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Has evolution made a mistake with prehistoric animals?
Let me start this by saying I have very limited knowledge in biology and evolution.
However, when visiting museums and watching documentary movies, I always get impression dinosaurs (and other animals in "dinosaur era") are very huge compared to today's animals, especially land animals.
So I wonder, was the this huge size actually an error in evolution?

You see them as unsuccessful? They roamed the planet for about 170 million years, which I find pretty impressive. If conditions change fast (like they did 66 Mio years ago) such animals cannot adapt fast enough.

Dinosaurs have been roaming the earth for 230 millions years. Birds are dinosaurs. Let's avoid fueling a weird non-monophyletic categorization to please a vague intuition.

You overlook one obvious factor.  It's a lot easier to find big dinosaur bones (or bones of any sort) than little ones.  I'd also guess that the bones of big creatures are more likely to be preserved in recognizable form...

@Chris I don't see them as unsuccessful. In fact, I'm very impressed by them. I am just curious was one trait of them, size, theirs disadvantage (especially when you compare them with todays land animals).

There are two questions here.

Dinosaurs were larger because their basic anatomy is better at being large than mammals. Their spine is better braced (no lumbar region), their breathing mechanism scales better, and their hip structure is stronger. This is called a preadaptation, or when an organism or group of organisms just starts with a head start on a particular adaptation due to unrelated reasons. It is the same reason mammals are the only terrestrial vertebrates to have echolocation: they are the only group with advanced amplification equipment in the ear to give it a head start.
Any era has its giants. Today is the time of the largest whales, largest trees, largest frogs, and largest horse to ever exist. Size is often a decent advantage: it makes you more resistant to resource fluctuation, it's just not a good for surviving global mass extinction inducing bolide impacts.

Evolution has no foresight. Evolution often produces and locks in counterproductive adaptations in the long run; while an adaptation may be an advantage in the short term, it may lock the organism into a disadvantaged position in the long run.
Sexual displays are a classic example: some quirk in peacock brains meant early female peacocks really liked more flamboyant males, that drove peacocks to the point modern males are incredibly vulnerable to predators and can barely fly due to carrying around huge superfluous tails. Both males and females would be better off preferring/having something less detrimental, but a feedback loop has locked in that detrimental feature. Males without it can't find mates, and females who do not prefer large tails male offspring also can't find mates. The term for this is fisherian or runaway selection. As an another example of counterproductive selection, many organisms when no longer controlled by predators or other factors will expand their numbers and consume resources to the point their populations collapse because there are too few resources to sustain them. Parasites often face this: a host with too many parasites dies, which is bad for the parasites but if the host can't fight off the parasites many are perfectly happy to kill their host and then starve.

Another aspect of evolution not having foresight is it cannot prepare you for extremely rare events, like mountains falling from the sky.

Runaway processes (and other evolutionary dead end processes that you quickly describe) is (are) not what killed the dinosaurs though.

no of course not, a mountain fell out of the sky evolution can't do anything to prepare you for that.

tl;dr

There is no mistake if there is no intention
pre-historic is not the term your were looking for
Some animals were big during the "dinosaur era" but not all and the largest animal to ever exist is extant today
Ancient dinosaurs have been around for 170 millions years. That's a very long time, much longer than anything you seem to be comparing to
Most lineages get extinct
NOT ALL DINOSAURS GOT EXTINCT! Some are still around

Semantic - On the concept of mistake
If you look to pretty much any definition of the term "mistake" (e.g. Merriam-Webster) you will find references to the concepts of choice and of intention. Indeed, in order to make a mistake one needs an intention, a goal.
Evolution is not some kind of mystical creature that has an intention for what ought to happen. Evolution has no intention. In this sense, it sounds very wrong to claim anything like "evolution made a mistake".
That makes your whole question (Has evolution made a mistake with prehistoric animals?) a little unclear.
Were pre-historic "huge?"
The concepts of historic vs pre-historic era are not concepts in empirical sciences but in history. The limit between the two is roughly placed at the invention of writing in humans. This boundary separate the past ~6000 years and the 13.8 billions years before it until the beginning of the universe (or the ~4 billions years of life on earth before it).
For the vast majority of these 4 billions years, life forms where definitely not all "huge". For most of this time, lifeforms were exclusively unicellular. First animals appeared ~550 millions years ago. And again, they were definitely not "huge" at the beginning. So a claim like "prehistoric animals are huge" would be very misleading.
Now of course, what you meant by "prehistoric" was actually "dinosaur era" but I still wanted to correct your choice of terms.
Were "dinosaur era" animals "huge"?
By "dinosaur era", someone probably refer to the period of ~170 millions years between the beginning of the triassic and the CP extinction event. Again, please note that in your comparison you are comparing a 66 millions years period to a 6 thousands years (0.006 millions years) period. To give you a little more perspective, there is about 170 millions years that separate a mid-triassic dinosaur (such as the Thrinaxodon) to a late Cretaceous dinosaur (such as the famous T-rex) but there is only ~66 millions years that separate a late Creataceous dinosaur to us, today!
Animal size varied a lot along these 66 millions years but yes, there were very big dinosaurs and also very large insects. This is mainly caused by a higher oxygen content in the atmosphere. Note however, that the largest animal that has ever lived is the blue whale who did not exist at that time but is extant today.
Extinction events
You probably meant to call "dinosaurs" a mistake because they do not exist today. First let me tell you that dinosaurs are not extinct, there are still a lot of dinosaurs alive today (see next section). Second, I would like to talk about extinction events.
Mass extinction events happen! In the phanerozoic only (that is in the past 500 millions years, that is a quarter of the time since life exist on earth), there are 7 commonly accepted mass extinction:

O-S
Late D
Cap
P-T
Tr-J
K-Pg
H

The last one, H refers to the holocene extinction and is the extinction event that is currently happening. Excluding the holocene extinction, the last mass extinction was the K-Pg (Cretaceous–Paleogene extinction event), which is the one who massively reduced the number of dinosaur lineages.
So really, don't think too much of modern life as being more "successful" that ancient dinosaurs because they are still extant. They just did not get extinct yet. If you want to call ancient dinosaurs a mistake, then you would have to call any lineage who got extinct a mistake and that represent the vast majority of all lineages that has ever existed. Also, these ancient dinosaurs have been around for 170 millions years! And also, ... as said above, dinosaurs are not extinct anyway!
Dinosaurs are not extinct
If by dinosaur, you mean Dinosauria, that is the monophyletic group that include all the things that you would typically call a dinosaur and all their descendent, then dinosaurs are still alive. Dinosaurs are still "flying around"! Birds are dinosaurs. They are not just distant cousins of dinosaurs but they are dinosaurs. It would indeed sound very wrong to state that dinosaurs are extinct just because we decided to name "bird" the dinosaur lineages that did not get extinct. For more information please have a look at the posts

If dinosaurs could have feathers, would they still be reptiles?
Were there any flying dinosaurs?

Whether or not you consider dinosaurs extinct depends on how you define "dinosaur". "Dinosaur" in the common sense refers to the extinct species.

That's right. I am using the only well defined definition that exists (the same used on wikipedia). I call a dinosaur any member of the clade Dinosauria

Downvoted because of the "birds are dinosaurs" nonsense.  By the same logic, birds, dinosaurs, and humans are just different kinds of fish :-)

Ha ha. Well, the point (maybe unclear; I tried to clarify that) is that stating dinosaurs are extinct is really silly because there are lineages that did not get extinct we just stopped calling them dinosaurs in the popular language. Nobody would say that all metazoa are extinct just because we got them more specific names.

Yeah, but what you've done is answer the question "what's wrong with this question [insert question]" in Semantics SE rather than try to answer the question that was asked in Biology, you could have probably condensed all the problems you have with it's wording into less than a 10th of this, defined what you thought he meant in less than that & then answered the question, which would have all been fine, you've only done the first bit ("your question is silly & this is why") & took a bleedin long time about it as well :)


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identification of differentially expressed genes in RNA-seq analysis
I am using four different packages (viz. EBSeq, DESeq2, edgeR, LPEseq) for identification of differential genes. Now I am confused whose fold change value should I take for further downstream processing.
Please give your suggestions.
Thanks in advance.

Why do you use four packages for one task?

Each package is using a different mathematic or statistical model and trying to fit that model to the data. Each model has different sensitivities and specificities, in different types of sample or experimental setup, so it can be useful to use more than one package. They are all asking a similar question in subtly different ways, so some people believe that taking a consensus can provide a more robust conclusion to the analysis.

Unless you have a good reason, stick with the ones that the community at large uses most frequently: EdgeR or DESeq2.

I would typically have an independently calculated fold-change that I use for QC and visualization.  I don't currently have a paper to reference to recommend doing some benchmarks for every project, where I would recommend testing DESeq2 / edgeR / limma-voom.  However, there are some papers that cite use of that strategy here in this acknowledgement.
In other words, one way that you could tell if a method may not be optimal for your dataset if you have a known perturbation, you can visually confirm the expected change with the directly calculated log2(FPKM + 0.1) value, but that gene isn't identified as differentially expressed with one of the methods.  It is kind of messy, but I do briefly mention this sort of troubleshooting strategy here.
In terms of comparing rlog values from DESeq2 and the direct FPKM / fold-change values, I do have this blog post: http://cdwscience.blogspot.com/2019/02/variance-stabilization-and-pseudocounts.html

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Bacteria as predators
Why do some bacteria kill each other? And how do they do that?
It's really a mind-blowing thing if you think about it. Please give me a simple answer.

Welcome. Have you done any research yourself?. I'm mod and cannot vote as such, but I would close it on the basis of underresearchedness. Adding prior research provides focus to your question. The post is too broad, which in turn attracts poor answers (and a lot of mod work :)

They do that because a bacterium contains all the molecules required for life, that is they are a source of amino acids, lipids, glucids and nucleic acids. This is the same reason why we eat in the first place: we need a source of these molecules to survive or, in other words, to allow our cells to carry out their tasks such as replicating the DNA or producing proteins.
Bacteria can kill other bacteria by a kind of infection: the predator bacterium enters a bigger prey and then start consuming the prey's molecules. By the same token, Mycobacterium tuberculosis enters the macrophages and used them for its own biochemistry, for instance.
Interestingly, this process of bacterial predation is under scrutiny for the development of a new breed of antiseptics in the age of antibiotic resistance (see https://phys.org/news/2017-03-predatory-bacteria-antibiotic.html).

Is it really always inside out? Couldn't a bigger bacteria eat and digest the smaller one?

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Learn biology without experimentations
I'm a high school student in a third-world country (Algeria).
My problem is with the way we are been taught biology. It's all about memorizing facts and procedures from a textbook without any application whatsoever due to the unavailability of laboratory equipments(there are some but they are either expired or useless).
My question: does this way of learning have any benefits at  all? Are we even learning?
I know what a lipid is because I've read its definition, but, is this enough? Is it enough to only read a paragraph that describes lipids and then see a model of it in order to know  what a lipid really is? Would it be useless if I go to a laboratory, extract some cholesterol, study its characteristics and see it with my own eyes to have a rough idea of what it is?
I've been seriously thinking about dropping out of school because I think the world doesn't need another indoctrinated kid who knows a bunch of facts and want to  earn some money with that knowledge.

there is a big difference between "no experimentation" and "only memorizing facts and procedures"  Are there explanations, examples, and discussion? Also what level of schooling is this? There are not many suitable experiments for the biology at the lower school levels.

There is typically little to no "experimentation" in math education, yet few would consider math as a boring list of facts to learn. You are definitely putting in opposition two concepts that should not be. Studying biology is much more than learning a boring list of facts (and it does not necessarily implies making any kind of experiment). That being said, if you find your class boring it might be a result of poor teaching skills of your instructor (it might be for some other reason).

If you want to study biology by yourself, you will find some ressources on this post.

I'm voting to close this question as off-topic because it is not about biology but about teaching practices. It is also slightly unclear by opposing two concepts that should not be opposed. The last paragraph of the post is clearly off-topic.

Not to be discussed on a biology Q&A site but earning money with your acquired knowledge is really not fundamentally wrong. Not being interested in class or not finding the point of studying can be a challenging sentiment. I would personally tend not to recommend dropping school but I am not trained to give such advice and would not know enough about your situation. In all case, you have my sympathy and I wish you good luck with whatever you'll end up choosing!


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What do phagocytes secrete?
What do phagocytes release after interacting with a pathogen? I know that this is a broad topic but I only need a general and concise answer.

Hi and welcome to Bio.SE! What type of phagocytes? I'm not an expert, but immunology responses like these are incredibly complex. What would also be helpful to a potential answerer would be your own attempts at an finding answer, and why those attempts didn't answer your question.

Wiki has lots of information about the interaction. They are secreted as purrulent flow. it sounds like a homework question which has been mixed up?

I think it would be hard to delineate what secretions are specifically because of phagocytosis, because in that sort of environment you have multiple types of cells secreting things, and multiple signals through such pathways as toll-like receptors (TLRs). So, I looked at papers involving activated professional phagocytes such as macrophages and neutrophils. The secretome of the activated cells follows a somewhat typical pattern for innate immune cells: IL-1ß, TNF family, interferons, IL-6, IL-8, and a host of other chemokines and cytokines (1, 2, 3). Mast cells of course secrete things such as histamine in response to Fc-receptor stimulation and TLR signaling.
Non-professional phagocytes like epithelial cells lack receptors to make phagocytosis efficient, but I'm far less certain about the body of data on non-professional phagocytosis. We know that activated epithelium and endothelium secrete inflammatory signals to attract immune cells, for example, like IP-10 which attracts CXCR3-expressing cells.

Phagocytes eat the pathogen cells by process of phagocytosis. They engulf the cell debris and pathogens by forming pseudopodia around them. However there are other cells which perform secretion. For example mast cells secrets histamine, serotonin etc. and fibroblasts secrets the blood matrix


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Biology and dna samples to determine parental lineage
How could you use nuclear and mitochondrial DNA samples run through electrophoresis to determine parental lineage.

Before DNA sequencing was widely available, some lineage information could be determined using restriction fragment length polymorphism, a kind of "DNA fingerprinting".
https://en.wikipedia.org/wiki/Restriction_fragment_length_polymorphism
Analyzing nuclear DNA would give information about both parents, while mitochondrial DNA would give information specifically about maternal lineage, as we inherit our mitochondrial DNA only from our mothers.


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Do you have nerves on the outside of your skull?
I have a spot on my skull that feels like a nerve or blood vessel. I know that there are many to the brain, however, it is the only one I have ever felt. So do we have nerves or blood vessels on the top or outside of the skull?

Are you talking about the surface of your skull, or anything/everything "outer" to it? If there were no nerve (endings) or blood vessels outside the skull, there would be no pain or bleeding with, say, scalp lacerations or hard bumps. So wording needs to be more specific. Generally the nerves and blood vessels of the scalp aren't easily palpable. Might you be feeling a skull suture line?

A soft or hard spot (bump) on the skull part of the head can be also a skin cyst or lipoma, for example. The nerves are flat and I'm not sure if you can really feel them. From vessels you would probably more likely feel the veins than arteries.

There are a number of nuerovascular bundles that exit the skull. Three involve branches of the trigeminal nerve.


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constitution of read and gene region (IGV)
I work with fastq files containing NGS reads for some human DNA regions. The reference genome is hg19. I had two fastq files (pair-ended). I generated alignment BAM files. I used "bwa" and samtools to find a possible target gene region (chr7:55,242,376-55,242,574,). This corresponds to a region of the EGFR gene.
Here is a screenshot of the gene region

And here is a screenshot of the primer region

I also have a list of primers and reverse primers:
FORWARD
1. TTGCCAGTTAACGTCTTCCTTCTCTCTCTG
2. CCCTTGTCTCTGTGTTCTTGTCCCCCCCA
3. TGATCTGTCCCTCACAGCAGGGTCTTCTCT
4. CACACTGACGTGCCTCTCCCTCCCTCCA

REVERSE
1. GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA
2. CCCCACCAGACCATGAGAGGCCCTGCGGCC
3. TGACCTAAAGCCACCTCCTTA
4. CCGTATCTCCCTTCCCTGATTA

And I have some adaptors
ADAPTORS 1
AAGACTCGGCAGCATCTCCA

ADAPTORS 2
GCGATCGTCACTGTTCTCCA

I have to answer to the following questions:
1) What is the constitution of each read (adaptor+primer+amplified region)?
The forward primer is obvious and corresponds to the first primer of the list
TTGCCAGTTAACGTCTTCCTTCTCTCTCTG

So why do we have the three other forward primers? I don't understand. And what about the correct reverse primer?
It seems to be the complementary sequence of the end region
GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA

Finally which adaptor is used?
Is [ADAPTOR1 - PRIMER1 - AMPLIFIED REGION] the correct answer? Are there other possibilities?
2) % of reads that map the human genome? what about the unmapped?
Can you please give me some clues about how to answer this question.
I just need some clues I want to do it by myself.
Thank you very much for your help.

You have asked quite a few questions here. I will try to answer a subset of them.
To answer your question, I started by going to the UCSC genome browser, and selected the BLAT from the tools dropdown menu. Then passing your primer sequences as queries, we can clearly see where they map to the reference genome.

Looking at the figure above, I can guess that your data comes from a targeted sequencing experiment (exome, or gene panel, etc); where you have primers around each exon of EGFR on two strands, on 5' end of exon sequence on each strand (think about DNA polymerase acting in PCR to amplify the number of DNA molecules before sequencing).
Regarding the adapter, I am not sure which read you are referring to. Can you clarify please?
About percentage of mapped vs unmapped reads, you can use bamtools.
Example Usage:
/user/me/src/bamtools/bin/bamtools-2.3.0 stats -insert -in my-sequence-file.bam
Example output:
Total reads:       103277668
Mapped reads:      90088436     (87.2293%)
Forward strand:    58136735     (56.2917%)
Reverse strand:    45140933     (43.7083%)
Failed QC:         6529806      (6.32257%)
Duplicates:        0    (0%)
Paired-end reads:  103277668    (100%)
'Proper-pairs':    87439672     (84.6646%)
Both pairs mapped: 87910438     (85.1205%)
Read 1:            51638834
Read 2:            51638834
Singletons:        2177998      (2.10888%)
Average insert size (absolute value): 6317.39
Median insert size (absolute value): 301

Thank you very much. They all use the same 2 adaptors. Is that possible? It's seems weird for me.

just one last question How do you pass your primer sequences as queries in BLAT? And obtain such a nice figure

Glad I was able to help. I generated a fasta format input with your eight sequences. Then after performing BLAT, selected the browser link for one one your sequences, zoomed out by a factor of 10 a few times so that all the query sequences are in the range. By default, one gets a crowded display in genome browser. You can press 'hide all' button below the genome view figure, and follow by setting BLAT and refGene/refSeq options to full.

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Links between Genetics and Personality Types
This topic was visited briefly in the thread, Genetic Effects on Personality, but I was surprised not to find more on it. (Is there a taboo I don't know about? What's the ethical stance on this nowadays?)
(An answer in that thread mentions serotonin receptor genetics specifically as having strong links to personality, but provides no explicit references.)
The question: What links have been measured between genotypes and personality outcomes within personality frameworks/models like the Big Five?
Related:
 - An Overview of Personality Models?
 - Genetics and Intraversion/Extraversion

Welcome to Biology.SE. This question is too broad. Also, the statistic you are interested in is called heritability. You should read Why is a heritability coefficient not an index of “how genetic” something is? to understand what it means.

One can find estimates of heritability on H2DB data base.

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Are some people more 'attractive' to mosquitos? If so, is that a hereditary trait?
Mosquitos clearly love me-- but I have been told I am just more reactive to mosquito bites. Are some people more 'attractive' to mosquitos (get bit more)? Or is it just that they are more reactive? If it is an 'attractive' trait-- is this hereditary?

There is a genetic component to mosquito's attraction to humans.

Female mosquitoes display preferences for certain individuals over others, which is determined by differences in volatile chemicals produced by the human body and detected by mosquitoes. ... Overall, there was a strong narrow-sense heritability of 0.62 (SE 0.124) for relative attraction and 0.67 (0.354) for flight activity based on the average of ten measurements. The results demonstrate an underlying genetic component detectable by mosquitoes through olfaction.

--Heritability of Attractiveness to Mosquitoes

However, analysis of a comparative rating variable "compared with your twin, who is bitten by mosquitoes more often?" indicated a strong genetic influence on frequency of being bitten by mosquitoes, with no significant differences observed between males and females.

--Twin study of adolescent genetic susceptibility to mosquito bites using ordinal and comparative rating data.
There are many other influences on how attractive people are to mosquitos, including diet, alcohol consumption, and various disease conditions.

extensive anecdotal experience confirms this, for some reason, I'm always ~10x more attractive to the local mosquitos than my frequent hiking partner.

So it's a complete myth about having a higher level of blood sugar and therefore having "sweeter blood"

I would distinguish two major types of mosquito bites "risk factors": genetic predispositions and transient attractiveness.
Mosquitoes utilize different senses to localise and choose a host. Olfaction seems to be a principal stimuli (constant, gradient measure, simple sensory system). Based form experience from studying other hematophagous ("blood-eating") animals carbon dioxide (CO) is a key feature of breathing living animals. Therefore, CO is an indicator of potential host suitability. Amount of exhaled CO may increase eg. with body mass.
Preferences are made based on excretion of (S)-lactic acid and products of skin bacteria, which may vary between individuals and be attributable to genetic background (eg. the immune system that may affect the composition of skin flora) and transient factors (eg. physical activity).
Skin temperature is another possible stimuli, that mosquitoes can detect. It is correlated with individual's metabolic activity and results from increased blood flow through the skin (increasing chances for tasty meal). So all factors that affect metabolism rate may make individuals more prone for bites, eg. pregnancy, physical activity or fever. The latter is essential for malaria spreading.
Some studies suggest blood type (unlucky type 0) or even beer drinking as an important factors.
As sugar is one of the main blood nutritional resources, it is reasonable to hypothesise that the blood sugar level may correlate with the number of mosquito bites, but relevant literature supporting this is lacking.
Sources and further reading (highly recommended):
Host Preferences of Blood-Feeding Mosquitoes
Annual Review of Entomology
Vol. 58:433-453 (Volume publication date January 2013)
Landing Preference of Aedes albopictus (Diptera: Culicidae) on Human Skin Among ABO Blood Groups, Secretors or Nonsecretors, and ABH Antigens Journal of Medical Entomology 41(4):796-799. 2004
Beer Consumption Increases Human Attractiveness to Malaria Mosquitoes PLoS ONE 5(3): e9546
Limburger cheese as an attractant for the malaria mosquito Anopheles gambiae s.s. Parasitol Today. 1996 Apr;12(4):159-61.


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Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?
I'm working on a problem where I'm given that the phenotypic variance of the parent, $p$, for trait $A$ is $175.2$ and the phenotypic variance of the offspring, $o$, for trait $A$ is $146.1$. However, I'm also given that the covariance between parent and offspring of a different trait, $B$, is $14.6$.
Can I still calculate the narrow-sense heritability of $A$ using
$$\begin{eqnarray}
\frac{h^2(A)}{2}&=&\frac{\text{Cov}(p,o)}{\text{Var}(p)}=\frac{14.6}{175.2}\approx0.0833 \\
h^2(A)&=&2\times0.0833\approx0.167
\end{eqnarray}
$$
even though they're different traits?
I'm also told that any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects. I've read that if this is the case, then $h^2$ is $0.50$, but I'm a little confused with it.

Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?

Yes. See below for more information.

Can I still calculate the narrow-sense heritability of AA [..] even though they're different traits?

No, you can't. A measure of heritability makes sense only for

a given trait
a given population
at a given time
in a given environment

[I'm also told that if any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects, then $h^2$ is 0.5, but I'm a little confused with it.]

The above is not a exact quote from you but the original sentence made no sense. I rephrase what I suppose you tried to say.
The formulation is inaccurate and could therefore be misleading. It is wrong to say that any covariance between parent and offspring is only due to genetics. In reality, environments between parent and offspring often covary. There might also have covariance due to epigenetic reasons and potentially many other reasons.
You cannot make any claim about what value should $h^2$ takes for the special case where covariance between parent and offspring is solely due to genetic variance (or any other special case considering only genetic variance). You still need to know the relative importance of the genetic variance to the total phenotypic variance. If any of this is unclear, then you should keep on with the recommended reading below.
Reading Recommendation
I recommend that you have a look at Why is a heritability coefficient not an index of “how genetic” something is? for an overview of the concept of heritability and common misconceptions.


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Why does M1 RNA together with C5 protein in 100mM Mg(II) fail to cleave tRNA?
Sidney Altman discovered that RNA moeity of RNAse P (M1 RNA) alone is able to perform enzymatic cleavage of ptRNA, which won him the Nobel Prize of Chemistry in 1989.
However, when I read the Nobel Lecture on Bioscience Report, Vol. 10, 1990, the figure on page 325 (the image below) confused me.

I listed the relevant parts of the figure legend as follows:
(R: M1 RNA was added, P: [C5]=2x10^(-8) M, 20P: [C5]=4x10^(-7) M)

Lane 3: R+P,   [Mg(II)]=10  mM.  ptRNA cleaved.
Lane 5: R,     [Mg(II)]=100 mM.  ptRNA cleaved.
Lane 6: R+P,   [Mg(II)]=100 mM.  ptRNA NOT cleaved.
Lane 8: R+20P, [Mg(II)]=100 mM.  ptRNA cleaved.

In Lane 3, RNAse P was formed and was able to catalyze cleavage; Lane 5 showed that M1 RNA with higher concentration of magnesium could function as enzyme.
But how did the addition of C5 protein, compared to Lane 5, inhibit the cleavage of ptRNA, as shown in Lane 6? (Or, how did raising [Mg(II)] to 100 mM compared to Lane 3 inhibit the reaction?)
And how come by increasing the concentration of C5 protein by a factor of 20 compared to Lane 6, M1 RNA was able to function again, as shown in Lane 8?
I would appreciate any kind of help, and sorry for my poor formatting.
Thanks.


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Is there a record of species kept in zoos worldwide and number of individuals? If yes, can one have access to it?
Looking for the number and species of wild cats kept in zoos to assess the potential pool of individuals available for reintroduction programmes.

A potential data source could the data base that stores zoo animal data, where the most comprehensive (to my knowledge) is Species360 ZIMS (Zoological Information Management System). It contains animal records and current breeding programmes, but also information on how to care for animals (best-practices and studbooks).
In your case, the ZIMS for Studbooks module should be relevant, which contains:

ZIMS for Studbooks improves Studbook Keeper efficiency and record accuracy with suggested animals, notification of records updates, and extensive data quality tools. [...] enabling users to conduct intensive population analysis, improving species and conservation management

However, I do not have access to the data base myself, so I cannot say how accessible the data is. If you are connected to a zoo, teaching institution or research facility you can however apply for access and a membership, but I don't know the specifics of this process (or possible costs). It might be worth checking out either way.


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Why do I feel nauseous at the sight of blood, despite not being afraid of it?
Every time I ask google this question, all it spits at me is info on blood phobias ^-^; basically, I've always been hugely interested in morbid stuff, but I noticed that I always feel sick when interacting with any sort of gore IRL - when I volunteered at a hospital to keep patients company, I had trouble staying calm around patients who had been in accidents when they were getting their bandages changes, or around patients who've had surgery when they drained their tubes. Yesterday in Anatomy we dissected a pig's heart, and I was super excited until we finally got them & I felt sick seeing it! I'm just confused because mentally I'm fine & don't mind being around that stuff, but physically I feel ill & its pretty annoying tbh :/
If it helps explain it at all, I do have issues with vasovagal syncope & tend to faint when getting blood drawn & being in a very warm, humid place, & I kinda have the same feeling with it? I'm not afraid of needles or heat, but I feel sick in those situations & end up fainting

Your last paragraph is helpful. A vasovagal response is not fear. Anecdotally, one of my medical school classmates struggled with this but was able to overcome the problem over time (by continuing to expose himself to the stimulus). Dissecting a human cadaver helped.  Posting this as a comment as it is anecdotal and I have no references at hand to back it up.

I usually experienced this as well in biology classes. I'm not particularly afraid of needles or anything. But in classes where we were talking about the internal body or blood (or similar topics), I would often get very dizzy--despite me finding it interesting!


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Help identifying plant
I saw this plant during the summer in Yorkshire, in the north of England. It was found near in a lowland area not too far from a river, but not in a boggy / marshy place. I’ve also seen them ok roadside verges as well.
I think it’s possibly related to a Lily, but I’m not sure at all about that.
Does anyone know what species this might be?

This plant is a bellflower. Either a Campanula Takesimana or a Campanula Alliariifolia

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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Rod and cone photoreceptors are neurons?
i mean the photoreceptors have axon and dendrite and body cell or it is not neuron
any more   . can we say outer segment of photoreceptor cell is dendrite ? of course these have body cells but i am not sure they are neuron or not

Photoreceptors are considered neural based on embryonic origin: they derive from neuroepithelial cells like neurons do.
Neuroepithelial cells also produce non-neuronal cells like some glial cells.
It doesn't make much sense to worry too much about whether a rod/cone photoreceptor is a neuron or not. They don't have long axons or dendrites, but they need not have either to be called a neuron. They make synapses, but these synapses are highly specialized and different from other types of neurons; that isn't sufficient to not call them a neuron. They don't fire action potentials, but they need not fire action potentials to be called a neuron. They do release neurotransmitter, but there are other cells that also release neurotransmitters that are not considered neurons. Ultimately, deciding whether a cell is a neuron or not is a matter of semantics, not biology.
Most texts I am familiar with consider them neurons because of their neural origin, which differentiates them from other sensory cells that derive from other tissue.


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What kind of fish is on the picture?
I saw these fish in a video at an art exhibition, I'd like to find out what kind they are.

This is an Atlantic wolffish (Anarhichas lupus). It's a very characteristic fish, with the teeth, the long dorsal fin and the small back fin.

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


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Are fruiting bodies, basidiocarps, heterokaryotic?
In that, if we have a mycelium with genetically compatible hyphae, will the fruiting body created by this mycelium be heterokaryotic, or will it just contain one dikaryotic organism's genetic material?


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Question: What is CINWntUp and CINnormL?
What is CINWntUp and CINnormL?
I read a paper that uses this two things as classes but Im not sure what they represent. I imply that CIN is referring to Chromosomal instability but I don't know what WntUp & normL refer to. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214593/)

From the paper:

The dataset contains six colon cancer subtypes: class 1 = CINImmune-Down (116 samples), class 2 = dMMR (104 samples), class 3 = KRASm (75 samples), class 4 = CSC (59 samples), class 5 = CINWntUp (152 samples), and class 6 = CINnormL (60 samples).

CINWntUp and CINnormL are therefore two classes of colon cancer. You are correct, CIN is for chromosomal instability; WntUp refers to upregulation of Wnt, a signalling pathway involved in some cancers and named for a Wingless/Integrated phenotype in fruit flies and the homologous gene in vertebrates. normL stands for "normal-like."
See the original paper describing these classes:
Marisa, L., de Reyniès, A., Duval, A., Selves, J., Gaub, M. P., Vescovo, L., ... & Kirzin, S. (2013). Gene expression classification of colon cancer into molecular subtypes: characterization, validation, and prognostic value. PLoS medicine, 10(5), e1001453.


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How does garlic preparation affect its active compounds or medicinal properties?
I read the following claims about how to consume garlic:

Consume immediately after crushing since the active compounds (allicin) is volatile and gets oxidized as soon as it's crushed
Allow to sit 10 minutes after crushing to allow time for allicin to form
Do not change the PH of garlic (i.e. mix with acid/lemon) in order not to disrupt the formation of allicin, during those 10 minutes
Allicin is completely lost within 20 minutes after crushing

If so:

Which of those claims is true? Is the wait-10-minutes practice is only recommended before heating the garlic? i.e. should you wait at all after crushing, when you consume it raw? (e.g. in a salad)
Given this is how I prepare a salad:
Cut vegetables and herbs
Crush garlic and mix in (no waiting)
Add lemon juice and vinegar and mix right away
Season with salt and pepper
Pour olive oil and mix right away
Let sit refrigerated in air-tight container 5-10 minutes
The salad is consumed at least 15 minutes after garlic is crushed, and it takes me another 15 minutes to finish eating the salad
By that time (30 min after crushing) are the active compounds in the garlic (particularly allicin) preserved or completely lost?
Will it make any difference if I mix the garlic in the oil first (to merely prevent oxidation), wait 10 minutes, mix in the acid, and pour everything over the salad right before serving?

This question has nothing to do with Biology in terms of SE Biology. You might try SE Nutrition as there doesn't appear to be a SE Quack Medicine.

@David I couldn't find SE Nutrition board, were you referring to SE Medical Sciences?

@David - that comment :D

Contrary to David's comment, there is no nutrition SE site. I inquired over at MedSci if this is ontopic there, but unfortunately not. Over here I see it as offtopic as it's more about the chemical properties of a compound. I've asked over at Chemistry. After that, I've ran out of ideas I'm afraid.

I doubt it would remain open on chemistry.se (I am a mod there, cc @AliceD). The question basically boils down to how is allicin formed when crushing garlic, and how stable is it after that, which is basically already answered on the Wikipedia page. (Questions about properties of compounds should be accompanied with the necessary literature research.) The other, principle, problem is that the conditions are probably producing a much larger uncertainty than you would be able to measure in the levels of Allicin, and all would not be reproducible.

I'm voting to close this question as off-topic because it's offtopic here as it's not a biological problem, but one of nutrition and chemical stability. I've inquired across the network, but unfortunately I can't find a suitable place, as mods of other sites have rejected it. Apologies.


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What is the consistency of cytosol?
Imagine you somehow got a cup of pure cytosol.  What would be its consistency?  That is, how thick, how sticky, and how viscous would it be?

pure cytosol - you just want the aqueous phase of the cytosol only? so wouldn't it have to be pretty much like water with some salt in it?  the really sticky stuff is in vesicles and/or it would be excluded from the aqueous phase with whatever filtration you apply.  the cell as a whole, however, does not behave like salty water, but rather like a gel

Cytosol is actually about as viscous as water
(i.e. ~1 cP or 1 mPa/s).
From the Introduction of Bicknese et al. 1993

In fibroblasts and several types of epithelial cells, fluid-phase viscosity was 1.1-1.5 cP, not much higher than that of water (1 cP) (Periasamy et al., 1992). Recent measurements of cytoplasmic viscosity in CV1 and PtK1 cells by a novel ratiometric method supported the conclusion that fluid-phase viscosity in bulk cytoplasm is similar to that of water (Luby-Phelps et al., 1993).

And from the conclusion:

Apparent fluid-phase viscosity near the cell plasma membrane was 1.1 ± 0.2
  cP (fibroblast) and 1.0 ± 0.2 cP (MDCK), not significantly different from the viscosity measured in bulk cytoplasm far from the
  plasma membrane.

Interestingly, the paper cites the following studies:

In fibroblasts, fluid-phase viscosity was weakly temperature-dependent (Arrhenius activation energy 3-5 kcal/mol) and nearly independent of cell volume (Fushimi and Verkman, 1991).

Note:
cP = centipoise

A centipoise (cP) is a non-SI (non-System International) measurement unit of dynamic viscosity in the centimeter gram second (CGS) system of units. It is multiple of the CGS base viscosity unit named poise (P)
1 cP = 0.01 g/cm/s
1 cP = 1 mPa/s

Source:
Bicknese S., N. Periasamy, S. B. Shohet, and A. S. Verkman. 1993. Cytoplasmic Viscosity Near the Cell Plasma Membrane: Measurement by
Evanescent Field Frequency-Domain Microfluorimetry. Biophysical Journal 65: 1272:1282

Further Reading:

Beals et al 1999
Gyurov & Token 2011
Guthrie & Nettesheim 2012
Kalwarczyk 2011

I can't comment about the consistency of this viscosity between all cell types or between taxa. I welcome suggestions to edit if anyone finds additional or more recent info.

Nice answer - I'm not an expert in plant physiology but that's one example where I might expect to see a higher viscosity, at least in some plant tissues (I don't mean that as a criticism of your answer but just a suggestion in case no one comes along to add on).

I do not agree, all your other sources report (slightly) higher viscosities. Based on those measurements I'd say it's more comparible with blood (3-4 cP). Still fluid, just a bit less than water. However, that's only for small molecules. If you're looking at bigger probes (>5 nm) the viscosity is 20-40 cP, comparable to vegetable oil (numbers according to your Kalwarczyk source). Also, based on the protein content alone you'd also have to assume a viscosity of 5-15 cP.


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Identification of Bioluminescent Species in South Carolina Marshlands
I was in the brackish marshlands in South Carolina and the water was lit with short flashes of greenish bioluminescent light from a species that seemed to be floating in the current.  The lights seemed to be associated with a crackling noise as well but I'm not 100% sure that the light and sound were related as there were so many flashes going off at a given.
When I turned a flashlight on I saw some quarter inch long bugs moving in the water but the light was too bright to confirm that the bioluminescent light was coming from those bugs.

Do you have a picture?

Quarter of an inch is quite large but it sounds like bioluminescent plankton. All lumped together by their behavior when we call them "plankton", there is tremendous variety of species of these animals and plants. Unfortunately, I think it might be impossible to identify which species you observed without a clear photograph or a microscopic image from a sample taken.

We tried to take a movie but it didn't come out.   The lights were just short flashes and a ton of them in the water, but they were spaced out fairly well. The plankton idea is probably correct we were thinking small pistol shrimp (Alpheidae) given the sound, but the light the cavitation produces is not supposed to be visible.

Confirmed by a number of locals later on to be a small species of pistol shrimp. It was a pretty cool phenomenon.  Thanks for the help here.


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Why isn't direct diagnosis of infectious disease through microscopes a common thing?
I'm not sure if I am being accurate about this but from what I know about diagnostics (watching House MD etc), if a doctor has a suspicion of a pathogenic infection then he/she usually prescribes corresponding medication without doing some kind of a confirmatory test. But isn't it possible to just have a look at the blood sample under a microscope and then confirm it? I guess it can't be done for viruses because they need an electron microscope to resolve them apart but I guess normal bacterias can be identified using more commonly available microscopes.

The problem with this is that A) the infection may be local, and very few if any bacterial cells may be in circulation, and B) even if the infection is systemic, there could be as few as a couple of bacterium per million red and white blood cells, making visual confirmation impossible. More often, if the attending physician feels the need for a direct ID in order to prescribe the correct medication, a culture is taken from the site of infection or blood is drawn, and then subjected to one of any number of different automated ID systems and/or culture conditions to identify the particular type of bacteria present. This can be as simple as Gram staining to identify Gram positive vs. Gram negative bacteria (different types of antibiotics work on the two classes) all the way to a full identification (genus, species, strain) based on molecular sequencing, typically of ribosomal RNA.

Could the person who didn't like my answer offer ways of improving it, including pointing out incorrect assertions (if any) or things I may have missed?


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Visibility of a cell membrane under microscopic Imaging
When we see any cell under a microscope the membrane surrounding the cell is opaque. But then if the cell membrane surrounds the cell in all the three dimensions how come we can see through the cell membrane and have a look at the organelles inside if the membrane is also covering the cell from the top and not just at the boundries on the object plane.

A little simplified: a glass (say a glass of water) is clear, yet if you look at it level with the water level, the sides are dark, as is the top of the water. Swiveling the glass doesn't change anything; the glass and water are very clear, but where there is an increase in the sheer amount of clear matter in the same plane, it appears darker. Same principle.

If you can see the cell's insides, the cell membrane is, obviously, not nontransparent

The membrane(and associated proteins) isn't actually opaque, it is just "more opaque" or "less translucent" than the cytosol: when you look through the microscope, you are utilizing this contrast to detect the edges.
In the center of the cell you observe, you see the membrane straight-on, and light is only affected by 1-2 layers of membrane. On the edge, you are viewing through the membrane somewhat "sideways" , so there is effectively more "thickness" of membrane. Maybe not an exact replica of the situation, but one that might be easier to visualize, is earth's atmosphere viewed from space. You can see the "blueness" of the atmosphere at the edges, but when you look straight down at the ground you see clouds, oceans, landmasses not tinted as blue.

I'm not sure if this answers my question. What I think of a cell is a three dimensional object surrounded by a cell membrane. Now if on looking at a cell 2 of microscope I can see the cytosol then it probably means that the cell membrane that should have been between the microscope and the cytosol is transparent but then how come at the same time I see the cell membrane in the same image as a dark boundary surrounding the cytosol.

In the center of the cell you observe, you see the membrane straight-on, and light is only affected by 1-2 layers of membrane. On the edge, you are viewing through the membrane somewhat "sideways" , so there is effectively more "thickness" of membrane. Maybe not an exact replica of the situation, but one that might be easier to visualize, is earth's atmosphere viewed from space. You can see the "blueness" of the atmosphere at the edges, but when you look straight down at the ground you see clouds, oceans, landmasses not tinted as blue.


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p53 gene in benign tumors
In a benign tumor, p53 gene does not work. I know that our cells constantly are mutating and the p53 fixes this. Hence, why does it take so long(or in some cases never) for a benign tumor to become a malignant one? I would imagine a malignant cell would rise rather quickly.

There are a number of main reasons for this: The main reason here is that there is more than one needed to transform a cell. This is usually the silencing of tumor suppressor genes like p53 and the activation of proto-oncogenes. Only one of these is not sufficient to transform a cell. This is also seen in melanoma, where nevi which carry the activating BRAF V600E mutation (which is the most often occuring activating mutation in this cancer) can stay silent for a lifetime. This is called the Knudson Hypothesis (a short overview can be found in reference 1)).
So the turn-off of the control system is not enough, the cell needs to be further pushed to become a cancer cell. More details can be found in reference 2
Then, our immune system is very good in catching cells, which have gone malignant. Most cells, which turned into cancer cells, are eliminated by the immune system. This idea has been first formulated by Paul Ehrlich in the late 19th century, see the references 3 and 4 for details. The figure from paper 4 shows this schematically:

References:

Two-hit hypothesis
Tumor Suppressor (TS) Genes and the Two-Hit Hypothesis
Cancer immunoediting: from immunosurveillance to tumor escape.
The Immunobiology of Cancer Immunosurveillance and Immunoediting


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Cloning DNA fragment - at least trying to
I`ve been trying to clone a fragment (about 1.6 kb) using pGEM system, unfortunately it was not succesful. Then, I moved to pJET, and guess what? Again, very low transformation efficiency. Now I am moving to pENTR. However, I am think about why I am struggling to clone this fragment.
I have tried to increase insert:vector proportion; plate a higher # of e. coli cells; left my ligation reaction overnight, but nothing is very helpful. Does anyone have any guess or suggestion about it? Does anyone think that the fragment is too long?
Thanks :)

The fragment size itself shouldn't be a problem in principle.
Cloning has many steps, so anything you didn't specifically test could be causing problems. If different vectors are also not the problem, you should probably look at your experimental steps:

One problem can often be residual EtOH from cleanup steps, which will make your ligation and transformation very inefficient.
You should also test your competent cells with another plasmid to be sure, that they are still viable
Have you checked that all fragments run at the correct size on a gel? You might have star-digestion or bound enzymes that cause problems. Additionally you could also check the ligation product on a gel (though you won't be able to use that for transformation), to see if the reaction works correctly

Hi Nicolai, thank you so much for your suggestions! I'll test it! Best regards, Matheus!


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What is the term for a given interpretation of a fossil record?
There exists a term, that I have heard and forgotten it appears, for taking a described species in paleontology and creating a version of what it was like in life.
For example, a prior [insert this term here] for T Rex had it upright and dragging it's tail, while a more recent [insert term again] has shown a much more horizontal and rigid body plan.
I know you 'describe' it formally when you identify it from remains, and 'mount' when you set up a specific set of remains. But what is it when you interpret those remains to a specific form?

Realization? Re-creation? Interpretation? Depiction? Illustration? Imagination?

The term you are looking for is reconstruction (as in
Forensic facial reconstruction).
You can find it used on the wikipedia articles for Fossil cave and for Transitional fossil or in the post In reconstructions, how are various shapes of facial features determined from skull only? for examples.


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Who cleans the cleaner fish?
Cleaner fish are those fish that eat the dead skin cells and parasites off from other usually larger fish.
( such cleaners include wrasse, cichlids, catfish, shrimp etc )
I wondered if the cleaner fish themselves ever receive this service from others, though understandably it is an added benefit rather than a necessary one for health.


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Linkage disequilibrium
I want to know what ranges of value can D' in linkage disequilibrium take? Because I read in my book (An introduction to population genetics by Nielsen and Slatkin) that D' is guaranteed to be between 0 and 1. Whereas at the link provided below, it says D' can be between -1 and 1.
http://csg.sph.umich.edu/abecasis/class/666.03.pdf
Could someone explain this discrepancy? Because now I am totally confused.

The whole point about using D' rather than D is because D' is bounded between -1 an 1 for any allele frequency, while the bounds for D depends upon the allele frequency of interest.
Recall the definition of D
$$D = p_{ab} - p_ap_b$$
Let, $D_{min}$ and $D_{max}$ be the minimal and maximal values of $D$ for a specific allele frequency.
For $p_a = p_b = 0.5$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.25$) and $D_{max}$ is when $p_{ab} = 1$ ($D_{max}=0.75$).
For $p_a = 0.8$ and  $p_b = 0.2$, the  $D_min$ is when when $p_{ab} = 0$ ($D_{min} = -0.16$) and $D_{max}$ is when $p_{ab} = 0.2$ ($D_{max}=0.04$).


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Which species of centipede is this and is it dangerous to cats?
My cat was "playing" (aka torturing) with this centipede:

I tried to measure its length with a measurement tape:

Since I know some species of centipede can be poisonous, I tried to find if centipedes can be dangerous to a cat, but the links said it depends of the species.
When the cat tried to catch it, the centipede ran fast to below the carpet or my slipper. Now, when I lift the carpet, it pretends to be dead, although in one occasion the arthropod moved its legs without changing position.
If it matters, I'm in Southern Brazil in a subtropical region and it's 01:30 AM. I don't think it bite my cat, since I'm not seeing any signals of health problems on the cat (also the anxiety of being forced out of my room so they can't interact until I solve the situation).
I think this animal is a Scolopendra, known here as "Lacraia".

The picture seems like this one, but it is from Tanzania (with invasive presence in Saint Helena, but not in Brazil): https://en.wikipedia.org/wiki/Scolopendra_morsitans

Also the Chinese red head is a subspecies of Scolopendra subspinipes species, which is present in South America:
https://en.wikipedia.org/wiki/Scolopendra_subspinipes

Visually it seems a lot like a younger Chinese red headed centipede since they average at 20 cm rather than 5-6, but it shouldn't exist here in Brazil. I tried finding a page in Portuguese but apparently there's only an English option.


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True or False: Dideoxynucleotide sequence analysis Question
True or false: Dideoxynucleotide sequence analysis is a template-directed method that makes use of chain terminators that stop DNA synthesis because they lack a 2'OH group.
The answer is false.
However I thought it would be true because dideoxynucleotide sequences stop DNA synthesis due to a lack of an OH group on a 2' and 3' group. What have I misunderstood?

you probably want to edit your question given that it's for homework...check out this link to understand how we handle homework questions on this site... http://biology.stackexchange.com/help/homework

Instead of posting here you should look up the structures of deoxy- and dideoxy-ribose, and that of the phospho-diester bond in DNA. (Learning them would be good.). Then the answer to the question will become obvious to you and you will have learnt something.

It is false, because DNA synthesis occurs via DNA polymerase,5' to 3'
By hydrolyzing activated nucleotides together. This occurs by nucleophilic attack of 3'-OH, of the last nucleotide in sequence, on alpha phosphate of a corresponding nucleotide triphosphates.

You should explicitly state that the 2' OH does not matter in this case, because all DNA nucleotides are missing the 2' OH, it's not needed for DNA synthesis and wouldn't affect chain termination.


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What Type of Mushroom is this?

Recently in Eastern Pennsylvania, there has been lots of rain and heat (90's) for a couple weeks now, so lots of mushrooms are popping up.
A neighbor posted a picture of this fungus in a community group, and was wondering if it is edible.

I found some images of Amanita rhopalopus that look similar, but I`m not totally convinced they are the same, as some look a bit different. Any one think they are Amanita rhopalopus?

You should not eat it if you don't know for certain what it is! E.g. here is a similar deadly mushroom: https://www.google.hu/search?q=gyilkos+gal%C3%B3ca&client=firefox-b-ab&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiOgqreh57OAhVB3SwKHYyqBDoQ_AUICCgB&biw=1536&bih=730#imgrc=nrVy5g6yIBrD-M%3A

Obviously no one should eat any unidentified organism without the guidance of an expert. Thanks for the possibility.

I am no mycologist, but I think it looks like the false death cap, Amanita citrina var. alba.
I'm basing this mostly on color, size, and the universal veil remnants on the cap.  Here is a picture for comparison:

Amanita citrina is now known to contain the toxin alpha-amanitin;
  however, if eaten in normal amounts it is considered the concentration
  is so low that it is unlikely to have any significant effect on a
  healthy adult. Of far greater risk is the possibility of confusion
  with one of the deadly Amanita species such as the Deathcap, Amanita
  phalloides, or the Destroying Angel, Amanita virosa. For this reason
  our advice is not to eat Amanita citrina, whether it is raw or cooked

Source: First-Nature

It could be an Amenita, another option is a Lepiota.

yes amanita sp. do not eat it at all. They come up in the grass after rain and hot weather.


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What organisms are Chloroperoxidase enzymes found in?
Are they found in humans? I'm wondering because they display a structural similarity to glucose-6-phosphatase, which is an important enzyme in gluconeogenesis.

Could you add some details of the structural similarity - from a quick search, I see that chloroperoxidases has a 3-layer sandwich (alpha-beta hydrolase) fold and G6P has a number of subunits.

I can look for more on that but my primary question is what organisms they are found in.

A good start is to look for the EC in RCSB  : http://www.rcsb.org/pdb/results/results.do?tabtoshow=Current&qrid=2F987A5C there's an 'organism' box on the left hand side

It is only found in an ascomycetes which is named Leptoxyphium fumago, also known as Caldariomyces fumago.
It isn't found in any other specie that we know of yet as searched on the RCSB PDB and Uni-Prot.
In researches that uses it they extract it from the organism, it is also available to buy from companies like Sigma Aldrich who extract it from the ascomycete too.
Sources:
Improvement of activity and stability of chloroperoxidase by chemical modification
Over-expression of chloroperoxidase in Caldariomyces fumago.
RCSB Protein Data Bank
Uni-Prot


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Difference between going against and going down a concentration gradient
The difference between facilitated diffusion and active transport is that facilitated distribution occurs down a concentration gradient and active transport occurs against a concentration gradient. I understand that, as a result of these differences, active transport uses ATP so that it can bind to the carrier protein, however I don't know what is meant by going against a concentration gradient or down a concentration gradient.
In short, I would like to know the difference between going against and down a concentration gradient. A definition of what a concentration gradient is might clarify things a little further as well, since the definition I have doesn't help much.

"Concentration" is "how much stuff is there someplace?" "Concentration gradient" is "how much is concentration changing from point A to point B?"
Imagine a terrain where concentration is represented by height.
"Down" a concentration gradient means from high concentration to low concentration - this is the direction things would move via simple diffusion.
"Up" or "against" a concentration gradient means from low concentration to high concentration. Moving in this direction requires some sort of energy input, such as active transport using ATP, or an electrical gradient, or something else.

Moving against a concentration gradient means that the substance is moving from a low concentration to a high concentration.
Moving down (descending) a concentration gradient means that the substance is moving from high concentration area to a low concentration area.

Welcome to Biology.SE! Your answer doesn't seem to be adding anything to the already existing answer. In addition, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


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What difference do trans and cis configurations of amide groups bring to the polypeptide chain?
Hi I was just wondering whether there would be any difference to the structure of the polypeptide chain, or any changes to a proteins characteristics, if it has more amide groups with a cis or trans configuration.
Apparently the trans configuration is more stable, so more amino acids with a trans configuration can be found within a polypeptide chain. Does this pose any significant characteristic to a protein, and if so what is this characteristic?

Apparently the trans configuration is more stable, so more amino acids
  with a trans configuration can be found within a polypeptide chain.
  Does this pose any significant characteristic to a protein, and if so
  what is this characteristic?

As you said, the trans- form is energetically more favourable. However, in proline the cis- form is energetically similar to the trans- form. The cis- structure introduces a kink or bend in the peptide chain which is seen in case of proline (see this section of wikipedia page on proline).


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Does cocaine bind competitively or non competitively to DAT?
I was just wondering whether cocaine, once reaching a synapse, binds to a DAT (Dopamine transporter) competitively or non competitively, or neither of them?

Cocaine binds competitively to DAT, though not in precisely the same binding site, rather there is overlap, and many of the same amino acids are involved in binding of each.
Amphetamine and benztropines also bind in the same region.
Beuming, T., Kniazeff, J., Bergmann, M. L., Shi, L., Gracia, L., Raniszewska, K., ... & Loland, C. J. (2008). The binding sites for cocaine and dopamine in the dopamine transporter overlap. Nature neuroscience, 11(7), 780-789.

Is this overlap also present when dopamine binds to the dopamine transporter?

@ModoUnreal I'm not sure what you are asking- this is all referring to competitive binding with respect to binding of dopamine. When you have competitive antagonism you can't really bind substrate and antagonist simultaneously, that's the whole meaning of competitive binding: they sit in the same place.

As in does dopamine overlap with the dopamine transporter when it binds to it, like cocaine does? Apologies for the confusion.

Overlapping is referring to the binding sites for dopamine and the binding sites for cocaine on the transporter. Each binds to some of the same amino acids so we say they are overlapping. It doesn't make any sense to say whether either overlaps with the transporter: the transporter isn't binding itself.


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Under what conditions do laboratories have the need to perform both, colony counting and cell counting?
It seems that the requirements to perform colony counting and cell counting in petri dishes are quite different. This is especially true, because colony counting can be done with the naked eye, even though it can get very tiring.
Since I am interested to find out what tasks most biological labs have to go through, I was wondering whether these two tasks might be requested by the same types of labs.

I don't think people actually count cells on Petri dishes. In my experience, cell counting is done for liquid cultures not for Petri dishes. In this case, you can use counting chambers (microscope slides with a grid)

There is a multitude of reasons to use one or the other.
Colony counting is often used on petri dishes for antibiotic resistance screening for practical reasons. One of the downside of this versus cell counting is the need to incubate the bacteria for 12h+ after you have done your experiment before having the result.
In some cases, you will need to know the concentration of cells you have immediately to perform specific dilutions or calibrations etc, you then use cell counting.
Cell counting is normally done with a liquid culture of the bacteria. it can be used to determine the concentration of the whole culture or count during or shortly after an experiment. Some bacteria will have a hard time growing on solid media or some molecules that you might want to test for resistance are not soluble, so you can't plate them to colony count.
So it basically all depends on your needs for the specific experiment and what you are working with (bacteria, medium, molecules etc.).

Any lab that would like to make the distinction between live and dead cells in a cheap way would use both techniques. You count colonies on petri dishes to get the number of living cells, and count in counting chambers under the microscope to get the total number of cells.
There are easier ways to do this though, for example using this: https://www.thermofisher.com/de/de/home/brands/molecular-probes/key-molecular-probes-products/live-dead-viability-brand-page.html in a flow cytometer. That's not that cheap though.

For mammalian cells (I don't know about bacteria/fungi), you can simply use Trypan blue exclusion or acridine orange/propidium iodide staining to determine the number of cells with intact vs. compromised membranes, which generally correlates to live and dead cells, respectively. Viability dyes are great if you're already doing flow, but I wouldn't use them just for determining live/dead status and nothing else.


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What does "genus VI" mean in mycology?
This Guidebook is called "How to identify mushrooms to genus VI". Some other editions/versions of it say "Genus III" or "Genus I". What does this mean?

This is a multi-part series of books, with each volume numbered with roman numerals I, II, III, IV, etc meaning 1, 2, 3, 4, etc, followed by a subtitle, in this case the subtitle is "Modern Genera."
There is no meaning to "Genus VI", the title of the book series is "How to Identify Mushrooms to Genus" which indicates it will help you identify mushroom genus but will probably not bother with differentiating species of the same genus (even that is quite a lofty goal).
The authors could have instead called this book "How to Identify Mushrooms to Genus; Volume 6: Modern Genera" to convey the same meaning.


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How Would I Isolate and Amplify a Viral Enzyme?
what procedures would I use to isolate and amplify integrase? If I am trying to study the integrase enzyme which is found in HIV how would I
1) destroy the viral capsule to release its contents.
2) separate Integrase from other enzymes and the viral DNA.
3) make copies of the enzyme for testing.
Any help would be greatly appreciated!!

This sounds rather like a homework question. Please see the site's policy on such questions and in particular the requirement to show you have attempted to answer yourself.

Each virus would contain extremely low amounts of enzyme (probably a few individual molecules, at best); collecting and concentrating enough viruses to extract a significant amount of enzyme would be long and difficult, if at all possible.
The usual strategy in research laboratories is to clone the nucleic acid sequence coding for this protein (either by direct amplification from an HIV-infected cell, or by synthesizing a piece of DNA in vitro) and integrate it in an expression vector, that is, a larger piece of DNA, usually circular, suitable for integration in a host cell (human, or even bacterial) and carrying the sequences necessary for persistence and gene expression. This way you can produce thousands of copies of the enzyme you are interested in in each cell, and you can then purify a significant amount of integrase to study it.
To make purification easier, it is common practice to add to the gene a sequence coding for a "purification tag", that is, a few extra amino acids that have special properties that make the final protein easier to purify. Stretches of 6-8 histidine residues are very commonly used. The assumption is that the protein carrying this tag will have an activity similar to the natural enzyme, after purification.


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Why don't the heads of phospholipid bilayers repel hydrophobic molecules?
What I Think I Know: Hydrophilic and hydrophobic things repel each other. Since the cell membrane contains hydrophobic tails, it is difficult for hydrophilic molecules to pass through the cell membrane.
Question: Why don't the heads of phospholipid bilayers repel hydrophobic molecules? In other words, if the phospholipid membrane has both hydrophilic and hydrophobic portions, why do only the hydrophobic portions act as repellents?
Stipulation: I need a quotation from a textbook, university, or other credible source.
Evidence of Prior Research:
Why lipophilic molecules can pass phospholipid bilayer, in spite of 2 hydrophilic layers?: This question has a comment that links a graph from a textbook. I can't understand the graph by itself. There are no other references.
Understanding what passes through and doesn't pass through the plasma membrane: All references discuss the topic, but none answer the question.
I understand that this topic is addressed quite frequently, but the question I'm asking is never answered. Texts tend to say something like, "Ions can't get through the core because of their charge" and completely gloss over the concept of lipids getting through the heads. Please don't dismiss this as a homework question that I didn't take the time to research. This is my second try asking this question (on this site); I have spent hours trying to find an answer.

Taylor, you've done an excellent job updating your question and providing evidence of additional research effort. Thanks very much for making the extra effort. I don't foresee this question getting marked/closed as homework now, and I hope you get a good answer! Good luck! :).

@Taylor Do you mean chemicals in the intra/extracellular fluid or chemicals embedded in the plasma membrane?

@Jam I'm talking about molecules/chemicals that pass from the intracellular fluid to the extracellular fluid, or vice versa.

Your question is rooted in a misundertsanding of the hydrophobic effect. Hydrophillic and hydrophobic molecules do not repel but, rather, attract one another through van der Waals interactions. The tendency of hydrophobic molecules to aggregate in aqueous solution (ie the hydrophobic effect) is, instead of some repulsive force, actually driven entropically. I don’t think I will go into this in detail since it has been explained well in many places. That said, it is also explained very poorly in many places (which I suspect you have encountered). I recommend this website to learn about it and other intermolecular interactions.
Once you have a firm grasp on that, consider that in order for a hydrophobic molecule to reach a plasma membrane, it must already be solvated by water. The transfer of a hydrophobe from one hydrophillic environment (water) to another (head groups of the phospholipids in the plasma membrane) should be energetically negligible. The limiting step for passive diffusion across a membrane is transfer from the hydrophillic environment of the phospholipid head groups to the hydrophobic environment of their tails. In fact, the rate of diffusion across a plasma membrane increases with hydrophobicity.


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Why does solute potential go up as temperatures go down?
So the closer a solution's solute potential is to zero, the more water potential said solution would eventually have. The solute potential equation is -iCRT. If the temperature is 0, -iCRT would be equal to zero, and because temperature is measured in Kelvin, this would mean the solution is at absolute zero. Things can't move at absolute zero. How is it that that water has the most potential to move at absolute zero?
Same with the opposite.
If the temperature is high, wouldn't that mean water potential would be at its highest because water molecules are at high energy, jumping around everywhere?

Welcome to Biology Stackexchange. It sounds to me like your question isn't actually about biology, so I've voted that it should be moved to Chemistry Stackexchange instead. https://chemistry.stackexchange.com/

this is where I got my water potential information: https://goo.gl/t6LgvX

@user1136 — Water potential may be of concern to workers in many areas of science, just as may pH and ionization, chemical bonding, electricity etc. That does not make any of these appropriate for a SE site dedicated to questions in biology when there are SE sites specifically dedicated to chemistry and physics. It also makes sense to ask chemistry questions on SE Chemistry because they are more likely to get authoratitive answers (which will show up when a scientist from any discipline makes an internet search) there.


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Why glycosylation of a protein increases its non-specific binding properties?
This doubt arose while reading this website: https://www.thermofisher.com/cn/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/avidin-biotin-complex-method-ihc-detection.html

I think it has something to do with lectins binding to the glycosylated moiety.


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How does the specificity to bind to antibody differs between 'hot' and 'cold' antigen in radioimmunoassay?
This question is in relation to radioimmunoassay. In this assay, the 'cold' antigen replaces the 'hot' antigen. Why is it so, if both the antigens are same and hence their specificity? Does the radioactive molecule change its specificity?

The specificity is the same, but protein-ligand binding is an equilibrium process. In other words, the antigen is constantly associating with and dissociating from the antibody. As a hot antigen dissociates, it is possible that a cold antigen can take its place, and vice-versa. As the ratio of cold to hot antigen increases, there is a greater probability that cold antigens will take the place of hot antigens.
You can read more on Wikipedia.

@Indresh You’re welcome. If this answered your question, you can mark it as accepted by clicking the check mark.


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Help me find out what this bird is (description, no picture)
A while ago I read about this bird(s) whose species status was not confirmed. This was because they had a very large distribution and birds in adjacent population could breed with each other but birds at each end of the distribution (western Europe and South Asia I think) couldn't. I am pretty sure that they were some kind of gull and from Europe to Asia their wings got lighter, from black to grey. I think I might have read about them in a Richard Dawkins book.
Does anyone know the species I'm talking about?

Do you have an image of that bird, and some more specifications?

You're describing a Ring Species: "a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population".
The classic ring species is the Herring Gull complex, and that's probably what you read about:

The classical example of the ring species model was originally based upon the herring gull complex (Mayr 1942). This group comprises more than 20 taxa of large gulls (Haffer 1982) which together occupy a circumpolar breeding range in the northern hemisphere. ... Mayr envisioned all taxa of the circumpolar chain to be connected by gene flow, while herring and lesser black-backed gulls in Europe, the hypothetical endpoints of the ring, have reached full reproductive isolation and now coexist as distinct species.

--The Herring Gull Complex (Larus argentatus - fuscus - cachinnans) as a Model Group for Recent Holarctic Vertebrate Radiations
However, recent genetic work shows that the situation is even more complicated than this, and it's questionable whether they really are "ring species":

Contrary to the ring-species model, we find no genetic evidence for a closure of the circumpolar ring through colonization of Europe by North American herring gulls. However, closure of the ring in the opposite direction may be imminent, with lesser black-backed gulls about to colonize North America.

--The herring gull complex is not a ring species.


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Equation relating probability of fixation and number of generations
I am trying to find an equation that relates the variables of probability of fixation and generations. Or, how does number of generations affect the probability a gene will fix, if population size doesn't significantly decrease or increase.

You may want to have a look at the notion of Moran process, that's pretty much what these models are designed for.

From Hartl and Clark's 'Principles of Population Genetics' Third Edition chapter 7: Kimura and Ohta (1969) showed that the mean time in generations until the allele of frequency p is fixed (ignoring cases where the allele is lost) is:
$$t_1(p) = -4N[(1-p)log(1-p)]/p$$
The mean time to loss of the allele is:
$$t_0(p) = -4N[p \cdot log(p)]/(1-p)$$
Thus the mean persistence time of an allele is:
$$t(p) = -4N[p \cdot log(p)+(1-p)log(1-p)]$$
Hopefully I didn't make any typos there, but I reccommend this book to learn all the ins and outs of popgen. There is a PDF of the third edition online in an archive. For more book recommendations, please have a look at the post Books on population or evolutionary genetics?
You can also find these equations in the original article: Kimura and Otha (1968)

By wrapping your equations in dollar signs, you can use LaTex type of formatting. For example $\frac{1}{\sqrt{2}}$ becomes $\frac{1}{\sqrt{2}}$. See your answer edited for more info. I also added the original article and a link to more book recommendations.

It seems like answer to your question can be related to effective population size and idealized population. One of the models to to consider is Wright-Fisher model:
$$\frac{(2N)!}{k!(2N-k)!)}p^{k}q(2N-k))$$
where N is individuals, so there are 2N copies of each gene, k is number of copies of an allele that had frequency p.


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I want to extract genes from genomes
I m a student at computer science and I'm working in a project called Plant Breeding and for moment I need to extract genes from a file with genomes.
I know that the start sequence of a gene is ATG and the stop sequences of a gene is TAA,TGA or TAG.Should I know about inside more apart of the fact that inside I will find only A,T,G,C and inside are exons and introns?

I would highly recommend you to look into the detailed descriptions (or even papers) of how gene prediction and genome annotation is done.
This is a very complicated problem and you seem to missing knowledge of many details that need to be considered, but also there is a lot known about how to do this right, so you don't have to solve this by yourself.
A few very important details, that you either haven't stated or are misunderstanding:

The the ATG codon is the start site of translation, but not the start of a gene. A gene encompasses a promoter (which are very hard to define/predict), 5' & 3' UTRs (untranslated regions) in addition to the open reading frame, which is marked by start & stop codons.
In addition the genomic (i.e. DNA) sequence will contain introns, which are usually much larger than the exons coding for the proteins, and may contain any sequences, so you can not look for codons there.
If you are working with species for which the genome sequence is already known (which is a big number of species), at least a 'rudimentary' gene prediction has very likely already been done. You can find the annotation of all identified features (like genes) in the genome annotation files corresponding to the genome, however this gets very detailed and complicated very fast.
If you are working with a newly sequenced species, where this has not yet been done you need to be aware whether you have genome and/or transcriptome sequences (the latter are important to find gene locations with high quality).

Can you tell me someyhing about introns and exons?
The rules to split them.

And something about the size of the genes for Brassica napus oleifera and Brassica rapa oleifera.

I agree with Nicolai's second point - has your species been sequenced and assembled previously? If yes, then search online for the genome annotation (https://www.ncbi.nlm.nih.gov might be a good starting point).
If your species has not been assembled and annotated, then you might want to look into de novo gene prediction software. This page has a list covering some of the various kinds https://en.wikipedia.org/wiki/List_of_gene_prediction_software


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How is the activation energy lowered in an enzyme by just orientating the reactants closer to one another?
If the activation energy is lowered, bond strength has decreased. How does purely orientating the reactants closer to one another lower the activation energy in a protein? The only thing I can think of is steric strain.

We welcome new posts to SE Biology, but ask that posters read the advice in the help about posting questions. Your question has problems which can be solved by clearly setting out your assumptions and their basis. You state "if activation energy is lowered bond strength is decreased". You do not say what bonds you are talking about (the transition state?) and your basis for this assumption. Then you say "how does purely orientating…" without saying that you have read (where?) that this is how enzymes works. Please revise carefully.

The activation energy is not only lowered by orientating the substrate but by stabilizing the transition state.
According to the induced fit model many enzymes show a higher binding affinity to the transition state of a substrate.

We welcome new participants to SE Biology, but this is a question and answer site, not a discussion site, so what we expect from an answer is more than the two lines here. First, you need to consider whether this question should be answered at all. It is so poorly constructed that I would say no. However if you must, you need to clarify the question and the false assumptions, porvide more detail, and provide external justification for your answer. Without links or references, how can anyone tell whether or not you are correct?


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Could you save a species if there were only two remaining?
Let's say an endangered species had only two left (male and female) and they produced 4 children (two male, and 2 female), and those produced? Wouldn't the incest slowly degraded their genes? (Assuming the pair of children created 4 children each, etc)
My main question is could you really save a species with only two?

Incest doesn't degrade genes. Incest increases the chance that alleles with deleterious mutations are paired and therefore expressed. (In other words, inbred offspring are more likely to have homozygous traits associated with deleterious mutations and therefore may experience decreased fitness). Good thing mutations can continue to occur....

"degraded their genes" needs definition

Depends on multiple factors (environment, genetic composition of the parents, the physiology of the species, reproduction rate, etc). I guess it is theoretically possible but the chances of extinction are very high. Therefore as your question stands, it cannot be conclusively answered.

Depends on multiple factors (environment, genetic composition of the parents, the physiology of the species, reproduction rate, etc). I guess it is theoretically possible but the chances of extinction are very high. Therefore as your question stands, it cannot be conclusively answered.


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Identify function of cluster with high identity of genes
Let's say there is a secondary metabolites biosynthesis cluster in fungi A.
and I just found out a gene B(identitiy>=50% with nrps gene located in the cluster) from fungi B and also found that gene B is located in some gene cluster in fungi B genome. My question is, with these two proofs can I say the gene cluster including gene B is doing same function with a secondary metabolites biosynthesis cluster in fungi A?

Welcome to SE Biology. Take the tour and read the help on asking questions. 1. Your "let's say" suggests that this is a homework question. Is it? 2. you need to set out the information (evidence, not proof in English) clearly, point by point. What does "nrps gene" mean? When you say there is a gene cluster in gene B, what is your evidence this is a "cluster"? You only mention geneB, which I presume is related to one of the genes in fungus A (fungi is plural). Do you know anything about the other genes in fungus B? 3. without demonstration of function you can only talk abut likelihood.


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Is feeding wild pigeons really "weakening the entire species"?
While reading about what foods are healthy for pigeons, I came across the following paragraph: (Source)

Human interaction and improper feeding of domestic and wild pigeons is believed to be one of the reasons for the birds' decline. While many urban areas claim that pigeon populations are out of control, the truth is that around 59 species are currently threatened by extinction, which is over 20 percent of the pigeon population. Since the 1600s, 10 species of pigeon have become extinct. While habitat loss and over-hunting are partly to blame, bird specialists believe that domestication and improper feeding has weakened the entire species.

There are no sources cited. What does "weakening the entire species" even mean? What evidence is there to support the claim that improper feeding is weakening entire species of pigeons? How would overfeeding by humans lead to extinction? And how would domestication be contributing?

This might be a good question for Skeptics.SE

I did wonder whether an ecology question was on topic for this site. But how would I migrate the question?

The quote is silly. All the declines noted are for species other than Columba livia, the domestic and common wild pigeon. Indeed other species have been lost to habitat loss and hunting, but not to feeding.  Feeding and human activity have helped C. livia explode in population, which is not a sign that (entire) species has been weakened.

It might also be noted that those extinct pigeon species might well include the dodo: https://en.wikipedia.org/wiki/Dodo

Yes, [tag:ecology] questions are on topic here.

Yes, my comment about Skeptics was about the form of the question, not the topic

Oh, and the passenger pigeon.  Extinction of those had nothing to do with feeding, everything to do with human hunting and the introduction of new predatory species.


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How many of their caches do chickadees retrieve?
Chickadees are scatter-caching birds and I've heard they can hide as many as 10,000 seeds for retrieval over the winter. How many of these cached seeds actually end up getting used in a typical winter? And can the chickadee really remember all of the locations?

I'd guess about the same percentage as squirrels and their acorns, and yes, they remember where every one is hidden, but they have a hell of a time finding their car keys.


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Snake Identification - St. Louis, MO
We found this tiny snake in the finished part of our basement today. We live in the St. Louis, Missouri area.

The snake is dark greenish-grayish and has very faint lines running the length of its body.  Any idea if it is dangerous/what we should do with it?

It might be a juvenile lined snake (Tropidoclonion lineatum). The What Snake Is That page for Missouri says they are native. In your photo, I see very faint black stripes with a central tan line, which matches a lined snake. Photos of juveniles seem to be rare though.
Lined snakes grow to about 2 feet long and are non-venomous. According to this natural history page, the only venomous snakes in Missouri are pit vipers (of which 5 are native).


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Where do I find the CO2 clearance rate for various plants?
I'm trying to get enough plants to bring my office from ~1k ppm of CO2 to ~300ppm of CO2. (If I can't get below the ambient 450ppm, that's fine too.) It'd be nice to know before I start buying plants if I can expect to reach that target without, say, having to turn a conference room into a greenhouse.
But I can't easily find a table that lists the rate at which various kinds of plants remove CO2 from the local atmosphere. I'm aware of the NASA Clean Air Study, which looked like it was mostly focused on other pollutants, and Kamal Meattle's conclusion that it takes 4 Areca Palms per person. But I want to know where that number of Areca Palms came from. Or, more importantly, be able to calculate it for other plant varieties. (He might have been optimizing for something different than I would want to.)
So where can I find this information?


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Absorbable stents
Stents are tubular scaffoldings, which are used to expand blocked arteries. Absorbable stents dissolve after few years. Shouldn't the blood vessel become narrow again once the stent has dissolved?

Blood vessel by that time gets remodelled.

"Restenosis" is a problem with both absorbable and non-absorbable stents.


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Function of testosterone in women and estrogen in men
I was recently surprised to find out that testosterone and estrogen are found in both men and women albeit in different amounts.
I know that testosterone is related to the development of facial, body and pubic hair, deepening of the voice, and muscle development in men.  And that estrogen helps in maintaining the condition of the vaginal lining and its elasticity, and in producing vaginal lubrication in women among other functions.
But what could be the function of testosterone in women or estrogen in men? A simple Google search could give me no good results except for here where it says:

In men, estrogens have no known function. An unusually high level, however, may reduce sexual appetite, cause erectile difficulties, produce some breast enlargement, and result in the loss of body hair in some men.

and that

Large deficiencies of testosterone may cause a drop in sexual desire, and excessive testosterone may heighten sexual interest in both sexes.

Does anyone have any further knowledge?


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Biological replicates
We are currently doing an screening where supernatans from a bacteria genus are tested againts a pathogenic bacteria cell culture in a 96-well plate where OD is measured each 2 hours.
Each supernatant from a strain has 3  replicates  and the control phatogenic bacteria cell culture has about 11 replicates inside the plate.
Once each experiment is finished cell growth curves are modelated and 3 growth parameters are determined (mu, lambda and max absorbance) from each supernatant tested and from the control. Then a Mann-withney U test is performed for each growth parameter from each strain againts corresponding control parameter to check if there's some kind of possible inhibition.
The strains which has some inhibition efect againts this pathogenic bacteria will be tested again in further experiments to confirm the possible positive.
I  have a doubt about if performing statistical test to compare supernatants from each plate againts its corresponding control is correct considering that the possible candidates will be again tested in further experiments to confirm its inhibition. Since there's loads of strains to test, repeating each single experiment more than 3 times would take too long.
What it is your oipinion? Is it correct to do statistics for single plate (technical replicates) to gather possible positive for a later confirmation (biological replicates)?
Thank you
Are biological replicates strictly needed in this case?

You might have better luck with this question on https://stats.stackexchange.com.

These might be interesting to you: http://www.nature.com/nature/journal/v492/n7428/full/492180a.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321166/


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Do all commercial ionizers produce harmful ozone?
I'm not a scientist. I have read that negative ions have health benefits. I am interested in increasing the ratio of negative to positive ions in the air in my home.
I see that ionizer machines exist (e.g. https://www.amazon.com/s/ref=nb_sb_noss_2?url=search-alias%3Daps&field-keywords=ionizer).
I have also read that such ionizers produce ozone and that ozone can damage the lungs. Also sorry for not knowing what tags to use.
Do all ionizer machines produce ozone and are the levels produced harmful?
Please forgive me for my ignorance. If this is the wrong place to ask this question then please help me to find the right place.

"Negative ions" in this context having health benefits is complete nonsense pseudoscience.

This seems more to be about the specifications of a commercial product or set of products rather than a specific biology question. To be on-topic, you'd need to ask about ozone concentrations that would be harmful - to perhaps specified tissues of a particular set of creatures - and you'd need to show your research. Finding out if such levels are produced by a commercial machine would be off-topic here.