been subject to taxonomic controversy. From the 1920s to the 1950s, authorities have classified them into between one and four species. Although Aldrich in 1946 asserted there was near-unanimous agreement among Arctic biologists that there were two species, from the 1950s Delacour's taxonomy was most often followed, which had one species (Branta canadensis) and twelve subspecies.(1)
What changed the consensus were DNA studies.  Mitochondrial DNA (mtDNA), which is passed on without recombination, showed distinct sequences supporting two species. One RFLP analysis of mtDNA suggested the split between these two species happened about one million years ago.(1)
The species divide mainly along size and breeding location lines.  The Cackling Goose (Branta hutchinsii) is smaller and breeds on the Arctic tundra. The (present) Canada Goose species (Branta canadensis) mostly takes a larger form and breeds mostly in non-tundra areas.(1)
(1) - Mlodinow, S. G., et al. "Distribution and identification of Cackling Goose (Branta hutchinsii) subspecies." North American Birds 62.3 (2008): 344-360.


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Do eukaryotes assimilate DNA that is floating in the extracellular membrane?
Prokayotes, which replicate primarily using binary fission, don't get much genetic diversity. For this reason, they take in any genetic material they encounter, in a gambit to help them better adapt to their environment.
However, Eukaryotes, most plant or animal cells that contain a nuclei, have great diversity from crossing over during meiosis, not to mention genetic materials from two parents.
Due to other means of genetic diversity, it seems that eukaryotic cells wouldn't need to take in foreign DNA as prokaryotes do. But sometimes life has redundancy, so:
Do eukaryotes assimilate DNA that is floating in the extracellular membrane?

+1 Horizontal Gene Transfer occur in eukaryotes too, therefore it must be somehow possible for a piece of DNA to enter a eukaryotic cell and nucleus.

@GyroGearloose the transfer of DNA via sex-pilus occurs from one bacteria to another and not from the environment. Perhaps you mean type-IV pilus.


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Why are bacterial cultures necessary?
I notice that in a lot of bacteria testing procedures the sample has to be cultured. You place the sample in agar or another growth medium and wait for the bacteria to proliferate before examining them.
Why is this necessary? If the bacteria are present in the sample, can't you just examine the sample directly with a microscope to find them? Is it a needle in a haystack problem?
For example, a listeria bacteria is about 1 micrometer in size and has a positive gram stain. So, at 1000x magnification the organism would be 1mm in size in the objective which is highly visible. Even at 100x magnification you should still be able to see a tiny dot and be able to zoom in on the dot.

With only a microscope, you might be able to find the bacteria, but how do you know what kind of bacterium it is?
Taking Listeria, under a microscope, it looks like a small rod. Well, so do lots of other bacteria. If you only see that one bacterium, you can't take it and do any further tests with it, you can only see it.
So we do cultures, where bacteria multiply and form colonies. Whether they even grow under these conditions already tells you a lot - a lot of bacterial species won't grow colonies on The type of colony is another factor in determining what bacterium we are looking at - does it have fuzzy or clear edges, what color is it, is it "shiny"?
And then, with that culture, further tests can be done, like what chemicals the bacterium in this colony can break down, what they produce, whether they can be stained with certain dyes, etc. Many times this is needed because bacteria look very much alike (round or rods).
For Listeria specifically, there are special plates used as a growth medium that has certain chemicals added that makes their colonies appear red-violet. Other bacterial species won't show this color even if they do grow on the plates.


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Can a hormone be absorbed into the body digestively?
Obviously, to act most hormones must be present in the bloodstream. What happens if a hormone or hormone-containing food is consumed normally? Is there any way for the hormone to reach the bloodstream?
A related question is whether hormones are destroyed by digestive enzymes and chemicals, which include hydrochloric acid and bile salts. If hormones are destroyed by these chemicals then it may be impossible for them to enter the blood stream.

Yes, some hormones can be absorbed from the digestive tract. Birth control pills are a perfect example.

@MattDMo Well in that case the drug is encapsulated a special "enteric coating" that protects it from stomach acid.

@ImprisonedRhesus peptide hormones (e.g. growth hormone, insulin, pituitary hormones, etc) are denatured by stomach acidity and digested by proteinases - as MattDMo says above the steroid hormones (testosterone, estrogen, bile salts, etc) can be absorbed by the GI tract

This entirely depends on the kind of hormone. Hormones can be chemically completely different things. For example, estrogen is a steroid hormone and is chemically very stable so that it can pass the stomach without being harmed by the acidic conditions (even without enteric coating. AFAIK enteric coating is only used in emergency contraceptives, not in regular ones. And for the emergency contraceptives it is used in order to reduce side effects such as vomiting). As such, estrogen in your food or drink will have an effect on your body and there are many studies suggesting that this is a reason for reduced fertility in men.
On the other hand, insulin is a peptide, which would be digested and its hormone function completely inactivated when swallowed.
There is even the notion, that the gas nitric oxide may have a hormone function. In that case, it could reach the blood stream even through inhalation.
In summary, whether or not a hormone can be active after ingestion entirely depends on the kind of hormone.


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What do leafcutter ants do with the leaves?
I have seen pictures of leafcutter ants carrying off leaves. What do they do with them? Make a house?

c'mon...https://en.wikipedia.org/wiki/Leafcutter_ant maybe?

Trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer.

I'm voting to close this question as off-topic because it is an underresearched trivia

As in the Wikipedia article, these ants have a mutualistic relationship with a fungus. They feed their leaves to the fungus and in return the fungus makes pellets of food to feed it to the ant larvae. Along with that, the fungus provides defense to the ants.
Ants and many other animals cannot fully digest leaves as they contain cellulose which can only be digested by certain fungi and bacteria.

@AliceD I have added some extra information.


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Product of reaction between HCl and bile
In the mammalian digestive system  HCl is the main acid and bile is the main alkali. What is the product of the reaction between these two chemicals?

HCl is neutralised by the bicarbonate in the pancreatic juice. I dont think it'd form any products of reaction with bile

@Polisetty On the Wikipedia page for bile it specifically says that bile is alkaline and that it neutralizes excess stomach acid.

General chemistry questions are off-topic here, but can be asked on [chemistry.se].

It's a simple acid-base-reaction. In order for bile to do its job, i.e work as an emulsifier, it needs to in a basic environment. Bile acids are therefore in their charged, negative state.
The reaction of HCl with bile acid would then be.
[BILE]-COO- + HCl --> BILE-COOH + Cl-
In the human body the reaction would be:
[BILE]-COO- + H3O+ --> BILE-COOH + H2O
There will be hardly any free HCl in the human body, it will immediately react with water to form H3O+ and Cl-. H3O+ will then react with ionized bile acid to give the neutral form of bile acid and water.
So, depending on how you look at it, the product is neutral bile acid and (water or chloride).

That is very interesting. What is "bilic acid"? When I do a web search on bilic acid it does not return any useful results.

What are bilic acids? A typo, I meant bile acids. The answer was updated accordingly.


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Is RFLP markers are dominant or codominant?
there are several markers used in molecular biology,. marker analysis. RFLP is most commonly used marker which having several advantages. is RFLP marker co-dominant or dominant ?

Your question doesn't make any sense. Do you know what a restriction fragment length polymorphism actually is? It's not a gene, so the terms "dominant" and "co-dominant" don't make any sense. It's essentially like asking if an EcoRI fragment is dominant. The terms don't apply.

I suspect that you "know" the answer to your question and are just seeking confirmation.  First, let's get some terms straight.  Dominant and recessive are used in reference to phenotypes, so one needs to have a transmissible phenotype to score among the offspring of our genetic cross.  Phenotype are usually due to (or caused by) mutations.  In a diploid species, if you can only score the phenotype in offspring that are homozygous for that mutation (denoted m/m) then the phenotype is recessive to the wild-type allele of the gene.  In other words, a heterozygous offspring, (m/+) will have a wild-type phenotype.  On the other hand, if a heterozygous (m/+) offspring has a mutant phenotype then we would say that the mutation is dominant over the wild-type allele.
Your question is asking about a test cross of a +/+ individual to a homozygous mutant (m/m), however, in this case the RFLP does not typically have any mutant phenotype, it is just a convenient genetic marker for the purposes of this discussion.  All of the cross-progeny will be (m/+), and if you go to the trouble of preparing genomic DNA from those F1 cross-progeny and perform a Southern blot with a probe that detects the RFLP, then you will be able to demonstrate this.  Typically, unless the RFLP-bearing chromosome is homozygous, the probe will also detect the wild-type restriction fragment, so there will be two bands on the film, one for each allele.  Since you can detect the genetic marker in the F1 generation, the RFLP is dominant, but since you can also "score" the wild-type fragment, the two fragments are indeed co-dominant (after you do the Southern blot).

Your answer gave a clear identification. thanks in advanced .


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Name this insect
This is the monsoon season and some black insects are flying in my house. They have a very bad smell. Does anyone know what is the name of that insect, including English and Hindi name?

It is a bit old but since I ended up here while searching for the same insect, here is what I believe is the insect in question (I also have an experience with it in our little garden).
Its name is: "burrowing bug" or sometime referred as "Cydnidae" (scientific name).

Also, check out this video (if it still remains) :
https://www.youtube.com/watch?v=FABjzwRTeR4
Best regards,

That's the earth boring dung beetle. It has a very bad smell and it belongs to the family Geotrupidae. You can learn more about it here https://www.britannica.com/animal/dung-beetle

Is there any way to get rid of them? As Their smell is very burst that if I flies on body and get rubbed. These insects are flying around my house as this is the rainy season.

@SagarGupta well you can check their source around your house and how they come into your house


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What is allele-specific binding?
So far all I have found is this:
https://www.biostars.org/p/132527/
My guess is that some alleles, for whatever reason, bind to things like transcription factors 'moreso' (for want of better word - affinity maybe) than others. Or maybe some alleles are more likely to get methylated, for example.
I feel my understanding is very much bare bones. Is anyone able to go through it a  little more comprehensively? Thanks


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How RNA primer on leading strand is removed during DNA replication and how the gap is filled?
Please can you explain me how the gap created by the removal of primer on 5'-3' leading strand is filled.

is this a homework question? have you tried other sources? if you can show us what effort you have put into trying to answer this question, then one of the community members will be more inclined to helping you out

The group of cellular enzymes that remove RNA primers include the proteins FEN1 (flap endonuclease 1) and RNase H. The enzymes FEN1 and RNase H remove RNA primers at the start of each leading strand and at the start of each Okazaki fragment, leaving gaps of unreplicated template DNA. Once the primers are removed, a free-floating DNA polymerase lands at the 3' end of the preceding DNA fragment and extends the DNA over the gap. However, this creates new nicks (unconnected sugar-phosphate backbone).
In the final stage of DNA replication, the enyzme ligase joins the sugar-phosphate backbones at each nick site. After ligase has connected all nicks, the new strand is one long continuous DNA strand, and the daughter DNA molecule is complete.

Source: Boundless. “DNA Replication in Eukaryotes.” Boundless Biology. Boundless, 08 Jan. 2016. Retrieved 14 Mar. 2016 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/dna-structure-and-function-14/dna-replication-101/dna-replication-in-eukaryotes-437-12941/


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how DNA controls properties of cell?
My textbook says:

DNA is the heredity material which controls the properties and
  potential activities of a cell.

I couldn't understand how it controls properties of cell?

I think your best plan is to keep reading.

What it means is that it controls the cells purpose. Skin cells have a different genetic makeup than brain cells.

This question is far to broad. You are essentially asking "what is molecular biology" - like @AlanBoyd suggests, keep reading, probably the rest of your textbook or one you will read in the future is about exactly this.

@BryanKrause,actually I want to understand the fact what is meant by property of cell?and what is meant by potential activities(transcription or translation...yeh??)

The production of all RNAs and proteins in the cell, including RNA and proteins that regulate expression of other proteins, and indirectly all the functions of those proteins. Everything. This is all of biology at the cellular level. That's why your question is too broad.


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Segmentation in Platyhelminthes
My text book says:

Platyhelminthes are unsegmented worms.

Moreover, tape worm (Taenia solium), which is segmented, is one of the examples of Platyhelminthes.
My question is: why a segmented worm is included as an example in Platyhelminthes (unsegmented worm)?

Welcome to Biology.SE. Could you please add the reference to your textbook? Thanks!


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How chameleons change color?
Well, I was watching a video about chameleons and I saw that their cells can change color. Can someone explain me how is this possible?

https://en.wikipedia.org/wiki/Chameleon#Change_of_color

When it comes to displaying color, most organisms use chromatophores. Chromatophores are pigment-containing and light-reflecting cells, or groups of cells. Chromatophores reflect the color that they look like.
Chameleons also use chromatophores. The outermost layer of the chameleon’s skin is transparent. Beneath this layer are the chromatophores. The deepest layer contains melanophores, which are filled with melanin. Above that layer are cells called iridophores, which have a blue pigment that reflects blue and white light. Layered on top of those cells are the xanthophores and erythrophores, which contain yellow and red pigments, respectively.
For a chameleon to change color, it must expand or contract certain chromatophores depending on the signal of the nervous system. The expanded chromatophores block the contracted ones and the color of the expanded chromatophores determine the color of the chameleon. For example, to make the chameleon green, the iridophores and xanthophores must expand, and melanophores and and erythrophores contract.
Reference
WIRED - How Chameleons Change Colors
More to read
This Nature article provides a detail description and explanation of how this occurs - Photonic crystals cause active colour change in chameleons


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What type of Bacteria?
I did some tests to a bacteria colony and I observed the following:
First of all let's start from the shape and after that we move on to the chemical tests that I did to them:

Form: Circular
Colour: Yellow-to-white (something like pale yellow)
Margin: Entire
Elevation: Flat

Chemical results:

Gram: Negative
Catalase: Positive
Oxidase: Positive

After some research to the databases, I figured out that it might be:
If it belongs to the family of Pseudomonas:

Chryseomonas luteola OR Pseudomonas luteola group Ve-1 with a chance of 48.21%
Flavimonas oryzihabitans group Ve-2 with a chance of 48.21%
Xanthomonas maltophilia OR Pseudomonas-like spp, with a extremely low possibility of 1.34%.

So, my question has 3 parts:

Can someone please tell me if my hypothesis is right?
And if it is possible which bacteria from the above is the correct?
If you manage to find the correct type of bacteria can someone tell me the ideal enviroment to study them better? (agar plates, temperature, time needed, etc.) Thank you for all the efforts made!

Important notice: I have used a blood agar plate with a concentration of 5–10%. It contains as far I know, mammalian blood maybe from sheep or horse. I forgot to check the temperature, but I don't think that it is very important.

Sounds a bit like homework/course work to me...
I don't have an answer for you immediately, but if your observation that the cells are circular (coccoid) is correct, it can't be Xantho/Pseudomonas. If the results are to be trusted, that they are G- cocci, there aren't very many options, just Veillionella, Moraxella and Neisseria, pretty much http://rx.osumc.edu/asp2/microbiology/gramNegOrganisms.pdf.
Try Bergey's Manual of Systematic Bacteriology (I can't find an online copy though).
Your use of media and temperature can be very important. How was it incubated? Anaerobically?

@JoeHealey 30 degrees, aerobically. I will check now the Systematic Bacteriology, thanks for that guide!

Aerobically would rule out Veillonella, but I haven't checked whether Moraxella/Neisseria are Catalase/Oxidase positive or capable of growing on blood agar.

Well I will let you do your research.. When done post the results to the answer. Thanks!

Consolidating my comments, and taking all the results at face value (though microbiology can be very tricky), the most likely candidates are Moraxella, or Neisseria spp.
Gram negative cocci (spherical cells) rules out a large number of possibilities, leaving just the above 2 and Veillonella as candidates.

The OP said that the culturing was done under aerobic conditions at 30˚C. Veillonella is an obligate anaerobe, and so wouldn't survive this. Both Moraxella and Neisseria are happiest at 37˚C but would no doubt grow at 30. Both are cultivable on blood agar. Neisseria is best cultured in a 5% CO2 atmosphere, so is probably somewhat less likely. Both appear as pale-whitish colonies on plates. The OP's observation of yellowish colouring could be artifactual of the plate colouring, I'm not 100% sure.
Both are positive for oxidase and catalase.
Neisseria on blood agar:

Moraxella on blood agar:

One final comment: both of these are pathogens, so continue with all due caution.
Moraxella, in particular, is a respiratory pathogen, so I would advise working in a biosafety cabinet. I'll assume you already have the relevant paperwork/permission to be handling > BSL1 organisms...

Lovely answer, covers me 100%. And of course I have permission to work on pathogens... besides thats my future job! Pathologist....(still studing and experimenting but ok)

Great, that's good - thought I'd check. If it was a school experiment or something, they may not have had the relevant safety frameworks, so thought it best!

University experiment in special labs... and tutors-personnel that are always watching us.


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Questions on adding a protein to a DNA library
Two questions regarding finding the DNA sequence of a amino acid sequence (AA):
1) If you are able to find out the mRNA sequence of an AA, then don't you automatically know the DNA sequence?
2) When determining the mRNA sequence of an AA, how do you account for the various permutations in the genetic code for a given AA. Ex. Leucine is CUU and CUC. Or does it not matter?

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.

@MattDMo This is not a homework question. I am just curious about the answer based on a lecture I attended and couldn't grasp. Thanks for the help

For 1, that is how retroviruses such as HIV work, and of which scientists have utilised to use in gene therapy. It requires a process called reverse transcription.
However, this would only show you the gene the mRNA was from, but no information about its location, or if it is repeated elsewhere.
As for 2, this is to do with the fact that one base cannot code for one amino acid; as there are 20 common amino acids used to make proteins. With 2 bases, you are only getting 16 possible codes from the various base pairs you can create. However, with 3 bases, 64 possible combinations are possible, more than enough to suffice for the 20 needed. This is called the triplet code;
and therefore, there are more possible combinations of the base pairs in DNA than there are amino acids to be made from them. The 'left over' combinations can code for the same amino acids as other combinations, making it the code degenerate. Therefore, it doesn't matter, as the combination is always read in 3s (non-overlapping), and if it codes for a particular amino acid, then that amino acid will be produced at the ribosomes when its corresponding code is read.
I hope this increases your understanding of the topic.
http://www.genetherapynet.com/viral-vector/retroviruses.html (Question 1)
http://www.chemguide.co.uk/organicprops/aminoacids/dna4.html (Question 2)

Excellent! It definitely helps @Butallati
For 1, is it every important to know where in the human DNA the gene if you have the mRNA sequence to make synthetic DNA?

Well, if we're talking about 'synthetic DNA', it's gonna be pretty difficult to create millions of pairs - so often scientists only create synthetic DNA in the form of genes, which are more...measurable. By taking the mRNA that you know will be used to produce a particular protein, and using a retrovirus, you will just be inserting that gene back into the DNA (just like how HIV will insert its own gene into your DNA, after all, it too is a retrovirus). Therefore the location of gene on the DNA is not particularly important for that instance.

If you wish to know more on the uses of retroviruses in gene therapy, feel free to google about "SCID" and gene therapy. There may well be some processes, or maybe just general knowledge of how DNA works, which requires knowing the location of genes on DNA, however I personally don't know any.

thanks so much for the exciting information! I'm a medical student whose eyes are just opening to the world of therapeutics and biotech start ups. Most of my experience has been in retrospective clinical research but I'll be taking a research year soon to expose myself to clinical trials and basic science work

Awesome, glad I could help. I'm just an A2 student (1 year prior to University), so it's nice to see possible applications of what I've learnt to this website. In addition to what I mentioned earlier, some other interesting things under the topic of DNA technology are the use of gene markers, in vivo gene cloning (using vectors such as retroviruses, as explained above) and in vitro gene cloning (using the polymerase chain recaction). Those should help further your understanding of DNA technology (which is closely related to your question)


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How do coyotes remove cactus needles from their paws?
Here, in Arizona, coyotes roam and hunt in the desert.

While hiking with dogs, I often see spiny bits of Teddy bear cholla cactus on the ground.

Dogs often step on these and get stung by the needles. Trying to remove them from dog paws with hands usually results in hands getting pricked too. A pair of stones, sticks, or tweezers usually works. I imagine letting the dogs chew off the needles would result in having needles in their lips/mouth.
Q: What do coyotes do with stuck cactus needles? Do they remove them, if so how? Do coyotes and perhaps other desert animals have special adaptations for removing/avoiding cactus needles?

Their paws might be more callous and have more padding for the desert adaptation. Things can still get stuck in their paws but not cause serious issues and can fall off in time because of the adaptations. Wild animals can still be susceptible to splinter infections but it would be rare compared to humans or pets. I found some studies regarding to camels but not specifically for coyotes.