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Restriction enzymes, how are the recognition sequences determined?
How were the recognition sequences (e.g. GAATTC of EcoRI, GGATCC of BamHI) characterised? Text books only list the recognition sites but never the methodologies used to determine the sequences.

This paper describes a simple method to determine restriction sites, which was used to determine the restriction sequence of the previously uncharacterised enzyme from Haemophilus gallinarum.
In short, a known sequence of DNA (from the phage $\phi \text{X174}$) is partially digested with the restriction enzyme, and the various digested fragments can be used to determine the relative distances between each of the restriction sites.
Then, the restriction fragments are extended using T4 polymerase and sequenced using $^{32}\text{P}$ labelled Sanger sequencing.

Once the restriction map of the enzyme on the known DNA sequence is completed, the individual fragments can then be checked for similarities. For example, HgaI has a recognition site outside of the restriction site. Therefore, when the individual restriction sites are compared, it can be seen that all of them have the recognition site GACGC.

Wonderful, the paper is also openly accessible without a subscription! Wonder if this is still the method of choice nowadays for sequence determination given the advances of next generation sequencing platform...

@Green Presumably for restriction enzymes, Sanger sequencing (albeit with improved methods, such as the BigDye-based sequencing technique) is likely to be still superior to high throughput sequencing, as the number of sequences required to determine the restriction recognition site is very small and not sufficient to make high throughput sequencing worthwhile.


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Any books/publications about what life was like before antibiotics?
Just wondering. We've been discussing antibiotic resistant bacteria a bit in lecture, and how we're slowly sinking into a pre-antibiotic era again.

Any medical literature before 1928 is about "life without antibiotics". Please add some details to your question. Have a look at the tag-wiki for [tag:book-recommendation]

A google search with "life before antibiotics" gives a nice list of sources.

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How to detect Zika in mosquitos
I'll keep this as brief as I can. I am an engineer and I have an idea for an early detection system for the Zika virus. I want to build it. However, first I need to do research on how one detects Zika in mosquitos.
I am under the impression that to detect it in a human you would wait for the appropriate antibodies to appear in the blood. I am assuming that I would need to culture anything I get from a mosquito.
Can someone point me at any research material they can find? All of the search terms are to ambiguous for mere non medical mortals like myself.

This might get a better answer on Biology.SE.

It would not be possible to identify the virus carried by the mosquito by simple visual examination of the mosquito. You can visually identify the species of mosquito (like Aedes, Anopheles or Culex) and select the species that are known hosts. You don't need to culture, you can dissect the salivary gland and use PCR primers specific to viral DNA to test the presence of virus. This is a cheap method but still you cannot make some kind of screen to filter out carrier mosquitoes from the rest.

The gold standard would be the isolation of infectious virus from mosquito saliva. Extraction of saliva from mosquitoes is fiddly if you have to do it in containment and the survival of mosquitoes collected from the field may be low. Alternatives, in roughly declining order of strength-of-evidence, would be

identification of virus from dissected salivary glands,
identification of RNA from saliva/salivary glands,
identification of virus or RNA from heads,
virus or RNA from whole bodies of insects that are not visibly
engorged with blood (and we're getting
into not-very-reliable-at-all territory at this point).
detection of viral RNA from pooled field-collected (unsorted) insects, possibly including those which have recently blood-fed.

There are also other technologies that are beginning to be used for field surveillance of arboviruses in vector populations, such as sugar-coated or honey-coated Whatman FTA cards (mosquitoes sugar-feed on the cards which preserve RNA).
Two other things are worth emphasising here. One is that not all mosquitoes which ingest infectious virus will develop a transmissible infection even if they survive to complete the necessary incubation period. Some will clear infection completely, others may develop a disseminated but non-transmissible infection due to the existence of barriers to replication within the vector's tissues (see this paper for a nice review).
The second is that the importance of a vector is not determined solely by its competence (the probability that a mosquito ingesting an infectious dose and surviving the extrinsic incubation period develops a transmissible infection) but also things like vector:host ratio, biting preferences, and typical lifespan. Vectorial capacity is more important (this is a recent paper pointing out the differences).

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Sexing fish from a tissue sample
I am a member of a local fish club, we have a lot of different aquarium fish and would like to trade them amongst us. We all have a few fish that don't form pairs and would like to see if they pair up with someone else's. But as you can imagine keeping track of all the fish would be extremely hard and pointless if they were the same gender, so someone suggested we should buy a microscope and sex them via tissue or blood sample. But none of us has any experience doing that or if that is even possible, so we need some expert advice on the matter.
I wish to know if you can tell the gender of a fish from a tissue or blood sample and what equipment do you need (how much magnification in a microscope)? We work with discus and other cichlids, and countless marine aquarium fish.
For the sake of being specific I restrict my question to Discus fish, however, I would like to know if any general principles of tissue-sample based identification exist, for different species of fish.

I know nothing about ichtiology but if you just google discus fish sexing you get tons of hits (including videos).

But it's not restricted to discus fish, they are just the most common fish with sexing difficulties that came to mind. As for the google results, they are useless copy-paste guesswork.

I might misunderstand your point. Discus fish are maybe just one example but it is impossible to describe sexing generally for all fish. Is it? Or maybe you are asking for a list of methods generally used for sexing without willing to discuss sexing for any specific species? However, question like the magnification will obviously vary between 1X to 500X I suppose.

Well if you have a tissue sample you may be able to do genetic testing (PCR and gel electrophoresis) but it depends on species - sex determination systems are variable in nature. Asking what magnification scope you would need makes it sound like you want it to be a visual inspection method.

Depending on the number of fish, sending tissue to sequencing might be cheaper than buying a microscope. But it only works if the species is 100% GSD (genetic sex determination) and this depend on the species (won't work for clownfish for example). Also karyotyping might be a solution for GSD that have sex chromosomes which also depend on the species. The feasibility of a non-lethal visual inspection (with or without a microscope) depends on the species. So really....it depends on the species

Ironically, assuming 100% GSD, FISH might be a good option :)

As already pointed out by Remi, you can identify the sex from a tissue sample only if there is a genetic (such as chromosomal) sex determination system (by using techniques such as PCR or in-situ hybridization). However, different species of fish employ different mechanisms of sex determination:

Focus on or attachment to genetic systems involving X and Y
  chromosomes must quickly be shed in studies of sex determination in
  fish due to the diversity of mechanisms utilized, and, by doing so,
  the researcher can explore alternative regulatory mechanisms that hold
  important clues for understanding sex determination in general. The
  biology and ecology of fish is sufficiently diverse to provide unique
  examples of sex-determination mechanisms, yet they possess many of the
  same processes and pathways that are used in other vertebrate systems.

 Devlin, Robert H., and Yoshitaka Nagahama. "Sex determination and sex differentiation in fish: an overview of genetic, physiological, and environmental influences." Aquaculture 208.3 (2002): 191-364.

Though Devlin and Nagahama comment (above) that fishes also employ the same signalling pathways as other vertebrates for sex determination, study of these pathways to determine the sex would be extremely difficult as you may be aware that the cell-signalling and the gene regulatory networks are highly complex.
Fishes are highly sexually dimorphic (including Discus) and the sex can be easily identified (with some practice) by visual inspection. Microscopic identification would be both money and time consuming. Morphology based identification can be automated (when the machine is trained sufficiently). You can have a look at this article1 which is about using image analysis to score salmons.

1.    Merz, Joseph E., and William R. Merz. "Morphological features used to identify Chinook salmon sex during fish passage." The Southwestern Naturalist 49.2 (2004): 197-202.


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Are the arrows in this diagram of ATP synthase correct?
I have a question about this image below.
Do you think that the pink arrow is actually going in the right direction?
I would suggest a LTO sequence and not LOT, since it is in the T state that ADP + Pi is converted in ATP.

I found this diagram in the book: Alison M. Smith, George Coupland, Liam Dolan, Nicholas Harberd, Jonathan Jones, Cathie Martin, Robert Sablowski, Abigail Amey, Plant biology, first edition                                           There is said that the pink arrow show how the protons rotate the complex, but to me the sequences of the three states are wrong anyway

Yes, the arrows are correct. However, it's not immediately clear what they're trying to show.
ATP synthase
ATP synthase can act as a generator or a motor. Interactions cause rotation of the F0 subunit and the  subunit's axle has a kink in it which deforms the stationary F1 subunits (the axle can turn either way to act as a generator or a motor). Read more at PDB's ATP synthase 101.

What The Asker's Diagram is Trying to Show
The black arrows in the asker's diagram are implying the movement of ADP or ATP (generation) in and out of the catalytic site. The pink line implies the movement of the axle kink and not the transition of ADP+pi->ATP.
Let's focus on the left-hand subunit across the subfigures and it makes more sense (ADP and Pi go in, protein "closes" and ATP is formed, ATP is released). Meanwhile, the "kink" completes a full rotation.

If the complex move clockwise, due to the H+ movement, (as the pink arrow should show) then the synthesis of ATP should not be clockwise too?

F0 rotates, F1 should not. Only the  subunit's axle is rotating in this figure. L/T/O are referring to different states of each (stationary) subunit.

Ok. If it does not move it makes sense. Just a last question: are these 3 states found for both alpha and beta subunits?

Yup: wiki


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Why would I see no bands in DNA gel electrophoresis of red blood cells?

For forensic inspection, you only obtained red blood cells from an individual and amplified for the D1S80 locus in chromosome 1. Twenty nine different alleles of D1S80 have been identified, and 435 allelic combinations are theoretically possible. Approximately 86% of the population is heterozygous at this locus. You set up a PCR reaction for this locus and ran a DNA gel electrophoresis. What would your expected results be based on the described protocol?

A) You would most likely see no bands
B) You would see more than two bands
C) You would see two bands for the heterozygous while one band for the homozygous
D) You would see two bands for the homozygous while two bands for the heterozygous
I thought the answer was C given that heterozygous people would have two bands, one for each allele, and homozygous people would have one band for their one allele. The answer points to choice A for some reason...

Good luck retrieving DNA from erythrocytes...

It is a trick question. Red Blood Cells (RBC) are anucleated in mammals. You are not going to be able to extract anything about chromosome 1 from RBC.
By the way, if you want to know how they got from 29 alleles to 435 possible combinations (in a diploid), you just have to do 29 + 28 + 27 + ... + 1 = 435.

Interesting, I thought the same. But given my miniscule knowledge on RFLP, I was guessing that the answer hid somewhere else in the question. Thanks!


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Is bad tasting food more likely to cause harm?
Taste is often referred to as subjective. For example certain foods taste bad to me, such as oranges, grapefruit, grapes, raisins, and sweet potatoes. However the wiki article on taste explains that from an evolutionary perspective, it's important that bad taste might indicate poison in the food; taste isn't an arbitrary matter of subjectivity.
With that in mind I pose the question if a food tastes bad to a particular person, is it more likely to be causing harm to that person than someone who finds the food pleasant? In other words, is the bad taste a sign that my body is not suited for some components in the food?

I vaguely remember a documentary saying that the bitter taste experience may have evolved as an anti-poison mechanism, for example when tasting new berries. Often poisonous ones are bitter. But cyanide tasting of pleasant almonds, or people disliking broccoli are both different - taste is not linked to harm/benefit. We did not evolve with cyanide, and broccoli doesn't trigger the strong "bitter" taste but is rather a childish preference.

@AlwaysConfused My answer wouldn't add much more than the comment. Some fowl tasting food is great for our health, some very tasty food will harm us when over-eaten for years, and some tasty or tasteless compounds are actively harmful, and in all the previously mentioned statements there are exceptions! Too broad for my liking.

Why on earth has this question picked up two close votes for a medical question?!

Take a look at this article: https://www.ncbi.nlm.nih.gov/pubmed/25286017 I hope you can acces it. @AlwaysConfused this article is consitent with your answer, citing this would imporve your answer.

LaLanne said his two simple rules of nutrition are: "if man made it, don't eat it", and "if it tastes good, spit it out.".

tl;dr; If someone likes a food item, then even if it taste not so great to you, it will probably not harm you. If a food item taste awful to everybody (in particular bitter), then it would probably be best to avoid it.
Taste perception per se is not subjective, you either can detect or not a defined compound at a defined concentration. Food preference however is of course much more subjective.
The most established theory in the field is that we evolved both bitterness and sourness as a warning signal for poisonous compounds and inedible food. Bitterness is often the most referenced as most poisonous substances taste bitter to humans (e.g. strychnine, nicotine, ...) and are detected at very low concentrations (in the nM to $\mu$M range) (Meyerhof W, 2005). In comparison, the threshold for sweet taste perception is well above > 100mM (Park DC, 2015), or put otherwise, humans are at least 1000x more sensitive to bitterness compared to sweetness. As a result, we evolved to detect small quantities of bitter compounds and to dislike food items that are bitter as they could be poisonous.
Now for your question, you are probably misusing the word taste when you meant flavor, which is a combination of both taste and aroma (i.e. taste perception and olfaction combined, for example the "taste" of a banana). Food preference varies from people to people based on both genetic, physiological and more importantly environmental factors, in particular food habits. Typical examples are spiciness and saltiness where you can slowly adapt to tolerate higher and higher concentrations, meaning that your own food preferences can shift over your lifetime. Another illustration is the common shift in food preferences between childhood and adulthood. In other words, food preference is not an excellent predictor of a harmful food item.

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Do human somatic cells have 46 chromosomes all the time?
As far as I know, a human somatic cell has the cell cycle:
Interphase and Replication (mitosis). In interphase, the cell has 2 growth phases (G1 + G2) and a synthesis one (S phase being in between G1 and G2). After G2 ends, the cell will start entering mitosis.
Until the S phase, the cell has only 23 chromosomes right? And only after the DNA has duplicated the number of chromosomes doubles (to 46).
Please correct me if I am wrong? And will the cell in the G0 phase (after duplication and before G1) have 23 or 46 chromosomes?

Is this question also considering chromosome aberrations like Trisomy 21? https://en.wikipedia.org/wiki/Trisomy#Human_trisomy        Because that would break the question wouldn't it?

No, it refers to a general somatic cell division, assuming no chromosome aberrations.

Most of the time DNA is not present as chromosome as  such.

It is also interesting to note that cancer cells often have more than 46 chromosomes due to mutations

Humans have 46 chromosomes, 23 come from the mother and 23 come from the father. I think The easiest way to remember this is to think of the sex chromosomes--if you are male, you have one X chromosome from your mother and one Y chromosome from your father. During S-phase, the cell will make another copy of the X chromosome and the Y chromosome, so you will (technically) have 4 sex chromosomes in the cell before it divides, although you only have 2 UNIQUE sex chromosomes. After division, each daughter cell will have 2 sex chromosomes (one X and one Y). The same holds for all the other chromosomes.
So, to answer your question, yes, in G2 phase, you have double the amount of chromosomes in your cell (46*2 = 92), but you only have 46 UNIQUE chromosomes in your cell.
EDIT: As many people have pointed out, there are examples that do not conform to this rule. For example, both skeletal and liver cells can maintain a second copy of their chromosomes (making them 2n). This, however, is the exception. In my opinion, it's more valuable to know the basic rules that govern chromosomal number.
As an exercise I'd suggest to think about what it means that a cell has '2n' chromosomes? What happens if a germ cell obtains 2n chromosomes and passes that to a viable offspring? Is that offspring now '2n', or do they just have double the number of chromosomes as the parent? When does a duplicated chromosome become an it's own chromosome and not just a "duplicate copy"?

So let me see if I got this right. In interphase(till S-pase you have 46 chromosmes not 23) and after you duplicate the number you will have in G2 phase a bigger cell nucleus with 92 chromosmes not 46. And in mitosis each daughter cell will have 46 chroosmes.

yes, minus some semantic issues, I think you have got it. I doubt you'll ever find someone agreeing that you "have 92 chromosomes". You merely have 2 copies of 46 unique chromosomes. BTW, if this answer is satisfactory, please accept my answer by clicking the checkmark next to my post

Liver cells can be polyploid...

Thank you @Istbl; but saying that you have two pairs of 46 chromosomes at one time is similar to having 96 chromosomes, still in interphase but after S-phase . @biogirl : Liver cells can have multiple chromosomes because they have more than one nuclei or in one of the nuclei they have more than 46 chromosomes ?

As @biogirl said there are somatic cells in the body of a human that do not conform to the single nucleus, 2n genomic DNA. Skeletal muscle cells are polynuclear, so they have multiple nuclei with their own set of chromosomes.

@Vladimir In one nuclei, they have more than 46 chromosomes. See http://www.nature.com/nature/journal/v467/n7316/edsumm/e101007-09.html


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In cancer, why do cells duplicate themselves?
In regards to cancer why do cells replicate themselves? If it's a mutation, what kind of mutation would this be classified as?

I would rephrase the beginning of the question, if you agree. Right now it seems a bit "backwards". Cancer is defined as an uncontrolled growth of cells, so there is no specific reason (finality) for cancerous cells to grow. When a mutation causes cells to grow in an uncontrolled manner then you have cancer.

This article covers some of the key issues of cancer in layman's terms.
Essential, cancer is caused by multiple mutations in key regulatory genes which function in maintaining the cell cycle. This provokes uncontrollably rapid cell division, with only furthers the problem with genetic mutation. Here are some quotes from the article to strengthen your understanding in cancer cell mutations.

Image source

The cells become progressively more abnormal as more genes become damaged. Often, the genes that are in control of DNA repair become damaged themselves, rendering the cells even more susceptible to ever-increasing levels of genetic mayhem.
[...] Most cancers are thought to arise from a single mutant precursor cell. As that cell divides, the resulting 'daughter' cells may acquire different mutations and different behaviors over a period of time. Those cells that gain an advantage in division or resistance to cell death will tend to take over the population. In this way, the tumor cells are able to gain a wide range of capabilities that are not normally seen in the healthy version of the cell type represented.
[...] Mutations in key regulatory genes (tumor suppressors and proto-oncogenes) alter the behavior of cells and can potentially lead to the unregulated growth seen in cancer.

Hallmarks of Cancer: The Next Generation is by far my favorite article at the moment explaining cancer in-depth. I'd recommend reading through it.
The cells replicate themselves, without regard for normal cellular restriction, due to a number of mutations that accumulate:

So our cancer cells are evading apoptosis. P53 might be knocked down, so cell cycle arrest cant occur, but what about when Akt is constitutively "ON"? Normally P53 can induce apoptosis via the following mechanism:

And as it turns out, Akt inhibits apoptosis in the following manner:

So the cells really aren't dying. What about replicative aging? We find cancer cells have telomerase activity which essentially makes them immortal.
There's also evidence to support regulation of pathways which promote epithelial-mesenchymal transition in tumor cells, and promote invasiveness and cellular motility in most cases:

For the sake of a short response that isn't a wall of text/images, this is a broad survey of some relevant cancer pathways which essentially make cancer what it is. It's more complex than this, but if you put in some research given these hallmarks of cancer, the answers are there.


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What is the lowest common denominator of cancer?
What is the lowest level attribute that all cancers share? Also, what is the highest level attributes that all cancers share?

What I'm trying to establish on this post is.. What do all cancers have in common? Even on the lowest level.

The answer is the question. If you can state the question with sufficient clarity, the answer can always be found. A thorough comprehension of carcinogens is but the start of prevention. The essence of Genetics is necessary to even start. We first seek also what is common that avoids cancer. To what extent is transmittal possible by plants, the animal kingdom, as well as the variety in mankind? Aging, timing, the critical factor of timeliness and thermal genetics are but a partial segment of immunity or cure. There is a huge gap between Cancer Research versus cancer treatment. Genetic pronenes

Hanahan and Weinberg's "Hallmarks of Cancer" articles should answer your question.
Their original, highly cited (14k+ citations), [Six] Hallmarks of Cancer article list these six common attributes of all cancers:

Sustaining proliferative signaling
Evading growth suppressors
Activating invasion and metastasis
Enabling replicative immortality
Inducing angiogenesis
Resisting cell death

The new article, Hallmarks of Cancer: The Next Generation includes additional "emerging hallmarks" and "enabling characteristics" (Figure 3) common among cancers:

The capability to modify, or reprogram, cellular metabolism in order to most effectively support neoplastic proliferation; and
The ability to evade immunological destruction, in particular by T and B lymphocytes, macrophages, and natural killer cells.

I would say angiogenesis, is Cancer's weapon of choice, please see this talk at TED

Cancer is such a diverse group of diseases that they really only share one commonality, unregulated cell growth with the potential ability to invade or transfer to other tissue types.
Many types of cancer share certain characteristics and can thus be grouped, but as a whole the only characteristic all cancers share is that they are classified as cancer. That classification is based on a number of markers and evaluations used to differentiate between benign and malignant neoplasms. Malignancy is determined by an expert pathologist who uses these markers and evaluations to determine his or her diagnosis based on experience. Some examples of indicators are circumscription, pleomorphism, presence of a capsule, nuclei number and morphology, amount of cytoplasm, number of mitoses, size, depth, particular gene mutations and so on. Even with all of these indicators, it can't be known with certainty beforehand whether or not neoplasms will metastasize.

Could you define your terms a bit more? How do you define levels?
The most common trait shared by cancerous cells is a regulatory malfunction somewhere. Whether it's a failure to regulate apoptosis, failure to recognize boundaries composed of regular cells, or failure to enter states of the cell cycle - a metabolic process somewhere goes awry, which leads to the unwanted proliferation of the cell and its daughter cells.
It was recently discovered that some (but not all) tumors spring from a set of "cancer stem cells" which originally incurred the mutation and serve as the epicenter. They have the capacity to regrow tumors if they are not destroyed or harvested during treatment.
I think the "highest" level trait they all share is that all cancers are unwanted. Other than that, cancers vary so widely that there's practically no universals between them that I'm aware of.
However, I'm not an Oncoligst or a researcher.

A reference would strengthen this answer, especially if you aren't familiar with the field. Although you are right: "cancer" is very much a blanket term for anything uncontrollable division of cells, whatever the cause.

All cancers are very different, even when they are the same type of cancer. Breast Cancer, for example, falls into ER+, HER+ and Triple Negative subtypes, all which have different survival outcomes and response to therapeutics.  We didn't realise the extent of diversity until we started to analyse the tumours at a higher level of resolution.
That being said, there can be some common pathways that are affected. p53 mutations tend be common in all cancer types, RAS, EGFR  are some examples. When we analyze the details at the genomic level(SNP level,Copy Number variants, insertions-deletions), mutations can be very variable, but as you zoom out we see that they target similar genes and furthermore similar pathways.
But recall: people used to die just of fever back in the day, we know now that fever is a symptom not the disease. Technology will allow us to understand whether Cancer is just a catch-all, or whether they are actually different diseases.

There definitely has to be an upstream factor that drives ALL cancers.  The fundamental common denominator of all cancers is growth and survival, basic life processes.  If you can figure out what ultimately drives these processes, you can figure out what ultimately drives ALL cancer types and subtypes.  Cancer is just diversified growth.  With an open toolbox to employ.  All cancer cells originate because of one point factor, one switch point that alters their developmental trajectory.  There are lot of variables it could be.

Mites are one of the biggest major causes of diseases including cancer. It's known that's mites change th1 into th2 effectively compromising the immune response. Scabies (scarcoptes var homis) is NOT the only mite that can infest a human being. In fact there s 250 mites that can.
This is an area that needs to be collaborated with veterinary medicine.
I think the rise of cancer in the UK over past years will correspond to the increased trend over recent years for designer dogs. There's zero awareness to general public about mites and majority of people do not realise small caged animals or birds require to be treated also.
There's plenty case studies and peer approved papers that highlight the diseases alternate mite infestations transmit yet the medical community are not being educated in this area.
As a point of interest I find it difficult to understand why the UK government are giving drug addicts and alcoholics an additional £20 per week for the keep of the addicts dog. To my mind it's blantanly obvious these people are not responsible enough to regularly worm or treat for parasites I  these animals. Perfect way to spears the disease. Look at studies on stray dogs abroad and wild animals and birds. Whether mites have always been in the environment I believe the assumption they are self limiting is utterly ridiculous and wrong.  Mites are a hugely under researched area and there is conflicting references with authors giving the wrong information which they cannot prove. The evidence is there to say alternate mites or pseudo scabies acariasis can host swap can complete their life cycle on the alternate host.

Link to papers?

Can you please add some references to back up your claims?


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Breakdown of energy expenditure at the level of a single cell
The metabolic rate measures how much energy an organism expends over a unit of time. Its breakdown for the human body in terms of its functions is well documented : so much for the heart, for the brain, etc.
In West et al, 2002 I have found an estimate for the metabolic rate of a single cell. But how does this breakdown in terms of elementary functions in the cell?
E.g., how much of the energy made available from nutrients is used in the process of replicating genome, of expressing proteins, of trafficking...?
Following Jeremy Kemball's link suggestions, I find in this paper the fraction of ATP consumption for the following processes:
Protein synthesis    0.34
Na+/K+ ATPase        0.16
Ca2+ ATPase          0.17
RNA/DNA synthesis    0.25
Unidentified         0.09

(which adds up to 1.01 rather than 1 for spurious reasons). Their measurement is indirect, based on $O_2$ consumption for an assumed steady-state regeneration of ATP. I wonder how GTP-based processes are accounted for? Or are they negligible compared to ATP ones?
This is for a specific cell type, rat thymocyte, is there a reason to expect that this will be hugely different for say a fibroblast? Also, they stimulate their thymocyte with concanavalin A. I understood they are not getting RNA/DNA consumption signal without Con-A, but didn't get why it would be so.
Finally, what would be in the remaining 9% ? One candidate for ATP consumption suggested by Jeremy Kemball is actin turnover, I guess it fits only in the "unidentified" line. Tubulin turnover is a GTP process, not sure about intermediate filaments (do they turnover?). All ATP-molecular motors (myosin, kinesin, dynein at least?) have to be there too.  What else?
I am particularly interested in the total amount of ATP energy that goes to myosin.

@DevashishDas: Maybe my question was not clear enough: I'm not looking for a description of ATP production from glucose (and other related processes making energy usable), but of its usage. Some of it actually has to go back to energy production, but some also goes to protein synthesis, etc. Besides, I am looking for numbers (e.g., DNA replication would consume so much over 1 cycle of 24 hrs, which makes so much % of cell metabolic rate)

My instinct is that these figures are going to be hard to find. PET scans and things using fluoridated glucose can pretty easily ballpark metabolic demand for individual organs, but tracking where and when ATP is consumed is going to be much more difficult. A fun complication: ATP consumption and production rates change wildly across an individual cell during normal cell replication, even if the environment is constant. I wish you luck.

@JeremyKemball: thanks for your message. Already knowing that these figures may be completely unavailable is helpful...! I would anyhow be interested in any estimate available: there may be some from a mixture of in-vitro and in-vivo approaches, e.g. a lower estimate for DNA replication might be around, as we know how many b.p. we need to replicate and probably how much energy it takes to replicate one.

@JeremyKemball: Do you have a reference for the fact that "ATP consumption and production rates change wildly across an individual cell during normal cell replication"? Cheers.

I need to get in the habit of finding sources for things I say, even in comments where they won't fit. Just because I say things that seem plausible but turn out to be wrong when you actually do the math, uh, fairly often. :/

Note that any GTP process gets its energy indirectly from ATP.

@forest: Thx for your comment, can you point to an explanation of these energy fluxes?  https://en.wikipedia.org/wiki/Guanosine_triphosphate#Biosynthesis e.g. is not that clear on this.

What do you mean by energy fluxes?

You were writing that GTP processes get their energy from ATP. In physics, you'd call this a flux of energy from one biochemical storage to another.

I was musing on this and did some strange googling, and have some ballpark figures  for a bunch of different organisms. It's far from a complete answer but it's at least a start, and all this won't fit in a comment.
DNA replication, I assumed, was a huge metabolic drain on the cell. Turns out that is far from the case. Many helicases are passive, requiring no ATP, and the amount of ATP-equivalent triphosphates to synthesize the entire genome is pretty small compared to the amount that gets used and recycled every day.
According to these guys humans go through their bodyweight in ATP every day, about 50% of which is actin turnover, and 30% is synthesis (60% or more in rapid bacteria). Proteins cost about 4-5 ATP per AA to break down and rebuild.
You're not going to get a really good general breakdown, I don't think, but in crop plants or E. coli there are numbers for this, sort of. A lot of them are based on indirect measurements of protein uptake/turnover and ATP cost per AA or BP. They're fascinating but insane and often contradictory.

The 50% going into actin turn-over is for brain tissue, probably over-estimated for other tissue. However your link about synthesis lead me to this paper where there are numbers for thymocytes: 1/3rd of ATP consumption for protein synthesis, 1/3rd for calcium+sodium cycling, 1/4th for DNA/RNA synthesis and 1/10th for "all the rest". Firstly, how does this fit with the ATP consumption of actin treadmilling that has to be expected? (it has to fit in the 10% for thymocytes?) What else can one expect to find in these 10%?

Actin treadmilling for neurons I expect to be a pretty big part of energy expenditure. They recycle neurotransmitters and rearrange their dendrites and things often, and all that has a cost. Thymocytes are just blobs, so they don't have to spend as much energy on the cytoskeleton. http://www.genome.jp/dbget-bin/www_bget?cpd:C00002 is a list of some of the things ATP does in the cell. Where and how the ATP budget is spent is going to vary a lot from cell type to cell type. Muscles and nerves do a lot of ion pumps, glands do synthesis, etc.

A significant amount of heat generated by the cell does not come from the hydrolysis of an NTP. ATP is generated by a H+ gradient in the mitochondria, and this gradient is created by mechanisms which rely only in part by ATP.  Most of the energy stores in our bodies are not in the NTP pool. This is why CO₂ and urine are used to measure energy expenditure during physical exercise. On the scale of individual cells, it is a challenge to conceive a protocol which would account for all confounding variables. However, on the scale of a human, confounding variables in energy use are easily controlled. If you are interested in the energy expenditure of a single biological process, this would seem a better project rather than quantifying all processes simultaneously.

Thanks for your answer. In the paper I mention above indeed, there's a lot of cell-scale respiration which is not accounted by ATP processes but attributed to "proton leakage", and I understand that this is linked with heat production. Anyway, what I'm interested in is really the cell-scale energy expenditure, within which I'd like to particularize ATP-based energy. Then, specifically, I am interested in energy consumption by myosin (in nonmuscle cells).


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PDB file for Osteopontin (SPP1)
I am looking for PDB file for Osteopontin (SPP1). The entry- 3CXD shows the structure of an Osteopontin antibody, not of the protein itself.
Thanks

Is the structure known?

Apparently osteopontin lacks secondary structures. Only a 4-residue beta strand is reported in Uniprot.

There doesn't seem to be a 3D structure of Osteopontin available, and after looking a bit at the literature about this protein I'm not really surprised.
Osteopontin is hypothesized to assume an elongated and flexible structure (Sodek et al., 2000). Flexible proteins are very hard to impossible to crystallize, typically the flexible parts are either removed or stabilized in some way. I'm not a crystallographer, but this protein doesn't look like it can be crystallized in the full form.
For NMR it is a bit on the large side, a full structure would likely be not feasible.
It also has extensive posttranslational modifications, which makes it much harder to produce in large amounts as needed for crystallography, and extremely expensive for NMR where you would have to isotope-label the protein as well.

Thank Mad Scientist, I wanted to docking OPN with a small molecule. It seems it is impossible.

only a small peptide of Osteopontin is available currently
http://www.rcsb.org/pdb/protein/P10451


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How does beta branching stop alpha helices from forming?
I am told that beta branching interferes with alpha helix formation.
Problem is that I don't see how beta branching has anything to do with alpha-helix formation. Beta-branches are on the outside of alpha helices and internal hydrogen bonding holds the helix together.
My book (Lehninger) also doesn't say anything about beta branching interfering with alpha helix formation.

Beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation. Does that answer your questions? If it does I can expand on it and post it as an answer.

Also it shouldn't be said that they stop alpha helix formation outright, it's really contextual. Generally, though, they are favoured in domains where the back bone is more extended than in a helix.

@canadianer can you expand

@canadianer can you post this as an answer. You may also add an picture of helical wheel or Ramachandran plot for these residues.

@WYSIWYG Yes I will when I have time. Feel free to answer if you wish

The answer to this, as said by @canadianer in comment, is that beta branched amino acids are bulky and can sterically clash with neighbouring atoms, forcing the backbone to adopt torsion angles which don't favour helix formation.
I couldn't find reference for these exact words, but similar one here:

amino acids such as Valine, Isoleucine, and Threonine all have branching at the beta carbon, this will cause steric clashes in an alpha helix arrangement... valine, threonine, and isoleucine will often destabilize the helix because of branching of the beta carbon. These three amino acid residues are more often found in beta-pleated sheets, where their side chains will lie in a separate plane than the main chain.

Also, for torsion angles, from same source:

The torsion angle is the measure in degrees in bonds between atoms. Folding of proteins are influenced by the degree of rotation amino bonds can hold. There are two different types of torsion angles existing in polypeptide bonds. Psi, ψ is the angle between the α-carbon and the nitrogen atom of a peptide bond. The other bond is called phi, φ which is the angle between the α-carbon and the carbonyl group.

See this table for details of which amino acid prefers which configuration:

Source


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What is NK-cell compartments?
with respect to the paper:
Adaptive reconfiguration of the human NK-cell compartment in response to cytomegalovirus: A different perspective of the host-pathogen interaction
What is meant by NK-cells compartment? I searched Google but couldn't find a proper text that would help me understand what it means.. Google search shows papers which has this term, but I need to understand what it means before reading the paper. Please help.

I agree that you need to know the basics. But I got answers to your term on googling. Here's one: NK Cell Compartments and Their Activation by Dendritic Cells. Read the first two paragraphs.

In my very brief search, it appears to refer to the expression of specific surface markers.

@anongoodnurse You can post that as an answer. This is not that obvious to be classified as homework (someone VTCed this as homework).


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Why do we find flowers attractive?
Given that we (humans) are not evolutionarily closely related to bees, why do we find flowers attractive?

Attractive to what sense, sight or smell?  Quite apart from individual preferences, there are some which have repulsive odors (notably Rafflesia, which is said to smell like rotting meat: https://en.wikipedia.org/wiki/Rafflesia ), many others which have an inconspicuous appearance.  Also note that many garden flowers have been selectively bred to be more attractive to humans than their wild progenitors.

I meant sight and, sometimes, smell.

Sure, flowers can be sign that the fruit is underway as @JonathanMoore said and viewing any trait as a result of selection is probably what the OP was waiting for. Thinking that if an organism produces a behaviour, then this behaviour must have been selected is wrong though.
The reality is that specific behaviours are affected by evolution of other behaviours and other traits as well as an by our environment (incl. social environment). It will be particularly difficult to hypothesize as for the different selection pressures that may have existed on a specific behaviour especially in animals with such high cognition as humans. Maybe we like flowers because we like colour contrast and maybe we like colour contrast because face with stronger colour contrast is more attractive because it is a sign of health. Maybe we like sunset because we like flowers. Maybe we like colour contrast because we like fresh fruits. Maybe, we like complex design because it makes us think about the possible complexity of shapes. Maybe we like complex shapes because we like to explore. Maybe we like simple design because we like clear skins. Maybe we like flowers because of the diversity of shapes. Maybe we like flowers because they are a sign of the end of the cold winter. Maybe we like flowers because we are being told that they are pretty things. Maybe we like flowers because it symbolizes abundance and reproduction. Anyone could formulate loads of hypotheses. Maybe we like flowers because we like any smell that is not the smell of something that is rotting. Maybe we like flowers because we like trees, leaves, mountains, rivers, lakes and pretty much anything else in our natural surrounding. Maybe we like flowers because flowers is a sign that there is not no pests in our garden or simply that the plant we are growing is healthy.

Re "...any smell that is not the smell of something that is rotting", there's for instance Fritillaria imperialis https://en.wikipedia.org/wiki/Fritillaria_imperialis which, while it's a striking flower, smells rather like a skunk.  Or some kinds of Iris which smell nice (to me) in moderation, but are rather sickening in quantity.

Flowers are a sign that fruit is on its way, so it would be advantageous for us to remember the place where we saw flowers.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Why is mRNA used as a biomarker for cancer over tRNA or rRNA?
I cannot find a clear explanation for why mRNA is used as cancer biomarker and not tRNA or rRNA. Is there something peculiar about mRNA which cannot be fulfilled by tRNA or rRNA?

@ParthReghav what source are you seeing that mRNA is used as a cancer biomarker? mRNA is the protein coding RNA and it is proteins that are tumor suppressors or oncogenes - the answer to you question likely has its roots in that explanation

mRNAs encode specific genes and perform specific functions whereas the other two perform housekeeping functions in all cells. Changes in their expression are related to global changes in the cell.
The expression of rRNA and tRNA is affected in certain conditions such as stress and also possibly cancer (may be due to high replication rates). However, even if they are affected in cancer you cannot use them as markers for specific cancers as they are present and highly expressed in all cells.
Therefore specific tumour suppressor genes and oncogenes are studied.


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Why is nitrogen isotopic labelling required for protein NMR?
Why is labelling required for Nitrogen (by 15N) for studying structure of a protein using NMR?

It is not strictly required. Isotope labelling is required when the usual isotope does not have a magnetic spin (for example 12C). 14N has a spin of 1 and exhibits 3 spin states: -1, 0 and 1. The isotope, 15N has a 1/2 spin. As noted in this book, analytical methods exist for both nitrogen isotopes.
However, 15N is preferred for NMR studies because the chemical shifts produced by 14N can be too broad to be detected by high resolution NMR spectrometer.
From wikipedia:

Nitrogen-15 is frequently used in nuclear magnetic resonance spectroscopy (NMR), because unlike the more abundant nitrogen-14, that has an integer nuclear spin and thus a quadrupole moment, 15N has a fractional nuclear spin of one-half, which offers advantages for NMR like narrower line width.

From http://chem.ch.huji.ac.il/nmr/techniques/1d/row2/n.html:

The 1D 14Nitrogen NMR experiment is much less sensitive than Proton (1H) but has a much larger chemical shift range. Its signals are broadened by quadrupolar interactions. The larger the molecule and the more asymmetric the nitrogen's environment, the broader the signal. Hence, the small and highly symmetric aqueous ammonium ion gives a very sharp line (fig. 3), less than one Hertz wide. Liquid ammonia, being less symmetric, is 16 Hz wide (on a 400 MHz spectrometer at room temperature). Urea is larger and asymmetric so the line-width is approximately 1 KHz. Molecules that are significantly larger than urea yield signals too broad to be observed with a high-resolution NMR spectrometer. However, the nitrogen chemical shift range is wide and so may be readily used for distinguishing nitrogen species for very small molecules.


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Mechanism behind energy generation
I recently read about methanogens and methanotrophs. One converts CO2 to methane and vice versa respectively.
I can't get exact mechanism for the methanotrophs and I know they can't be reversed because this would result, in both directions being unable to produce energy.
Any information elaborating on the mechanism responsible for the generation is greatly appreciated.

"Methanotrophs oxidize methane to CO2 via a series of two electron steps with methanol, formaldehyde, and formate as intermediates."  from https://link.springer.com/chapter/10.1007%2F978-1-4020-3163-2_7 (link to a book that I can't access right now).


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Can anti-aging cream work?
I have a friend who told me that anti-aging cream cannot work to reduce wrinkles as it only penetrates x amount of skin layers and can never make a long term effect. Me not knowing much about how penetrative skin actually is, I was wondering if anyone knows if this is true and if anti-aging products are only working like a temporary moisturiser?

Welcome to Bio. Your first sentence "...not based on whether anti-aging products actually work..." does not match with your concluding question: "...if anti-aging products are only working like a temporary moisturiser...". Be specific - what do you want to know? I certain compounds can penetrate deeply enough, or whether anti-aging creme is bogus?

@AliceD Hi, you're right, I wasn't being clear. I've just removed the first line.

You mean anti-aging cosmetic cream in the sense that they remove wrinkles etc.? These cannot work, as they are not allowed to go deep into the skin, otherwise they would be classified as medical drugs. As such they would need licensed by the regulation agencies, undergo extensive testing and so on. These creams are mostly useless beyond moisturizing the top skin layer.

@Chris Yes that's what I mean. When you say "not allowed to go deep into the skin" do you just mean that the cream physically cannot penetrate that far down?

@SaturnsEye Yes, that's what I mean.

@Chris Why can they get away with selling such a product then :/

I have once been told that if the effects of anti-ageing cream were to be real, then one would need a doctor's certificate to buy one. In other words, companies building these products are not allowed to make products that work otherwise nobody would be allowed to buy the products. But it might be totally wrong.

Because their claims are vague enough and it doesn't do any harm.

Since there are different formulations for anti-aging creams, it would be helpful to focus on the specific compound or combination of compounds.
According to a comprehensive literature review done in 2007, certain compounds (Vitamin C, alpha-hydroxy acids, Vitamin A, Vitamin B derivatives, and botanicals) have had varied success in literature demonstrating anti-aging efficacy with Vitamin C and alpha-hydroxy acids being the better candidates.
Vitamin A/retinols have been shown to reduce wrinkles in some studies but no large studies have been conducted to show efficacy, Vitamin C has been shown to be the most effective (statistically significant improvement in texture, wrinkling, etc.) and alpha-hydroxy acids have been shown to increase collagen density, for example among other improvements.  A lot of these and other compounds have had positive or encouraging results replicated in literature, on mostly animal and human cell models so whether they actually have a significant effect on a large group of people needs to be looked at but to assess whether or not they actually "work" depends on what issues of skin damage as a result of aging one is targetting, the severity, the age at "treatment" and whether you're referring to over the counter or prescription-strength.
Huang, C. K. and T. A. Miller (2007). "The truth about over-the-counter topical anti-aging products: a comprehensive review." Aesthet Surg J 27(4): 402-412; quiz 413-405.


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Are there plants that produce (audible) sound?
Are there any plants that are at least able to produce some sort of sound? Actively, I mean - depleting energy reserves to produce an audible output, preferably with no experimental amplification. Ultra- or infrasound is also ok.
Edit: I guess a different way of asking this is, "Are there any plant parts whose function is to produce sound?"

I have heard anecdotally that you can hear the corn fields growing (at the peak time of growth). I am sure some of this is wind blowing but also the new growth rustling the drier outside leaves in thousands and thousands of plants.  Bamboo I have heard the same thing about.

There are several plants, which, as a way of seed spreading, "explode", which will make an audible sound. Plants that do this are for example: lupine.

These are good points, but the sound here is a byproduct - the plant "doesn't care" whether or not it is produced. I've edited to maybe make the question clearer.

Do you mean, 'intentionally' produce sound? Intentional would be only for communication, right?

@Polisetty well, not necessarily - perhaps as a warning, or attracting something, or to generate vibrations for some other reason. Communication would entail a) also a listening apparatus and, more importantly, b) some way of actually interpreting the sound - some sort of neural system.

@Zubo: I don't think a listening apparatus is necessary.  After all, plants communicate with pollinators & seed dispersers by using odors and visual cues.  I can't think of any fundamental reason they couldn't have evolved to use sound cues as well, though I don't know of an example.

It seems like Ritman and Milburn have done some work on acoustic emissions from plants. These two articles might be a starting point for you @Zubo : Acoustic Emissions from Plants: Ultrasonic and Audible Compared and Monitoring of Ultrasonic and Audible Emissions from Plants With or Without Vessels

arthropods can probably hear plants hydrating, through their leg vibration sense. Sound is air displacement born of fast mechanical movement/diaphragms. few plants have mechanical movement. Sound has little use in defense, even insects don't use it, arthropods mostly use it for advertising their presence and strength and energy. investing in an auditory structure isn't economically and ecologically documented for a plant.

not audible to us humans without some tweaking, but apparently plants do! https://www.cnet.com/news/listen-to-the-sound-of-plants-responding-to-the-world/

Plants make noise all the time as they transport water but that is believed to be an unintentional by-effect. As to the possibility of plants intentionally making noise,
my intuitive answer was no but I might well be wrong, there is actually increasing evidence that plants might produce vibrations for communication.
Two examples: Gagliano (2012) discovered that young maize roots subjected to a 220 Hz sound (check out the figure, not sure if I'm allowed to copy it here) grow towards the sound source and additionally emit periodic bursts of sound themselves for as of yet unclear reasons.  Gagliano, Renton, et al. (2012) demonstrated that chili plant seedlings grow faster in the presence of an adult fennel plant even though this adult plant was isolated in a such a way that it could not communicate via any known mechanism (chemical, light) with the seedlings, indicating influence through an unknown mechanism. The authors consider both magnetism and sound as possible unknown communication methods.
I don't think any of these sounds would be audible for humans though.
Acoustic emission analysis and experiments with physical model systems
reveal a peculiar nature of the xylem tension.
Laschimke, R., Burger, M., & Vallen, H. (2006).
Journal of plant physiology, 163(10), 996-1007.

Towards understanding plant bioacoustics
Gagliano, Monica et al.
Trends in Plant Science , Volume 17 , Issue 6 , 323 - 325

Out of Sight but Not out of Mind: Alternative Means of Communication in Plants.
Gagliano M, Renton M, Duvdevani N, Timmins M, Mancuso S (2012)
PLoS ONE 7(5): e37382. doi:10.1371/journal.pone.0037382

This is a more anecdotal answer, and it may not be what you are looking for, but I had a couple of water-hungry leafy plants in the past (Cannabis spec) that would look something like this -

Source: Sensi Seeds
...Note that mine were a lot bigger. After watering them and leaving them in the sun (enhances re-hydration by promoting water flow through evaporation of water through the leaves) you could literally see the leaves and stem erecting themselves again by the re-hydration process. If I remember correctly, some of those leaves would make audible sounds when they became dis-entangled from underlying leaves (popping sounds). They would look something like this after watering them.

source: AllBud
Note that these audible effects likely only happen in leafy, swift-growing (rapid metabolizing) plants like Cannabis.


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Simplest known form of aerobic glycolysis
What is the simplest known way that an organism performs aerobic glycolysis? In other words, what is the simplest known way known to convert glucose into $\ce{H2O}$ and $\ce{CO2}$, other than by burning it?
In general, the (relatively conserved) pathway is glycolysis $\ce{->}$ pyruvate decarboxylation $\ce{->}$ citric acid cycle $\ce{->}$ oxidative phosphorylation, but perhaps there exist simpler pathways with possibly a lower energy yield.
I am interested in a way to convert glucose into water and carbon dioxide under (near-)physiological conditions, with a reaction timeframe of 12 hours, give or take. Specifically, I'd like to get rid of sugar as tidily as possible, disregarding energetic benefits. In that sense, I am interested in the (bio-)chemistries of organisms, not in the energy yield.
I am aware, of course, that sugar is used as an energy source by organisms, and they generally want to accumulate it, or at least, decompose it as efficiently as possible. It may well be that the "shortcut" I'm looking for is not known.
Several publications sort of address this topic, but I haven't found a fitting answer so far. In fact, the closest research to what I'm looking for I've found is a publication from 1931 by Degering and Upson; they describe iron pyrophosphate as a catalyst for sugar oxidation. However, they work with far higher reaction times (up to about 3 weeks) and somewhat high temperatures (around 40-90 °C as opposed to 0-35 °C) than I'd like.
I've also tried looking for shortcuts within the pathways using KEGG database. Glucose is COMPOUND C00031 and is referenced in 32 pathways; I've looked at the Glycolysis pathway (map00010) and have found no pathway other than the generally known one.

Do you know why organisms converting glucose to carbon dioxide and water? It is unclear whether you do and what precisely you are asking. Do you think it is an end in itself? Why are you interested in aerobic glycolysis rather than anaerobic? Are you interested in energy yield or the varieties of chemistries in organisms? What do you mean by ‘efficient’? Have you consulted any of the numerous articles on glycolysis? Please clarify your question.

@David Thank you for your valuable remarks; I have edited the post to cover all your questions. Hopefully, it makes more sense now.

@David I see from your profile that you are also competent in the field of Bioinformatics, very nice! I will add some more info on what I've tried, then.

Protists are the thing. Not my field, but I found this review in following up a question (since closed) recently.


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Can someone who cannot talk still whistle?
Can someone who has a damaged larynx, which does not allow them to talk, still create a tune when they whistle?
I know that the larynx is what allows a person to manipulate their pitch and volume, but whistling sounds are just air making a noise as they are through the lips.
Would a person with a damaged larynx be able to whistle physically, but it would just be a toneless noise?
If this is so, is there any situation where a human would not be able to talk, but could still whistle with a tune and understand the speech of others perfectly? (i.e. having not suffered brain damage or are deaf)

Whistles, trees and other objects can whistle with a wide range of frequencies...

This is an entirely new question. Perhaps you could roll back these edits, restore the original question and pose this question as a new one. Changing a question entirely into a new question is not recommended, the.more since it has been answered already,  this answer has been upvoted and quite extensively edited.

Sounds such as certain phonemes are made merely with the use of air flow and movement of the lips or tongue, without the need for action of the vocal chords. Think of 'f', 's', 't', k in the English language. These are called unvoiced phonemes in phoniatrics (see the phonemic chart). Also, clicking sounds and whistling can be made without use of the vocal chords.

Could you provide some references that this really works?

I sometimes fell the same, yet what I think simple basic stuff for me might not be for someone else.. also for me pronouncing letter b does resonate my vocal cords unlike the other letters you listed. In the link you provided B is listed as Voiced Consonants..... it's a bit controversal I think.

@poka.nandor - auch, the 'b' was incorrect (only without the 'e' it is unvoiced), thanks! I added a ref to a chart. Thanks. Is this OK? Mostly I seek journal papers, but this is so basic that it is textbook stuff and I don't have any phoniatric stuff around I'm afraid. I used to work at an ENT department, that's why it was so natural for me to answer without backup :) Thanks for the downvote, that was necessary (and for the undownvote :-).

Thx for the update :) I think by the way that voiced and unvoiced phonemes might be a little language specific.

@poka.nandor - yes! Next edit underway :)

Yes, as long as the person is able to blow air and 'shape' it using their tongue+lips, a person can whistle; even if it means this person lacks the ability to create the vibrational patterns necessary to talk.


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On which chromosomes were the traits studied by Mendel?
In his experiment with peas, Mendel mainly studied two traits : yellow/green colours and round/wrinkly shapes.  I've heard that the pea genome is very large and its sequencing is a challenge. However, is there any information about the chromosoms involved in the traits on which Mendel worked ?

The yellow/green color of seeds is on chromosome 1, but the color for for the pods is on chromosome 5. The smooth/wrinkly seed shape is on chromosome 7; however for the pods a similar contrast is governed by chromosome 4. The pea has 14 chromosomes (diploid).

What you mentioned however are not all of the pea genes Mendel studies. He actually studied 7 genes (see table above) but only 4 chromosomes host all of the genes he studied. Mendel was lucky that two combinations don't usually show linkage because of the large distance between them (on the chromosome 1 and 4 respectively). There was one linkage which he should have detected though between plant height and the shape of the pods (both close enough on chromosome 4); apparently Mendel never published anything on that combination though. I don't know whether it was because it befuddled him or he just didn't study it.
Referernce: Blixt, S. Why didn't Gregor Mendel find linkage? Nature 256, 206 (1975). doi:doi:10.1038/256206a0


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How would I represent this on a cladogram?
So, right now I am making a cladogram (More of a dendrogram) for a kingdom of fictional species, and I'm not exactly sure how to represent a certain relationship.
Let's say that the oldest class in the kingdom is Clade A. And, while it is a clade in itself, it also evolved into two other classes. The first class it evolved into was Clade B, but Clade A still persists. Then, later on, Clade A evolves into Clade C - but still persists.
If I was to represent this on a dendogram, how would it be done?

The short answer is that cladograms are not compatible with Linnean taxonomy.
The longer answer explain how and why. First, there aren't enough ranks in Linnean taxonomy to cover all the cladogram nodes. The "kingdom-phylum-class-order-family..." was originally based on similiarity and not on phylogenetic relationship. For example: the class Reptilia is no longer a clade, and the class Aves is a subclade of the order Sauroschia (of the "super"-order Dinosauria, which is a clade of Diapsida which includes modern reptiles and crocodiles). The birds (Aves) are evolution descendants of dinosaurs but they ranked by Linneous as class while dinosaurs, according to Linnean taxonomy were at most super-order.
So you need to choose: a pseudo-Linnean relationship tree or a cladogram phylogenetic tree (and then you should omit the ranks' names "class", "order" etc.
I'll try to sketch the tree you described:

 A
 |
 |-- B
 |-- C
 |
 .
 .
 .

Okay, I changed "Class" to "Clade".

A clade is a common ancestor and all of its descendants. So if "Clade A evolves into clade C" then clade C is a subclade of clade A. As long there are descendants of the common ancestor of clade A, clade A does not go extinct.

Note that clade A still includes clades B and C!


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Which plants are healthy to keep in the bedroom at night?
I know that there are no plants which release oxygen in the dark (Can plants produce oxygen at night (without light)?).
I also know that some plants can clean toxic agents from the air (Nasa Clean Air Study).
Are there any plants which have health-beneficial properties specifically at night, i.e. in the dark?
Assume, if you'd like, that 12 leprechauns bring the plants to your bedroom the moment you turn off the lights and place them outside your house when you turn on the lights in the morning. Can bedroom plants still be beneficial to your health in this case? If so, which ones and why?

...leprechauns?

@Dubukay The reason I bring up leprechauns is that I have noticed many autistic people are active on SE. These people malfunction when you leave any room for interpretation. E.g. if I had only said 'at night' instead of 'in the dark', they would complain that artificial light could still result in photosynthesis. This is obviously besides the point and, to non-autists, need not be made explicit. Therefore, I used a tongue-in-cheek method to make such nuances explicit here.

Why have some people -1'ed? The question is well posed, has references and fits within the scope of this SE. If you -1'ed, explain yourself.

There exist a diversity of flora you may select relative to the antigen or noxious chemical you seek to reduce.
Pursuant to the British Medical Bulletin, the critical indoor pollutants are the polycyclic aromatic hydrocarbons like furanes and benzenes, ethanal (formaldehyde) and carbon monoxide. Depending upon which gaseous or volatile compound you seek to reduce in your household, you may select Chrysanthemum morifolium for the reduction of ammonia gas, xylene and alternative respiratory irritants; Chlorophytum chomosum for formaldehyde; and Dracaena genus concerning and trichloroethylene.
If you should suffer any infestation of Penicillium mould, then it is advised that one tackle the source of the infestation directly - areas rich in cellulose and moisture.
Further information regarding is available from the following links:
9 Air-Cleaning plants that are almost impossible to kill, https://greatist.com/connect/houseplants-that-clean-air
British Medical Bulletin, https://academic.oup.com/bmb/article/68/1/209/421251

Thanks, but this is not what I was asking.

As far as I understood the question, this answer should be perfectly suitable (though lacking references to substantiate the claim of those plants doing what is claimed). If not this, what are you asking for?

@Armatus Wow, seriously? My question, so obviously, is not about reducing toxins in general. In fact, I preface my question by stating that I am already familiar with the air-cleaning capabilities of some plants. I am not looking for more references about that. As stated multiple times in my question, I am interested in the effect of plants specifically at night, i.e. in the dark. I even wrote an entire story about leprechauns in the hope to make this more clear, with a further explanation in the comment.

While I think you should rethink your communication strategy, I see your point. As a suggestion, when you know what kind of information you're not looking for, it generally helps to specify that in your question.

@Armatus I fully agree with your last sentence, that is why I started with those 2 points which I already knew. But it seems that wasn't clear enough. Unrelated: please use the @[name] in your comments, such that I get a notification about comments directed at me.


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Is it possible to be allergic to the yolk of an egg but not the egg white?
At lunch one day, my friend had a hard boiled Easter egg. When he pealed it he squeezed the yolk, or yellow part, of the egg out. I asked him what on earth he was doing and he said, "I'm allergic to the yellow part of the egg not the white." I was very confused by this, he also sad he was allergic to tomatoes but could still eat pizza with sauce on it, apples but only the skins, and some other strange things. I didn't think this was possible at all. Can anyone explain this and tell me if it's even possible to be allergic to one part of an egg and not the other, or is it all in his head. If this is possible, is there an actual name for this condition?

It's plausible, on first thought, if the yolk contains different antigens than the white or the antigen in tomatoes is heat labile.

This isn't really a biology point but I've known a few people who use "allergic" as a shorthand for any similar condition (e.g. lactose intolerance) so your friend may not necessarily have an allergy (in the sense of an antibody mediated reaction)

The protein composition of the egg white and egg yolk differ appreciably. Hence, it is plausible for one to countenance symptoms of indigestion when consuming the egg yolk as opposed to the albumen, egg whites. It is important to stress that your friend may only an indigestion towards egg yolks as opposed to an immune response to an antigen.
If we consider the protein family, the egg yolk comprises a family of phosvitins, a group of highly phosphorylated proteins capable of mustering iron and calcium metal cations - serving a role in embryo development.
These are primarily absent from the albumen which comprises (with an unexpected name!) a highest percentage of suspended ovalbumin, ovotransferrin and ovomucoid. As demonstrated by the American College of Allergy, Asthma & Immunology, it is feasible to suffer an intolerance towards the egg yolk and yet suffer no gastro-enteric indigestion to the egg whites.
More information regarding the American College is available from: https://acaai.org/allergies/types/food-allergies/types-food-allergy/egg-allergy
Your friend evidently does not suffer a severe anaphylactic shock after consumption of the egg yolks otherwise he/she may be adverse to both the egg whites and egg yolk. In conclusion, it is possible that he/she may simply have a mild intolerance towards certain proteins in the egg yolks.


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Calculate growth rate of a population by Leslie matrix
We can calculate growth rate of a population by calculate the dominant eigen value of a Leslie matrix. What does this growth rate mean? I think that the growth rate N(t+1)/N(t) is depend on the age structure of N(t)? If the growth rate of a population is less than 1, will the population go extinct?


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Does this leaf belong to carissa macrocarpa?
I have a picture of a leaf and I am trying to find it's scientific name. The closer I got is Carissa Macrocarpa based on thorns alignment. If I am wrong, I need help in identifying correct species.. Thank you very much in advance!
Edit: Adding some more images

Can you give more pictures (e.g. the thorns you mention, and of course any flowers, the overall growth habit - tree, shrub etc) and location?

Hi Bryan, I added few more images.

I think you are close with your ID, certainly down to the genus.  However, all the pictures I can find of C. macrocarpa have leaves which are slightly more peaked/acute, and have a tiny little spine-like structure at the end.  Also, it looks like the thorns are bifurcated, but your specimen has simple spines.  Since this plant is used in landscaping, there are various cultivars available which may combine characteristics of the cannonical species.  You might need to find a key to this genus to be sure.

Try to find a key for Carissa for your area if this is a "wild" plant, not landscape specimen.  I found several by googling.

Thanks Bryan, that suggestion helped! It is highly likely that this specie is Carissa carandas which I found out grows in and around my locality.

Put it as an answer then with a little info about how you decided. It’s perfectly OK to answer your own question. Thanks for posting the question, I actually knew that plant indirectly from when I grew up in Southern California, where it was used as a landscape plant (and hurt a lot if a child tried to hide in a hedge of it!)

This plant seems to be Carissa carandas. With the thorns placements besides leaves, I was sure that this plant belonged to genus Carissa. Taking advice from Bryan Hanson, I searched for the plants in the same genus in my locality(Hyderabad, India). The white flowers and their rosy stalk made it easier for me to search. I found out that this is a common plant in country side and is used in many dishes. Thanks Bryan for pointing me in the correct direction.


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What is the full name of E. G. Gray?
E. G. Gray is Neuro scientist who found and described first the two major morphologically defined synapse types (Gray Type I (asymmetric) and II (symmetric)) in his work
E G Gray (Oct. 1959). “Axo-somatic and axo-dendritic synapses of the cerebral cortex: an electron microscope study”. In: Journal of Anatomy 93.4, pp. 420–433
However I am unable to find his full name nor further information about his life.

Is this really a biology question?

@Amory I think questions on the history of the science are pertinent to its future study, but others may not share that opinion

See http://meta.biology.stackexchange.com/questions/51/should-questions-about-the-history-of-biology-be-considered-on-topic

I couldn't agree more, but I don't know that this is history so much as a question involving an historical biologist.  "Initials" aren't exactly history, but I admit I'm not sure there's a better place.

It's about his bio, isn't? * ironic smile *
I shared your doubts, but I think this question will be useful especially for people using this SE site. Though I have to admit that main reason I asked it here instead of a more general site like Yahoo answers, is that I knew the people here were most likely to answer this question correctly. And Indeed it was correctly and comprehensively answered within minutes by @jonsca. Thank You very much therefor!

Edward George Gray went by the first name of George, which isn't evident from his initials (he was born Edward George), but I happened to stumble upon the Wikipedia article below.  From there, I found his obituary.
From his obituary:

GEORGE GRAY was a pioneer in the study of brain ultrastructure. He was Professor of Cytology in the anatomy department at University College London from 1967 to 1977 and then headed the Laboratory of Biological Ultrastructure at the National Institute for Medical Research.

From the Wikipedia article for synaptosome:

In a collaborative study with the electron microscopist George Gray from University College London, Victor P. Whittaker eventually showed that the acetylcholine-rich particles derived from guinea-pig cerebral cortex were synaptic vesicle-rich pinched-off nerve terminals.  Whittaker coined the term synaptosome to describe these fractionation-derived particles and shortly thereafter synaptic vesicles could be isolated from lysed synaptosomes

Might be worth putting in his full name in there, Edward George Gray

@Amory Good idea

@Amory made the edit.


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What are the differences between dual vector CRISPR/Cas9 lentiviral plasmids Lenti‐Cas9‐2A‐Blast and lentiCas9-Blast?
There are multiple  widely-used plasmids for using CRISPR/Cas9 with a dual lentiviral vector strategy (Cas9 & sgRNA on different vectors) in mammalian hosts with a Blasticidin selection selection marker.
In particular:
Lenti‐Cas9‐2A‐Blast(#73310) and lentiCas9-Blast (#52962)
What are differences between the two? Which vector is recommended (for use in mouse small intestinal organoids) and why?

You will have to include a lot more details about your protocol in order for anyone to give you pros and cons abot those two vectors. What kind of mammalian host? Please edit your question accordingly.
If there's a protocol in your lab, just use that one and see if it works. But I recommend that you do your own research and learn about the purpose of each and every entry of both plasmid-charts, so you know what you're doing.

I tried to to ask the question in way that the answer is useful for many people, but I included the host now.

It might also help if you add the type of host cells that produce your lentivirus.

I see these differences in lenti-Cas9-2A (compared to lenti-Cas9):

Absence of a bleomycin resistance. That just affects cloning
Changing from a CMV- to a RSV promoter for lentiviral mRNA production: That promoter is used for the host cells that produce your lentiviruses. They might react differently to different promotoers. So in the end, your viral titers might differ, when switching these plasmids.
Changing from a bGH- to a SV40 polyA signal  polyA signal. That might affect (production and) half-life of lentiviral mRNA both in your lentivirus producing-host cell culture and your mouse small intestinal organoids after transfection. You might want to start your research here: Humes et al. 2020

Together, I think both plasmids should work just fine. I'd say that the observed differences affect mostly how well your host cell culture performs in producing lentivirus. And these difference might differ a lot between cell types. But like I said, it's just the lentivirus production. If you got enough virus to apply to your mouse organoids for gene editing, it doesn't matter.


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Identification: Stinging walking/flying skin cells
Here I was, sitting in the veranda, minding my own business. Kids were playing outside, and I wasn't in charge of watching them. While browsing my stack overflow feed, I felt a pinch in my left arm. Like a very tiny needle just fell from the sky and decided to 'bug' me in my free time.
I looked at the spot where it hurt and saw a minuscule insect. It looked like two shedded skin cells crawling around slowly. Just very flat and small. What surprised me is that it kept hurting for approx 30 seconds afterward.
Not knowing what it was, I decided to get the camera. But how to photograph such a tiny creature, if you do not have the proper gear. Thankfully my wife remembered a trick where you can turn around the lens of the camera (if it's detachable), and take a picture while holding the lens firmly against the body. This way you get a sort of macro. Very difficult to hold it steady and to focus, because the focus field is extremely shallow.
Nevertheless, I managed to take some shots, and now my question is.. what is this stingy little buggy? I obviously let it live after the photoshoot and most likely it's a very common insect, but I've just never seen it in my life. Especially not something that stings like that.
Ah yes, apparently it can fly. Little bugger (literally) tried to flee the scene a couple times.
Additional info:
Origin: Romania, Targoviste (DB)
Date/time: 06 July 2018, 18:30, sunset
Warm sunny but windy day, still warm, 25 degrees Celcius

That is a Lace bug (Hemiptera). Family Tingidae. https://en.wikipedia.org/wiki/Tingidae.
From Wikipedia: "Lace bugs sometimes fall out of trees, land on people, and bite, which, although painful, is a minor nuisance. No medical treatment is necessary."


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Is anything known about the speed with which viruses spread geographically in R. affinis (or at least bats in general)?
RaTG13, which is the closest known relative of SARS-CoV-2 at full genome level, was sampled (just) in a R. affinis (bat) specimen in Yunnan Province... which is about 1,500 km away from Hubei, the epicenter of the first Covid-19 cluster.
So, what if anything is known about the speed with which viruses spread geographically among bats, particularly R. affinis? Basically, do we have any idea how long it would take a virus to "travel" in (R. affinis) bat populations 1,500 km?
A paper still in draft estimates that the most recent common ancestor of SARS-CoV-2 and RaTG13 "lived" around 2009.

the inferred the time to the most recent common ancestor in the recombinant region of the clade leading to RaTG13 and SARS-CoV-2 is no later than 2009 (2003-2013, 95% HPD limit).

I'm trying to figure out if this time frame is compatible in some sense with the speed with which viruses are known to spread in bat populations.

You can make SIR model acquire the diffusion equation characteristics by adding the spatial variables. That will give you the spatial diffusion (spread) speed.

Look at the sarbecovirus phylogeny and add the precise locations and years. @Hans we don't have any model for how the different bat caves/species exchange viral strains from years to years, we need to built it directly from the sparse data..


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Can you recognize this grape?
This gorgeous and sweet grape I collected in central Italy. I would like to know the name of this variety to get more information about it. I tried to compare with some pictures in Google but I am no grape/wine expert so it's really hard to figure it out for me.

I'm Italian, and that's an example of what we called uva da tavola , so these grapes aren't used for wine production. I think is the crimson variety.

Not sure at all.

@Marzipanherz — Because a proper answer would specify the grape variety in a scientific manner. The answer just makes the point that this is a table grape (uva da tavola in Italian), not a wine grape (which are not generally particularly sweet) and that it is sold under the name "Crimson". He also provides no evidence for his assignation (photo). Crimson appears to be an example of Vitis labrusca but may be an interspecies hybrid. However I am not competent to say if this is indeed Crimson.


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How are lesions in the RNA corrected?
I quite understand why thymine is present in DNA. So we can mark it out where cytosine undergoes a reaction and is converted to uracil. Then we can repair the DNA.
But how can we make that out in RNA ??

Note that the nucleobase is thymine not thiamine. Thiamine is vitamin-B1 and is a cofactor for certain enzymes. I corrected it and this is just for your information.

Actually very good question.

RNA is shortlived and need not undergo repair. A "mutated" RNA will degrade and will be replaced by the correct RNA.
Even though RNAs are shortlived compared to DNA (which does not really undergo turnover), some RNAs are stable and have low turnover. Nonetheless RNA would be present in multiple copies it is improbable that all of them would have undergone mutation.
Moreover RNA with certain mutated codons e.g. non-sense mutations are cleared off by the exosome.
Thanks to har-wradim for pointing out about RNA repair mechanisms. There are few reports that say that methylations in the RNA can be corrected by the enzymes AlkB (in E.coli) and its eukaryotic homologue hABH3. These enzymes were known to repair methyl lesions in the DNA (1-methyladenine and 3-methylcytosine), but it was subsequently shown that they can act on RNA as well [1,2].
However there seems to be no mechanism for repairing deamination damage; this study has demonstrated an artificially designed system which is capable of targeted RNA deamination (but there is no system yet that can fix a deaminated base in RNA).
This article comments that AlkB is tightly regulated because if uncontrolled it can demethylate functional methylations too. Overexpression of AlkB is actually toxic to the cells unless they are under alkylation stress by agents such as EMS/MMS (Ethyl/Methyl MethaneSulphonate).
But IMO RNA repair is not as essential as DNA repair because of aforementioned reasons.

RNA repair does exist: http://www.ncbi.nlm.nih.gov/pubmed/18289040

@har-wradim Was not aware of that. Let me see; it seems to be only in the case of alkylation

+1, of some relevance here is also the fact that there are proofreading mechanisms acting during transcription: http://www.sciencedirect.com/science/article/pii/S0959440X09001626

I forget the reference, but mRNA is also checked during the first round of translation, after the ribosome reads the mRNA the first time the proteins bound the mRNA are changed to mark it as okay, if the ribosome fails to successfully a protein the mRNA is marked for destruction.

@user137 perhaps you are referring to NMD and nonstop-decay

authors: موقع شقق العقاري


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Can someone help me analyze this article?
I need to read this article — "Beyond the rainbow" by
Marie-Claire Koschowitz et al., for an exam.
Following are some questions for which I could not figure the answer out after reading.
1) Why does this miniaturization necessitates insulation ? Following is quote from article: "For fast-growing, presumably warm- blooded animals , such miniaturization would only have been possible with sufficient body insulation. "
2) Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ? Why does the article mention reptiles before that ? Are birds reptiles ?
3) The article starts talking about how mammals develop fur and lost their highly differentiated color vision because they gave up structural color signaling. What is the direct connection between mammals and the dinosaurs ? I don't see the parallel here....why bring the mammals into the discussion ?
4) What is the connection between pennaceous feather and planar feathers ?
Any or all questions answered is welcome ! Thanks !

You cannot ask for an explanation of an article. A) It would be too broad B) Homework questions are considered off-topic unless you show an effort. It is fine to ask something that you do not understand from a paper but that has to be a precise point. And the article is in clear and understandable english.

could you provide an actual link?

@shigeta Link provided

I do not think it realistic to expect anyone can explain an entire paper here. If you have a particular question, that is, if you do not understand a particular sentence, or small paragraph (that is, something concise) you may try to ask that.

@WYSIWYG I have updated the question to reflect effort and understanding. Please unmark it from "hold" so that I may receive some answers.

I think the question, although still broad (i.e., multiple questions) is eligible for re-opening. I have adapted my answer.

you guys are too tough on newbies - asking for clearer question should be first resort. closing second.

@JennaMaiz If you can then please ask some points as a new question. For example the vision part can be separated from the feather/fur part. Miniaturization can also be another question and there are some posts here related to that topic already; you may also have a look at those. I am voting for reopen but it would be nice if you narrow the question down.

Agree with @WYSIWYG. Also voting to reopen but there are probably too many different questions.

@WYSIWYG  What are the guidelines for asking a question like this ?(Can I even ask something like this ?) Moderators on this site are way too strict closing the question immediately and asking to show effort, reword, edit the question. I understand they have a job to keep this site clean-but all the same, my impression was this kind of site is not a good place to get a rapid response(like before a final as was my case). Anyways, if necessary, you can delete the question if it doesn't fit this sites guidelines.

@JennaMaiz: did you get a useful answer in time for your test? I admit some questions are shot at too quickly at times. I tried to do my best answering it, and we have re-opened the question for you, despite the fact that the question was, admittedly, too broad. We all do our best :) Good luck in the future and please don't hold back asking more questions. This question was very interesting and the article you linked was of notable quality and I loved reading it.

@shigeta I do think we should be a bit more friendly towards newbies, but don't necessarity find it hostile to close a question if the reason is communicated clearly and in a nice manner. In this case, the question is really broad, and it is asking several separate questions that should be posted separately. There are cases where several subquestions for a single paper/issue are suitable (e.g. clarifying several methodological steps). However, in this case, the subquestions are unconnected and they sometimes seem to deal with tangential statements in the paper (so dependent on other papers).

@shigeta Oops, sorry for reviving a really old discussion - didn't notice the timestamp.

I will answer the questions one by one-

Why does this miniaturization necessitates insulation ?
An organism's volume determines the total amount of heat that can be stored. The loss (exchange) of heat between the body and external environment mainly occurs on the skin's surface. Hence, body volume determines how much heat is stored, while body surface determines how fast that heat is dissipated to the environment. Volume increases with a power of three with radius, while surface increases with a power of two. Hence, smaller animals have large surface-to-volume ratios, which decreases rapidly with body size. Hence, small animals will dissipate relatively more heat per unit of time.
Dinosaurs suppose to have tetrachromacy. The article mentions "dinosaurs were endowed with the highly differentiated color vision of birds". Does this mean Dinosaur's "inherited" their tetrachromacy from birds ?
No, birds are the closest living relatives to dinosaurs, and birds can be said to have inherited tetrachromacy from dinosaurs - see the cladogram below.

Why does the article mention reptiles before that ? Are birds reptiles ?
Birds are not reptiles, they are separate classes within the animal kingdom.
What is the direct connection between mammals and the dinosaurs ? ... why bring the mammals into the discussion ?
Here below is another cladogram; there is no obvious, direct (evolutionary) connection between dinosaurs and mammals. The thing is that dinosaurs ruled the world before the last mass extinction, thereafter it were the mammals. That's why the authors discuss them both, I guess. Especially since we are mammals it may make sense to draw parallels.

What is the connection between pennaceous feather and planar feathers
As far as I could track the two down, they are the same (Prum, 2006)

Lastly, in response to your original question, before edits: Here is a link with a plain-English popular-scientific web article published online by the first author.


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Identifying a tree with an image
I have trouble identifying a tree that I saw on a vacation. This is the image:

I would like to know the name of the tree, I only know that its not European.

Where did you take this image?

I took it in southern france but I asked the owner about the tree and she said that its not from there.

but it still could be european

I think you should look into trees in the Rubiaceae family (which is very large with ~6500 species in total). Many species there have spherical inflorescences, and some are somewhat similar-looking to the ones in your picture, e.g. Neolamarckia cadamba or species in the Nauclea genus. This is however just a suggestion to guide you, and not a species determination. Note also that spherical inflorescences are relatively common in many plant taxa, so it might be found in another family than Rubiaceae.
This is what Nauclea orientalis (photo from Wikipedia) looks like, just to give you a sense of the basic similarity:

The individual flowers are however much smaller than the flowers in your picture.

@tly Very generous to "accept" my answer, but in fairness I don't think it is a full answer to your question.

@AlwaysConfused That is why I wrote: "..just a suggestion to guide you, and not a species determination". I'm suggesting a family, not a species.

The fruit strongly resembles immature lychee (Litchi chinensis). Since I have only seen the fruit, I cannot comment on whether the flower looks correct. The flowers appear to be slightly different from those in Wikipedia, especially in the number of "stamens"(?) per flower.

I don't think this is correct, since the picture in the question seems to show spherical inflorescences (clusters of small flower buds) and not fruits. The inflorescences to the right have started flowering. Lychee (and the related Rambutan) have spiked fruits, but these are not flower beds (rather the result of flowering).

@fileunderwater You're right, which is why I said that the flowers appear to be slightly different. I would consider this a partial answer, perhaps the actual plant would be phylogenetically related.

In what season was the picture taken?
Can you give an idea of the size of the objects present on the photo?
Based on the rough surface of the fruits, I would suggest having a look at Moraceae, and in particular at the Artocarpeae tribe within this family.


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How many cells should be seeded for passaging?
Do you count cells when you passage them?
I found that many people will according to a ratio (maybe 1：2 or 1：3，etc.) to subpackage. It is so indistinct!
What is the optimal seedling density or optimal original confluent in various sizes of cell culture dishes and flasks?
that's all, thank you!

This answer is relevant in case of cell lines and not so much for primary cultures

When I first started doing cell culture, I used to count the cells before passaging. The idea is to seed enough cells to keep the population viable but not so much that you have to re-passage within 2 days. However as I became good with the technique I stopped counting as I would have a decent estimate of how much to seed. For seeding cells for some experiments (transfection/drug treatment etc) it is crucial to count the cells.
How much to seed depends on what the division time of the cell type is and how much you need after a given duration of time. You have to calculate it accordingly. For example a fully confluent well of a 6-well plate will approximately have 1 million Hela cells (this number would vary for different cell types because of the difference in sizes). Hela cells have division time of ~17h (see this post). If you need ~70-80% confluency after 17h then you should seed ~0.3 million cells.
Likewise, a T-25 flask would have ~3 million cells in full confluency. So, if you need a confluent flask in 3 days you can calculate how much cells to seed.
See this table in Nunc website for number of cells at confluency and optimal seeding density for different culture vessels.
Note that some cells (mostly primary cultures) may need to be seeded at high densities because they may need contact with other cells for survival. So, I cannot give any authoritative answer for primary cultures. Moreover, since it depends on the cell type, all examples cannot be listed here.

I'd also argue that for special cases like transfected cells, where expression is subject to drift, you have to make a judgment call (based on experience) on whether you want to maintain or expand.

Cells should be seeded when they reach 70 percent confluence as a visual measure. Even though it is not a specific number of cells the quantitative  amount of cells can be roughly measured. It is standard practice. Cells are counted with a haemocytometer they are counted and then a calculation is made for number of cells to derive a growth curve or growth rate through successive passages measured in doubling times.


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Why does carbon dioxide diffuse easier through the bilipid layer than oxygen?
When gas exchange occurs during respiration, the pressure of oxygen in alveoli is around 105 mmHg, whereas in the blood vessels in close contact with alveoli is 40 mmHg. For carbon dioxide the values are 40mmHg in alveoli, and 45mmHg in vessels. So the difference in pressure for oxygen is 65 and for carbon dioxide 5.
The fact that the pressure difference required for oxygen diffusion to occur is greater than that of carbon would mean that is diffuses with more difficulty. But how is that possible since the oxygen molecule is smaller and non-polar, so would technically pass easier through a hydrophobic membrane?

Note that the difference in CO₂ concentration between arteries and veins in much less (quite similar) compared to that of oxygen. BTW, CO₂ is non-polar as well.

@WYSIWYG And yeah, my mistake, I meant that CO2 atoms had partial charges instead of non-polar, but perhaps it doesn't change it's diffusion rate. That makes sense

I'm not conclusively sure if that answers your question. Hence the comment. If you think you found out the answer then please feel free to answer it yourself. It's good if a question is answered.

After diffusion the partial pressure of both O2 and CO2 in arteries become almost equal to the atmospheric values(100mmHg and 40mmHg), regardless of partial pressures in veins. Rate of diffusion through membrane is roughly the same, it's the solubility that is different, as CO2 is about 22 times more soluble than O2 (it can be stored is water as HCO3-).
  However, oxygen still can easily enter and stay inside the blood vessel because it's bound to hemoglobin inside the erythrocyte. Hence there is no significant difference between the diffusion rates.