text:
Regulation of the concentration of precursors of DNA and RNA synthesis
What is the specific cellular process for regulating the amount of the four DNA bases (adenine, thymine, cytosine, and guanine) that are present in the cytoplasm of a cell?
Basically, how do the cell's mechanical processes "know" that there are enough of these present in the cytoplasm for DNA/RNA processes to operate effectively?
From what I understand, DNA/RNA sequence production involves simply grabbing these out of the cytoplasm as they randomly pass near the sequence assembly protein.
As a side topic, but also important here, the cytoplasm is apparently just a random fluid containing all sorts of molecules flowing and diffusing in random directions via Brownian motion. I do not know if there is a specific direction cytoplasm flows around the inside of a cell, and if so, how the cell would manage to coordinate that either.
There does not seem to be a way for cell processes to "read" the proportional molecular contents of the cytoplasm to know if there is sufficient numbers of these present for proper cell function.
If there is a lack of any one of these four base molecules, DNA/RNA processes will slow or stop functioning, leading to systemic failure and potentially cell death.
If there are too many of any one of them, the cell could become so packed that nothing can move around and the cell's function is impaired. Possibly the cell wall could rupture if there are too many.

The specific cellular process that regulates nucleoside synthesis has chapters in books dedicated to it, but I think the question is still good and can be answered with an overview. You're side topic may be better off as an entirely different question. Diffusion is definitely important but, as a start, you can look up cytoplasmic streaming and cytoskeletal transport.

@canadianer, nice mention of cytoplasmic streaming and cytoskeletal support: Brownian motion is only an approximation, and a very over-simplified one. However, keep in mind a whole different question may be needed to discuss the answer in the case of prokaryotes vs. the case of eukaryotes. Also, I believe you meant Your (not You're)

No no, I did mean "you are side topic", my grammatical mistakes came later ;)

There is an area of biological science called Biochemistry that includes the processes by which cellular chemicals are interconverted — metabolism. You are correct in assuming that metabolism, including the pathways for the synthesis of nucleic acid precursors, is regulated, and in general this operates by certain intermediates acting as sensors, modulating the activity of key enzymes. Your question regarding the eight precursors of DNA and RNA synthesis is far too broad, and I have voted to close. I recommend Chapter 10 (Regulatory Strategies) in Berg et. al. (NCBI Bookshelf, online).

You would also benefit from reading the details of nucleic acid synthesis and that of its precursors, which are not free bases, but nucleoside and deoxynucleoside triphosphates. Again, there are chapters on this in the previously mentioned Berg et al. and other biochemistry texts.

I am not a biologist, just someone with a casual interest. Is there a reason why these are being posted as comments and not as answers, if you are suggesting these are answers to the question and reasons to close? Is distillation of the overall mechanisms not easily summarizable within a few paragraphs?

This information does not appear to be accessible online for free in any sort of open format. Is it possible to summarize it here? https://www.ncbi.nlm.nih.gov/books/NBK21158/#NBK21158_dtls   "By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed"

If they are not the originator of the post (question or answer), you need to @'user' for them to be notified of your comment. That being said, I believe that David is saying that this is too broad a question (it would require multiple book chapter to adequately answer). Unfortunately the book @David recommended is no longer available — perhaps he can make an alternative suggestion, but you can also search for resources using the key words he mentioned. I have also found that Khan Academy can be very helpful when starting to learn about a new area.

@tyersome — It was available in 2017, and so the OP had a chance to consult it if he wished. As it is only a comment, my only update is to suggest purchase of a second-hand copy.


text:
Food safety during roadtrips
I will be moving across the country in the coming weeks, and I have realised that I will likely have leftover perishable food in my apartment before I leave and I was thinking of trying to prepare some of it the night before I leave to bring with me. The trip will take me four days, and I was going to cook (extra thoroughly) hardboiled eggs, pork, bacon and sausages. I might even add some salt or something. And keep all of my packaging as sanitary as possible, eg. straight from pan/pot to sterile ziplock.
The eggs I'm unsure of because of the protective outer layer that is chemically removed during processing. The pork and bacon, I feel like they will be alright if they're eaten first. And I'm not too worried about the sausages because they've been processed and cooked.
I think a visual and olfactory test of the foods before I eat them would be wise - especially if nearing day 4. But, realistically, if I keep the food out of the sun covered up it will probably stay safe to eat, right? Or is this a bad idea?
I think that the food would definitely be safe to eat up until the end of the second day. But, what about any longer than that? How did people back in the old days travel with food?
Edit:
Just to clarify my question. I am not asking about whether or not my apartment is sterile. And I'm not asking about whether or not bacteria can multiply. I'm very well aware of these answers.
I'm looking for a realistic estimate on food longevity - not the food-standards enforced onto food manufacturers or restaurants by the FDA/Health Canada.

I'm voting to close this question as off-topic because better suited for Health.SE imo

@AliceD Is Health.SE for food science? I figured since food scientists rely heavily on microbiology this would be the ideal place for answers.

I think this is a biological science question. Food science, but still science.

The biggest factor in whether bacteria can grow in food is water bio-availability. Most non-sterile methods of preserving food (note that canning IS sterile) utilize this fact. Over salting while curing, adding lots of sugar, and dehydrating (or freeze-drying) all either remove water or remove the ability of the bacteria to utilize the water and hence grow in that medium.
This is the biggest reason that a hamburger from McDonalds can seem to petrify without devolving into an ugly mess. If the burger and bun and condiments dry out, bacteria can't grow on it. Put that same burger in a ziplock bag with a few drops of water and you will have the nastiest mess possible in a few days.
Honey and jams can remain at room temperature for months or years, even after opening despite being "watery", and this is because there is so much sugar in the solution, that all water tightly bound to the sugar molecules, leaving none for the bacteria to use (Note that some yeasts still can). Similarly, because of lack of water, crackers last for years, while bread spoils.
For your question with eggs and bacon, unless it was a hard-boiled egg that was cooked twice as long to ensure pasteurization throughout the yolk and you left the shell on, I wouldn't risk it after a couple of hours.  Bacon, once cooked, very little water activity. Fat doesn't count for bacteria propagation, they need water. I take cooked bacon on camping trips all the time. I also take sharp cheeses with me and they are good for days.
Your other option is cooking beans (with seasoning) or something and dehydrating them in the oven on a cookie sheet before you go. Then you just need to add hot water. I do this for camping as well.
Edit:
I didn't mention that high salt solutions (see pickling) function outside this paradigm somewhat, in that you are creating such an isotonic concentration in which bacteria membranes lyse.  I also didn't mention methods of pickling like kimchee and sauerkraut that use salt to positively select for species of bacteria (that aren't pathogenic to us) that can tolerate that salt concentration (mainly lactobacillus) as well as some yeasts.
Edit2: With a Source about water activity

How did people back in the old days travel with food?

Keeping said food alive until needed. Salting. Curing with smoke. Drying.Canned food. Buying it on the road.
Bacon and sausages. Have a lot of preservative in them (salt). So if you fry them, it will keep for a few days. Keep the oil on to stop exposure to air. Boiling on the other hand will remove said preservative, reducing your food shelf life.
Hard-boiled eggs.. so long as the shell remains intact..it will last the day and very likely last day 2.
The food listed would almost certainly last 2 days if kept in an air tight zip lock and kept in a cool place.
Day3 and Day4? It depends on the ambient temperature.
If it is below 10 Celsius. My guess is that the food will last till day 3. Probably till day 4.
However if it is above 20C, I don't know. My guess is that the food will be going bad.
Now... you have to realize that you are risking food poisoning (day3-day4). And this is the 2010s not the 1850s. You are not traveling the Oregon trail by wagon. Food is available everywhere.
So my recommendation, well if you want to boiled eggs and sausages. Sure, eat them on day 1 (and maybe day2, breakfast). But for day2, day 3 and 4, go out and buy some food. Moving cross country is an experience in itself. Experience the food from all the small towns that you pass through. These are parts of the country that you would rarely if ever visit.

Your apartment isn't sterile, and cooking kills many but not all bacteria - cooked food isn't sterile either, no matter how thoroughly cooked. No matter how well you pack things, they will have bacteria on them. Without refrigeration, that bacteria will multiply and may make food unsafe, or at minimum unpleasant to eat. Also, some forms of food decay aren't because of bacteria, but due to chemical changes in the food itself - protective layers won't prevent these types of spoilage.

Please note the use of the word: sanitary

Also note: protective layer removed

@Bob Sanitary isn't the same as sterile. There are bacteria floating all around the air around you all the time. Sterile devices (for example, for surgical procedures) are produced in special facilities and use chemical processes to ensure sterility. Cooking food is usually enough to kill bacteria that are present in quantities that could be harmful, but if you leave that food at room or elevated temperature, it is going to grow. You might not like this advice but please don't dismiss it.

I am aware. Please refer to my edited question.

I'm going to take issue with how you worded your response, "cooked food isn't sterile either, no matter how thoroughly cooked".  This is not true, else canned goods would not be good for years. The issue is that, absence of a sterile environment, he can't get it from a covered pot into a container and it still remain sterile.

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Does liver regenerate quicker if idle?
I recently heard a proposition that fasting (especially fruit-only diet) can improve liver function because it removes the load usually induced by toxins in common diets, thereby allowing the liver to regenerate itself quicker.
This is a common proposition in "detox diets" but I am not sure if it has any ground in science? Does consuming less toxic food allow liver to "recover" and regenerate quicker?

Welcome to Bio. Could you add your source to your claim? It may be a mythbuster-typed question and sourced are especially  relevant with those.

Thanks. It was a Facebook discussion from a closed group. Not sure how that fits with the rules here?

That'll do I guess. It's not the most reliable source, however. Was there a consensus in the whole group that this diet helps? How many folks were in the group? Sorry for the questions, just trying to get this clear. Personally I like the mythbusters, but they often hinge on the source of info.

Well it was a skewed crowd, the group is Bali based, and Bali is huge on veganism, detox, organic juices etc, so alternative propositions are usually threated like heresy. Not really a fact-based, paper-supported discussion, but I'd like to improve my own arsenal to participate in these discussions better.

This idea is prevalent in naturopathy and with popular health enthusiasts so I think it's a relevant question. Scientific consensus is a bit more elusive. Here's a link to one article: https://www.sciencedaily.com/releases/2016/05/160509085347.htm

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An efficient and free method of assembling a large number of Sanger sequencing reads?
I have a rather large number of Sanger Sequencing reads.
Is there a automated method in either Ugene or a similiar freeware that allows you to quickly assemble forward and reverse reads. Ideally something where the suffix of the filename will allow the software to automatically know which is the forward and reverse read.
Any help would be much appreciated as I'm not keen to do each sequence by hand in Bioedit.

Have you considered SPAdes? It's a popular, state of the art assembler that should work with Sanger sequencing reads.
http://cab.spbu.ru/software/spades/

What about the old Phred, Phrad and Consed suite of programs?

Thank you for answering, but it would be appreciated if you could at least provide a link to these programs. As it is anyone would have to search.


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What is this structure in human brain?
Scientists made a new image of brain.
I wonder, what is this arc (denoted by blue)?

Is it the caudate nucleus?

That blue outline is huge and honestly I can't see what structure you wish to show us with that?

See at right, it is clean there.

is that blue line outlining something or did you exactly trace the structure? Could you work with a few arrows with their tips just touching the structure of interest? Your blue outline would be a huge structure. It's probably the corpus callosum you are after that lies within the blue outline afaik.

@AliceD see my update please

Short answer
Based on shape and approximate position, I think it is the corpus callosum.
Background
I think it is the corpus callosum (Fig. 1). The corpus callosum is approximately 10 cm in length and is C-shaped. It becomes thicker posteriorly, as is also evident in your image. The corpus callosum is a structure consisting of white-matter, containing about 200 million axons.

Fig. 1. Mid-saggital section of the brain showing the corpus callosum. source: University of Central Florida
I think it is not the caudate nucleus, alhough it has also the curved shape. The caudate is positioned more laterally than the corpus callosum and by the looks of it your picture shows a mid-sagittal section of the brain. The caudate seems to be positioned too far laterally in the brain as far as I can see (Fig. 2).

Fig.2. Nucleus caudatus. source: Brain Notes


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Are four-leaf clovers mutations, developmental errors, or something more complicated?
What causes about 1 in 10,000 clovers to have four instead of three leaves? Will progeny(?) grown from its flower's seeds have a higher probability than that of also having four leaves?
From the Wired article The Mysterious Genetics of the Four-Leaf Clover

A clover’s lucky fourth leaf is presumably specified in its DNA. But the clover genome is surprisingly complicated, and finding the genes responsible—and under what conditions—for the four-leaf mutation is a still-unsolved biological puzzle.

From the Wikipedia's Four-leaf clover: Cause  (emphasis mine):

It is debated whether the fourth leaf is caused genetically or environmentally. Its relative rarity (1 in 10,000 clovers[ref]) suggests a possible recessive gene appearing at a low frequency. Alternatively, four-leaf clovers could be caused by somatic mutation or a developmental error of environmental causes. They could also be caused by the interaction of several genes that happen to segregate in the individual plant. It is possible all four explanations could apply to individual cases. This means that multiple four-leaf clovers could be found in the same clover plant.[citation needed] (emphasis added)

A recessive gene for four leaves has been identified (Tashiro et al., 2010). The clover is a tetraploid species and together with the fact that environmental conditions may also suppress the development of the fourth leaf, it indeed takes a lot of luck to find one. If it will bring you any is another question though.
In fact they are aiming at making a four-leaved cultivar (source: New Scientist).
Reference
- Tashiro et al., Crop Sci (2010); 50: 1260–8

That was quick! OK I'll give it a read.

Some of the links in the New Scientist paper aren't working, but I did find this one :)  Also this is interesting.


text:
Cartilage regeneration
Why can we not regenerate cartilage in our ear and nose, while bones and flesh can heal?
What makes it so resistant to regeneration. Can we artificially create it in the lab?

The reason that cartilage rarely is able to regenerate is that it is poorly vascularized and innervated. It doesn't have its own blood supply to deliver signaling molecules that promote regeneration and repair after injury.
There has been some recent progress on getting the body to repair and replace cartilage with lab created biogels detailed here.


text:
Difference between Peptone, Peptide and Proteose
In my school textbook, it is given that Pepsin converts proteins to peptones, proteose and peptides.
What is the difference between the three products? On googling the terms, the definition was similar.
Peptone: a soluble protein formed in the early stage of protein breakdown during digestion.
Proteose: A proteose is any of various water-soluble compounds that are produced during digestion by the hydrolytic breakdown of proteins short of the amino acid stage.
Peptide: a compound consisting of two or more amino acids linked in a chain, the carboxyl group of each acid being joined to the amino group of the next by a bond of the type -OC-NH-.
Peptide has a different definition, but it can be applied to the other two too as all are degraded proteins but not amino acids.

This, from Collins dictionary, claims peptones come from proteoses. But i am not sure if there is a definitive line between a peptone and a proteose.

And, a peptide, is just a molecule containing a peptide bond: amino group bound to carboxyl group, as you stated. Therefore peptones and proteoses, and I guess maybe even proteins can all be considered peptides.

Personally, I hate biological semantics.  I once had a professor tell me that it's better to understand a chemical process than be able to define mundane boundaries between said processes. This same professor taught genetics, but admitted to not knowing the dictionary-defined stages of the cell cycle.

Burn your school textbook! That's the only way it will provide any illumination. Nobody talks about peptones or uses the term proteose.

Quick Answer

Peptide refers to at least two amino acids joined by amide bonds.
Proteoses are products of acid proteolysis which precipitate with saturating ammonium sulfate.
Peptones are products of acid proteolysis which do not precipitate with saturating ammonium sulfate.
While peptide is a term of significant relevance today, proteose and peptone are anachronistic.

Long, Confusing and Out-Dated Details
The terms peptone and proteose were first used in the late 19th century, which makes finding substantive definitions, well, difficult. I refer you to the following paper (yes, 1891...). It is not the first to discuss proteoses, but I can't find any earlier ones and the explanation is quite clear (emphasis added).
Chittenden RH, Hartwell JA. 1891. The Relative Formation of Proteoses and Peptones in Gastric Digestion. J Physiol 12:12-22.

In the digestion of proteid matter by pepsin-hydrochloric acid there are three well-defined products or classes of products, viz. acid-albumin or syntonin, albumoses or proteoses, and peptones. We look upon the first as the initial product of gastric digestion and identify it by its well known precipitation by neutralization. In the filtrate, the [proteoses] can be detected... best by saturation with ammonium sulphate, while the true peptones... are found in the filtrate from the latter precipitate... True peptones are bodies not precipitated by saturation with ammonium sulphate, and are the final products of pepsin digestion.

NB: proteid = protein
So, according to this paper (and apparently "all physiologists" at the time, see below), there are three main products resulting from pepsin-acid digestion of protein:

syntonin - the initial product, precipitates upon neutralization (likely due to acid denaturation)
proteose - the main product after continued digestion, characterized by precipitation with saturating ammonium sulfate

Study of the individual proteoses formed in the gastric digestion of albumin, fibrin, globulin, myosin, casein and other proteids has seemingly already shown that these so-called preliminary bodies are the main products of the digestive action of pepsin

peptone - the final product of digestion, does not precipitate with saturating ammonium sulfate

All physiologists are presumably agreed that peptone is the final product of gastric digestion

They further emphasize that peptone is a product of continued proteose digestion:

Since the discovery of the [proteoses] and of their characteristics, frequent study of digestive mixtures has given convincing proof that in an ordinary gastric digestion of any common proteid only a comparatively small amount of peptone is formed; peptonization in the true sense of the word results only from the long-continued action of pepsin-acid, and even then complete peptonization rarely if ever occurs. The... proteoses are to be considered as the primary products of gastric digestion, while peptones are the end products of proteolytic action, the latter being formed by the gradual hydration of the primary products...

It would seem that peptone differs from proteose only in the length of its constituent peptides, with peptone containing shorter peptides due to continued proteose digestion. However, a more recent paper (with more recent meaning 1924) challenged this view and claimed that both proteose and peptone consist of small peptides which differ in amino acid composition rather than length. In their view, different composition rather than length explains their differential solubility in saturating ammonium sulfate.
Rudd GV. 1924. Proteoses, Peptones, and Polypeptides. Aust J Exp Biol Med Sci 1:187-190.

...each fraction must consist of a mixture of comparatively simple peptides, which differ among themselves in the amino-acid units of which they are constituted. The fact that some, at least, of these peptides are precipitated by ammonium sulphate shows that they belong to the group of proteoses, which therefore are partially, if not entirely, made up of simple peptides.
It is possible that the terms, "proteose," "peptone," and "polypeptide,*' will all have to be considered to apply to substances of the nature of peptides... each built up of a small number of amino-acid units and differing from each other, not so much in the number of amino-acids in the molecule, but rather in the variety of these acids. The differences in solubility in various solutions shown by these compounds are thus to be attributed to differences in their chemical constitution, rather than in their molecular complexity. If this be so, these substances would be considered, not as successive stages in hydrolysis, but as products of one completed stage, differing in their solubility's.

They also quote another paper with supporting evidence:

Fischer produced tripeptides and tetrapeptides of known composition and structure, which were precipitated when their aqueous solutions were saturated with ammonium sulphate. If these peptides were found in the solution obtained by the hydrolysis of a protein with pepsin they would be classed as proteoses.

I wasn't able to find any subsequent research. Nevertheless, such definitions from this period are based on macroscopic physical, rather than molecular, properties of the substance. This old terminology is not particularly informative in modern biology, and it would seem that they remain in use only as historic anachronisms. Today, both peptone and proteose are terms used almost exclusively when describing microbiological culture media (which dates from the period) or when making general reference to digestion products. In fact, they are often used in conjunction (ie proteose-peptone) which suggests they are now synonymous.

Let me first give the definitions of the three terms before differentiating them.
Peptide: Peptides are biologically occurring short chains of amino acid monomers linked by peptide (amide) bonds1.
Peptone: Peptones are derived from animal milk or meat digested by proteolysis. In addition to containing small peptides, the resulting material includes fats, metals, salts, vitamins and many other biological compounds2.
Proteose: any of a group of compounds formed during proteolysis that are less complex than metaproteins but more so than peptones3.
Now, peptides are the most basic components. Like proteins, they too are polymers of amino acids, the difference being that they are just shorter than the original protein which the protease acted upon.
Peptones can be considered as derivatives of peptides i.e. they also contain some other substances like fats, salts, vitamins, etc. in addition to peptide.
At last, there does not seem to be a clear definition of proteose. The only definition (that I found informative) was from Collins, according to which proteose is also derived from proteins, which are quite more conplex than peptones. Meaning, in the order of decreasing complexity:

Proteose > Peptone > Peptide

Yet, the final verdict would be that there is no clear cut difference between the three terms4. I hope this helps a bit (if not much).
References:

Peptides - Wikipedia
Payne JW (1976). "Peptides and micro-organisms". Advances in Microbial Physiology. Advances in Microbial Physiology. 13: 55–113. doi:10.1016/S0065-2911(08)60038-7. ISBN 9780120277131. PMID 775944.
Proteose - Collin's Dictionary
Proteoses, Peptones and Polypeptides, by G. Vincent Rudd


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When is an anatomic entity named "laterale" vs. "lateralis"?
I'm trying to learn the latin names of anatomical entities and I have a hard time remembering whether it's "Os cuneiforme laterale" or "Os cuneiforme lateralis".
In that case it's "laterale". But in a case like "Nervus cutaneus antebrachii lateralis" it's "lateralis". What's the logic here? How do I remember the right one?

Though I answer the "whats the logic here" part of the question in my answer, I don't really mention how to remember the right one. The simple (but awful) answer is to memorize a ton of Latin (and Greek) grammar and inflection rules and memorize a bunch of declensions ;p.

This is actually much more of a lesson in Latin linguistics/grammar.
The root, Lateral, comes ultimately from latus meaning “side" or "flank” in Latin. [Source].

By adding one of these suffixes we instead create an adjective meaning "of the side."

However, the suffixes differ in their inflection (specifically their gender):
Laterale has the neutral, singular suffix of the nominative 3rd declension.
Lateralis has the masculine, singular suffix of the nominative 3rd declension.

 Source: Wiktionary

The difference between the gender-assignment of these suffixes is due to Agreement.

[Agreement] happens when a word changes form depending on the other words to which it relates. It is an instance of inflection, and usually involves making the value of some grammatical category (such as gender or person) "agree" between varied words or parts of the sentence.

More specifically, adjectives must agree with the nouns they modify in case, number, and gender.

Let's break down each of these anatomical structures to understand the agreement-induced inflections [Source]:
os cuneiforme laterale - each of these words is neutral/singular:

os = noun, declension 3, nominative, neutral, singular
cuneiforme = adjective, declension 3, neutral, singular
laterale = adjective, declension 3, nominative, neutral, singular

nervus cutaneus antebrachii lateralis - the 2 adjectives match the  masculine/singular noun they describe:

nervus = noun, declension 2, nominative, masculine, singular
cutaneus = adjective, declension 2, nominative, masculine, singular
antebrachii = noun, declension 2, genitive, singular
lateralis = adjective, declension 3, nominative, masculine, singular

 Note: you see a shift to the genitive case for antebrachii because in this instance this phrase means "Lateral cutaneous nerve of the forearm."

Latin Linguistics  For Dummies:

Declension = category of nouns in Latin and Greek with broadly similar case formation (i.e., they are inflected/conjugated similarly).

Inflection = the modification of a word to express different grammatical categories such as tense, case, voice, aspect, person, number, gender, and mood.

Nominative = The case used to indicate the subject of a finite verb.

Genitive = The case used to express some relationship such as possession or origin. It corresponds roughly to the English preposition "of."

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Validation of houskeeping genes in a mixture of cDNAs of two species
I have a parasite sample (mixed with host blood) and I need to check gene expressions of parasite using relative quantification (RT_qPCR). For this, I need a good housekeeping gene. I chose 10 genes (suggested as housekeeping) that I need to validate and after choose the most stable one(s). My problem is that my parasite cDNA is mixed with host cDNA and it is impossible to separate them or count the parasite. I do not know how I could choose the best housekeeping gene in this case? I do not have the real amount of parasite cDNA used for qPCR, and I do not have any good internal control. Basically, it is circular problem: In order to validate my target gene I need a good housekeeping gene for internal control, but I do not have an internal control to make relative quantification of my housekeeping genes and to chose the best one. Could you please suggest any study or method that deals with such a case?

Is the parasite genome sequenced?  If so, you may be able to identify a gene that is different enough from host to parasite to design parasite specific primers?

Your qRT-PCR primers should be specific to one species or another in at least one of the housekeeping genes you choose, it's unlikely all 10 primer pairs work on both species.

Two possibilities:

Design primers based on differences in the sequences of the gene for the same protein between the two organisms. (Suggested by @Artem)
Identify an aspect of the metabolism of your parasite that is not present in the host, then use enzymes from that pathway. If the parasite is a worm and the host a mammal, for example, you should surely be able to find something.

We have primers that distinguish mouse and human Beta-Actin and GAPDH for engraftment experiments. It's not difficult to simply design primers to target one species and not another.

@Artem — Don't tell me, tell the poster in an answer. Only comment on my answer if you think there is a flaw in it, not to point out an alternative.

Because comments are not answers, and SE Biology has a specific question and answer model I have incorporated Artem's comment into my answer. This way it will be useful for anyone else with the same question. (I do not need the points that will accrue when it is marked up or accepted, which should now be done, I think.)


text:
Preserving/disinfecting meat with alcohol?
I'm considering safer ways to handle raw meat and it occurred to me that alcohol might be useful.
I'm considering, say, sealing pieces of meat in a container with 40% alcohol or higher in fridge or possibly freezer.
My question is what effects will this have on potential bacteria/parasites in and on the surface of the meat, and what will happen over time.
Different results as per higher concentrations/volume of alcohol and various temperatures are a plus.

Since, then the solution is more concentrated than the eco , osmos will take place, resulting in dehydration of cells , ultimately cells collapse.

So it will actually dry it out in the center?


text:
Can NADP be converted to NADPH using d glucose?
For one of our reaction, we require NADPH enzyme. We have NADP in our stock. Is it possible to convert NADP to NADPH using D-glucose anhydrous and if so please provide me how to go about it?

Reduction potential of NADP⁺ is -0.32 and that of glucuronic acid to glucose is 0.05. So, I guess that glucose oxidation to glucuronic acid cannot reduce NADP⁺.

@tomd you would also need the enzyme. I assumed that OP wants to use the property of reducing sugars to reduce NADP.


text:
What kind of spider is this (reddish spider)?
I just saw this spider on my door and was wondering what kind of spider this is.
information

Country: The Netherlands (Europe)
Color: quite reddish (maybe an idea why this one is reddish?)

pictures

This most likely is Microlinyphia pusilla. Note that this is a male, females look quite different. A picture that closely resembles yours can be found here

https://www.ispotnature.org/node/402405
And in case you want to know, the Dutch name is 'kleine heidehangmatspin'


text:
Sense of rotation of DNA motors
DNA motor will rotate during transcription instead of reciprocal.

What others will rotate?
Does it rotate in a fixed sense?
Why do they rotate?


text:
What is this colourful insect with a large thorn?

Someone sent me the picture so I don't have a lot of details. Is it a real insect or is it fake?

It might not be fake, it looks like a thorn bug

As @Kiritee mentioned this is actually a treehopper, due to thier unusual shape they are of long interest of naturalists.
This is a female Umbonia crassicornis.
Here's a female with her colourful nymphs captured by
C. D. S. Molinari
.

Facts:

The females have a pointed pronotal horn (spike), the males' are blunt, with a flat top.

The adults display variation in colour and size.

The pointed pronotal horn is an adaptation as the insectivorous birds mistake them as thorns (on stem) and do not consume them.

This is a variable species as to size, color and structure, particularly the pronotal horn of males (which is more angled posteriorly than the females' and often somewhat expanded apically).
This tall, essentially perpendicular thorn-like pronotum discourages birds and other predators from eating it, if only by mistakenly confusing it with a thorn.
Typically, the adult is green or yellow with reddish lines and brownish markings.
The range of this species is from Northern South America all the way to Mexico and Florida. Its preferred hosts are ornamental and fruit trees of subtropical regions.

Parental care: The females on sensing an intruder would rush to her nymphs and would charge the offender by kicking her legs, fanning her wings and sometimes even buzzing. The females communicate with the nymphs to ensure that they are in a group.
References:
Encyclopedia of Land invertebrate behaviour, Encyclopedia of Insects and Libraries of life

Picture References:

A female with eggs.
Two males (blunt top)
Original size

Good reads:

Thornbug to Thornbug-The inside story of insect song

Libraries of life (audio clips)

Your edits really elevated this answer. Nice picture :). +1.

Wow, are the wings functional?

@AntonSherwood Yes, they are. The males are detectable when they fly from one branch to the another in search of female.


text:
How thick is the neural tube at Stage 10 in a chick embryo?
As the question states - I am really struggling to find ANY website/paper/article which states this. I want to know if the neural tube is still one cell thick and stage 10 of development. Any evidence that can be supplied to show this would be useful.
Thanks


text:
What is the depression between bridge of nose and brow called?
In a human being, what is the depression often found between the bridge of the nose and the brow called?

Nasion [New Latin nāsion : nas(o)- + Greek -ion, diminutive suff.] is the region below glabella , also known as the bridge of the nose.

The nasion is the midline bony depression between eyes where the frontal and two nasal bones meet, just below the glabella.It is one of the skull landmarks, craniometric points for radiological or anthropological skull measurement.

Source:https://radiopaedia.org/articles/nasion


text:
Can you identify this wasp-like insect?
I've never seen anything like it, although I suppose it could be a wasp or an ant with wasp-like colour bands. Found in our garden today (Cambridge, UK). It's about 1.5 cm (half an inch) long.

Thanks!

It looks like the parasitic wasp, Ichneumon stramentor, as found by my amazing girlfriend, and discussed on Nature Spot (UK). And it's a female to be even more precise:

Description: Length 13 to18 mm. Female - Long tapered abdomen, first half yellow and rear half black, with yellow spot at the tip (both on the top and beneath. Legs have black femora; tibiae are half yellow blending into brown that exceeds to the tarsi. Black thorax (with yellow spot) and black head. Long dark antennae with broad white patch about half way along its length. Wings have a brownish tinge. Male has all dark antennae, no yellow spot to the tip of the abdomen. (emphasis mine)

It can be seen from April to July, commonly in meadows, hedgerows and woodland edge.
The adult wasp lays its eggs inside caterpillars which, after hatching,  eats the caterpillar from the inside. Hence the "parasitic" descriptor.
Further reading at Paul's Back Garden Safari
Wiki article on Ichneumonoidea

We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed. Besides it is good to avoid writing personal information in your posts in both question and answer on the main site.

@qris: Sanjukta is right: please add some info from one or more (reputable) source(s) providing a bit more support for your answer. We like to differentiate ourselves from most sources of species ID by providing  detailed and referenced answers.... Other than that, awesome find by your girlfriend -- wasps are not easy to ID!! :D.

Qris, I took the liberty to edit your post to bring it within site guidelines. If the edit is unacceptable in any way, please feel free to roll back. Good find!


text:
Can LSD in very small amounts increase mental ability?
Can one take a small amount of LSD(acid) and not trip but still benefit from the intended purpose? It was said the military experimented with it for extra sensory abilities. It has also been said it could increase your hearing or sight?

What is the source of this rumor? Could you link it here?

LSD was developed by the chemist Albert Hoffmann. Please have at least a look into the relevant Wikipedia article, which gives you a lot of information. It can be found here.

@Chris I have seen a documentary on it. I stated the reason it was developed. All I can site that it was om the discovery channel.

The acute mind enhancing effect of an LSD microdose is less than running off 1000 calories. LSDm acute effects are mood related, it's not racily imaginative. Einstein didn't microdose, nor do most great scientists. Physical fitness, mental effort and cerebral tasks and challenges increase IQ. Microdosing enhances serotonin and is appreciated for depression and positivity. it doesn't score for creativity. If the person has a very healthy, interesting and energetic research lifestyle, they could try a drug for imaginative dizzyness. High drug lifestyles often correlate with demotivated people.

There is no evidence so far that this is the case. Try reading https://en.wikipedia.org/wiki/Psychedelics_in_problem-solving_experiment and especially  https://peerj.com/preprints/1202.pdf

I saw a video of a woman who microdoses on TV, it was a documentary interview. Her mental clarity was... "Fucked"... she looked like she had low energy and was fairly confused and full of ticks. I understand that people dying of cancer should definitely take mushrooms one time to give them a new perspective of their mental map, but microdosing LSD is probably only good for artistic persuits and people who can't achieve high physical health through natural means.. artistic, and not logical or rigorously intelligent ones. if you want to do some surrealism and forget your keys in your car, ++lsd

Did you read about project MK-Ultra, that is when the US military experimented with reprogramming brains. https://en.wikipedia.org/wiki/Project_MKUltra

The phenomenon you are referring to is called microdosing. It was brand-new in terms of research focus when you initially asked your question, and it is still a fairly novel and little-studied subject.
A lot of interest in this phenomenon stems from anecdotal evidence by microdosing users, who report beneficial effects. This is however not necessarily an indicator of neuroenhancing potential, since psychopharmacological agents are known to modulate subjective evaluations of performance more than constrained objective measures of it (compare tables 3 and 4 in this article, which does not discuss LSD or microdosing per se, but illustrates this psychopharmacological phenomenon).
Anecdotal findings regarding LSD are substantiated in an article, which found that microdosing LSD improved the self-reported mood of participants.
Additionally, this article showed an improvement of vigour (as per the POMS scale) at the highest dose.
This is, however, still not a behavioural effect, as POMS is a psychometric assessment method.
Still, this further substantiates the mood-enhancing effects beyond direct self-reporting.
Another article reported increases in creativity, focus, and well being, though again, it should be noted that all of these metrics were assessed using participant reporting, and not evaluated based on behaviour.
So to conclude, there is to date no convincing evidence that microdosing LSD improves “mental ability”.
There is however a growing amount of evidence that LSD microdosing improves mood, which in and of itself can be a desirable effect, and can further be argued to contribute to improved “ability” in more complex behaviours such as sustained deductive reasoning or social interaction.
Conjecturing from the first cited article on methylphenidate, modafinil, and caffeine, it is conceivable that a similar effect:

In conjunction with results from neuropsychological testing we conclude that modifying effects of stimulants on complex cognitive tasks may in particular result from more reflective decision making processes. When not under time pressure, such effects may result in enhanced performance.

as the one seen with modafinil and methylphenidate could be present with LSD microdosing.
Appropriate data to address such complex evaluations is however very scant in general, and to date wholly absent for the emerging phenomenon of LSD microdosing.
TL;DR
No but maybe.

There was UK program interviewing people that microdose and they appeared slightly/considerably insane.

@LifeInTheTrees that hardly sounds rigorous. People willing to experiment with currently-unproven cognitive supplements might not appear to be the most "sane" people, even if their actual experimentation is minimal. The perceived sanity of self-experimenters in a documentary is no indicator of the pros or cons a substance might offer when used in a scientifically-optimized manner.

Aldous huxley was a famous psychadelics experimentor who took quantities that most scientists would consider high, since he was 40-50. He did appear cognitively able and a bit disctracted, fairly on the ball in his later days. Carlos Castenada, on the other hand, told one of his disciples, a little blonde girl, to drive to the middle of Mojave desert and walk to meet him in the center, after he had died, and they would both dissapear together in a ball of light everywhere in the univese, and so she go there. That is not sane advice.

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


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Is co-transport within a cell active or passive transport?
ATP is used to actively transport H+ out of the cell against the concentration gradient. The H+ & sucrose cotransporter, for example, then uses this proton gradient for transport. H+ goes back into the cell with the gradient (passively) with concomitant sucrose transport across the membrane. Is this active or passive transport?

Co-transport, also called secondary active transport, is a form of active transport because it is using the energy from one concentration gradient to transport another molecule across the membrane against its concentration gradient. The concentration gradient which drives this process requires energy to set up in the first place, which is why co-transport is considered active.


text:
Effect of cold showers after intense training
What is the effect of cold showers after very intense training (body fully covered in sweat, high pulse, increased body temperature)?
I'm especially interested in how it affects perspiration.

I haven't done a full case-control study on this but I'm pretty confident one will stop sweating a few seconds after entering a cold shower ; ) What do you mean  exactly?

I assume, because the pores close, but after the shower the body would continue sweating, at least if the temperature is still too high, I guess? Also are there any health issues involved in this delayed perspiration?

A shower is very good at transferring/absorbing heat, if anything your body temperature will cool down significantly faster in a cold shower then by sweating alone. The recommendation of cold showers/cooling post exercise has to do with reducing inflammation in the muscles.

Taking cold showers(10-15 ℃) after training or workout have many benefits:

It helps in lowering the damaged tissues temperature by constricting blood vessels.
Cold helps numb nerve endings which provides instant localised pain relief.
Brings down heart rate and increases circulation.
It minimises inflammation and help you recover faster.
It is more effective in relieving delayed-onset muscle soreness,
which generally occurs one to four days after any physical activity.
It reduces uric acid levels, so it is beneficial for people suffering from gout.
It boosts glutathione levels in the body which is a very beneficial antioxidant.

Those who should avoid cold showers:
1] Those who suffer from heart diseases as constriction of blood vessels can lead to a heart attack.
2] People having high blood pressure, because blood vessels will constrict and can reduce the supply of blood to different organs, especially the brain.
Ice bath:

In sports therapy, an ice bath, or sometimes cold-water immersion or cold therapy, is a training regimen usually following a period of intense exercise in which a substantial part of a human body is immersed in a bath of ice or ice-water for a limited duration. While it is becoming increasingly popular and accepted among athletes in a variety of sports, the method is controversial, with a risk of hypothermia, with the possibility of shock leading to sudden death. Many athletes have used cold water immersion after an intense exercise workout on the belief that it speeds up bodily recovery; however, the internal physical processes are not well understood and remain elusive. Generally research into the health effects of cold water immersion as part of an athletic training regimen is inconclusive, with some studies suggesting a mild benefit such as reducing muscle damage and discomfort and alleviating delayed onset muscle soreness, with other studies suggesting that cold water immersion may slow muscle growth and interfere with an overall training regimen.

[Source 1]
[Source 2]
You also maybe interested in:
[Question 1]
[Question 2]

References:
 - A cold shower maybe more beneficial to your fitness[Dr. Mercola].
 - Cold shower after exercise.
 - Effects of hydrotherapy on various systems of the body(NCBI)
 - The effects of cold water immersion and recovery of inflammation
 - Ice bath (Wikipedia)
 - 8 do's and don't's of Ice bath

Thx for the answer! Could you add some information on the effects of showers below 10-15 ℃? And are there any side effects, because of (possibly temporarily) suppressed perspiration due to closed pores?

Almost all of the claimed benefits you list here are unlikely to be true, even your own reference (http://onlinelibrary.wiley.com/doi/10.1113/JP272881/full) doesn't support your claim about inflamation! A Cochrane review of Ice Baths found only Delayed Onset Muscle Soreness showed any effect, and even here the evidence was weak: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008262.pub2/abstract

The claims you make may or may not be in your references, it's hard to tell since you don't link your claims to particular references, but your references are a pretty mixed bag - including a link to a site that credulously discusses Spleen Qi, for example - and the more credible of them are more skeptical.

Dr. Mercola is, at best, highly controversial and, at worst, a dangerous AIDS-denialist and anti-vaccine crank, q.v. https://en.wikipedia.org/wiki/Joseph_Mercola. I do not consider his site "credible".


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Example of invertebrates that are attracted to heat?
I would like to test a device that outputs heat in order to attract schistosome parasites in water. However, I would like to use a substitute, since I cannot find schistosome parasites for sale.
Are there any organisms that are attracted to heat and are easily accessible?

The tendency to be attracted toward heat is called thermotaxis.
Documented cases
Thermotaxis has been documented in

C. elegans

Ploff and Sokut 2010

Slime molds Meloidogyne incognita

Pline et al 1988

Drosophila

Rosenweig et al. 2004

Mosquito Aedes Aegypti

Patterson and Brown 2009

Lake sculpin (Cottus extensus) larvea

Wurtsbaugh and Neverman 1988

Mammalian sperm cells

Bahat et al. 2003

The best documentation is on C.elegans. There are probably many undocumented species that display thermotaxis but above are the only documented cases I could find.
Many of these species are easy to find in biology labs. Mammalian sperm cells are very easy to find if you are a male but it may take complex methodology to observe thermotaxis on cells. Bigger organisms are of greater interest. Drosophila might be the way to go.
Do you really need to test with another species?
Whether the test is a good idea was not part of your question but I thought I would comment on it anyway!
I am wondering whether testing your device on a different species is of much interest to you. Testing that your device creates a thermal gradient is sure of interest but one species may react very differently to a specific gradient than another one and it feels a priori to me that you'd be waisting your time by testing it on a different species.
I think it would be more interesting to just place thermometers (if you have access to good accurate thermometers) along space and measure temperature to ensure that a gradient exists and make sure that the temperatures and steep of gradient are within the range of what schistosome may experience in nature.
I am not involved in this research and you may have good reasons of yours of testing your device on a different species.


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What's this black, white and orange beetle?

Found in Toronto Canada.
Maybe 1-2 mm long but I'm not a good judge of measurements.
Should I be concerned it has friends? I've dealt with carpet beetle larvae in several homes over 7 years and an praying this isn't an adult.

Rulers are good judges of measurement ;)

Related, but no real duplicate (different species).

Yes this is an adult carpet beetle.
Specifically,  this is a Common carpet beetle (Anthrenus scrophulariae)

See here for more info.

2.5 to 3.8 mm in length.
Black head (mostly hidden by the prothorax) + black  thorax and elytra with distinct scale patterns.

The thorax is covered with white scales except for a large midline.
The elytra have orange to red scales down the midline with variable patches of white scales.

Note: in older individuals, some or all of the scales may be lost and the color pattern may look different.

This species is found worldwide.
Unlike the larvae,  the adults are primarily pollen grazers.


text:
How is sebum secretion regulated?
The principle of homeostasis in biology says that living organisms try to maintain some sort of equilibrium. Doing that requires the use of feedback mechanisms to regulate things like temperature, salinity, etc. Are there any feedback mechanisms the body uses to regulate the output of the skin's sebaceous glands? If so, what are they, and on what timescale do they operate?

Nice question! Unfortunately, the complete list of pathways involved in regulation of sebum production and secretion rate by sebaceous glands are not understood yet (Picardo et al, 2009). However, we know that sebum production is continuous and is not regulated by neural mechanisms (Thiboutot et al, 2004). Retinoids, hormones, and growth factors are known to influence sebaceous gland growth and differentiation (Zouboulis et al, 1998). Also, androgens and growth hormones are known to promote sebaceous gland differentiation (Deplewski et al, 1999, Rosenfield et al, 1998) whereas estrogens and retinoids, like 13-cis retinoic acid, inhibit their differentiation (Strauss et al, 1962).
In retinoids, isoretinoin is shown to have greater sebosuppressive action as compared to all-trans or 9-cis retinoic acid (Hommel et al, 1996). In androgens, androgen receptors have been localized to the basal layer of the sebaceous gland and the outer root sheath keratinocytes of the hair follicle, and testosterone and dihydrotestosterone are the major androgens that interact with these receptors (Liang et al, 1993). However, the molecular mechanisms through which androgens interact with these receptors and sebaceous glands are not understood yet (Thiboutot et al, 2004). Apart from this, insulin and Insulin-like Growth Factor 1 (IGF-1) also play a critical role here. Acne is considered as IGF-1 mediated disease, and high levels of sugar (caused due to diet) induce high levels of insulin and IGF-1. Both these hormones amplify the stimulatory effect of GH on sebocytes and augment mitogenic downstream signalling pathways of insulin receptors, IGF-1 receptor and fibroblast growth factor receptor-2b (Melnik et al, 2009).
Other (known) substances which are found to regulate sebum secretion include histamine (due to presence of H-1 receptor on sebocytes, Pelle et al, 2008), LXR ligands (due to presence of Liver X Receptor, Zouboulis et al, 2009), PPAR ligands (due to presence of Peroxisome Proliferator-Activated Receptor, Trivedi et al, 2006), vitamin D deficiency (Yildizgören et al, 2014), neuropeptides (Ganceviciene et al, 2009), etc. See the image below (from Makrantonaki et al, 2011) for visual representation:

In spite of this, elucidating the mechanism of regulation of sebum secretion by sebaceous glands is a difficult task since, although evidence suggests that nonendocrine factors may also be an important part for regulation along with endocrine factors, the nature of this secretion and the regulation of the secretory process seem to differ among the various types of glands which, in spite of being similar in structure, might be different in function and regulation (Thody et al, 1989).
References:
 1. Picardo, Mauro et al. “Sebaceous Gland Lipids.” Dermato-endocrinology 1.2 (2009): 68–71. Print.
 2. Diane Thiboutot, Regulation of Human Sebaceous Glands, Journal of Investigative Dermatology, Volume 123, Issue 1, July 2004, Pages 1-12, ISSN 0022-202X, http://doi.org/10.1111/j.1523-1747.2004.t01-2-.x.
 3. C.C. Zouboulis, L. Xia, H. Akamatsu, H. Seltmann, M. Fritsch, S. Hornemann, R. Ruhl, W. Chen, H. Nau, C.E. Orfanos
The human sebocyte culture model provides new insights into development and management of seborrhoea and acne
Dermatology., Volume 196, Issue 1, 1998, pp. 21–31
 4. D. Deplewski, R.L. Rosenfield
Growth hormone and insulin-like growth factors have different effects on sebaceous cell growth and differentiation
Endocrinology., Volume 140, Issue 9, 1999, pp. 4089–4094
 5. R.L. Rosenfield, D. Deplewski, A. Kentsis, N. Ciletti
Mechanisms of androgen induction of sebocyte differentiation
Dermatology., Volume 196, Issue 1, 1998, pp. 43–46
 6. J.S. Strauss, A.M. Kligman, P.E. Pochi
The Effect of Androgens and Estrogens on Human Sebaceous Glands
J Invest Dermatol., Volume 39, 1962, pp. 139–155
 7. L. Hommel, J.M. Geiger, M. Harms, J.H. Saurat
Sebum excretion rate in subjects treated with oral all-trans-retinoic acid
Dermatology., Volume 193, Issue 2, 1996, pp. 127–130
 8. T. Liang, S. Hoyer, R. Yu
Immunocytochemical localization of androgen receptors in human skin using monoclonal antibodies against the androgen receptor
J Invest Dermatol., Volume 100, 1993, pp. 663–666
 9. Melnik BC, Schmitz G. Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris. Exp Dermatol. 2009;18:833–841
 10. Edward Pelle, James McCarthy, Holger Seltmann, Xi Huang, Thomas Mammone, Christos C. Zouboulis, Daniel Maes, Identification of Histamine Receptors and Reduction of Squalene Levels by an Antihistamine in Sebocytes, Journal of Investigative Dermatology, Volume 128, Issue 5, May 2008, Pages 1280-1285, ISSN 0022-202X, http://doi.org/10.1038/sj.jid.5701160
 11. Zouboulis, Christos C. “Sebaceous Gland Receptors.” Dermato-endocrinology 1.2 (2009): 77–80. Print.
 12. Nishit R. Trivedi, Zhaoyuan Cong, Amanda M. Nelson, Adam J. Albert, Lorraine L. Rosamilia, Surendra Sivarajah, Kathryn L. Gilliland, Wenlei Liu, David T. Mauger, Robert A. Gabbay, Diane M. Thiboutot, Peroxisome Proliferator-Activated Receptors Increase Human Sebum Production, Journal of Investigative Dermatology, Volume 126, Issue 9, September 2006, Pages 2002-2009, ISSN 0022-202X, http://doi.org/10.1038/sj.jid.5700336
 13. Yildizgören, Mustafa Turgut, and Arzu Karatas Togral. “Preliminary Evidence for Vitamin D Deficiency in Nodulocystic Acne.” Dermato-endocrinology 6.1 (2014): e983687. PMC. Web. 23 Apr. 2017.
 14. Ganceviciene, Ruta et al. “The Role of Neuropeptides in the Multifactorial Pathogenesis of Acne Vulgaris.” Dermato-endocrinology 1.3 (2009): 170–176. Print.
 15. Makrantonaki, Evgenia, Ruta Ganceviciene, and Christos Zouboulis. “An Update on the Role of the Sebaceous Gland in the Pathogenesis of Acne.” Dermato-endocrinology 3.1 (2011): 41–49. PMC. Web. 23 Apr. 2017.
 16. Thody, A. J. & Shuster, S. Control and function of sebaceous glands. Physiol Rev 69, 383–416 (1989)


text:
To what extent are lifestyle factors taken into account in medical testing?
A glance at any official health bodies advice will show that we are entreated to eat more healthily, take more exercise and reduce stress. Presumably, there is some reasonable evidence that these factors play a relatively significant role in disease formation and response (otherwise, one would presume they would not be within the remit of such organisations).
In what little opportunity I've had to read primary research on medical testing, however (I'm a statistician, not a biologist), I've not come across any attempt at stratification for these factors.
If one is, say, testing the response to a new medicine, presuming these factors will promote recovery in your test subjects, then the apparent efficacy of the medicine might be affected by the distribution of these "lifestyle" factors within your test and control groups.
Similarly, on the other side of the coin, if you are testing the response to a new health threat by epidemiological study, a quoted Odds Ratio of 1.2 might be quite radically different for individuals of different general health, yet (in the studies I've read) there seems to be simply a presumption that the control group and the test group will have a similar spread of lifestyles.
It certainly seems to be a relevant factor in some cases as individuals with a history of smoking are almost always controlled for in such epidemiological studies (especially related to lung conditions), but I have never come across similar treatment of individuals in high stress jobs, eating fewer than 5 fruit and veg per day, taking less than three hours exercise a week etc.
For large effects, these factors would probably be insignificant, but where the effect is small (say a slightly efficacious new treatment, or a low risk environmental contaminant), failure to take account of these factors could theoretically lead to the conclusion that the drug is a slight improvement on what we have, or the threat requires some moderate mitigation, when if fact the drug is virtually ineffective in people who are otherwise unhealthy, or the threat is actually zero to a healthy individual, which would be really important conclusions for public health.
My limited interaction with epidemiological studies was quite a few years ago now, so my question is, have things moved on to start controlling for these factors now we have a better idea of their impact, and more significantly, if they have, have any studies from the past been revised in the light of such controls? Also, does anyone know of any accessible studies on the impact of these factors on epidemiology in general?
To clarify in the light of the close reason. The question is a single one which can be simply answered by anyone involved in epidemiology or researching pathology. Do modern epidemiological studies of disease causal factors control for lifestyle factors, such as diet, obesity, exercise and stress? The answer I'm looking for would come from someone who is either involved in epidemiological research or reads a significant number of epidemiology papers and the would at it's simplest be " Yes, they do" or "No they don't". I'm not sure how much less broad it can get.

I'm voting to close this question as off-topic because it is much better suited for Health.SE.

I don't understand why you think this question would be better suited to Health.SE. That site seems to be primarily about health questions, this question is about pathology and epidemiology research methods. Both tags exist here. If you're suggesting it's off topic simply because it relates to a health issue, then what questions could possibly fall under the epidemiology, health or pathology tags?

While it's true that the majority of questions on that site are personal medical questions, this is the kind of question they would welcome. Tags existed before Health.SE went into public beta.

A well intentioned consideration that another site might like to tackle the question, and voting to close as off-topic are two quite different things.

One of the close reasons is that 'this question is better suited to another SE site.' Not sure of the exact wording, but it is right there. I have nothing against this question; closing it would most likely lead to migration. I simply think there is a better site; both actions ate well-intentioned.

Most studies aren't large or sufficiently powerful enough to consider too many intervening factors. Only the largest trials could even attempt this. Most drug trials are basically as small as they can be, because they are 1) expensive, and 2) you are testing an unknown medication, so you don't want to unnecessarily expose patients to risks that might not yet be understood.

@anongoodnurse The answer to the question here https://biology.meta.stackexchange.com/q/3416/23094 seems to state quite specifically from a diamond mod that "Questions on medical science are on-topic here"

I disagree with the reopen, and the edit does not actually make it more specific. If you really want an answer as simple as that, it isn't really an appropriate question to ask here. The actual answer is obviously it depends: some studies will and some studies won't. Explaining all of the causes and reasons etc to make a solid answer is where it becomes too broad.

@BryanKrause I'm afraid I don't understand your comment at all. You seem to be saying that If I want a short answer the question isn't suitable for this site, but if I want a long answer it isn't suitable either. Also how does "Explaining all of the causes and reasons etc to make a solid answer" make the question too broad. To suggest that the choice to include lifestyle factor stratification in a control group is made considering reasons so vast and complex they couldn't even be summarised in an answer is ludicrous.

I worked (rather tangentially) on statistics for epidemiological studies a few years ago and in that limited experience absolutely none of the studies, no matter what size, stratified their control and test groups for any lifestyle factors, so if it's so "obvious" that some do, simply linking to one of them would have made a simple informative answer. The fact that, instead, everyone just seems to want to dodge the question has served as an answer in itself.

I wouldn't expect subjects to be stratified over lifestyle factors, since the number of groups would get prohibitively large as you add multiple dimensions of factors. However, demographic data is often included and analyzed, the whole fields of population health and epidemiology deal with these factors all the time, just not every factor in every study. Since you are a statistician, I am sure you are aware of the problems with testing too many factors simultaneously. You can design a better powered study if you focus on factors most expected to be of interest.

Testing two factors simultaneously is relatively simple, one only has to use an interactive term on one of the coefficients in a regression analysis, neither is dealing with multiple lifestyle factors complicated where the null hypothesis would be that lifestyle factors did not affect one's risk from the chemical concerned, a compound score for "general healthiness" can be used (and has been in the many studies correlating social status and health). Only if the null hypothesis is rejected would there be any interest in which lifestyle factor had most influence.

Additionally, as I requested in my previous comment, if " the whole fields of population health and epidemiology deal with these factors all the time". I really would be very grateful if you could point me in the direction of one of those many studies, that really was the point of me asking the question. You've twice asserted that at least some studies do take account of lifestyle factors sometimes and yet in my experience I've come across none that do, I'd really like to see an example of how it's done. Some links to the papers that have lead you to this conclusion would be much appreciated.


text:
Are we going against nature?
Nature selects those who leave more progeny (reproductively fit) according to natural selection. But nowadays we are going in for family planning. So are we in a way going against Nature?

I'm confused about what you're asking. Can you please clarify? For example, are you asking if we are becoming less fit?

Your brain is a product of evolution; so technically whatever you decide to do is pretty much natural. Please clarify your question or else it would be put on hold.

Are you suggesting that Homo sapien development is some form of supernatural progression?

I mean to say that nature selects those who leave more progeny according to Darwin.But as we are now going in for family planning, we are going against what Darwin said.So how will we be selected by nature and exist thereafter

I think yes. In most cases we( man ) is against the nature .

If the "more progeny" claim was true, codfish would rule the universe.  Sarcasm aside, you might note that it's SURVIVING progeny that matter.  If your species produces more progeny than can be supported by the environment (food supply &c), then most of them will die.  See Malthus.

Issue in the post
The question is based on a false dichotomy between what is natural from what is not. This non-existence of the concepts of natural vs artificial is a matter of analytical philosophy, therefore your question is non-sensical for philosophical reasons.
Some insights despite above issue
In several species that have advanced cognitive abilities, there are traditions and culture. This culture may affect the number of offspring that individuals will have. This effect exists in humans for sure. There is nothing unnatural to it (but again it depends what you want to call natural and artificial)!
In a comment you say

I mean to say that nature selects those who leave more progeny according to Darwin.But as we are now going in for family planning, we are going against what Darwin said.

There are at least 2 issues here
Misrepresentation of evolutionary biology as being Darwin's saying
Evolutionary biology is so much more that Darwin's work. Of course Darwin was a very important scientist that contributed a lot to evolutionary biology but summarizing any saying from this field of science to Darwin's saying is very downgrading for evolutionary biology.
It feels like nature is an active character
In saying nature selects those who leave more progeny, it feels like "nature" would be some kind of character that actively chooses those that leave more progeny. This is wrong. Genomes that leave on average more copies of themselves will tend to become predominant in the population. Selection is just the consequence of fitness differential and not a choice that is made by looking at fitness differences. If you are unused to the term "fitness" as used in evolutionary biology, please have a look at the wikipedia link. This term is completely different from the concept of body-building in sport.

You might want to have a look at Understanding Evolution by UC Berkeley, a free online very introductory course to evolutionary biology.

@user31223 You already accepted the answer but I would like to attract your attention to the fact that I edited the answer to add some information about a comment of yours.


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What is Genome wide analysis and Locus specific analysis
I am reading some articles on genetic variations and I see there are two types of analysis one is genome wide genetic variation analysis and second one is locus specific genetic variation analysis. I don't understand what these two, genome wide and locus specific analysis mean and what is the difference between these two analysis or why do we need both type of analysis?

Welcome to Biology.SE!
A locus (plur. loci) is a region of arbitrary size on a chromosome. A locus can be a single nucleotide or it can much larger (like $10^7$ sites).
A genome-wide analysis is therefore an analysis using the whole genome at once while a locus-specific analysis is the same analysis performed at the level of individual loci.
To make an analogy, if a genome-wide analysis is like a country-wide analysis, then a locus specific analysis is like a city specific analysis.
Without more context, it will not be possible to say more than that!

So what I understand is that, Genome wide SNP analysis means detection of SNPs in whole Genome, this gives us the location of the SNP and then this Location specific analysis is done on different people to find out if that SNP is present in certain group of people(Europe/Asian for example)?

I would need to read the paper to know what they really did but the term "locus-specific" does not mean "individual-specific" or "subpopulation-specific", it means "locus-specific", where locus is an arbitrarily defined genomic regions.


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No. of meiotic divisions to produce specific no. of seeds
If I want to produce 100 seeds. Then the no. of meiotic divisions is 125 which can be calculated by the formula x + x / 4.
x = no. of seeds produced.
How is this formula derived?

Assuming that you have studied megasporogenesis and microsporogenesis. To produce a seed, you require the production of pollen(n) and egg(n) and their fusion.
Let's start with pollen grain(n):

4 pollen grains are produced after 1 meiotic division in the pollen sacs.

$$4~\text{pollen grains} = 1~\text{meiotic division}$$

To produce 1 pollen grain.

$$ 1~\text{pollen grain} = 1/4~\text{meiotic division} $$

For production of $x$ pollen grains.

$$ x~\text{pollen grains}=x/4~ \text{meiotic divisions}\quad(1) $$
Now coming to egg(n):

Only 1 egg is produced after 1 meiotic division in the megasporangium.

$$ 1~\text{egg}= 1~\text{meiotic division}$$

For production of $x$ no. of eggs.

$$ x~\text{eggs}=x~\text{meiotic divisions}\quad(2)  $$
For production of $x$ no of seeds(2n):

$x$ pollen grains and eggs are required. No. of meiotic divisions to produce $x$ pollen grains and eggs.

$$x~\text{seeds}=x + x/4~\text{meiotic divisions} \quad\text{From}~(1)~\text{and}~(2) $$

For producing $x$ number of seeds (or say zygote) $x$ number of egg cells must fuse with $x$ number of male gametes.
In angiosperms, 1 meiotic division of Megaspore mother cell leads to formation of one egg cell.
So $x$ egg cells are formed from $x$ number of meiotic division.

But 1 meiotic division of Sperm mother cell (2n) leads to formation off 4 haploid cells (male gametes).
So by Unitary method,
4 functional male gametes are formed from 1 Meiotic division
$x$ functional male gametes are formed from 1/4 x $x$ Meiotic divisions

So total number of meiosis needed to produce $x$ seeds = $x$ + $x$/4.

Prerequisite: Knowledge about Sexual reproduction in Angiosperms (ncert)

@Mesentery It's alright.


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Why mosquitoes sit on wall vertically (head upper side)?
I was curious to know why mosquito sit on walls or trees vertically like head towards sky, unlike other insects like fly, ants, termites sit with any direction.
Also, what they do sitting doing nothing (rest/digestion may be)?


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What is this beautiful pink flower plant seen at Bodnant Gardens?

Seen at Bodnant Gardens, North Wales UK.

Please include as many details as possible. I can't tell if it's a tree, a shrub, or a tall plant. It certainly is beautiful, though!


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What do sphingolipids do in humans?
I want to know the significance of sphingolipids in human.
I have learnt that sphingomyelin is the most significant type of sphingolipid in human.
Also that the sphingomyelin serves as a structural constituent of myelin sheath of nerve fibres.
Is that all? I need to clarify this. Please help me. Thank you

cross-posted http://chemistry.stackexchange.com/questions/71897/what-is-the-significance-of-sphingolipids-in-human

It turns out sphingilipids have many functions in humans, many of which might still remain unknown. I will discuss here only the general, known functions  of sphingolipids, not about specific sphingolipids (as it'll make the answer too long).

Sphingolipids are believed to protect the cell surface from harmful external factors by forming a mechanically stable and chemically resistant outer leaflet of plasma membrane lipid bilayer.
Certain complex sphingolipids are known to be involved in cell signalling and cell recognition. It has been suggested that ceramide on the cell surface of one cell can be recognized by proteins on another cell's surface. Also, antibodies have been created which recognize the ceramide on a cell's surface1. All this suggests that sphingolipids play an important role in cell-cell interactions which lead to cell recognition and cell signalling.
Some simple sphingolipids, like ceramide and sphingosine-1-phosphate, have recently been shown to be mediators in signalling cascades involved in apoptosis2, proliferation3, necrosis4, inflammation5, autophagy6, senescence7, etc.
Ceramide-based lipids self-aggregate in cell membranes and form separate phases less fluid than the bulk phospholipids. These sphingolipid-based microdomains, or lipid rafts were originally proposed to sort membrane proteins along the cellular pathways of membrane transport8.
Studies indicate that proper sphingoid base synthesis is required to control protein phosphorylation events that are crucial for endocytosis and overexpression of protein kinase C1 (PKC1) and PKH1 or PKH2 (ortholgues of mammalian protein-phosphoinositide dependent protein kinase 1 or PDK1) restores the actin localization defects in the lcb1-100 mutant9,10. A suggested pathway representation would be like this11:

Decreased levels of ceramide and increased levels of sphingosine-1-phosphate are known to be mechanisms of tumor progression and drug resistance in cancer cells, and are hence being targeted in pharmacological experiments as possible cancer cures12.
Sphingolipid (mainly sphingomyelin, ceramide and gangliosides) reorganization and interaction with proteins within cellular membranes is suggested to cause many neurodegenerative disorders13.
Sphingolipids are also known to play an important role in microbial pathogenesis since in the context of bacterium- and virus-host interaction, the host is typically the source of sphingolipids, whereas in the context of the protozoan- and fungus-host interaction, both host and pathogen sphingolipids are involved14.
Sphingolipids also act as immune response modulators. Exogenously added sphingolipids (especially sphingosine) changed the receptor expression in immunological synapses, including CD3, CD4, CD8, CD45, CD54, etc. disrupting T-helper cell differentiation and prevelance of Th2 cells over Th1 cells. Sphingolipids activate macrophage function via elevation of receptor F4/80 expression and chemokine production. Fumonisin B1 regulates memory cell formation and secondary immune response, and inhibits the DNA synthesis in normal lymphocytes in response to mitogenes, more effective in T cells compared with B cells15.
Sphingosine-1-phosphate (S1P) level in lymphoid tissues, especially in thymus, is lowered as compared to blood. This creates S1P gradient that attracts lymphocytes and promotes S1PR1-dependent egress into the blood. When T cells are ready to exit the thymus and enter the blood, S1PR1 is re-expressed so that T cells can respond to the chemotactic effect of high S1P levels in circulation. When T cells re-enter the blood, S1P downregulates S1PR1. Increased lymphoid tissue S1P. blocks egress of lymphocytes by disruption of the S1P gradient or desensitization of S1PR1 on T cells. See the diagram below for representation16:

References:
 1. Gerrit van Meer, Sandra Hoetzl, Sphingolipid topology and the dynamic organization and function of membrane proteins, FEBS Letters, Volume 584, Issue 9, 3 May 2010, Pages 1800-1805, ISSN 0014-5793, https://doi.org/10.1016/j.febslet.2009.10.020.
 2. Hannun YA, Obeid LM (July 2002). "The Ceramide-centric universe of lipid-mediated cell regulation: stress encounters of the lipid kind". The Journal of Biological Chemistry. 277 (29): 25847–50. doi:10.1074/jbc.R200008200
 3. Spiegel S, Milstien S (July 2002). "Sphingosine 1-phosphate, a key cell signaling molecule". The Journal of Biological Chemistry. 277 (29): 25851–4. doi:10.1074/jbc.R200007200
 4. Hetz CA, Hunn M, Rojas P, Torres V, Leyton L, Quest AF (December 2002). "Caspase-dependent initiation of apoptosis and necrosis by the Fas receptor in lymphoid cells: onset of necrosis is associated with delayed ceramide increase". Journal of Cell Science. 115 (Pt 23): 4671–83. doi:10.1242/jcs.00153
 5. Snider AJ, Orr Gandy KA, Obeid LM (June 2010). "Sphingosine kinase: Role in regulation of bioactive sphingolipid mediators in inflammation". Biochimie. 92 (6): 707–15. doi:10.1016/j.biochi.2010.02.008.
 6. Lavieu G, Scarlatti F, Sala G, Carpentier S, Levade T, Ghidoni R, Botti J, Codogno P (March 2006). "Regulation of autophagy by sphingosine kinase 1 and its role in cell survival during nutrient starvation". The Journal of Biological Chemistry. 281 (13): 8518–27. doi:10.1074/jbc.M506182200
 7. Venable ME, Lee JY, Smyth MJ, Bielawska A, Obeid LM (December 1995). "Role of ceramide in cellular senescence". The Journal of Biological Chemistry. 270 (51): 30701–8. doi:10.1074/jbc.270.51.30701.
 8. Brown DA, London E (June 2000). "Structure and function of sphingolipid- and cholesterol-rich membrane rafts". The Journal of Biological Chemistry. 275 (23): 17221–4. doi:10.1074/jbc.R000005200
 9. Friant S, Zanolari B, Riezman H. Increased protein kinase or decreased PP2A activity bypasses sphingoid base requirement in endocytosis. Embo J. 2000;19:2834–2844.
 10. Friant S, Lombardi R, Schmelzle T, Hall MN, Riezman H. Sphingoid base signaling via Pkh kinases is required for endocytosis in yeast. Embo J. 2001;20:6783–6792.
 11. Rao, Raghavendra Pralhada, and Jairaj K Acharya. “Sphingolipids and Membrane Biology as Determined from Genetic Models.” Prostaglandins & other lipid mediators 85.1-2 (2008): 1–16. PMC. Web. 5 May 2017.
 12. Oskouian, Babak, and Julie D. Saba. “Cancer Treatment Strategies Targeting Sphingolipid Metabolism.” Advances in experimental medicine and biology 688 (2010): 185–205. Print.
 13. Elena Posse de Chaves, Simonetta Sipione, Sphingolipids and gangliosides of the nervous system in membrane function and dysfunction, FEBS Letters, Volume 584, Issue 9, 3 May 2010, Pages 1748-1759, ISSN 0014-5793, https://doi.org/10.1016/j.febslet.2009.12.010.
 14. Heung LJ, Luberto C, Del Poeta M: Role of sphingolipids in microbial pathogenesis. Infect Immun. 2006;74(1):28–39. 10.1128/IAI.74.1.28-39.2006
 15. Sphingolipid modulation of immune cell function: The Association of the Sphingolipidologists
 16. Maceyka M., Spiegel S. Sphingolipid metabolites in inflammatory disease. Nature. 2014;510:58–67. doi: 10.1038/nature13475.

An interesting note about S1P: it mediates leukocyte trafficking. The major source of S1P in the blood is erythrocytes. What you can imagine is a gradient of S1P exists where it's high in the blood and perfuses to the tissues. Leukocytes express an S1PR that promotes re-entry to the blood, which is blocked by known tissue retention signals such as CD69. Fingolimod (FTY720), an S1PR inhibitor, is used to prevent T cell egress from lymphoid tissues in the treatment of multiple sclerosis. You can add sphingolipids to your list as immune response modulators!

@CMosychuk thanks, thats a very nice point! But I can't add it now since I've got some work, I had to finish it up at this much...but I'll do that as soon as I get free. Thanks again :)


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How can I calculate alpha helix content from molar ellipticity?
How can I calculate the alpha helix content (i.e. percent) in a protein from a given molar ellipticity of 222 nm, without using any software. I have tried the Greenfield-Fasman equation, but the answer doesn't seems to be correct.

You can use the information at this site, especially section 3. (https://www.photophysics.com/resources/tutorials/circular-dichroism-cd-spectroscopy)
Notice the different CD spectra for alpha-helix, beta-sheets and random coil. If your protein is measured at 222nm you need to compare your measured values to the the spectra at 222nm, this will allow you to guestimate the secondary structure of the protein, but if you want to be accurate, you will need to measure at several wavelengths to determine the distribution of alpha helix, beta-sheet and random coil. This is because all three contribute to the measure spectra and as such you need several measurements to figure out the relative contributions of each secondary structure.


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Twist in the DNA double-helix
DNA, has a deoxyribose sugar — phosphate backbone with the purine and pyrimidine bases, adenine, cytosine, thymine, and guanine connected to the deoxyribose sugar. (The base–sugar molecules are nucleosides, and those with phosphate, nucleotides.) In the double helix structure of DNA the two strands are twisted and connected by hydrogen bonds between the bases.
How is this "twist" created in the cell, and why is it necessary?

@heather, you are a middle school student (therefore max 14 years old I guess), you ask a good question about molecular genetics and in the meantime you have on github some Python and $\LaTeX$ code. You also have some notes on calculus, trigonometry, Collatz Conjecture and general relativity. You also have 5.5k reputation on Physics.SE with a number of quite highly upvoted answers. I must say, I am impressed!

@Remi.b, thank you =) I just read about your research on your website, and you said that much of your work falls within the realm of computational biology - what is the sort of "standard" programming language for that? I am aware that R is used a lot for data analysis, but didn't know if that was what you used.

Let's continue this discussion in chat.

@heather I have deleted my comments and converted them to an answer. Let me know if something needs to be explained better. We can talk in chat, though I do have to leave soon.

I have cut your question drastically, replacing your query about the basic structure with a statement of fact which can be found in Wikipedia or any basic biology or biochemistry text. This allows the focus to fall clearly on the single question appropriate to this forum (and we like single questions) — that about twist. Please don’t be offended. It makes your question clearer.

First, your description is accurate. The only pedantic critique I would make is that the technical term for nucleotides in DNA is deoxyribonucleotide.
Second, I don't want to say that non-helical DNA never occurs since the structure of any macromolecule is dynamic, but I am specifically avoiding exceptions to the rule to avoid confusing the issue.
The helical structure of DNA is a low energy form which makes its formation thermodynamically favourable. Chemical bonds in DNA (and every molecule) have conformational flexibility which means that the molecule as a whole can adopt different structures. If you picture two DNA strands joined by hydrogen bonds but in a non-helical, straight form, you can simply twist the strands about their central axis to form a helical structure. This twisting is allowed because of the conformational flexibility of the chemical bonds. The helical structure is more stable than the "straight" form (because of base stacking interactions), and so it forms spontaneously. I struggled in vain to find a good animation of this, but came up short. You can skim through this video to see an example of what I'm talking about. It's subtle, but you may be able to see, or conceptualize, that as the two strands are twisted around each other, the adjacent bases in a strand come closer together. This permits stabilizing interactions between the adjacent bases which favours spontaneous helix formation (I briefly discuss this at the end of another answer).
As for how frequently the "rungs occur", this is dependent on the specific helix geometry. In B-form DNA, the geometry thought to occur predominantly in vivo, the helix completes one full turn approximately every 10.5 bases and the spacing between adjacent bases is ~3.4 Å, as shown below:

One key point for someone coming to structural biology from another disciple is to understand the basic thermodynamics underlying the concept of ‘stable’ structure. This is described in an introductory chapter of  Berg et al. online. Although it is strictly necessary to consider the entropy of the total system, in many cases the most important factor is the (Gibbs) Free Energy of a structure. If one compares two (or more) structures, the most thermodynamically stable is the one with the lowest free energy.
Factors contributing to a low free energy state in a structure (‘stabilizing it’) are presence of chemical bonds and lack of steric or electrostatic repulsion. The double-helical structure is stabilized by hydrogen bonds between the bases of opposite strands, and stacking interactions between the aromatic rings above and below one another in the helix. This is mentioned by @canadiener, although the perspective of his diagram is not optimal for showing the stacking. Frame (a) of my diagram below views the DNA helix from ‘above’ with the purine bases red, the pyrimidine bases blue and the sugar–phosphate backbone white.(Frame (b) shows the hydrogen bonds as broken lines between the bases, although the blue half does not show up well.)

The reason for the ‘twist’ that is the basis of the helix in the DNA is simply that it is part of the structure that allows the strongest hydrogen bonding and base stacking with the lowest amount of steric or electrostatic repulsion. This will be the structure with the lowest free energy.
[See also the description of the double-helix in Berg et al., which includes a diagram of base stacking. I would very much advise refering to the biochemistry and molecular biology texts online at NCBI Bookshelf for standard material rather than Wikipedia. The scholarship, refereeing and consistency of the latter are generally much higher.]

Maybe my diagram isn't optimal because someone changed the question ;). Nevertheless, good answer.

@canadianer — Whoa! I wasn't criticizing your diagram I was describing it. Your diagram isn't optimal to show the base stacking because it is optimal for showing the hydrogen bonding and other features. My diagram does not show the hydrogen bonding at all. In general one needs two diagrams to describe the structure of the DNA double helix: you provided one, I provided the other.

@canadianer — Actually your diagram does not show the hydrogen bonds, so I added a second frame.

I was just kidding. The more information the better and I like your explanation better. I just added that diagram to show the spacing between bases and the number of bp/turn.


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Positive control for microorganisms
I'm planning to test the antimicrobial activity of endophytic fungi (their secondary metabolites) against Gram-positive bacteria, Gram-negative bacteria, and one fungus (Candida).
I was wondering what could be a suitable positive control for them? One kind of control each for the Gram (-), Gram (+), and the fungus? If yes, what kind? Or is there one kind of substance that would work against them all?

Do you mean "I'm planning to test the anti-microbial acrivity"?

Yes. Sorry for that.

Streptomycin or penicillin/streptomycin, and potentially amphotericin B. If you need a penicillin-free alternative, gentamycin is a good option.
I think streptomycin is a good candidate with a broad enough spectrum to target Gram positive, negative and yeasts. You can buy from Thermo Fisher a 1000X penicillin/streptomycin cocktail that you simply add at 1X to your medium, and the spectrum is broader. Due to penicillin allergy, you may need to find an alternative. Gibco markets gentamycin in 10mg/mL and 50mg/mL formats, but I think with gentamycin you definitely want to add amphotericin B. Use the same cocktail across all three types of control.
You can even go as far as to test your antibiotic cocktail in advance, in triplicate on your strains of interest, to ensure you have a valid positive control.
I find these compounds to be quite common and so there are other anti-fungals you could use, but I can't attest to their efficacy.


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What is this insect from India called?

It was found on a roof in Jaipur, Rajasthan, North-Western India.

Can you add some more details, like its size?

It appears like a pellucid hawkmoth (Cephonodes hylas; also called coffee bee hawkmoth). This belongs to the same family as the hummingbird hawk moths.

  From wikipedia

Many photographers have misidentified this one as the hummingbird hawkmoth (See the picture and the link below. So if you google hummingbird moth india, you'll get pictures of the pellucid hawkmoth too).

  Courtesy: Nitin Prabhudesai


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Do Archaea have membrane-bound organelles?
From Campbell Ch. 6 Intro to the Cell,
Which of the following statements concerning bacteria and archaea cells is correct?
A) Archaea cells contain small membrane-enclosed organelles; bacteria do not.
B) Archaea cells contain a membrane-bound nucleus; bacteria do not.
C) DNA is present in both archaea cells and bacteria cells.
D) DNA is present in the mitochondria of both bacteria and archaea cells.
(A) is correct. My logic was that Archaea and Bacteria were originally from the same family as they are prokaryotes with membrane-less organelles. Is this thinking correct? If not, where am I wrong?

Surely the answer is C.

A) Archaea cells contain small membrane-enclosed organelles; bacteria do not.

FALSE. As you said, Archaea and Bacteria are prokaryotes: that don't have any nucleus nor membrane-bound organelles.
B) Archaea cells contain a membrane-bound nucleus; bacteria do not.

FALSE. See comment above.
C) DNA is present in both archaea cells and bacteria cells.

TRUE. Apart from some kind of viruses, all living organisms* have DNA as the support of their genome. It confirms that other choices are false.
D) DNA is present in the mitochondria of both bacteria and archaea cells.

FALSE. See comment for answer A: neither of them have mitochondria.
More info: Archaea on Wikipedia
(*) Viruses aren't always considered living organisms.