What is the normal blood water content What is the normal water volume per 1 L of blood, and how much deviation from that norm causes dehydration or hyponatremia?

The human blood contains about 45% of erythrocytes and 54.3% of plasma by volume. The plasma contains about 92% water, while the erythrocytes, about 64% by weight.

The blood is slightly less than 80% water.

Dehydration occurs when water intake is insufficient to replace free water lost due to normal physiologic processes (like sweating, urination etc). Hyponatremia is low sodium concentration in the blood. Usually, the Sodium and water concentrations in blood are regulated independently. Hyponatremia can be caused by intake of to much water, which reduces the sodium concentration.

References: The sodium, potassium, and water contents of red blood cells of healthy human adults by L J Beilin, G J Knight, A D Munro-Faure, and J Anderson, J Clin Invest. 1966 Nov; 45(11): 1817–1825.


What kind of fish is this? Spotted or largemouth? I don't know if this is a weird looking largemouth bass or a spotted bass. It was caught in southern Oklahoma. Please help! Thanks.

This looks like a spotted bass (Micropterus punctulatus).

Here's an image showing some quick differences between some common bass species:

Using the above photo and this source to guide our judgment we can see your specimen appears to:

Have a jaw that does not go posterior to the eye (as it otherwise would in a largemouth).
Have rows of pigment towards its ventral side (below the "lateral line").
Not have the typical darker horizontal line of scales characteristic of the largemouth bass .
Have smaller-sized cranial scales (those around the eye) characteristic of the spotted bass.

If you can provide additional pictures of the following, I can provide a more definitive ID:

Both dorsal fins -- if the 2 dorsal fins are connected, it would further suggest a spotted bass (as largemouth bass dorsal fins are not typically connected)
Tongue -- evidence of a tooth patch is more likely on the spotted bass.

According to the International Game Fish Association:

  Spotted bass can be found throughout the central and lower Mississippi basin to the Gulf of Mexico (from Texas to the Florida panhandle), including Georgia, Alabama, Tennessee, Kentucky and other nearby states where it occurs naturally or has been introduced.


What is the best way to orally administer a water insoluble powdered drug to macaque monkeys? They typically need to be given ~150mg, once a day, and it'll last for two weeks. The drug is very water insoluble, becomes almost like a paste, not suitable for tube feeding. And yes, this is for for real lifesaving medical research.

The best we can come up with right now is putting them to sleep, mixing the powder into Nutella, and putting it under their tongue. The idea being they'll wake up and swallow the mixture.

If it is not water-soluble (lipophobic or hydrophilic), the only other alternative would be that it is fat-soluble (lipophilic or hydrophobic). Consider adding the powder to fatty solids or liquids which can be absorbed from the GI tract into the vascular system, if that is where you'd like the drug to go to be distributed throughout the body. Ideally, you would need to look up the target concentration of the drug within the blood in order to be effective, its volume of distribution, its bioavailability, its half-life, mechanism of metabolism, and calculate from there how much you would really need in order to last the full 2 weeks.


how do they identify different protein chains? Can someone please explain how different protein chains occur exactly? I'm not talking about the side chain, but the protein chain which is typically labelled as A,B,C etc in the PDB. I'm curious as to how they are first found and what causes them? As far as I understand, the protein backbone could be in any of several conformations and each conformation has a label? Is that correct?

Chains are individual polypeptides that make up a multimeric protein complex.

  I'm curious as to how they are first found and what causes them?

SDS-PAGE will resolve all the different chains (if they are different in molecular weight). Chains are products of translation (and some modifications such as clipping and/or other PTMs etc) and they assemble to form final protein complex.

  As far as I understand, the protein backbone could be in any of
  several conformations and each conformation has a label? Is that
  correct?

Yes. The labels are assigned as per the reported conformation.

  Is one chain more common than the other? What causes translation to
  produce different chains in this case? And finally, during the x-ray
  crystallography, how do they identify them when they grow the crystal?

There can be different kinds of multimers. There can be homomultimer or a heteromultimer or a multimer of this configuration $(XX)_2$-$(YY)_2$ (a heterodimer of homodimers- just one arbitrary case) etc.
Each chain is a polypeptide and is encoded by a distinct gene. It is possible that in a multimer there are more number of a certain chain than the other for e.g. $X_3$$Y$. This is not because $X$ is produced more then $Y$ but rather because of the way the multimer is assembled.
In X-ray crystallography you basically get the arrangement of atoms. You can also understand which atom is what and similarly the termini can be found out. In any case people don't just proceed to crystallography without understanding the subunits and other biochemical properties.


Mutation-immunity in Luria-Delbruck experiment If experiments like those of Luria and Delbruck on E. coli and T1 phage are the main source of our confidence in the mutation-immunity model, is it then highly unlikely that there are other types of bacteria for which an encounter with a phage is the mutagenic (or immunity-conferring) event?

Are the two possibilities in principle mutually exclusive?

No. Surprisingly, there is an adaptive immune system in prokaryotes. This is still widely unknown. The newest review is

S. Al-Attar, E. R. Westra et al: Clustered regularly interspaced short palindromic repeats (CRISPRs): the hallmark of an ingenious antiviral defense mechanism in prokaryotes. In: Biological chemistry. 392, 4, April 2011, 277–289. doi:10.1515/BC.2011.042. PMID 21294681. (Review).

Cited from abstract:

  Many prokaryotes contain the recently discovered defense system
  against mobile genetic elements. This defense system contains a unique
  type of repetitive DNA stretches, termed Clustered Regularly
  Interspaced Short Palindromic Repeats (CRISPRs). CRISPRs consist of
  identical repeated DNA sequences (repeats), interspaced by highly
  variable sequences referred to as spacers. The spacers originate from
  either phages or plasmids and comprise the prokaryotes' 'immunological
  memory'. CRISPR-associated (cas) genes encode conserved proteins that
  together with CRISPRs make-up the CRISPR/Cas system, responsible for
  defending the prokaryotic cell against invaders.

and

  An application of the CRISPR/Cas system is the immunization of
  industry-relevant prokaryotes (or eukaryotes) against mobile-genetic
  invasion. In addition, the high variability of the CRISPR spacer
  content can be exploited for phylogenetic and evolutionary studies.
  Despite impressive progress during the last couple of years, the
  elucidation of several fundamental details will be a major challenge
  in future research.


What tree has three balls I have seen this tree in Spain and Portugal. Its leaves and bark bring to mind the American Sycamore or London Plane Tree, but not exactly. Also, it has three spherical fruits, an arrangement I am unfamiliar with. Like an idiot, I left my tree identification book at home and the Internet has failed to satisfy my curiosity in this matter. Any help would be appreciated.

As you noticed this is definitely tree from Platanus order.

The London plane which is Platanus acerifolia, which is more casual is actually a hybrid of two platanus. Those two names are Platanus occidentalis and Platanus orientalis.

Frankly, I think the one of what are you looking for is that Platanus orientalis. See it on a picture of seeds taken from Wikipedia.


Patterns/Motifs Repository I am new to this area. I am a researcher working on fast pattern searching in general scenarios (e.g., regex in string matching).

I am curious about the "regular expression (regex)" (pattern/motif) in bioinformatics. Can anyone help point out some repository where I can see some "regex" instances (used by people in real cases)?

So that I can get a sense how complex they are and the possibility to apply our techniques.

Thank you!

Regular expressions are not commonly used for DNA or Protein analysis, but many people use Hidden-Markov-Models (HMMs).

If you are looking at protein domains, you can find many HMMs here:
http://pfam.xfam.org/


Why sleep? No, actually, why wake? I was just reading the sleep threads, and I wondered, why is the body so constructed so that sleep is necessary? (Is it just a design error?) But then, how do things come to be awake at all? How did this happen? Yes, I can see the advantages, but how did it happen? What is "awake"? Are single-cell animals awake?

The question I want to ask is, how did things progress from just sitting around ingesting and growing, like plants, to being something more? Is it more? What do "wakers" have that the rest don't?

Sorry, I'm not a biologist, this may be a foolish question, or in the wrong place.

Based on various comments, I've expanded this answer. Though long, I cannot cover the depth of the topic of sleep but I tried to address the issues asked in the original question while broadly highlighting various aspects about sleep research. I welcome any suggestions for improvement.

What is sleep?

To know what it means to be awake, you must know what it means to be in a state of sleep. These are two alternative states for animals that sleep.

Finding a concise scientific definition of sleep is difficult, probably because sleep is a very complex process. For example, Diekelmann and Born (2010) state that,

  Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory...

and later

  Sleep is characterized by the cyclic occurrence of rapid eye movement (REM) sleep and non-REM sleep, which includes slow wave sleep (SWS, stages 3 and 4) and lighter sleep stages 1 and 2....

Most attempts to explain what sleep is include the four stages of sleep along with REM (rapid eye movement sleep). The stages are nicely explained by this National Institutes of Heath website on Brain Basics: Understanding Sleep. Each stage of sleep can be identified by specific types of brain waves, shown below (image from here).

Notice that the first wave pattern is characteristic of being awake.  The wave patterns change as an individual becomes drowsy and then falls asleep. While asleep, the brain cycles through the different stages, each with its characteristic brain waves.  Associated with these stages are changes in metabolic activity and physical capabilities. For example, the Brain Basics site notes that we become less responsive to external stimuli and metabolic activity slows. During REM, breathing becomes rapid and we can't move the muscles in our arms or legs. Similar states are found in other invertebrate and vertebrate organisms, which suggests that these are common indicators of sleep or a sleep-like state. Some examples of these states are given in the citations and links below.

Defining "awake" seems just as difficult as defining "asleep" but once again neural activity seems to be key indicator. As shown in the figure above, being awake has characteristic wave patterns in the brain that are distinct from the wave patterns associated with sleep. In addition, none of the physiological/physical states associated with sleep stages are present when you are awake.

In both cases, asleep and awake, the indicators seem to be based on characteristic neurological activities in the brain or, in the case of some invertebrtes, the organized nervous system.  This interpretation is important when considering whether organisms without any type of nervous system is capable of sleep or the alternate state: awake.  More on this at the end.

Why sleep?

Science magazine, in the 125th anniversary issue, made a list of 125 big questions that remain to be answered by scientists. One of those questions was "Why do we sleep?" The role of sleep remains elusive but many ideas have been put forth about the role of and the evolution of sleep. The leading idea seems to be memory consolidation. This article by Kavanau (1997) reviews ideas about the function of sleep and why it evolved.  He suggests that sleep and memory evolved as as ways to improve or maintain effective connections among the nerve cells in the brain. Some circuits are used frequently, such as those used to process sensory information like vision. Other circuits are used less frequency, such as circuits that can be used to store memories. Sleep may allow those infrequently used circuits to be activated and used without causing conflict with the circuits used during "restful waking." In other words, sleep may allow the lesser used circuits to be exercised, which can help to consolidate memories. So, at least one function of sleep may be to help maintain efficiency in how information is moved around the brain by maintaining the brain circuitry.  See also this review by Siegel (2005) and the previously mentioned article by Diekelmann and Born (2010).

This Scitable article has a nice overview of the importance of sleep for humans, as does the Brain Basics site.

What organisms sleep or have sleep-like activity?

Sleep has been well-studied in vertebrates, from fishes (Marshall 1972) to mammals (Pace-Schott and Hobson 2002). However, not all vertebrates necessarily sleep (Kavanau 1998). For example, continuously swimming fishes like some sharks and blind cave fishes may not sleep. These are just three references of many about sleep in vertebrates.

Sleep and sleep-like activity has not been as well studied in inertebrates. As noted in this thread, there is evidence for sleep in at least some insects. Cephalopods like octopuses show signs of sleep (Mather 2008). Caenorhabditis elegans, a nematode worm and model biological system, shows sleep-like states tht are similar to mammals and fruit flies (Raizen et al. 2008). The most basal organism that shows evidence of sleep-like patterns is a jellyfish called Chironex fleckeri (Kavanau 2006). Cnidarians like jellyfishes are the basal (most "simple") group of organisms with an organized nervous system. Interestingly, C. fleckeri process a lot of visual information obtained through their 24 eyes. Twelve of the eyes are simple, light-receiving structures but 8 of the eyes are camera-like, meaning they have a lens.  Kavanau (2006) argued that sleep (up to 15 hours) in this jellyfish allows time for its simple nervous system to process the visual information obtained while it is awake. The presence of sleep-like activity in jellyfish and nematode worms suggest that sleep is an evolutionarily ancient phenomenon.

This Wikipedia page on sleep in non-humans overviews evidence for sleep in vertebrates and invertebrates. It's not clear whether androids sleep or what they dream about if they do sleep.$^1$

Do single-celled organisms sleep?

This is (to me) a tricky question. Sleep is associated with specific types of neural activity in the brain or nervous system. In addition, sleep-like neural activity has been found in diversity of organisms with some type of nervous system, and seems evolutionarily old. I therefore think that any organism that has some form of organized neural center (brain, brain-like organ or centralized nervous system) has the potential to show some type of sleep-like patterns.

In contrast, organisms lacking any type organized nervous system would not be capable of sleep, at least as currently defined. If they do not sleep, then they also cannot be awake because being "awake" seems to be recognized as neural activity not typical of sleep.  Therefore, it seems to me that single celled organisms like bacteria and paramecium are neither sleeping nor awake.  Plants are neither sleeping nor awake. They are metabolically active but they are neither asleep nor awake because they do not have any type of neural activity.

I'm not a sleep researcher (but sometimes I am a sleepy one) nor am I a neurophysiologist. I just walked through my train of thought. I welcome contrary views along with the supporting science.

Literature Cited

Diekelmann, S. and J. Born. 2006. The memory function of sleep. Nature Reviews Neuroscience 11: 114-126.

Kavanau, J.L. 1997. Origin and evolution of sleep: Roles of vision and endothermy. Brain Research Bulletin 42: 245-264.

Kavanau, J.L. 1998. Vertebrates that never sleep: Implications for sleep's basic function.

Kavanau, J.L. 2006. Is sleep's 'supreme mystery' unraveling? An evolutionary analysis of sleep encounters no mystery; nr does life's earliest sleep, recently discovered in jellyfish. Medical Hypotheses 66: 3-9.

Marshall, N.B. 1972. Sleep in fishes. Proceedings of the Royal Society of Medicine (abstract).

Mather, J.A. 2008. Cephalopod consciousness: Behavioral evidence. Consciousness and cognition 17: 37-48.

Pace-Schott, E.F. and J.A. Hobson. 2002. The neurobiology of sleep: Genetics, cellular physiology and subcortical networks. Nature Reviews Neuroscience 3: 591-605.

Raizen, D.M. et al. 2008. Lethargus is a Caenorhabditis elegans sleep-like state. Nature 451: 561-572.

Siegel, J.M. 2005. Clues to the functions of mammalian sleep. Nature 437: 1264-1271.

Footnote

I could not resist.


Amino Acid requirement + intake in relation to diet + meat type I was arguing with a friend:

I said: The Yulin festivals cannot be condemned by western culture, as we also kill animals in equally cruel ways.

She said: It isn't just that the killing is cruel, but it doesn't help us, as humans do not derive the same essential amino acids from consuming these less traditional meats (e.g. dogs, cats, etc) like they would from consuming more traditional meats (e.g. cow, pig, goat, etc) She cites her father, a geneticist, as her source.

Question one:
Are my friend and her father correct? Does the consumption of a less traditional meat (e.g. cats, dogs, etc) provide fewer essential amino acids than the consumption of traditional meats (e.g. cows, pigs, chickens, etc)?

Question two:
My friend also made a comment about veganism and vegetarianism (I am a vegetarian), stating that for the same reason as her and her father's above comment, people who exclude meat from their diet need to use supplements. Is this correct, or would it also be possible to just vary diet to obtain these essential amino acids?

There is a difference between animals in their requirements for amino acids. For example, cats need high amounts of taurine (and can't make it) and when fed diets lacking enough can go blind. This is why vegans trying to feed vegan diets to their pets can be very bad for the pet. Animal proteins have sufficient taurine for the cat.

However, the meat of a cat or dog is just as a complete source of protein for humans as any other meat. All essential amino acids are there in sufficient ratios. Suggesting otherwise by her father suggests some confusion between the dietary needs of cat vs. the nutritional value of the cat to another predator.

Your second question is easily answered by looking up essential amino acids.  Wiki is plenty sufficient to get the gist Wiki Link. In short, most plants don't contain the full complement of amino acids that humans require (and can't make on their own). So to get this full complement, it requires eating multiple plant products that together contain the required amino acids.

From Harvard School of Public Health

  Protein is built from building blocks called amino acids. Our bodies make amino acids in two different ways: Either from scratch, or by modifying others. A few amino acids (known as the essential amino acids) must come from food.

  Animal sources of protein tend to deliver all the amino acids we need.
  Other protein sources, such as fruits, vegetables, grains, nuts and seeds, lack one or more essential amino acids.

  Vegetarians need to be aware of this. People who don’t eat meat, fish, poultry, eggs, or dairy products need to eat a variety of protein-containing foods each day in order to get all the amino acids needed to make new protein.


Why some muscles have more tendons than others? Very interesting examples to me are Trapezius or Latissimus - they both have places with more tendons than muscles. Taking into account that now they contract weaker and slower with all these tendons, what are the profits?

If you observe the general structure of the locomotor system, you will be able to roughly separate muscles in two main groups:

the muscles used for static work and position maintenance.
those exclusively used for manipulation of the external world.

You will also notice that most muscles with extensive tendinous attachments reside on the axial skeleton (i.e the trunk). This is because they are used for maintenance of the upright position, and examples of those are: Trapezius, Latissmus dorsi, Rectus abdominis, and many more... Given their static nature, they contain a lot of slow muscle fibers, allowing them to keep working over extended periods of time without rest. However, this does not make them weak. If the postural muscles were to have a structure similar to more peripheral muscles, for example biceps brachii, they would require an enormous number of different circular tendons extending in every direction to account for all the different body positions they act to maintain. To build a progressive example:

the biceps brachii is a fusiform muscle including two main parts. It is designed to pull hard in a limited range of movement types (i.e arm flexion). For that, it has evolved a small number of strong tendon attachments.
the serratus anterior was designed for a more extensive panel of moves. It therefore possesses several main bodies of muscles extending in different directions, with their own tendon attachment on the ribs.
the trapezius muscle has been designed to allow the head to keep its upright position (among other functions), and therefore is used as a positional link to guarantee the positional relation between head and shoulders. Its a static muscle and must be able to pull efficiently in a wide range of different directions, so its tendinous apparatus is extensive.

There are also special cases. If you take the digastric muscle of the neck for example, the tendons are used as attachments, but also as a kind of hinge to redirect the directional strength of the muscle.


How to set threshold in ImageJ for quantifying relative fluorescence? I have taken images from two different samples that have uptaken EdU during DNA synthesis (S-phase). The experiment setup is to find which condition had uptaken more EdU. Therefore I am detecting EdU with fluorescent to be able to quantify them in two conditions and compare them. The images are taken under same exposure. However in ImageJ when I want to adjust threshold I am not sure if I need to have the same threshold for both images or they can be different? Any tips are appreciated and let me know if I need to provide more info.

cheers!

You need to normalize both images to the background. This can be done in many softwares including photoshop.

When I was learning this starting to do it with something more simple like SDS page protein bands helped me a lot. The principles are the same you are still subtracting background. Look at this tutorial:

http://m.youtube.com/watch?v=JlR5v-DsTds

However, when analyzing intensity values in fluorescent microscopy the most important parameter is area of your analysis. This needs to be an objectively applied as much as possible, and that can be by increasing the number of replicates whose area you analyze. Your going to look at pixel intensities for many many cells and average those intensities. Using the imagej cell counter plug-in is helpful to see how to determine cell area.


Help me identify this caterpillar looking insect Can someone please help me identify this caterpillar looking insect from the Caribbean?

Thanks.

They look like the caterpillars of Alope sphinx (Erinnyis alope)

There is a webpage on a dedicated website here:
https://www.butterfliesandmoths.org/species/Erinnyis-alope

Among the pictures in the linked website you can find one with the green and brown morphs/stages of the caterpillars.


Why is there no U3 snRNP in the spliceosome complex of transcription initiation? snRNP U1,U2,U4,U5,U6 are present in the spliceosome but there is no mention of U3.

U3 RNA with its proteins forming a complex is localized at nucleolar. The box C'/D motif in U3 snRNA is responsible for this localization. Therefore U3 snRNA does not have a chance to go to mRNA transcription active sites. Instead, U3 snRNP play important roles in ribosomal-RNA processing.
Because of necleolar localization, U3 snRNA is called U3 snoRNA alternatively.

https://en.wikipedia.org/wiki/Small_nucleolar_RNA_U3


Do macrophages get nutritional value from the pathogens that they eat? X-posted on reddit AskScience here.

I know that macrophages engulf foreign bodies and transport them to various waste excretion pathways (sorry if the terminology is wrong), and if the foreign bodies are cellular in nature, they get trapped in phagolysosomes and get digested by enzymes.

Does the macrophage get any "nutrition" by destroying the cells, the same way that a person would if those same cells were to pass through their digestive system? Is there any chemical energy produced by the catalysis that the macrophage then uses, e.g. pyruvate for its mitochondria? Or scavenged cellular components that it can use to build its own cytoskeleton?

In this article it is described that starved macrophages 'consume' heat inactivated bacteria through phagocytosis with enhanced ability. Starving can also induce (macro)autophagy and the pathways are connected with phagocytosis,in the macrophages under investigation it was shown that autophagy did not play role in the enhanced ability of phagocytosis. The paper however does not mention anything about macrophages utilizing the resources obtained by the digestion of the bacteria. although it would seem logical. I'll keep looking.

Edit:

I found a text book that says:

  in general cells of the macrophage series have two major functions. On f their functions ,as their name ("large eater") implies, is to engulf and, with the aid of all the degradative enzymes in their lysosomal granules, break down trapped materials int ismple amino acids, sugars and other substances, for excretion and reutilization.

Source : IMMUNOLOGY A Short course 3rd edition by Eli Benjamini, Geoffrey Sunshine and Sidney Leskowitz 1996 pages 23-24. ISBN 0-471-59791-0. I only have printed copy, but I'll try to find online version.
The other function is antigen presenting.

Thus I can say that yes macrophages and other cells do utilize resources from digested pathogens.


Do non-human animals suffer from insomnia? And how do we know whether they do or not?

§

If sleep is a physiological need, it seems weird that we become unable to fulfill on demand even in the absence of any obvious physical issues. We would all probably would like to be able to fall asleep on demand on a long flight and we all know this can be hard even when we are tired.

Thus, my question is whether this is a mostly human dysfunction or a common animal property.

Insomnia most certainly occurs in other animals. One interesting example is the case of insomnia in Drosophila melanogaster. In this study 3 day old male and female flies that demonstrated reduced sleep time were crossed together over 60 generations to create flies insomnia-like (ins-l) that sleep less than 60 minutes a day compared to 800 min a day in their control flies, which are generation 0 (Fig 1B). These (ins-l) flies exhibited difficulty initiating sleep, maintaining sleep and showed cognitive impairment. They also had difficulty maintaining balance with elevated levels of triglycerides, cholesterol and fatty acids and although their core molecular clock remained intact, ins-l flies lost their ability to sleep in constant dark. Using whole-genome transcriptome profiling using Affymetrix high density nucleotide microarrays, these flies are compared against the control flies and many genes were over-represented (changed in expression compared to control flies) which are involved in metabolism, neuronal activity, behaviour and sensory perception with changes in lipid metabolism and synaptic transmission being consistent with increased adiposity and learning defects in flies. In addition, these ins-l flies were hyperactive and hyper responsive to environmental simulations and the over-representation of genes associated with sensory perception suggests that hyperarousal in insomnia may be attributed to increased activity in the sensory system and that these processes are under genetic control. Two genes in particular Filamin-A (Cheerio) and Malic enzyme (Men), which were found to be differentially regulated (changed in expression) in files are also modulated (changed) by sleep loss in humans, showing that the same processes are involved/get effected in humans and flies during insomnia.

The research above clearly demonstrated the genetic regulation and effects of insomnia in other animals and shows that its not just a human dysfunction.


How could humans have interbred with Neanderthals if we're a different species? To be clear, I'm not doubting that homo sapiens and homo neanderthalensis did interbreed: of that much I'm convinced.

Within the past few years I've seen an upcropping of pop-sci articles discussing the interbreeding between pre-historic species of humans. In everything that I see in these articles, as well as in scientific literature (my college Bio textbook, among others), I see these different humans being referred to as separate species.

This conflicts with my understanding of a species. Given the following definition, wouldn't homo sapiens and homo neanderthalensis be the same species?

  A species is often defined as the largest group of organisms where
  two hybrids are capable of reproducing fertile offspring, typically
  using sexual reproduction.  ~Wikipedia

Is this definition incorrect?
Are the publications using "species" colloquially, as opposed to scientifically?
Is "species" still a poorly defined concept? (see Ring Species)

Thanks!

Short answer
The concept of species is poorly defined and is often misleading. The concepts of lineage and clade / monophyletic group are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.
Note that Homo neanderthalis is sometimes (although it is rare) called H. sapiens neanderthalis though highlighting that some would consider neanderthals and modern humans as being part of the same species.
Long answer
Are neanderthals and modern humans really considered different species?
Often, yes they are considered as different species, neanderthals being called Homo neanderthalis and modern humans are being called Homo sapiens. However, some authors prefer to call neanderthals Homo sapiens neanderthalis and modern humans Homo sapiens sapiens, putting both lineages in the same species (but different subspecies).
How common were interbreeding between H. sapiens and H. neanderthalis
Please, have a look at @iayork's answer.
The rest of the post is here to highlight that whether you consider H. sapiens and H. neanderthalis to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.
Short history of the concept of species
To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see Aristotle and Plato's thoughts). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.
Charles Darwin already understood that as he says in On the Origin of Species (see here)

Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.

You might also want to have a look at the post Why are there species instead of a continuum of various animals?
Several definitions of species
There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".
I will below discuss the most commonly used definition (the one you cite) that is called the Biological species concept.
Problems with the definition you cite

A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.

Only applies to species that reproduce sexually
Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.
In practice
In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.
How low the fitness of the hybrids need to be?
One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?
Type of reproductive isolation
We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see wiki). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:

Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?

Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?

Under what condition is the hybrids survival and fertility measured
Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?
Ring species in space
As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post Transitivity of Species Definitions). Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
Species transition through time
Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.
Practical issue - Renaming lineages
How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.
Time
Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.
Special cases
When considering a few special cases, the concept of species become even harder to apply.
The Amazon molly (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (Kokko et al. (2008)).
In an ant "species", males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (Fournier et al. (2005)).
Bias
It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this TED).
So why do we still use the concept of species?
Naming
IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.
The alternative use of the concept of lineage
It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.
In consequence
In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).
Homo lineages
I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the Homo sapiens and the Homo neanderthalis lineages. The issue is a matter of the definition of species.
Video and podcast
SciShow made a video on the subject: What Makes a Species a Species?
For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at podcast.unil.ch > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon

Here is a related answer


"50% of the variance in antisocial phenotypes is the result of genetic factors" means what? How can i understand the following sentence:

  Overall, the conclusions reached by these studies have been highly consistent in showing that approximately 50% of the variance in antisocial phenotypes is the result of genetic factors.

Is it saying genetic factors have a weight of 50% in the total influences on antisocial behaviour?

Source: "Natural born killers: The genetic origins of extreme violence" by Christopher J. Ferguson , Kevin M. Beaver

In a population the phenotypic variance can be caused by several underlying variance including the variance in the environment and the genetic variance (among others). The fraction of the phenotypic variance that is caused by the genetic variance is what we called the heritability in the broad sense. The fraction of the phenotypic variance that is caused by the additive genetic variance is what we called the heritability in the narrow sense.

So the sentence

  50% of the variance in antisocial phenotypes is the result of genetic factors.

can be rephrased as

  Antisocial phenotypes have a heritability of 0.5.

The concept of heritability is useful as it gives us an idea of how well selection can act on the changing the frequency of phenotypic traits in the population (see How to interpret the breeders equation?). Please have a look at Why is a heritability coefficient not an index of how “genetic” something is? for more information.


What kind of house plant is this? This is a house plant I have that I love but I don’t know what it’s called. I’d love to research it and even buy more but it’s name is a mystery. Picture taken in Ontario, Canada.

It looks to be a Clivia; The English common names are Natal lily or bush lily.

It's a plant that comes originally from Africa but it now commonly sold as house plants.

The Wikipedia article give a good information about that plant.

Example:

Picture taken from this site.

You have also to notice this is a toxic plant and to keep away from small children or pets.


What is this hairy, striped orange-black caterpillar? There are so many these hairy, striped orange-black caterpillars in my backyard.

What are these caterpillars? Are these dangerous?

It's a woolly bear caterpillar which will later grow to become Isabella tiger moth.


How is it decided what type of food we want to eat? How is it decided what type of food we want to eat? For example, sometimes you would like to eat some sweets but not a full meal, other times you'd like to eat some fruit, sometimes not and so on.

I have read somewhere that organism can detect whether we are hungry or not and it gives the effect so that we feel that we are actually hungry. But the question is: is there something that measures for example what is level of glucose or aminoacids or some fats in blood and specifies not only whether we are hungry or not but also what type of food we should eat to replenish lacking resources?

I'm no biologist but here are two answers to your multidimensional question. "How is it decided what type of food we want to eat?"
There is new research into neuroscience and microbiological science about a phenomena where bacteria in our gut that produce vitamins and digest things that we cannot digest, contribute to the choices we make for our diet. Don't ask me how, but from my understanding they must somehow communicate with the brain to release dopamine while stimulating neurons responsible for choosing a certain food to crave. "Is there something that measures for example what is level of glucose or amino-acids or some fats in blood...?" Well yes actually, let's take the pancreas for example. It knows when blood sugar is high from digested materials and will begin to produce insulin. I won't go much further because already there is a response based on the detection of sugars. Your entire digestive tract is based on these detective processes in order to appropriately digest and react to digested material. Are there processes that tell your brain what to eat next? Well besides the bacteria, there are plenty of hormones produced by your gastrointestinal tract such as Ghrelin which is the most common "hunger hormone" and is responsible for homeostasis aka energy regulation/distribution throughout your body.

It's better not to ask how but to ask why when researching topics similar to this, the how is almost always provided. I'm not entirely sure how those hormones communicate with the brain, my knowledge of the brain is less biochemical and more neurological (e.g. neuron formation).


Agony, Hydrophobia and viruses in the light of evolutionary principles I'm undergraduate physics student, but I've always been interested in biology. So I have a couple of questions about an application of the evolutionary principles to practice.

Agony as the last stage of dying.
Hydrophobia as symptom during Rabies.

Now I'm going to clarify what exactly I do not understand. In the first case it's not clear for me how this mechanism helps to survive, how it can help at all? In the second case it's not obvious why this virus causes such a symptom. As I think virus always create favorable environment for himselve (for reproduction). But how could water prevent it?

The hydrophobia symptom is most likely a bi-product of the effects the virus has on the brain and not an evolutionarily derived strategy to create an appropriate environment to reproduce in. Just the same as other symptoms the infection causes, like fever for example, is a reaction the body has to the presence of the virus and not something the virus is doing on purpose to set up a better environment.

A bit old, but check out [1]: "Hydrophobia may represent an exaggerated respiratory tract irritant reflex with associated arousal potentiated by the selective destruction of brain stem inhibitory systmes."

So basically the virus is indirectly causing a fear of water. The destruction of brain cells and inflammation caused by the presence of the virus in the central nervous system cause a reflex in the respiratory tract which manifests as muscle spasms and renders the patient, who is already pretty out of it at this stage, unable and very unwilling to drink any fluids [2].

[1] http://europepmc.org/abstract/MED/982512 (Warrell DA, Transactions of the Royal Society of Tropical Medicine and Hygiene [1976, 70(3):188-195])

[2] http://publichealth.lacounty.gov/vet/rabiesmanual/clinical.htm


Black insect with antennas and large abdomen I found this insect crawling outside near my house, and I have never seen anything quite like it!

It was found in the summer in Denmark.

Length is approx 4 cm (1.5 inc) with the antennae.

What species is this insect from and what is the insect called? Is it rare? What caused it to have such a large abdomen?

What species is this insect from and what is the insect called?

This is a Meloe proscarabaeus, most commonly known as a black oil beetle. Looking at the antenna of the insect in your provided image, it's clearly a female.

M. proscarabaeus

Males have a "kink" in their antennas, females don't.

  What caused it to have such a large abdomen?

The primary reason/cause for the large abdomen is eating. Initially, the abdomen is much smaller, but after eating it will rapidly swell. Another cause for such an abdomen is pregnancy.


Why is your taste affected due to sinuses? I heard someone say "My sinuses are acting up, I can't taste the food." I don't think the person is lying, they probably believe this but I'm having trouble seeing how the sinuses would affect the taste buds. I realize smell helps identify foods, but it seems like not smelling a food wouldn't affect taste so severely as people make it sound.

I don't have sinus troubles much and haven't experienced this, so I'm not claiming it's fake, I'm just curious to understand how that works.

The first thing which is important to note is the difference between taste and flavor.
Taste refers to the chemical sense performed by taste buds present on the tongue, and to date there have been identified 5 tastes: sweet, bitter, sour, salty and umami. Thus I understand obstructed nose and sinuses should have no significant effect on taste.
Flavor, on the other hand, is the final sensation that conveys the information about the food we're eating, and involves not only taste, but also smell, mechanical sensation (like that smooth flavor from cream) and pain and temperature pathways (hot and spicy food, like peppers). Part of the signals from all these receptors located on the mouth (and nasal) cavity ultimately converge to the same location in the brain, where they are processed to create the final flavor (I know taste and smell do converge to the same region, cannot tell the others with full certainty).
So, having obstructed sinuses and nasal cavity can interfere with the smell detection (by not allowing molecules to bind to receptors on the olfactory epithelium), and thus interfere with flavor.

You can check this site which I think explains very well what I am trying to pass on, it is very clear and covers all the physiology that I talked about, allowing you to go deeper into details if you are interested: http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/taste.html and also http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/olfact1.html (you have to scroll down to the main text)


Death because of distilled water consumption One of my friends said that I would die if I drank distilled water (we were using it in a chemistry experiment) I gave it a go and surprisingly did not die.

I did a bit of Googling and found this

It said that drinking only this kind of water could definitely cause death, as distilled water was highly hypotonic and it would make the blood cells expand and finally explode and ultimately cause death.

I wanted to know exactly how much of this water on an average was needed to be consumed to cause death.

I'm extremely skeptical of @leonardo's answer.  I suspect that what would happen if you drank only distilled water is nothing perceptible.  The only place where concentrations of distilled water would ever be high enough to conceivably matter is in the tissues of the mouth and throat, and even there, the effect would be temporary.

Compare drinking 8 glasses of either distilled or tap water every day.  With tap water, you're looking at less than 200 ppm of Mg, Na, K, and Ca combined.  That's less than 400mg of total mineral content per day.  Given that the combined RDA of all of those minerals is on the order of 7g for an adult male, this is not nothing, but it's certainly small.  Your dietary intake of these minerals probably varies by more than this daily, and your intestines, kidneys, sweat glands and mineral storage organs (like your bones and muscles) are constantly maintaining the mineral blood levels within a very narrow range, despite handling a throughput of several pounds of water and food daily.  They might have to work slightly harder to manage this range if you drank nothing but distilled water, but in a healthy adult, normal intakes already vary by more than this amount without major problems.  For example, the average American consumes more than 3.4 grams of sodium daily, while a low-sodium diet is on the order of 2g.  Low-sodium diets have been widely studied in the medical literature, and are considered safe.

As for pH, the lowered pH is caused by increased carbon-dioxide absorption to form carbonic acid.  Just as carbon dioxide is more soluble in distilled water, it is less soluble in stomach acid, and may be burped out.  Would you die of acidosis from drinking seltzer water all the time?  If that were the case, I'm sure there would be big health warnings about drinking soda, while it seems relatively benign. Furthermore, your body produces and excretes (through the lungs) around 1kg of CO2 daily, dwarfing any extra CO2 you might get by drinking distilled water.  If the small amounts of CO2 found in distilled water were dangerous, jogging would be invariably fatal.

If you were to drink nothing but distilled water, and eat no food, you probably would die of hyponatremia within a few weeks.  But you would also die of hyponatremia if you were to drink nothing but tap water, though perhaps slightly more slowly.


Species Identification : Worm like insect but broad at back Can anyone help me identify this insect

Location: Southern India

Size: About 2cm

It looks like a worm but has a broad back, it seems like (not very sure) it tucks it's thin head inside the broad shell like body to ward off.

Here is the picture,

That actually looks like some sort of caddisfly larvae in its case to me.

Are you sure that's it's 'body' & not a case?

Did you find it in water?

Or a Case Bearing Clothes Moth (Caddisfly are closely related to moths).

This one (a clothes moth larvae) looks very similar to your image.


Is it more likely to develop a throat-ache at night? I have noticed that I rarely develop phlemmy throat-aches in the daytime, but often notice them after I have been sleeping.  Is this a recognised phenomenon?  Could it be because viruses or bacteria aren't being flushed out by food, water and vibration of the throat from speaking or that one's immune system is lower at night? If it is the latter, why is this?

It's because your mouth and tongue are stationary at night, so you don't move the slowly-drying saliva around to lubricate tissues. The mucous tissues dry out, resulting in greater friction with muscle movements (like swallowing), and your body is slightly dehydrated after 6-10 hours without water. If you've ever undergone surgery where they intubated you (stuck a tube down your throat to ensure air supply), afterwards it's a very similar feeling to waking up with a soar throat because your throat dries up and the anesthesia prevents muscle movements.

Your immune system actually works better at night and requires rest to work efficiently. Bacteria and viruses don't really care about the time of day, although the muscles of the larynx do ensure that the mucous layer is continuously circulated. The continual circulation helps prevent debris and bacteria/virii from establishing themselves, although the magnitude of the effect isn't on the same scale of other tactics taken by your body.

Several factors can affect mucous/phlegm/saliva production - including infections, hydration levels, environmental temperature, smoking habits, diet, environmental humidity, and lots more. If it's a constant trouble, you can try drinking more water during the day, a steam humidifier, or talking to your doctor.


What is this beetle? Found in heather in snowdonia We were walking in the hills of snowdonia the other day and my girlfriend found this in the heather:

I've never seen anything like it. Can anyone identify it? It was the biggest beetle I've ever seen.

I believe it's the Violet Ground Beetle -
Carabus violaceus. This is a close relative to the Carabus coriaceus posted by Jon.

The purple colour is a give away, but as in many insect groups there are often very similar species. As pointed out in the comments to this anwer, this is the case for C. violaceus and C. problematicus (differences)

There are websites  like observado.org where sightings can be added as a species or for instance "unknown beetle", where they are reviewed (depending on the availability of the volunteering experts) or identified.


Why didn't the human Cerebrum evolve to have granule cells like the Cerebellum does? The Cerebellum is much smaller compared to the Cerebrum yet it contains more than half of the total neurons contained in the brain.

That's mainly due to the granule cells in the Cerebellum which allows it become so densely packed with neurons.

But why is the Cerebrum not like that? Why isn't it as "compressed" as the Cerebellum? Doesn't it make sense for it to be more smaller and compact?

By "cerebrum" I assume you really mean the cerebral neocortex, since the cerebrum includes other subcortical structures that themselves are quite distinct (e.g., the basal ganglia).

Simply, the neocortex and cerebellum have completely different functions. The cerebellum performs a particular class of computations that are very different from the variety of computations performed by the cerebral cortex. They have completely different laminar structures, with neocortex being a ~6-layer structure, the cerebellum has just 2-3. There are a much higher diversity of connections and cell types in neocortex compared to cerebellum.

It seems like an optimal configuration for the cerebellum is a very high cell density. More cells doesn't necessarily mean "better", because the more cells you have the less space you have for connections. There is no unused or empty space in the neocortex: if you packed in some more cells you'd have to lose something else.

Doya, K. (1999). What are the computations of the cerebellum, the basal ganglia and the cerebral cortex?. Neural networks, 12(7-8), 961-974.


Cyanobacterial photosynthetic oxygen yield I am somehow not convinced that biotic factors are solely responsible for creating 21% of atmosphere (around 40 million moles of oxygen).
There may be additional issues here. Since cyanobacteria produced oxygen, it should have developed antioxidant machineries. By the time cyanobacteria flourished, some dependent heterotrophs must have evolved and they also would need antioxidants, as they are expected to thrive in close proximity to the autotrophs. There is a likelihood that aerobic respiration co-evolved with biotic oxygenesis. This would have further delayed the build up of oxygen in the atmosphere.

Does anyone have an idea of what is the photosynthetic oxygen production rate per gram biomass of cyanobacteria? Since photosynthesis must have happened mostly at the surface of the water (limnetic zone), the total biomass would be restricted. Then it might be possible to calculate the time required to achieve the oxygen levels of 21%.

This measure can indicate whether the current theory is plausible or not.

This is a study on the O2 production rate of one of the fastest growing species of cyanobacteria. The theory is not just someone's idea, it's a conclusion made from trends which were discovered during the course of conducting countless experiments.


Will modern-day insects grow to massive size in a high-oxygen environment? It's a reasonably well-known fact that insects grew to massive sizes due to the excessive concentration of oxygen in the prehistoric-Earth's atmosphere.

If one were to try to recreate this high-oxygen environment in a lab setting, would insects reared within grow to massive size?

While @CalendarJ comments "Yep!" above, a quick search suggests that experimental hyperoxia typically only increases insect body sizes slightly. Everything below is from VandenBrooks et al. 2012 (of course there could be other sources that contradict this!)

  A few beetles have been reported to reach larger sizes when reared in hyperoxia, but most of the species examined reach similar body sizes in 40% oxygen as in normoxia (Harrison et al. 2009).

and:

  Here we investigated the impacts of Paleozoic oxygen levels (12–31%) on the development of Blatella germanica cockroaches. Body size decreased strongly in hypoxia, but was only mildly affected by hyperoxia.

and this figure:

These results show that male cockroaches grow much larger under present-day (normoxic; 21% oxygen, highlighted box) and elevated (hyperoxic; >= 24% oxygen) levels than under low (anoxic; 12%) conditions, but the hyperoxia-grown roaches are only a bit larger than normoxia-grown ones. (Similar results for females not shown.)

VandenBrooks, John M., Elyse E. Munoz, Michael D. Weed, Colleen F. Ford, Michael A. Harrison, and Jon F. Harrison. “Impacts of Paleo-Oxygen Levels on the Size, Development, Reproduction, and Tracheal Systems of Blatella Germanica.” Evolutionary Biology 39, no. 1 (March 1, 2012): 83–93. https://doi.org/10.1007/s11692-011-9138-3.


If the body continuously produces new sperm, how is there room for it? If you never ejaculated, how is there room for the constantly generated new sperm? I mean, is there always room for more?

Your testes are a sort of waiting room where sperm hang out, and if ejaculation does not occur, they eventually die, just like red blood cells (or any of your body's cells). Once cells in your body die, they are broken down, and your body uses the components and nutrients to create new cells.

So it's a continual cycle of replacement and death.

Read more here


Which cryogenic vials and caps are ideal for storing glycerol stocks? There are internally threaded, externally threaded, natural caps. For the vials, there are skirts, star-footed, and various bottoms. Why do any of these things matter?

For any kind of frozen cell stock (for cell culture or bacteria) we routinely use freezing vials similar to these: http://www.sigmaaldrich.com/catalog/ProductDetail.do?D7=0&N5=SEARCH_CONCAT_PNO%7CBRAND_KEY&N4=V9255%7CSIGMA&N25=0&QS=ON&F=SPEC

These tubes are internally threaded with a rubber grommet to seal the lid and make the tube air and water tight. I suspect the air tight seal prevents condensation from entering the tube and freezing within the tube, but I've never had a problem with either choice of tube.

The tubes don't really matter at -80 C for a glycerol stab. Freezing cells in liquid nitrogen on the other hand has a huge impact when storing in liquid nitrogen. Some tubes are meant to be stored in the liquid versus the vapour phase of nitrogen and not matching the tube to it's intended storage condition can result in explosion of the tube.


What is this insect, the bite of which is causing deaths? This insect is currently found in Kolkata, and in many parts of West Bengal, India. Its bite results in a fever, and if not treated immediately, the victim dies. This is the insect:

It seems that the insect belongs to the family of spiders due to its eight feet. But I can't conclude any more. Does someone know what this insect is, and how to be safe from it?

You were right to suspect arachnid. Its a red clover mite. But they normally don't bite humans or cause diseases. Could you post some links to news articles talking about the disease?


Somatosensory System I have a test in my upcoming Neuroscience class, one of the items on the study guide is:

Identify 2 means by which a maintained, constant stimulus produces only a transient excitation of the Pacinian corpuscle (phasic receptor). How does adaptation occur?

I would consider physical filtering properties of the corpuscle sheath as well as adaptation of the neuron or downstream targets.


Why my proteins are migrating like this on SDS-page? I'm trying to make a SDS-page of total proteins extracted from algae but I'm encountering two problems. First, when I depose my proteins in the wells the sample goes down and then it starts to move up the sides of the well. Second the result of my run looks like this:

so my bands are not visible and I have like a vertical smear on the sides of the lane.

The buffer used to extract proteins contains Tris, NaCl, EDTA DTT and Glycerol and my loading buffer is a 5x commercial dye with B-mer.

Thank you!

It's a guess, as I haven't run a algae sample on SDS-PAGE, but your migration problems might be due the algal polysaccharides that are present in your sample. Check if your protein purification protocol is specific for algal proteins and see if there is any step dealing with the algal polysaccharides.


How can hyperthyroidism induce osteoporosis? It says in my physiology notes that hyperthyroidism can cause osteoporosis.

I've been trying to figure out how this could be possible for a little more than an hour now. Every article that I look at seem to agree with the fact, but I can't find the explanation as to why it is that way.

In MarieB, it says T3 and T4 favor bone growth. Calcitonine also favors bone formation.

How can.... too much of an hormone that favors bone growth, cause bone resorption?

T3 stimulates osteoclast formation. Osteoclasts are cells that break down bone tissue. They are essential for bone growth in children, because they allow bone remodelling. However, elevated stimulation of osteoclast formation leads to osteoporosis in adults, where bone remodelling is not necessary.

In hyperthyrodism, T3 levels positively correlate with levels of calcium ions in blood, which confirms the break down of bone tissue. Calcium ions are then excreted in urine, because they cannot be efficiently reabsorbed. This constant loss of bone tissue cannot be reduced with high calcium diet, only by drug treatments that affect T3 levels.

Definitely can recommend further reading, especially regarding different types of thyrodism:

DOI: 10.1002/jcp.20041


How to find sequencing data of a specific drosophila strain I'm trying to correct low coverage parts of an assembly of these PacBio reads with Illumina data. According to PacBio they "have sequenced adult males from a subline of the ISO1 (y; cn, bw, sp) strain of D. melanogaster.  This is the same stock used in the official BDGP reference assemblies since the first genome sequence release in 2000."

Unfortunately the Illumina data sequenced by the same guys (also  ISO1 (y; cn, bw, sp) but 2057) "revealed significant differences" to the official reference strain. Something I found out as well.

Now I'm trying to find Illumina data for the reference strain at NCBI, but I'm pretty lost. There seem to be dozens of different strains and I can't figure out which one is the reference strain, mostly because I'm completely unfamiliar with the biological nomenclature like ISO1, (y; cn, bw, sp) and 2057 or D8, D20-C2, mbn2 and so on.

So I guess my question is: What strain exactly is the drosophila melanogaster reference strain used in BDGP and how do I find SRA data of this strain on NCBI?

As described in File S1 of Gutzwiller et al (2015) the relationship between the sub-strain of the ISO1 reference strain used by BDGP for the original Drosophila genome proejct, and the sub-strain in the Bloomington Drosophila Stock Center is complicated:

  "We investigated the cause of the discrepancy of Wolbachia sequences in the Berkeley Drosophila Genome Project (BDGP) and Bloomington Drosophila Stock Center (BDSC) ISO1 genomic data by first establishing the provenance of these lineages. As documented in the BDSC database, the BDSC ISO1 sub-strain was donated directly to the stock center by Jim Kenni- son in 1994. The ISO1 sub-strain used by the BDGP was obtained from Gerry Rubin’s lab in the late 1990’s (Roger Hoskins, personal communication). The Rubin lab ISO1 sub-strain was obtained in the mid-1990s from Jim Kennison via at least one intermediate lab (Todd Laverty, personal communication). Thus, in contrast to naive assumptions, the ISO1 sub-strain at the Bloomington Drosophila Stock Center is neither a direct descendant nor progenitor of the ISO1 sub-strain used in the D. melanogaster genome project, and these two sub-strains have had independent trajectories since at least 1994."

The PacBio dataset you refer to was generated using the BDGP sub-strain. The Illumina data you refer to was generated using the BDSC sub-strain and is available here: https://www.ncbi.nlm.nih.gov/sra/ERX645969[accn]


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


Recording policies in functional magnetic resonance imaging Assume that the areas in a single-subject's brain that are involved in solving a task are supposed to be visualized with fMRI. The dynamics of the task solving process shall not matter (which areas are active first, which second?).

  How, i.e. by which policy, are the data collected to give the final image?

I believe to have understood that data are collected per slices (of some millimeters thickness) and later postprocessed to give the final image.

For the sake of definiteness, let $T$ be the overall time it takes to complete the task (e.g. 10 seconds). Let $t$ be the time it takes to simultaneously take the BOLD data of one slice (e.g. 100 milliseconds). Let $N$ be the number of slices to be recorded (e.g. 20). Let $n$ be the minimal number of recordings of one slice that is necessary for statistical analysis ($n=?$). So there are $N n$ recordings of slices necessary which takes $N n t$ milliseconds, if only one slice could be recorded at once. If $T$ is too short, the experiment would have to be repeated $N n t/T$ times to get all of the required $N n$ slice recordings.

If $m$ slices could be recorded simultaneously, a single run of the experiment would suffice, when $m > N n t/T$.

  In any case: In which order are the slices to be recorded chosen (in
  case they cannot be recorded all at once)?

Possible policies:

always from top to bottom (along the z-axis) in time $T$?
repeatedly from top to bottom in some time $T'=T/k < T$?
alternating between top-bottom and bottom-up in repeated experiments?
in a random order?
in an order informed by knowledge of the stages of the task (when different slices are primarly active at different times during the task)

Or is my picture of the recording process all too naive? Or is the question somehow meaningless (for reasons I do not see, but would like to learn about)?

If I recall correctly, in BOLD fMRI an echo-planar imaging (EPI) sequence is typically used. In one example:

  44 slices were acquired, every 3 seconds, 96 times in a row, leading
  to a total number of 4,224 images acquired in 4 minutes and 48
  seconds.

— https://www.imagilys.com/functional-MRI-fMRI/

You can read more about EPI here. I think you will find the zig-zag pattern in this link interesting. See also this link for a description of EPI.

fMRI is slow and has a low temporal resolution, because the hemodynamic repsonse of the blood is around 6 second long. This is perhaps a limiting factor for fMRI, which is why there is a limit to optimizing the sequences. However, one real impact of faster sequences is to capture head movement artifacts more accurately. Other sequences are used in anatomical MR imaging, such as FLAIR.


Why metacarpus is considered hand proper? This textbook states

  The hand (or manus) consists of the following parts: (a) wrist or carpus, (b) hand proper (or metacarpus), and (c) digits (thumb and fingers).

How could I justify why are digits not considered as hand proper? Hand is a prehensile organ and digits are of primary importance for prehension. So then how could metacarpus be considered as hand proper?

Proper in this instance means the main body of the hand, the part that has no other identifier. the fingers and wrist have other terms to identify them, the hand proper does not. If I say the the hand you are not sure whether I mean the hand as a whole or that part in particular so it is called the hand proper. Its an old usage of the word, but that is common in anatomy text.

From webster it is the 6th definition. Proper: strictly limited to a specified thing, place, or idea


If so many different hormones/molecules work by activating adenylyl cyclase, how do they have different effects? It seems that many hormones and molecules work by activating adenylyl cyclase to convert $\text{ATP}$ to $\text{cAMP}$, such as adrenaline and glucagon. Both of these seem to bind to $\text G$ protein receptors, cause an alpha subunit to dissociate and bind to adenyly cyclase to activate it, and then adenylyl cyclase forms $\text{cAMP}$. If so many molecules work in the same way, how can they have different effects?

My guess is that perhaps they may have different molecules inside which respond differently to elevated levels of $\text{cAMP}$? I presume both cells affected by adrenaline and by glucagon have the protein kinase which, when activated by $\text{cAMP}$, is able to activate glycogen phosphorylase to break down glycogen, as both adrenaline and glucagon increase blood sugar levels. Perhaps liver cells have more of the glycogen phosphorylase enzyme for a greater rate of breakdown of glycogen?

But then when I consider the heart, adrenaline increases heart rate but glucagon does not. If they have the same mechanism of action, how can this discrepancy arise? Could it perhaps be that adrenaline increases heart rate not by acting in the heart cells but in the medulla oblongata to increase the heart rate? But then again I come to the problem of why glucagon does not have the same effect. In this case I could hazard a guess that the glucagon molecule is too large to pass across the blood brain barrier.

But this is just one example of a possible problem in how two different molecules use the same mechanism. Although I cannot find a link now, I think I remember that long term potential ion to for new memories involves activation of adenyl cyclase. If that is so, it doesnt make much sense becaus adrenaline certainly doesn't help in the formation of new memories!

EDIT: I have just also read that insulin works by activating cAMP in hepatocytes/muscle cells, however it also seems that glucagon works by activating cAMP in the same cells! Two directly opposing effects using the same mechanism in the same cells- I'm very confused now!

How can hormones/molecules have different effects if they all work through cAMP? The short answer is that receptor expression on cell types is highly specific, and only if a cell has a particular receptor will it respond to a particular hormone. Thus two different hormones can have different biologic effects because the cells that contain those receptors are highly specific. Overall it is the presence of specific cellular receptors that determines the specificity of hormones and their effects.

A little more in depth of an answer... This is a classic concept from graduate physiology and was a real step forward in our understanding of hormone action in the 1950s/1960s. Earl Sutherland, who received the Nobel Prize in 1971 in Physiology or Medicine for this work, was on the faculty at Case Western Reserve University (and later at Vanderbilt University). Dr. Sutherland was studying the actions of hormones that were involved in glycogen metabolism (i.e. glycogen synthesis and glycogen breakdown). These classic studies identified a substance, now recognized as cyclic AMP (cAMP), whose intracellular concentration was increased in liver cells that were treated with hormones that stimulated glycogen breakdown. Conversely, cAMP was decreased by hormones or other conditions that were associated with glycogen synthesis. Most interestingly, it was identified that different hormones that either increased or decreased glycogen synthesis/breakdown had similar effects on the intracellular concentrations of cAMP (e.g. epinephrine, glucagon). This suggested that somehow cAMP was a common signaling molecule (or "second messenger") that transmitted the extracellular hormonal signal to the inside of the cell to have a biochemical effect (in this case stimulating glycogen breakdown).

In the case of Sutherland's studies, the increased concentration of cAMP stimulated the activity of Protein Kinase A (PKA), and the lack thereof decreased PKA activity and allowed the actions of protein phosphatases to predominate. For example, when glucagon binds its receptor on hepatocytes (liver cells), that receptor is coupled to an intracellular enzyme ($G_S$) that is activated and then can activate an enzyme called adenylyl cyclase, which increases synthesis of cAMP from ATP. The increase in cAMP then binds to PKA and phosphorylates the glycogen synthesis enzymes and breakdown enzymes. When the glycogen synthetic enzymes are phosphorylated by PKA they are inactive and, conversely, when the breakdown enzymes are phosphorylated they are active. Thus, glycogen receptor activation leads to activation of the glycogen breakdown machinery and inhibition of the glycogen synthetic machinery. This makes sense physiologically if you think about it - glycogen acts to increase hepatic glycogen breakdown and increase hepatic release of glucose into the circulation.

In brief, once Sutherland's group demonstrated the importance of cAMP as a second messenger protein within the cell, other groups began realizing that many other hormones led to changes in intracellular cAMP but each had there own effects. The differences in these effects were determined by the cell type that the hormone was acting on and whether or not that receptor was coupled to a particular second messenger system. Thus, you could have any number of receptors on the cell surface that are available to bind extracellular ligands (e.g. hormones, nutrients, drugs). However, each of these different hormones can be "coupled" or linked to different types of intracellular "second messenger" processes to transmit a signal. There are many types of second messengers that help transmit extracellular signals to the inside of the cell.

As you mention in the question, cAMP is a common second messenger system for a variety of different cell types. However, those different cell types have different receptors that are coupled to cAMP. Thus, hormones can have different effects depending on the tissues that express the receptors. For example, the glucagon receptor is expressed on hepatocytes which increases $G_S$ activity and thus cAMP, leading to glycogen breakdown and increased hepatic glucose production. Similarly, the $\beta_2$ adrenergic receptor that binds epinephrine/norepinephrine on smooth muscle is also coupled to $G_S$ which increases cAMP and leads to smooth muscle relaxation. These very different hormones have different biologic effects in different tissues, even though the effects are both driven by cAMP-dependent mechanisms. Briefly stated, it is the receptors that are present on a cell, that determine the response of a particular cell to that hormone.

This is graphically shown in the image below from this medical biochemistry link in adipose tissue - though the same concept is true for liver cells. Glucagon signals through its receptor to increase adenylyl cyclase, cAMP and then PKA activity, while insulin inhibits that activation by increasing the activity of PDE (a phosphodiesterase) that works on breaking down cAMP and subsequently keeping PKA in its inactive form.


Homeopathy is placebo, but isn't placebo good? I never considered homeopathy as a serious and scientific medicine, and now we have plenty of evidence supporting this (http://www.theguardian.com/commentisfree/2015/mar/12/no-scientific-case-homeopathy-remedies-pharmacists-placebos).

But placebo effect is also a thing that works, strange as it may be. The placebo effect deals with the importance of the brain's role and perception in physical health. So, in my understanding, placebo is better than nothing.

But now I can't treat myself with homeopathy, because I don't believe on it. Other people believe, and are happy with it (benefiting from the placebo effect).

So, my question is, wouldn't be benefitial to illude someone (or yourself) in order to achieve the placebo effect?

The point of a double-blind trial is that treatments are compared to placebo effect. Therefore, conventional treatments that "pass" double-blind trials are better than placebo.  If homeopathy is equal to placebo, that means that homeopathy is worse than conventional treatment.  Therefore, people who treat with homeopathy are giving worse than standard care.


How does Trifluralin kill newly germinating seeds, with almost no effects on established ones? Trifluralin (2,6-Dinitro-N,N-dipropyl-4-(trifluoromethyl)aniline) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

From what I understand, the mode of action is as a mitotic inhibitor, which disrupts the microtubules that pull the cell apart when it divides (stops cell division).

How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?

Mitotic (cell division) inhibitors in plants are pretty much what a chemo therapeuticum means for cancer, i.e., rapidly dividing tissues will be affected most. Germinating seeds depend on mitosis for growth. An established plant will also be affected (it will stop growing), but it will stand its ground. To push the analogy - chemotherapy is often commenced after surgical removal or irradiation therapy to remove the tumor, and then chemo is applied to make sure any surviving tumor cell will not start to divide. Your herbicide will prevent germination (cf. cancer re-growth), but will not grossly affect established plants (cf. existing tumor).


The use of cytotoxic T-cells The video below mentions whether the dendritic should call in a 'anti-virus force' or an 'army of bacteria killers'. The video goes on to talk about how bacteria is killed, using B-cells, but there's no mention of cytotoxic T-cells. Is the cytotoxic T-cells only for viral infections or is it for both?

https://youtu.be/zQGOcOUBi6s?t=2m42s   <-video is time stamped.

I don't study biology and the internet is confusing sometimes.

I didn't watch the video, but the answer you're probably looking for is that cytotoxic T cells are for intracellular infections -- that is, CTL target pathogens that grow inside one's own cells.  All viruses grow inside cells. Some bacteria also grow inside cells (e.g. tuberculosis, Listeria); those bacteria can (often) be effectively attacked by CTL. Many bacteria do not replicate inside cells, and for those, CTL aren't effective, but B cells (via antibody) and T helper cells (by recruiting other cell types and modifying inflammation) can still be effective.


Redox potentials in photosynthesis light dependent stage In my lecture notes, it states

...there is a significant thermodynamic problem due to the respective redox potentials of the half reactions:
H2O<--> 1/2 O2 + 2H+ +2e-      pE=+0.82V
NADP+ +2H+ +2e- <--> NADPH +H+      pE=-0.32V

Could someone please explain what the 'pE' is? I thought it would be just ordinary redox potential, however the redox potential for water is apparently +1.23V not 0.82V. I cannot find anywhere a source stating the figures given above or what they mean (I have also consulted Biochemisty, Stryer et al)
Could it have something to do with this being the potential in the conditions present in a typical chloroplast as opposed to standard conditions?

You are right about the conditions in the chloroplast stroma vs. standard conditions. The pH is high (i.e., low H+) in the chloroplast compartment where the reaction takes place (within the stroma), so the pE is shifted from the nominal "pE0", which is +1.23V (effectively you push the equation to the right by low concentration of H+).

See this for a textbook-like summary of the important reactions and this for a quick problem on the math behind pE in different conditions, as well as this for more on the stroma.


Menstrual cycle and luteinizing hormone (LH) What is the effect of increased concentration of LH on the follicle at the start of the menstrual cycle?

I know that increased levels of FSH at the beginning causes follicles to mature and release estrogen, but I cannot seem to be able to find what the effect of increased levels of Luteinizing Hormone at the beginning of the cycle would have.

Luteinizing hormone (LH): A hormone released by the pituitary gland in response to luteinizing hormone- releasing hormone. It controls the length and sequence of the female menstrual cycle, including ovulation, preparation of the uterus for implantation of a fertilized egg, and ovarian production of both estrogen and progesterone. Theca cells in the ovary respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells. In women, ovulation of mature follicles on the ovary is induced by a large burst of LH secretion - the preovulatory LH surge. Residual cells within ovulated follicles proliferate to form corpora lutea, which secrete the steroid hormones - progesterone and estradiol. Progesterone is necessary for the maintenance of pregnancy, and, in most mammals, LH is required for continued development and function of corpora lutea.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136063/


How does glutaraldehyde kill bacteria? How does glutaraldehyde kill bacteria?

After disinfecting, does it leave the corpses of the bacteria to count?

Does it leave bio-film in tact?

Gluteraldehyde interacts with amino groups to block the dynamic movements that biology requires.

Yes the corpses of the fixed bacteria can be counted and bio-films will be intact but the bacteria will be fixed in place.

Biofilms that are fixed with gluteraldehyde may shrink when prepared for imaging due to the effects of dehydration.


Does playing music during sleep actually suppress rather than rouse the brain? I've long been interested in the effect of music/sound on dreaming, and even built 2 apps that play music during REM period. Now I'm looking at this article about FMRI studies of a sleeping brain, and I see that it mentions:

  During wakefulness, acoustic stimulation elicits activation of the
  auditory cortex (red). Similar stimulation during light NREM sleep
  stage 2 evokes transient downregulation of widespread cortical areas
  (blue), supposedly a sleep protective mechanism.

and

  Acoustic stimulation in REM (rapid eye movement) sleep revealed a
  different brain activation pattern during phasic and tonic REM
  periods, with strongest suppression of cortical reactivity during
  phasic REM sleep periods.

Can I interpret information on that site to suggest that auditory stimulation during sleep actually makes the brain less active? Can one assume that playing audio during REM would disrupt dreaming due to transient downregulation?

This is a very interesting but difficult to answer question. That is because scientists are still debating about the various stages of consciousness. As it stands, there is evidence that people can learn even though they are asleep indicating that it is likely that sensory channels are open and information is being processed even when asleep. That likely means the brain is behaving as if it were awake at certain times during sleep. In this article they interpret the lack of blood flow seen by fMRI as less active which is mostly correct. Playing audio during REM is a tricky question because as you know dreaming does not require sensory input so that channel(hearing) may be free to receive information although your guess may also be true if if the music was loud enough to interfere with other cognitive processes.


Why don't plants get hot under sunlight? I've read that efficiency of photosynthesis is only like 5%, and it operates on visible light spectrum, not infrared (which is heat radiation). Which means light should either be absorbed and increase plant temperature, or reflected, and heat what's around the plant. But when you get near or touch plants under sunlight, they are at ambient temperature. In contrast, if you touch a metal plate, ceramic tile, rubber, plastic, asphalt, concrete, sand etc, that's exposed to strong sunlight, they are very hot, either because they reflect heat onto you (sand), or because they absorb heat and their temperature is high (asphalt). But with plants, it seems like neither happens, and it stays cool. How does that work?

Take a look at the Temperature paragraph from this reference:
Ecophysiology

  Plants can avoid overheating by minimising the amount of sunlight absorbed and by enhancing the cooling effects of wind and transpiration.

They seem to have several ways to counter the heat as we do with transpiration, wind etc.

This article is more complicated but as really useful informations on the effects of wind on the plant's temperature:

Leaves in the lowest and highest winds: temperature, force and shape


Does body temperature affect human lifespan? If a human body were somehow to be kept at a cold temperature (say 30C) for the entire life of the given individual. And somehow the brain could be fooled into thinking that this 30C feels nice and warm.

Would that given individual live longer as a consequence?
What effect does a tempreature have on lifespan?

I am assuming that you are referring to a baseline human cooled to a core body temperature of 30C from birth. I am also assuming that you are ignoring the fact that the environmental temperature (and thus the temperature of the extremities) has to be much lower than 30C to cause a core temperature of 30C. Thus, I am ignoring hypothermia-based gangrene, necrosis, and extremity loss.

If you had a normal human with a 30C core temperature starting at birth, I have doubts that it would live any longer than a human at 36.8C. Unlike flies, which are ectotherms, humans need to have a more or less constant temperature to successfully complete most of their metabolic processes efficiently. Since humans are not built to withstand extremely low temperatures, it is likely that lowering the core body temperature to 30C will cause it to have organ impairment, causing organ failure, followed by death. Though you might be able to "fool" the brain on thinking that 30C is normal, it is unlikely that the organ functions can follow. It could be possible to breed successive generations of humans in ever-lower temperatures, but it is unlikely for a baseline human to withstand such a large temperature drop. Sensory neuron adaptation =/= bodily adaption. However, lowering the core human body temperature by 1-2 degrees (typical of sleep) may have a chance of altering a human's lifespan in a more meaningful way. Though cooling may prolong the lifespan of temperature-conformers and single-celled animals, it is unlikely that the same can be said for endotherms. Endotherms have had biological processes that run on a fixed temperature for a long time already.  One more thing: @Hermann: Their core body temperature may not have been much lower than the baseline.


Degree of complementarity Apologies in advance for asking bit naive question. I have looked up for this concept a lot but didn't find anything.
The wikipedia (I know its not authentic all the time, but I think works well for definitions atleast) page on Complementarity says:

  The degree of complementarity between two nucleic acid strands may vary, from complete complementarity (each nucleotide is across from its opposite) to no complementary (each nucleotide is not across from its opposite) and determines the stability of the sequences to be together

This is quite new concept for me and how come we can have basepairing between opposite nucleotides if there isn't 100% complementarity? Any evidences behind it?

This can happen when DNA separates after melting and then reanneals.

You likely will not see this in chromosomal DNA in the cell, but I would assume it can happen to RNA molecules sometimes as they are single stranded and can self-anneal.

Mostly though, we think about this issue when performing PCR or DNA/RNA hybridization assays. Shorter pieces of DNA will be more likely to bind and anneal incorrectly, especially if the DNA is rapidly cooled after it has been melted.

Rapid cooling does not give the DNA time to "test" the different combinations of complementarity and sometimes can get stuck in a place where there is very little complementarity.

You also need to remember that while A-T G-C hydrogen bonding is favored, bases are able hydrogen bond to other bases, it just makes the double stranded molecule less stable.


Find Mutations Frequencies by Cancer Type Is there somewhere that has mutation frequencies by cancer type? So if I were looking at CML, AML, or even more generally at something like leukemia. Is there some database that would contain mutation frequencies? So that I could find that in leukemia 50% of cancers contained a T100G mutation.

I have looked through COSMIC but haven't had much luck.

There is one paper called "Mutational heterogeneity in cancer and the search for new cancer-associated genes" from the "The cancer genome atlas" which should be interesting for you. This project aims to map the mutations occurring in different cancers, one of the results is this figure (from reference 1):

The project itself has numerous data on the different cancers available on the project website, which can be found in reference 2.

References:

Mutational heterogeneity in cancer and the search for new
cancer-associated genes
The cancer genome atlas project website


Tropical Plant Identification After searching extensively I have been unable to find a name for this plant. It was found growing in the Eden Project Tropical biome in the UK. The flowers were approximately 7-8 cm across.
Any help greatly appreciated!

After continuing to search I have located the name of this plant. It is Ipomoea alba or 'Tropical white morning glory'.
On locating the area of the Biome on a map where I had found it, I could conclude it grew in tropical and sub-tropical areas of South America and north of there. This narrowed down the search somewhat.
Thanks again to all involved for helping to identify!


What is the difference between Crossbreeding, Outbreeding and Outcrossing? I only found one book which isn't a textbook  named Storey's Illustrated Guide to 96 Horse Breeds of North America By Judith Dutson (not sure if it is good enough to follow) that defined these terms.

Outbreeding/ outcrossing is deliberately crossing one line of horse within a breed to a very distant or unrelated line. The term is also occasionally used as a synonym for crossbreeding.
Crossbreeding is the deliberate crossing of horses of different breeds.

My understanding:
Outbreeding or Outcrossing is the mating between two individuals of a  breed but different varieties/sub-varieties.
Crossbreeding is the mating between two individuals of different breeds (could be intraspecific or interspecific as well).
Are these definitions correct?

Answer in keywords

Inbreeding : related individual,same breed

Outbreeding

Cross breeding : between different breeds
Outcrossing : unrelated individual,same breed,no common ancestor

Detailed answer

Inbreeding it is a mating within the same breed between different superior male and superior female. Inbreeding between close relatives can cause inbreeding depression like decreased Vigour , fertility and productivity. It is therefore advisable to mte superior animals of different population of the same breed .

Outbreeding is mating between unrelated animals of same or different breeds.

Outcrossing is mating between unrelated animals of same breed with no common ancestor for at least 4 to 6 generation. Offspring formed from such a cross is called out cross .

Cross breeding is mating between superior animals of different breeds for raising new breeds for improving local breeds.

Please note: Outcrossing and
cross breeding are two types of Outbreeding.

If you have any further doubts please ask .
Hope it helps!!