Identity of strange bird with fish net tangled around one foot This bird was photographed at a small beach in Rio de Janeiro, Brazil.

What kind of (ocean?) bird is this??

This could be an immature black-crowned night heron, Nycticorax nycticorax.
Lines of evidence:

pale yellowish bill
thick neck
hunched back
orange eyes
head feather patterning consistent with "black crown" in adults

See these photos and captions published by the Cornell Lab of Ornithology:

Juvenile Black-crowned Night Heron
Thick-necked heron with a thick bill. Juveniles are brown and streaky overall. Note pale yellowish bill.
© Evan Lipton

Immature Black-crowned Night Heron
Immature birds have a mix of juvenile and adult plumage. This individual has faint streaking on the chest, a dark gray cap, and a nearly complete dark gray back.
© Alex Lamoreaux

Adult Black-crowned Night Heron
Stocky and compact heron. Often tucks neck into its body creating a hunchbacked look. Adults have a black cap and back that contrasts with its whitish to pale gray belly and gray wings.
© Jeff Timmons

Note the fishing line tangled around the adult bird's feet.  Must be a common trait!


how to find accurately the closest species to my plant species? I'm working on some bioinformatic analysis of a non-model woody plant within the family with least information. So, I'm looking for a closest species to my plant. Any suggestion would be highly appreciated. Also, It will be great if I have know about the divergence time (? million year) between two species. Is there any documents or website to address this issue? Thanks

If you know the species name, you can search TreeBase to find previously published phylogenetic trees which will point you towards close relatives to your species. Depending on how obscure your taxon is, though, you might not find much.


Can CRISPR also remove DNA viruses? If I'm not mistaken only RNA viruses insert themselves into the host genome. As an example of DNA viruses, herpes viruses for example do not insert themselves in the host genome.

Can CRISPR cut DNA that isn't in a chromossome, like a DNA virus?

Yes, this should in principle work, and a number of groups have shows that it works in cultured cells:

  We found that CRISPR/Cas9 introduced InDel mutations into exon 2 of the ICP0 gene profoundly reduced HSV-1 infectivity in permissive human cell culture models and protected permissive cells against HSV-1 infection.... Combined treatment of cells with CRISPR targeting ICP0 plus the immediate early viral proteins, ICP4 or ICP27, completely abrogated HSV-1 infection. We conclude that RNA-guided CRISPR/Cas9 can be used to develop a novel, specific and efficacious therapeutic and prophylactic platform for targeted viral genomic ablation to treat HSV-1 diseases.

--Inhibition of HSV-1 Replication by Gene Editing Strategy

There's also been at least one trial in an animal model:

  Using a hydrodynamics-HBV persistence mouse model, we further demonstrated that this system could cleave the intrahepatic HBV genome-containing plasmid and facilitate its clearance in vivo, resulting in reduction of serum surface antigen levels. These data suggest that the CRISPR/Cas9 system could disrupt the HBV-expressing templates both in vitro and in vivo, indicating its potential in eradicating persistent HBV infection.

--The CRISPR/Cas9 System Facilitates Clearance of the Intrahepatic HBV Templates In Vivo


What is the function of epidermal ridges on human fingers (that produce fingerprints)? What function is served by the epidermal or capillary ridges on human fingers, the supposedly unique impressions of which are known as fingerprints?

I found many plausible claims that fingerprints increase friction. However, the following article claims, at least under their experimental conditions, that fingerprints actually decrease friction with smooth surfaces by reducing contact area.
Fingerprints are unlikely to increase the friction of primate fingerpads.

It is generally assumed that fingerprints improve the grip of primates, but the efficiency of their ridging will depend on the type of frictional behaviour the skin exhibits. Ridges would be effective at increasing friction for hard materials, but in a rubbery material they would reduce friction because they would reduce contact area. In this study we investigated the frictional performance of human fingertips on dry acrylic glass using a modified universal mechanical testing machine, measuring friction at a range of normal loads while also measuring the contact area. Tests were carried out on different fingers, fingers at different angles and against different widths of acrylic sheet to separate the effects of normal force and contact area. The results showed that fingertips behaved more like rubbers than hard solids; their coefficients of friction fell at higher normal forces and friction was higher when fingers were held flatter against wider sheets and hence when contact area was greater. The shear stress was greater at higher pressures, suggesting the presence of a biofilm between the skin and the surface. Fingerprints reduced contact area by a factor of one-third compared with flat skin, however, which would have reduced the friction; this casts severe doubt on their supposed frictional function.

That said, the author does later discuss their potential role in gripping of rough or wet surfaces:

So why do we have fingerprints? One possibility is that they increase friction on rougher surfaces compared with flat skin, because the ridges project into the depressions of such surfaces and provide a higher contact area. Experiments on materials of contrasting known roughness are needed to test this possibility.
A second possibility is that they facilitate runoff of water like the tread of a car tyre or grooves in the feet of tree frogs (Federle et al., 2006), so that they improve grip on wet surfaces. Though there is evidence that friction falls on fingers coated with high levels of moisture (Andre et al., 2008) it is possible that it falls less quickly on fingertips than on flatter skin. Once more, suitable experiments could test this idea.

There seems to be more consensus on the idea that fingerprints are useful for tactile sensation. The following are just some articles which discuss this.
Effect of fingerprints orientation on skin vibrations during tactile exploration of textured surfaces.

In humans, the tactile perception of fine textures is mediated by skin vibrations when scanning the surface with the fingertip. These vibrations are encoded by specific mechanoreceptors, Pacinian corpuscules (PCs), located about 2 mm below the skin surface. In a recent article, we performed experiments using a biomimetic sensor which suggest that fingerprints (epidermal ridges) may play an important role in shaping the subcutaneous stress vibrations in a way which facilitates their processing by the PC channel. Here we further test this hypothesis by directly recording the modulations of the fingerpad/substrate friction force induced by scanning an actual fingertip across a textured surface. When the fingerprints are oriented perpendicular to the scanning direction, the spectrum of these modulations shows a pronounced maximum around the frequency v/λ, where v is the scanning velocity and λ the fingerprints period. This simple biomechanical result confirms the relevance of our previous finding for human touch.

The role of fingerprints in the coding of tactile information probed with a biomimetic sensor.

In humans, the tactile perception of fine textures (spatial scale <200 micrometers) is mediated by skin vibrations generated as the finger scans the surface. To establish the relationship between texture characteristics and subcutaneous vibrations, a biomimetic tactile sensor has been designed whose dimensions match those of the fingertip. When the sensor surface is patterned with parallel ridges mimicking the fingerprints, the spectrum of vibrations elicited by randomly textured substrates is dominated by one frequency set by the ratio of the scanning speed to the interridge distance. For human touch, this frequency falls within the optimal range of sensitivity of Pacinian afferents, which mediate the coding of fine textures. Thus, fingerprints may perform spectral selection and amplification of tactile information that facilitate its processing by specific mechanoreceptors.

This paper also asserts a reason for the elliptical nature of fingerprints:

In humans, fingerprints are organized in elliptical twirls so that each region of the fingertip (and thus each PC) can be ascribed with an optimal scanning orientation.


Identification of store-bought succulent plant I bought this succulent in the Bronx Botanical Garden Shop, but it was unlabeled. On the photo it is about 4" high:

Can anyone help identify this? Could this be Echeveria haagai? It's indoors in NYC.

The only reason I have any clue as to what this could be is because I have one that looks exactly like it and, in a stroke of sheer genius, I wrote the name on the bottom of the pot. I think it is some member of x Pachyveria, which are intergeneric hybrids of Pachyphytum and Echeveria. Because there are so many, determining the exact cultivar may prove difficult. Mine is "Blue Pearl" and it looked very similar until it's untimely demise.

You can check out this website to see some different varieties. Actually, some of the Pachyphytum look pretty close too.

Compare w/ x Pachyveria "Cheyenne" (source):

and x Pachyveria "Little Jewel" (source):


Genotoxic agent and their metabolic pathway What are the mechanics (set of biochemical reactions) allowing a given genotoxic agent

to modify the mutation rate at a given spot?
to induce only a given type of mutation (from Gs to Cs for example)?
some other consequence of the kind that you think is worth talking about!

I am not necessarily seeking for a very detailed explanation of the biochemical pathway but rather some kind of understanding of how such things are possible (not evolutionary speaking but in terms of physiology and cytology).

This question comes in reaction to this post.

In terms of DNA mutations, it's usually just pure chemistry.  The mutagens article gives a brief rundown of some of the usual suspects, but to pick a few of the ones I'm familiar with:

UV light can cause pyrimidine dimers, which clearly is a dimerization of Cytosines or Thymines, which can cause replication issues.
Deaminases, which remove amine groups, is probably the coolest example.  Deamination can occur naturally, turning Cytosine into Uracil, but is often done deliberately as part of bisulfite sequencing to determine methylation status.
Alkylation can occur, in particular of Guanine, which can lead to a preference in binding for Thymine; subsequent replication will result in an Guanine to Adenine conversion.

Similarly, there are many base analogs that will fill in for a given nitrogenous base.  These analogs often prefer to bind to an "incorrect" base as above (and in the figure below with 5-bromouracil) which will lead to specific errors.

On a more intentional basis, biotechnological tools such as zinc finger nucleases, TALENs, and the (oh-so-sexy) CRISPR system can be used to specifically alter genome sequences of choice.  ZFNs are in particular being used as a gene therapy tool for just that reason.

Otherwise, viruses (and transposons) that insert into the genome can cause specific mutations or errors if they do so non-randomly.  Figuring that out, though, can be tricky; most oncoviruses cause mutations through specific genes that allow uncontrolled growth and tumorigenesis, not in a site-directed manner.  There is, however, a growing hypothesis that certain retroviruses which tend not to cause cancer, in particular HIV, may be inserting into sites with certain characterizations, such as chromatin level.  That is far from known, though.

If you're looking for random causes, that's easy.  Anything that disrupts DNA repair mechanisms such as p53 or Rb will do that.  For chemicals, intercalators such as ethidium bromide and thalidomide insert in between DNA bases and prevent proper DNA repair.


How is propagation of action potentials terminated once the "message" has been sent/received? I'm thinking about neurons in the brain that are used for "thinking". As I read about action potentials, I see that an Axon is connected to a Dendrite of a neighboring cell and that there are neurotransmitters involved in the signal propagation from cell to cell.

I'm interested in learning how action potential propagation gets terminated. Let's say a message from the brain region A to brain region B has been delivered through action potentials.

How does the region B know not to "route" the action potential further down the chain of neurons?
How does the region A know that the message has been sent, to stop sending more messages?

I'm not a Neurologist or Neuroscientist, so I can only share what I know about the subject!

TL:DR

Cease sensation
Neuronal recovery period prevents further signaling
Neurotransmitter inhibition prevents ligands from binding to receptors (usually Feedback mechanisms)
Neuronal hyperpolarization prevents signaling
Creation of signal (can be perceived as cessation of signal)

It's important to note, first and foremost, that a cessation of stimulation will result in a cessation of the propagation. This is one of the simplest ways that neurons can stop firing - you're no longer touching, tasting, hearing, seeing, smelling, or thinking of what you were previously.

Because of the way Neurons are constructed, and as far as I'm aware, signal propagation will persist as far down the line as possible. I don't believe there's a discrete point where an Axon will simply not send a signal once a dendrite on the same neuron has received the order.

What can happen is that a competing signal has exhausted the propagation potential for the next neuron in the chain (the neuron is still recovering), or a competing signal has released inhibitors that prevents the neurotransmitters from another Axon from affecting the target neuron. Competing signals is particularly common in the neurons of your eye, since the Amacrine cells fire depending on the competitive input of the Cones if I'm remembering everything correctly.

Then there are also substances like Benzodiazepines which block propagation by opening Cl- channels and hyperpolarizing a neuron's membrane, which prevents it from firing. Only a subset of GABA receptors have sites for benzodiazepines, but it's one more way that signals will cease.

Another way to cease a signal, or at least the perception of a signal, is to actually induce propagation. The Rods in your eyes only fire below a certain lumination threshold. What you perceive as light is them not firing, and darkness is what happens when Rods fire at full strength.

I'm not the last word on neurobiology, but I hope I've given you a good start!


What Effect would Cannabinoids have on the Acute Porphyrias? I should be clear in saying that this question is NOT intended for personal medical advice. Rather what I am looking for is journal articles and/or books that touch on this subject because I think it would be quite an intriguing topic to probe. I am unaware of any interaction between the endocannabinoid system and the formation of haem and porphyrins in general.

Yes, they can induce an acute attack.

  Drugs metabolised by cytochrome P450 (CYP) such as analgesics may induce acute attacks in patients with hepatic porphyrias. In recent years, preclinical and clinical studies have suggested that cannabinoid pharmaceutical preparations may be potentially useful in the treatment of pain [1].

There is even a clinical case about acute intermittent porphyria in a marijuana user:

  Mr. G is a 55 year old Caucasian male with a past medical history significant for acute intermittent porphyria (AIP), chronic back pain, renal insufficiency, hypertension, and nicotine dependence. The patient has presented to the hospital with multiple AIP exacerbations since diagnosed eleven year prior to the current case. [...] Urine drug screen was positive for cannabinoids, which he admitted to frequent marijuana use [2].

But an experimental study on mice failed to prove that:

  Our findings indicate that CP-55,940 (a cannabinoid CB1 receptor agonist) and its metabolites do not behave as porphyrinogenic drugs and may potentially be safe for treating pain in patients with acute porphyrias [1].

References:

Fontanellas A, Manzanares J, García-Bravo M, Buzaleh AM, Méndez M, Oliva JM, Batlle A, Palomo T, Enríquez de Salamanca R. Effects of repeated administration with CP-55,940, a cannabinoid CB1 receptor agonist on the metabolism of the hepatic heme. Int. J. Biochem. Cell Biol. 2005 Aug;37(8):1620-5. doi: 10.1016/j.biocel.2005.02.010. PubMed PMID: 15896668.
Ware SK. Acute Intermittent Porphyria With Psychiatric Manifestations: A Case Report. Ment Health Clin. 2013;3(5):100. Available at: http://cpnp.org/resource/mhc/2013/11/acute-intermittent-porphyria-psychiatric-manifestations-case-report. Accessed July 27, 2014.


What is the name of this tiny creature? It looks like a tiny piece of moving cotton? By chance, I saw this tiny insect on my bag a few days ago in Sydney. Am I the first person who has pinpointed this animal?! If not can you please let me know its name?

From your image, it looks like it might be a woolly aphid. I just did a bit of cursory research, and it looks like they're often described as floating pieces of fluff, that seem to wander instead of directly heading somewhere. The fluff on their back is actually wax produced as a defense mechanism from predators and the like. I hope this is what you were looking for!


What is projected to go extinct first? Though a number of animals have been going extinct at alarmingly quicker rates (so called anthropocene extinction), a number of 'star'  threatened animals are still alive.  Which of the following charismatic endangered species is modeled or expected to die off soonest: polar bear, panda, black rhino, african elephant, mountain gorilla,bengal tiger/ tiger.

Where can I find population projection models for each of these species?

Mountain gorillas  have the current smallest population,  but polar bears are clearly in  a lot of (and quickly widening)  trouble due to melting ice. African elephants are seeing species loss due to poaching,  and drying conditions making food/water scarce,  which could also speed their decline, but they have the largest of the populations.

Since WWF and other conservation organizations use these charismatic species to 'sell' conservation and raise interest, awareness and funding,  losing one (or many) of these species could affect conservation considerably. This will either be positively via a reactionary  disappointment by the public or negatively by losing a "poster species".

Black Rhino, status: critically endangered

With around 5000+ black rhinos left in existence, and population numbers seemingly recovering (up from ~2400 in 1995), the black rhino is not really under any immediate threat.* The major threats to black rhinos is poaching (for the rhino horn trade), and, with prices for rhino horn increasing, it looks like it will be a problem for a while to come. Furthermore, corruption, war/civil unrest, easy access to guns, poverty, funding cuts (etc.) contribute to make the battle against poaching more difficult.

African Elephants, status: vulnerable

There are around 470,000 African Elephants left in the wild, and 25-30% of these are the Forest Elephant subspecies, so they aren't going anywhere soon.* Numbers are steadily increasing (~4% per year), although some populations are reducing. Poaching for ivory and bushmeat are signficant problems, but habitat loss and fragmentation is a massive issue. Elephants occupy a large number of habitat types and populations cover vast ranges, it is very difficult to protect an entire population range such that elephants could freely and safely move throughout their range (particularly at national borders), but things are getting better in many cases and efforts are ongoing.

  An increasing number of transboundary elephant populations are co-managed through the collaboration of relevant neighbouring Range States. Large-scale conservation interventions are also planned through the development of conservation and management strategies at the national and regional level.

Polar Bear, status: vulnerable

Population estimates range between 20 and 25 thousand polar bears in the wild, and populations are on the whole fairly stable at the moment (in population studies, for populations where enough data was available, 1 grew, 6 were stable, 3 declined over a 12 year period). These animals are dependent on sea ice which, with human caused climate change, is rapidly declining. Climate change poses a more serious threat to polar bears. Relative to many things, like poaching and habitat fragmentation, it will take a very long time to reverse the tide; it may even be too late to prevent fatal damage to the polar bear habitat. They are also at risk from hunting, pollution, and habitat disturbance. Realistically, it is hard to predict when (or if) polar bears will go extinct because there is so much variance in the prediction of climate change and loss of habitat (sea ice).

Giant Panda, status: endangered

Less than 2000 pandas are left in the wild. Hunting and habitat loss remain to be enormous problems for wild pandas; masses of deforestation and fragmentation is occurring in their range. The chinese government has established >50 panda reserves, but this covers around ~60% of the population. The population trend is a decreasing one, which is serious cause for concern, and fragmentation of populations could reduce genetic diversity (increasing inbreeding depression and reducing adaptive capacity). Despite popular belief, pandas reproduce fairly well in the wild, it is in captivity that we have struggled, and that causes problems for breeding programs that can boost numbers and restore genetic diversity to sub-populations.

Mountain Gorilla, status: endangered

Fewer than 1000 mountain gorillas are left in the wild and populations are declining. Habitat encroachment, deforestation for the charcoal industry, bushmeat, and poaching are major issues affecting populations, and much has been fuelled by conflict (e.g. the 1990's war in Rwanda) in their range (in the last 20 years, 140 Virunga rangers have been killed trying to protect Gorillas). Also affecting them is human disease including the common cold which is often fatal to gorillas.

Bengal Tiger, status: endangered

Currently with a population of >2500, and with populations stabilising, and even rebounding in many areas (I was in Ranthambore last year, numbers have risen from ~20 to ~60 in the last 10 years), it seems the Bengal tiger is no immediate threat of extinction.* The major threats are poaching, population fragmentation, and habitat encroachment which leads to conflict with (and killing by) humans in the areas. Project Tiger is a major programme in India which has greatly contributed to successful growth in tiger numbers. The range of tigers is under increasing pressure from encroachment.

Summary

In summary, few models will be able to predict when or if any of these species will go extinct. Even if the short-term problems can be overcome, loss of genetic diversity prevents issues for the long-term prosperity of these species. Many of the problems are fixable in a relatively short time but will take a lot of effort and money, (such as poaching, hunting, deforestation) because they are mainly about cultural and social issues.

Climate change is perhaps more concerning because reversing the effects of human caused climate change will be extremely difficult (social and economic pressure), and slow to reverse; by the time we reverse the trend of rapidly declining sea ice it may be too late. Therefore, out of your species I'd say it's a close call between polar bears (despite good numbers they perhaps have the worst prospects of rescue) and mountain gorrilas (because numbers are so low and conservation projects are fighting difficult problems such as poverty and the effects of decades of civil wars and unrest). This article from national geographic suggests mountain gorillas may have as little as ten years left, while polar bears may be able to cope with some amount of warming, but the rate of warming is a major concern.** The WWF has also warned that pandas are not far from extinction.

What happens if we lose these species?

Many of these species are very attractive to the general public. The loss of some species would likely be worse than others; many of these are used to promote ecotourism and this would have varying effects for each. For the cases of black rhinos and african elephants many of these areas have many other species which are of interest to ecotourists (lions, leopards, cheetahs, white rhino, giraffe, crocodiles, buffalo, and many other mammals and birds, even sharks). However, if black rhinos went extinct then there would probably be losses in those species too (they face many of the same problems). Ecotoruism in the relevant areas tigers and pandas on the other hand are hugely important draws, India and China simply don't have the same diversity and abundance of highly sought after species with which to boost ecotourism should either go extinct (there are other nice species in these areas, but few are as highly sought as tigers and pandas). It's much the same for mountain gorillas and polar bears, these areas have less to fall back on should their species go extinct, so in many cases these species are of major economic importance.

That said, losing one or two of these species could cause some good. The outrage at losing some of the most popular animals in the world would be enormous. Funding for conservation and social pressure would likely swing massively more in favour of conservation efforts, making the fight to protect other species easier. Personally I don't hope we will ever have to rely on this strategy.

* Relatively speaking

** Strong selection may not get adaptive responses to occur quickly enough because generation times, standing genetic variation etc. such that while populations may adapt they don't adapt quickly enough.


Why do surface mole tunnels follow directly below the electric fenceline I have electric fencing enclosing five acres, and moles always seem to tunnel in a straight line just under the electric fence - are they following a force field? Can that be?

Rumor has it that some moles, such as the star nosed mole, have electroreceptors in their nose.

  In 1993, Gould and colleagues proposed that the star-like proboscis had electroreceptors and that the mole was therefore able to sense the electrical field of its prey[24] prior to mechanical inspection by its appendages. Through behavioral experiments, they demonstrated that moles preferred an artificial worm with the simulated electrical field of a live earthworm to an identical arrangement without the electrical field.

They may thus be sensing the electrical field of the fence, and interpreting it as a nearby tasty worm.


How does the adaptive immune system store information? I am quite curious about this:

Where and how is knowledge that the adaptive immune system accumulates stored?
What is the "memory size limit" of this storage method if there is any?
Why cant this knowledge be transferred between individuals like we transfer computer antivirus definitions?

There is probably no precise answer to this question since, as others pointed out, the adaptive immune system is not really comparable to a computer. That said, here are a some items you might want to look into.

Question 1: the main site of information storage for the adaptive immune system is a special region of DNA in T and B lymphocytes that encodes immunoglobulins, the proteins that these cells use to recognize foreign organisms. The sequence stored in this special DNA region can be rearranged by hypermutation and recombination mechanisms. This occurs early in the life of T and B lymphocytes, so that each cell gets a unique DNA sequence. Those cells that later on happen to recognize invaders will multiply as part of the immune response, and they will later survive as memory cells, so that their specific DNA sequences are retained. If the same infection happen again later in life, these memory cells will help the immune system respond more quickly.

Question 2: the region of DNA used is on the order of 1 million bases long, and it has been estimated that the human immune system can generate around $10^{11}$ different immunoglobulins. How to interpret these numbers in terms of "memory size" is not clear to me though. On one hand, 1 million bases is equivalent to 250 kbytes (each nucleotide base storing 2 bits); but on the other hand, $10^{11}$ as an integer can be stored in 37 bits. I guess it depends on what level of information you consider.

Question 3: there is no mechanism for directly transfering information between lymphocytes. Lymphocytes cannot read and write their DNA at will, and they are not able to simply copy sequences from each other. Rather, their diversity comes from first randomly re-shuffling their immunoglobulin-coding DNA, followed by selection of the successful cells --- this is a brute-force, random-search method, like evolution itself. Also, lymphocytes from unrelated individuals will generally interpret each other as invaders, causing an immune response. However, it is possible to experimentally "edit" the "memory" of lymphocytes extracted from blood using genetic techniques. This has for example recently been explored to "train" cancer patients own lymphocytes to attack cancer cells, in some cases with remarkably good results.


Why are urban birds still scared of humans? I understand that animals are naturally scared of humans because we basically slaughtered every living thing we found in our way for millennia. How long does it take for them to genetically 'forget' we are a threat?

Perhaps counter-intuitively, fear of humans is often a learned behaviour. There are accounts, such as one made by Charles Darwin following his visit to the Galapagos islands;

In Charles Island, which had then been colonized about six years, I saw a boy sitting by a well with a switch in his hand, with which he killed the doves and finches as they came to drink. He had already procured a little heap of them for his dinner, and he said that he had constantly been in the habit of waiting by this well for the same purpose. It would appear that the birds of this archipelago, not having as yet learnt that man is a more dangerous animal than the tortoise or the Amblyrhynchus, disregard him, in the same manner as in England shy birds, such as magpies, disregard the cows and horses grazing in our fields.
From "The Voyage of the Beagle" - http://www.ling.upenn.edu/courses/hum100/Beagle17.html

Birds born and bred in proximity to humans will have learned that we are actually to be avoided.
Ducks and swans, for instance, (and this is quite anecdotal) live in very close proximity to a lot of humans in cities, and feel confident walking picking up food. However if you try to get close to one they are very quick to get out of the way. The only exceptions to this are learned behaviours, such as when someone stands and feeds them.
In the wild animals may be cautious of humans if we are much bigger than them, but if they have no experience at all of human contact they  may just ignore them. This quite often happens with film crews in Antarctica, as in the below image from the BBC's Frozen Planet series.


Question regarding the number of alleles Why is it that in biology we often say that a gene has two alleles? When we analyze allele frequencies (e.g. using Hardy-Weinberg Equilibrium), formulas are often generalized for two alleles of a gene.

Given mutations, isn't it quite likely that a population will have more than two alleles for a gene?

The two-allele scenario is often used in genetics teaching because of its simplicity. However, quite a few genes have more than two alleles. Some examples that readily come to mind are:

The ABO gene in humans: This determines ABO blood group, and has six common alleles. Many more rare alleles have been described [1].
The human leukocyte antigen (HLA) genes: These are well-known for their allelic diversity. One of them, HLA-A, alone has over 6,000 alleles [2].

Reference

Seltsam A, Hallensleben M, Kollmann A, Blasczyk R. The nature of diversity and diversification at the ABO locus. Blood 2003; 102(8):3035–3042. https://doi.org/10.1182/blood-2003-03-0955
Robinson J, Halliwell JA, Hayhurst JD, et al. The IPD and IMGT/HLA database: allele variant databases. Nucleic Acids Research 2015; 43:D423-431. http://hla.alleles.org/nomenclature/stats.html


Do animals get sick from eating dirty food or eating off the floor? Humans have very strict tradition of hygiene, such as washing hands before eating, using utensils, and in general keeping as much distance between food and dirt as possible.

At the same time, most animals would eat off the floor or eat food with foreign particles stuck to it ( after being dropped on the floor). Many animals, like cats groom themselves, practically licking off (and swallowing?) dirt off their coats.

Do animals suffer adverse effects, such as indigestion or disease from consuming food that is dirty by human standards?

Or is it something about the human digestive system that cannot handle the same kinds of dirt that animals can?

I'm sure it varies wildly based on the animal and what they're eating.  In general, if in the course of an animal's natural feeding process it picks up a little dirt, it has evolved to cope with that.  Animal's behaviors and guts have evolved to fit their food source and lifestyle.  For a behavioral example, seals will eat rough rocks to help breakdown bones (and barf them up when they get too smooth).  Guts have evolved symbiotic relationships with microbes that are specifically adapted to the food source, termites have microbes to help them break down wood, whereas we don't have the microbe population to pull that off.  Interesting side note: it was found that one of the gut microbes in some Japanese people has gotten a horizontally transferred gene from a bacteria that lives on seaweed, probably helping them break down seaweed.

There could be a problem when the body is challenged with dirt that contains uncommon substances that the body isn't adapted to.  I'm sure if a cat rolled around in soil contaminated with a lot of arsenic it probably wouldn't be doing very well after licking off all the dirt.

This does bring up an interesting current medical hypothesis called the Hygiene Hypothesis.  Basically, these things you are talking about, utensils, antibacterial soap, etc. are all very very recent developments in human evolution.  As a result, proponents of this hypothesis think that our bodies are adapted to challenges by microbes and parasites, and depriving our bodies of that exposure when we are young totally screws up the development of our immune systems.  This would explain why we see a huge increase in allergies and autoimmune diseases in the developed world, our immune systems are totally miscalibrated, and freak out over harmless things like pollen (allergies), or worse, attack self-antigens (anti-insulin antibodies in type I diabetes).  Human children are animals, and baby animals should play in the dirt!


Is it possible for any impurities to get through the apple peel? My parents always told me not to eat from the apple trees near the  road, because some kind of bad toxic dirt might get through.

This sounds to be physically possible but not really probable in my view. In the time apples grow on the tree they never rot. The rotting procces starts as the apple falls down and damages - the wound will quickly change its colour and it begins to decay - from this I assume the peel is almost perfect defense against bacteria & toxic penetration.

I think the only danger may come from the dust microparticles spread by the cars - which can be easily washed by water or wiped off with a piece of cloth. Am I right? What about other types of fruit?

The answer I got from Jan Kolář of Charles University:

The spores of fungi or bacteria in apples don't just emerge from nothing, they have to get into it from the surroundings. I often see apples, which rot while still hanging on the tree, the hole needed for the infection of the apple is usually made by a worm. The problem of the apples near roads isn't that they would rot. Indeed, plants can absorb all kinds of harmful substances from soil, water or air, including heavy metals, chlorinated organic compounds or organic compounds from the exhaust gases of cars. How much and which substances, that usually depends on the type of plant (specifically on where it stores most of the substances).

It's not enough to wash an apple because the impurities are absorbed in the fruit itself as well. And on the surface of the peel, there are waxes and other unsolutabe substances which can absorb toxic aromatic carbohydrates from the exhaust gases, and can't be simply washed off.

The greatest risc near the roads used to be contamination with lead because petrol used to contain it. Many of the plants can recieve the lead and hoard it up in some organs. Now, when the lead petrols are forbidden, the biggest risc pose the fumes from the diesel engines. So I'd rather not eat fruit near the roads (especially near the busy ones).


Can mammals and/or birds see / detect infra-red light? Wondering if there is any evidence that mammals or birds eyes can detect light emitted in the infra-red?  The reason I'm asking relates to the use of nest cameras to detect predators, using infra red LED light to take pictures at night.  New technology allows a picture to be taken every 3 seconds, throughout the night.   Clearly if these can be seen - then a mammal, or nocturnal bird could quickly learn to look for the flashes of light and find a tasty source of food...

Infrared is a fairly large part of the electromagnetic spectrum, so to get an answer best suited to your specific case, you should specify the wavelength of your LED. There is at least one study showing that ferrets (not sure if it's the best predator to worry about for what I assume is a suspended bird's nest) can see up to 920nm.

So to answer your question, yes, at least some can, but the further into the spectrum you go, the fewer there will be.

I am much less certain, however, that this would attract danger. Nocturnal predators in biomes inhabited by humans generally evolve to avoid rather than seek out artificial light sources.


Expected reproduction rate of a dandelion and/or fern I am working a basic mathematical/computer simulation of an ecosystem, and I need to know the birth rate of each organism in my simulation. However, I could not find any data for how often a small, asexually-reproducing plant, like a fern or dandelion, reproduces. Does anybody know either a) the time to reach sexual maturity and the expected offspring of one dandelion or fern OR b) when starting with one plant, the expected living dandelion or fern plants after a year?

In other words, if I plant one dandelion or fern in a closed system (providing it with requisite water, food, sunlight, etc), how many can I expect to find at the end of the year?

These values don't have to be exact, I can adjust them later, but I need something to use as a baseline.

Dandelions may have "from 54 to 172 seeds per head and a single plant can produce more than 2000 seeds" (https://fyi.uwex.edu/weedsci/2002/11/12/dandelion/), but the number of inflorescences depends, for example, on the age of the plant. It should also be remembered that some individuals repeat the blooming in autumn, although it is not so abundant (usually only one inflorescence). That, what is called a dandelion (Taraxacum officinale) is a collective species, which actually consists of several hundred microspecies, which may differ in the amount of seeds produced. Thus, the given data is only quoted.


Why does looking at bright light trigger sneezing in some people? Why does looking at bright light trigger sneezing in some people?

Are there any recent studies that have found a cause for this Photic sneeze reflex? The Wikipedia article only references studies pertaining to the effect, stating that the cause is unknown. The article also states that "the condition affects 18–35% of the population", which seems to be quite a large percentage.

What could have lead to the development and persistence of such a genetic trait in humans? Are there any evolutionary advantages to this?

You are talking about the photic sneeze reflex.

The mechanisms are not entirely understood, but it affects 18-35% of the population.

According to Wikipedia (although this passage is not sourced):

  The probable cause is a congenital
  malfunction in nerve signals in the
  trigeminal nerve nuclei. The fifth
  cranial nerve, called the trigeminal
  nerve, is apparently responsible for
  sneezes. Research suggests that some
  people have an association between
  this nerve and the nerve that
  transmits visual impulses to the
  brain. Overstimulation of the optic
  nerve triggers the trigeminal nerve,
  and this causes the photic sneeze
  reflex.

And, it could  be advantageous:

  On the other hand, some people with
  the trait feel that it is
  advantageous. In the event that nasal
  discomfort occurs, but to an extent
  that is insufficient to induce a
  sneeze, intentionally seeking and
  finding a light source facilitates the
  sneezing process and is in turn a mode
  of relief.

Also, anecdotally, as I too photosneeze, I can see an advantage: should the atmosphere become weaker in the future, and allow more light to enter than we are accustomed to, it would discourage looking directly at the sun.


GC content of a protein-coding region I have computer science background and I am trying to understand the equation below.

The average value of the G + C content of a protein-coding region is
given by :

(G+C)=  $\sum_{\alpha} (I_\alpha *f _\alpha$ )/3

$I_\alpha$ = Maximum number of nucleotides C and G that appear in one of the
synonomous codons for given amino acid

$f_\alpha$ = Frequency of amino acid α.

Where does the 3 in the denominator come from ?

Each codon codes for one amino acid and every codon contains 3 nucleotides.


Why do oviparous animals not have ears? I was chatting with my friend, and we both found that there's a relation between putting eggs and ears; we count animals and we found that if an animal is oviparous (birds, snakes, etc.), then it does not have ears. We really did our best but we did not find anyone!!

So, Is there any scientific reason laying behind this difference, I'm a little bit curious? Thanks!

Interesting hypothesis! - all of those animals you mentioned in fact do have ears, they just don't have external pinnae. You are probably thinking of these external structures when you are thinking of ears.

Importantly, pinnae are unique to the mammals, and not even all mammals have them. Since most mammals do not lay eggs, that is probably the joint relationship you are recognizing. Monotremes (egg laying mammals) also don't have external pinnae (for example see this book). So, the scientific reason is that both non-egg laying and external pinnae evolved in the mammalian lineage around the same time.

I don't know of any shared benefit for these traits to go hand-in-hand, but you could probably come up with more traits that also largely follow these ones, again because of shared lineage rather than a particular synergy.


Antihistamine's effect on insulin secretion and tiredness? Antihistamines are known to cause tiredness.
The essential hormones of the body are insulin (glucose), parathyroid hormone (calcium) and aldosterone (Na-K ATPase, sodium).
I am thinking how this tiredness symptom can come.
There are so many different antihistamines so I am confused about the mechanism how they cause tiredness.

Histamine acts on parietal cells of stomach via H2 receptors to stimulate hydrogen ion secretion - cephalic phase.
Excess of antihistamines can lead to decreased acidity of stomach so change in conversion of pepsinogen into pepsin.
So less pepsin breaking down peptides and proteins.
Body has to do something else to break those components - and this consumes much energy and makes you tired.
Small mucus food mass stays in the intestines.
Delayed absorption.
Nutrients needed so liver has to work and make essential things - amino acids and something else.
Some waste management also may happen - because of tiredness.

Changes in blood sugar level.
Delayed most probably after food intake.
Very fast and fast insulin secretion mechanism starting during wrong times - all of the sudden.
So less insulin secretion cumulatively:

very fast mechanism - change of permeability of membranes (Na-K ATPase and sodium channels) reacting during times when not suitable - long after food intake
fast mechanism (phosphorylation of different things) happening more, since sympaticus apparently is not so inhibiting here
slow and very slow mechanisms however preferable (increased permeability of amino acids and mitoses)

So I think the tiredness of antihistamines is because of the increased amount of active fast mechanisms of insulin secretion, while less very fast mechanisms.
To carry the raw food mass in the intestines also require much energy.

What is the physiological mechanism behind the tiredness of excess antihistamines?

Thanks to studies on animal behavior and on histamine dection in the Central Nervous System, researchers found out the "histaminergic system".
It's thought that histamine-containing neurons regulate sleep-wake cyrcle, immunity, memory, body temperature, drinking, feeding rhythms. By the way, knockout rats who lack of histamine system don't show big defects in any function.

H1-Receptors for Histamine are distributed in the CNS and in the rest of the body. H1-antagonists (such as Promethazine, Chlorcyclizine, Loratadine...) have different effects on CNS, depending on dose. At conventional doses central depression appears and patients are sedated. They can even experience an antihistamine "hangover" in the morning, even if they take these drugs at bedtime. By the way, antihistamine overdose typically shows with convulsions.

The "non-sedating" H1-antagonists, or "second generation" have a lot less effects on CNS. They have polar chemical structure: they can not cross the blood-brain barrier.
By the way, a lot of typical and atypical anti-psychotic drugs have H1-antagonism effects on the brain (with H2 and H4 antagonism): their main goal is sedation to stop the patient from hurting himself (or others) during manic episodes.

So I think the last two sentences explain that sedation is almost a totally CNS-mediated side effect of antihistamine drugs.

H1-antagonists don't suppress gastic secretion, do not inhibit salivary, lacrimal or other exocrine secretions. Older H1-antagonists have an anti-colinergic effect on muscarinic receptors: they may reduce ACh-mediated secretions, typically in mouth and in the respiratory tree.

H2-antagonists are used to treat acid-peptic desease (as PPIs, proton pump inhibitors). CNS-related side effects are not commons, and include: confusion, delirium, hallucinations, slurred speech and headaches. These effects are mostly related with IV infusion of the H2-antagonist.

I just made a very small research on PubMed. I found this:
http://www.ncbi.nlm.nih.gov/pubmed/3529778
as you can see it is a study (on only 9 patients, in 1986), about insuline-glucose-Cpeptide and ranitidine (H2-antagonist) relations. Their conclusion is "Ranitidine significantly increased the area under concentration/time curves for glucose and insulin but not that of C-peptide. Our data indicate that ranitidine does not affect pancreatic insulin release nor peripheral glucose utilization and are consistent with the hypothesis that ranitidine influences the hepatic clearance of glucose and insulin both of which undergo high first-pass liver extraction."

I think that tiredness is a typical CNS-mediated side effects of H1-antagonists (anti-allergic) but is not a side effect of H2-antagonists (anti-acid). Maybe H2-antagonists affects insulin action via hepatic effects.

*I'm italian (sorry for any english mistake) and I am a last-year medicine college student.
I wrote trying to summarize some chapters (8, 32 and 45) of:
- "Goodman & Gilman's The Pharmacological Basis of Therapeutics" - L. Brunton, B. Chabner, B. Knollman - 12th edition; McGrawth Hill 2011


Does NADH inhibit gluconeogenesis? I was told in a physiology lecture that alcohol inhibits gluconeogenesis because 'NADH produced from ethanol catabolism leads to product inhibition'.

But is NADH not a reactant coenzyme of gluconeogenesis? It would make more sense if NADH inhibits glycolysis by product inhibition.

So, what is wrong here? Or is it because of some other reason why alcohol inhibits gluconeogenesis and leads to hypoglycemia?

Yes, this is the effect of metabolizing ethanol and also the reason why excess ethanol can lead to hypoglycemia.

Ethanol is oxidized by the alcohol dehydrogenase to acetaldehyde. This reaction consumes one molecule of NAD+ per molecule ethanol oxidized:

Ethanol + NAD+ <=> Acetaldehyde + NADH + H+

Acetaldehyde is oxidized by the acetaldehyde dehydrogenase in a second reaction in the mitochondria to Acetyl-CoA, which produces another molecule of NADH:

Acetaldehyde + NAD+  + CoA <=> Acetyl-CoA + NADH + H+

If you now take a look at gluconeogenesis, there is one critical step which needs NAD+: the oxidation of lactate to pyruvate by the lactate dehydogenase which then cannot be processed into oxalacetate, phosphoenolpyruvate and so on.

Adding excess NADH shifts the reaction equilibrium completely to the side of lactate and also leads to the production of additional lactate, leading to hypoglycemia and lactic acidosis. Excess NADH from the ethanol oxidation inhibits the oxidation of fatty acids in the liver - this process also generates NADH for the production of ATP. NADH signals this process that enough energy is available in the cell. And finally excess NADH also inhibits the malate dehydrogenase reducing the amount of oxalacetate for gluconeogenesis further.


Determining if a Protein Model Contains a Backbone Clash I have an ensemble of homology models of a protein, and I now wish to remove those models which have backbone clashes. I could obviously check by eye but this is subjective and probably will not be accepted for publication.

What is the best (reproducible) method to determine if a particular protein model contains a backbone clash?

The way to check for steric clashing between any two atoms, backbone or otherwise, is to compute their Euclidean distance. If a and b represent two atoms (with a_x being the X coordinate of atom a and so forth), you can calculate their Euclidean distance as follows.

  d(a, b) = sqrt( (a_x - b_x)^2 + (a_y - b_y)^2 + (a_z - b_z)^2) )

So essentially the idea would be to calculate the pairwise distance between each of the backbone atoms. For any pair of atoms, there is steric clashing if the distance between them falls below a certain threshold. If I remember correctly, this threshold is the sum of the van der Waals radii of the two atoms.


Why do I feel my schoolbag to be heavier after meals? I am not sure this is related to psychology or not.

My friend casually commented to me that he feels his bag to be heavier after his meal. So I started observing my perception of weight of school bag after every meal. I did this for 3 weeks ( 1 log per day i.e. lunch, 5 days a week, 15 observations).

For 15 observations, 13 times I felt my bag to be heavier. These 13 times I had regular class after lunch. The other 2 times, I had an exam an hour later my lunch.

Is it psychological and / or body function related ?

Could certainly be physiological. After eating more blood is diverted towards the smooth muscles around organs for digestion. This will mean your skeletel muscles have decreased blood flow so less nutrients such as Glucose available to make contractions. As you have less energy available to contract the skeletal mucles you're more than likely to feel slightly weaker.

On the contrary it may he purely psychological! :) Good question though!


Math behind the Genetic Relationship Matrix The genetic relationship matrix (GRM) can estimate the genetic relationship between two individuals ($j$ and $k$) over $m$ SNPs and $i$ representing a specific SNP. What I don't understand from their equation is why we divide our summation by $m$ (the number of SNPs). $x_{ij}$ is the number of copies of the minor allele for the $j$-th individual in SNP $i$. $p_i$ is the frequency of the minor allele for SNP $i$.

This expression is a mean
$$\frac{1}{m}\sum_{i=1}^m ...$$
($m$ is the number of SNPs) of the ratio
$$\frac{numerator}{denominator}$$
where the numerator is a covariance
$$(a_i-C)(b_i-C)$$
and the denominator is the expected heterozygosity (it is also the variance of binomial distribution with n=2)
$$2p_i(1-p_i)$$
Therefore, it represents how much do two individuals covary $(x_{ij})(x_{ik}-p_i)$ respectively to what is expected on average $2p_i(1-p_i)$ averaged over all SNPs $\frac{1}{m}\sum_{i=1}^m...$, where $m$ is the number of SNPs.
It is a relative measure (relative to the expected heterozygosity) of covariance between each individual (averaged over all SNPs).
Does it help?


Neuron stimulation experiments Has anyone extracted a class of neurons (or a connected set of neurons) and stimulated them electrically to get an understanding of their behavior?

If so, could someone point me to papers along these lines? If not, do people have an idea of why this is not been technically feasible yet? As I would imagine this would be tremendously useful in building neuron models.

Short answer
Although outside my direct area of expertise, there is quite a lot of literature on the topic. The trick often is to use the correct keywords. Key in "recording + stimulating + ensemble + neurons", or "Utah + neuron + implant".

Background
There is quite some literature on this topic. For instance, a much used device in this arena is the Utah implant (Fig. 1), which can be used to record and also stimulate neurons (e.g., Nordhausen et al. (1994)). It has 100 penetrating electrodes and is even used in humans. There are also other approaches, e.g. by implanting a bunch of microwires (e.g., Nocolelis et al (1997)). In scientific jargon, the recording of multiple neurons simultaneously is often referred to as 'ensemble recording' (Nicolelis, 2008).

Fig. 1. Utah Implant. Source: WebVision

References
- Fernandez & Normann, Introduction to Visual Prostheses. In: WebVision, online book
- Nicolelis, Methods for Neural Ensemble Recordings, 2nd ed., Front Neurosci, CRC Press/Taylor & Francis; 2008
- Nicolelis et al. Neuron (1997); 18(4): 529-37
- Nordhausen et al., Brain Res (1994); 637: 27-36


Why do we have to move in the cold for higher chance of survival? To survive in the cold temperatures, a person should move as much as possible so that they do not freeze to death. But constantly moving also leads to the body becoming more and more exhausted.
Why doesn't the human body "know" that it is better to invest energy directly in heat rather than in movement and the resulting heat?
After all, the body already optimizes blood circulation, protecting the inner organs better than limbs like hands and feet.

As with any evolutionary "why" question, most any answer will likely involve some speculation. But we can still think about what we do know in relation to the question.
First, lets think about thermogenesis in humans. As your questions mentions, humans move to stay warm. This is because the conversion of chemical energy (in the form of ATP) into kinetic energy in our muscles is inefficient, resulting in some of the kinetic energy dissipating in the form of heat (instead of moving your body). Shivering is actually a cold-induced reflex that helps our body maximize the amount of chemical energy converted into heat through skeletal muscle contraction. So, in a sense, you body does "know" how to invest in generating heat without moving (without moving as much at least).
A different mode of non-shivering thermogenesis in mammals is mediated by a specialized type of fat called brown adipose tissue or brown fat. This brown fat is used by some animals to generate heat during periods of hibernation. However, adult humans tend to have very little of it. Human infants on the other hand, carry can carry quite a bit (up to 5% of total body weight). This could relate to a number of factors that make infants more sensitive to cold than adults, including having less developed skeletal muscles that are unable to generate much heat though movement or shivering.
It seems like one reason we can't generate heat very well without moving is that we don't carry much of this brown fat around. So, why don't we then? It could be that it's just energetically expensive, and those resources can be better spent elsewhere. Or maybe there could have been some negative health effect associated with carrying excess brown fat in adults. Whatever the reason, it comes down to a lack of selective pressure to maintain this extra tissue into adulthood.
But there's one other, more behavioral solution that might be worth consideration (although it's purely speculation at this point). In most naturally occurring scenarios where the body would be approaching a state of hypothermia, simply staying put and waiting for the temperature to change will seldom be your best chance for survival, even if you are doing burpees to stay warm. In order to ensure continued survival, one may need to actively change their condition of being in an environment that's too cold to maintain sufficient body heat. Humans are pretty good at changing their immediate circumstances. It might involve getting up and finding/building shelter, gathering fuel to make a fire, or migrating to someplace warmer. But in any case, it would require some amount movement accompanied by a cognitive motivation to move. Feeling less cold seems like a powerful motivator to me. If we had more robust means stationary thermogenesis, it's possible that we'd be able to survive a longer spell out in the cold just by conserving our energy a bit better, but that might not be the most effective survival strategy given the situation. Calories and liquid water can be hard to come by in extremely cold environments, and waiting for some other physiological need to motivate action might be less advantageous than proactively moving around to alter one's state of being too cold. Just a thought.


What is this insect in North Carolina? This insect is in my house in North Carolina, USA. I think it shares similar body features of that of a wasp, but it is far too narrow and has what appears to be a long stinger. What is it?

This is some species of ichneumon wasp.

The ichneumon wasps are parasitoid wasps in the order Hymenoptera. They commonly parasitize other invertebrates, especially larvae and pupae of Coleoptera, Hymenoptera, and Lepidoptera.

Specifically, this appears to be Dolichomitus irritator.

 Photo credit:  Thomas wilson

Here's another specimen of the same species found in Weymouth Woods-Sandhills Nature Preserve, Southern Pines, Moore County, NC:

 Photo credit:  Dorothy Pugh

You can find additional high-quality images from Jeff Tome's Flickr page.

I could not find too many sources with good information about this specific species. Fontanelle Forests' Nature Search provided the most complete info:

Description: 7/8 inch long, not including the ovipositor.  The head and thorax are black.  The abdomen is red-orange.  The legs are yellow and orange.  The antennae are black.  The black ovipositor is at least as long as the body and head.
Ecology: Parasitoids of many woodboring insect larvae including long-horned beetles, weevils, metallic wood-boring beetles and some moths that are wasp look-alikes.
Taxonomy: In the subfamily Pimplinae, which has 180 species in 28 genera in North America.


Non toxic low melting point alloy I am looking for an alloy with low melting temperature (< 350°C) which is not toxic when in direct constant contact with skin, food and overall in domestic environment. My application is a solder that can be used for soldering a ring.

I'm not a metallurgist, which you should probably ask... but there is this that I found:

Low Melting Fusible Alloys

Both Cadmium and Lead are toxic, but Bismuth, Indium, and Tin are not. An alloy of those might be what you're looking for. Indium raises the price-point considerably, as it's a few magnitudes more expensive than Bismuth and Tin.


Can any protein be phosphorylated? I am working with an Arabidopsis mutant with an F-box protein knocked out. It has been shown that F-box proteins targets must first be phosphorylated (Skowrya et al., 1997). I have heard of phosphorylation sites, but I can't find out whether every protein has them. Can any protein be phosphorylated?

Skowyra, D., Craig, K.L., Tyers, M., Elledge, S.J. & Harper, J.W. (1997) F-Box Proteins Are Receptors that Recruit Phosphorylated Substrates to the SCF Ubiquitin-Ligase Complex. Cell. 91 (2), 209–219.

Phosphorylation can occur on specific amino acids only, what you have called phosporylation sites. These amino acids are Ser, Tyr, Asp, Thr and His. In theory any of these amino acids may be phosphorylated, but in reality it may not actually occur for a number of reasons. Some of these are because of the change in overall charge of the protein which can influence the 3D conformation, or the amino acids are not accessible to specific kinases, etc. If you ask for the purposes of doing a Western blot, then the antibody specification sheet should indicate whether a phosphorylated form exists and there should be a reference to the literature describing this modification.


Why is haemophilia unviable in later stages of life? A sentence in my textbook is:

The possibility of female being haemophilic is extremely rare because mother of such a female has to be at least carrier and the father should be haemophilic (unviable in the later stage of life)

I know that haemophilia is an X-linked recessive disorder. Hence mother should be carrier and father must be affected for daughter to get affected. But I'm unable to understand what "unviable in the later stage of life" means.

I think what they mean is that those affected with haemophilia rarely survive to the adult life. This is less of a constraint for women, since a woman carrying only one recessive gene will not be affected by this disorder.


Could one hear without his ear? Might be a stupid question, but I'm quite curious about finding out ^^

If someone looses his ear, or for example cuts it of, just as Van Gogh did. Would he still be able to hear, since the actual organs that are responsible for hearing are on the inside of your ear canal? The ear itself more or less is just flesh, right?

Short Answer

Yes, you could hear, but it would be harder to localize sounds.

Longer Answer

The "ear" from a biological perspective includes the inner ear which is all of course necessary for hearing.

The external part of the ear is called the pinna/pinnae (plural), and yes, you can hear without pinnae; that's essentially what you do when you use in-ear headphones since they project right into the auditory canal and don't use the pinnae at all.

However, the pinnae are important both for collecting sound (therefore increasing the amplitude) and for sound localization, because they both shape the volume of sounds depending on direction (you can localize continuous sound by turning your head back and forth) and have a vital contribution to the head related transfer function that is crucial for localizing sound in elevation.

Sound localization experiments that use in-ear headphones sometimes first record the head-related transfer function with a microphone in the ear to then apply this filter to sounds that are played. This varies somewhat from individual to individual and captures the unique shape and position of the pinnae.

Note that sound localization is not only important for knowing where sounds are coming from, it can also be important to identify and pay attention to auditory objects, especially in noise, like one person talking in a cocktail party.

Algazi, V. R., Duda, R. O., Duraiswami, R., Gumerov, N. A., & Tang, Z. (2002). Approximating the head-related transfer function using simple geometric models of the head and torso. The Journal of the Acoustical Society of America, 112(5), 2053-2064.

Batteau, D. W. (1967). The role of the pinna in human localization. Proc. R. Soc. Lond. B, 168(1011), 158-180.

Brungart, D. S., & Rabinowitz, W. M. (1999). Auditory localization of nearby sources. Head-related transfer functions. The Journal of the Acoustical Society of America, 106(3), 1465-1479.

Hofman, P. M., Van Riswick, J. G., & Van Opstal, A. J. (1998). Relearning sound localization with new ears. Nature neuroscience, 1(5), 417.

Wenzel, E. M., Arruda, M., Kistler, D. J., & Wightman, F. L. (1993). Localization using nonindividualized head‐related transfer functions. The Journal of the Acoustical Society of America, 94(1), 111-123.


How do baby animals that primarily subsist on cellulose get their initial gut flora? In the case of mammals like giraffes and koalas, is that bacteria common on the plants they eat so when a baby starts to try to stick something besides its mother's milk in its mouth, it can't digest the cellulose at all the first time, but along with the cellulose, into its mouth went some cellulose-digesting flora that then begins a lifelong colony in the animal's gut? Is that about how it happens?

I would not expect this to be any different than other animals - they get the flora from the environment. Key components of the environment for newborns are:

Birth canal
Den / living quarters
Skin / fur of mother, especially near the teats
Diet
Feces of family members (animals sniff this and aren't so clean)


How was the resemblance between apes and humans explained in pre-Darwinian biology? Humans and apes have somewhat obvious similarities, these must have been apparent to natural philosophers before the possibility of a common ancestry was first proposed in the mid-1800's. These proposals were not formally made in Darwin's On the Origin of Species (1859), but his general ideas of common ancestry were built upon in Thomas Huxley's Evidence as to Man's Place in Nature (1863) and then Darwin's The Descent of Man (1871).

How was the resemblance between apes and humans explained prior to this shift in thinking?

The time before Darwinism, people believed life as an entity which is created rather evolved. But there were great biologists interested in the relationship between species, who deliberately thought of evolution ideas and some of them believed in ape-human similarities and placed humans and apes in same group.

In 1699, Edward Tyson, an English anatomist, dissected an ape specimen(chimpanzee) and showed that its anatomy closely approaches ours.But he didn't established any relationships between humans and apes. It was first done in 1738 by Swedish scientist  Linnaeus in his book Systema Naturae .After that in 1759, Lamarck, a French naturalist  who was Darwin's predecessor in general theory of evolution, stated that humans were derived from up-right walking apes.

  In 1759, just half a century before Darwin was born and precisely one hundred years before he published his famous book , "Origin of Species", Linnaeus, the great Swedish scientist, discovered that man was a mammal. He then placed man in the Order of primates, which means literary the first, or the highest,order of mammals.It comprises all the monkey like forms, including the man-like apes.
  Reference

References

Primate Evolution and Human Origins - Russel L. Ciochon & John G.Fleagle

Human Evolution: A Guide to the Debates - Brian Regal


Is this panspermia mechanism feasible? One episode of Cosmos: A Spacetime Odyssey describes a mechanism by which microbes could travel between planetary systems. As a star's orbit takes it around the galaxy, it occasionally passes through dense interstellar clouds. Rocks thrown into space at that time from the surface of a microbe-harbouring planet could carry life to temporarily nearby planets of another planetary system, before cosmic radiation would sterilise such rocks.

It's an interesting idea for TV; but scientifically, how plausible is this mechanism? My main concern is whether the average number of "infected" planetary systems per passage through an interstellar cloud is estimable as non-negligible.

Note: the use of "panspermia" in the title refers only to the question of whether an occasional interstellar transfer of microbes is tenable, not whether Earth's life originated outside this planet. As I understand it, the mechanism described above is lithopanspermia.

The theory is staggeringly improbable. However, so is life. The probability of life emerging from non-life is the basis of the misguided idea of intelligent design (a thinly veiled repackaging of creationism). Bear with me: the probability of life on Earth is 1. It is here, and this is the only observation of Earth we have. But the thought of complex life appearing out of some molecular soup by chance (abiogenesis) is also staggeringly improbable. But as I said, life is here. How did it get here? There are only three possibilities: Abiogenesis, divine creation, or from panspermia (which kicks the can down the road, because it had to have begun somewhere). God is no explanation at all, because even a mystical imaginary creator would have needed some mechanism besides waving a finger. So in terms of probability, both abiogenesis and panspermia would be astronomically improbable, but since life is here (probability of life is 1), then one of these two is the source of it. We have no hard evidence to choose between them.


How to define ammonites? I miss the definition of ammonite. In my opinion, many authors confuse the term "Ammonite" and "Ammonoid". Ammonoids (Ammonoidea) are large group of cephalopods including for example goniatites (Goniatitida), ceratites (Ceratitida) and ammonites (Ammonitida?).

But what do we call "true ammonite"? Is it an ammonoid with ammonitic suture? This way, many triassic, jurassic, creataceous and possibly paleogenic (danian) ammonoids could be called true ammonites, because they have complex (ammonitic) sutures.

Can you show me where ammonites are on phylogenetic tree? Can we call phylloceratina, psiloceratina, lytoceratina, ammonitina, haploceratina, perisphinctina and ancyloceratina ammonites? Can we call phylloceratina, psiloceratina, lytoceratina ammonoids, but not ammonites?

Ammonites are not strictly defined. One can reffer to ammonites as to the whole group of ammonoids (Ammonoidea, ammonites sensu latto). This is common, but not supported by most researchers. Researchers use the term "ammonoid" for paleozoic ammonoidea and "ammonite" for Jurassic and Cretaceous Ammonoidea (ammonites sensu stricto). Ammonites sensu stricto reffer to ammonoids with complex (ammonitic) sutures, which are typical for Jurassic and Cretaceous ages. However, complex ammonitic sutures are not exclusive for Jurassic and Cretaceous ammonoids. Ceratitic sutures are not exclusive for Triassic either and occur in Jurassic ammonoids, too.

  So caution must be exercised when using suture lines as a means of
  classification. To obviate some of the problems posed by this
  simplistic classification, Wedekind, in 1918, introduced the terms
  palaeo-, meso- and neoammo-noids to classify ammonoids better.

(PDF) Goniatites. Available from: https://www.researchgate.net/publication/262048294_Goniatites [accessed May 12 2019].


What would happen if some neurons are unmyelinated? I know that cold receptors have myelinated axons and heat receptors don't.

From a physiological perspective, what could be the consequences if cold receptors were unmyelinated? Would that pose some detrimental effect?

From a physiological perspective, what could be the consequences if cold receptors were unmyelinated?

Per the resistor-capacitor model of a neuron, one would expect signals conducted through myelinated axons to be faster, more sharply localized in time (spikes don't broaden out as they propagate down the axon), and less costly of energy, vs in unmyelinated axons.

I wouldn't read too much into significance as there's all kinds of ways to accomplish the same effect at any level, e.g. faster conduction is also accomplished through larger axon diameter, and better temporal localization is also accomplished through signal coding, and energy consumption is also modulated by tweaking membrane composition of ion channels etc.

  Would that pose some detrimental effect?

Generally, if it's normal for axons to be unmyelinated then one would expect things to be running normally. Demyelination of normally myelinated axons pretty much always leads to loss of function in sensation or motor control.

The question to ask here is rather "Would myelination of normally unmyelinated afferents pose some detrimental effect?" I'm actually not aware of any disorders in which there is "extra myelination" -- Even the dysmyelination disorders are all loss of function in the proteins, not extra insulating myelin or myelination in the wrong place. That doesn't mean there aren't overmyelination disorders, but does suggest that our nervous systems are less sensitive to overmyelination if it is a thing that happens.

One would expect conduction velocity and energy consumption to decrease, okay. Probably not an issue unless temporal synchronization in that signal is important; even then "plasticity" usually irons out these problems.

If the normally unmyelinated afferent axon normally has synapses homogeneously distributed along its shaft, then abnormal myelination could cause abnormal development of these synapses. As contact area would only be available between myelin "nodes," synapses would be crowded into smaller area. Also depending on how development works in the systems you're considering, overmyelination might affect the spatial pattern of secreted growth factor concentration which could affect synaptic development along the axon shaft. But this is all completely hypothetical.


Competition with other individuals of the same species vs. adaptation pressure from predators It is often said "You don't need to outrun the cheetah, just the other gazelles", thus emphasizing that greater part of the adaptation pressure comes from competing with other individuals of the same species and not directly from predators/parasites (which are seen as more indirect forces similar to the living conditions imposed by the environment (climate, geophysical factors, etc.))

My question is:

Isn't there a difference between competing with other individuals of the same species for food, habitats (i.e. resources) and competing with them in avoiding being eaten?

The correct answer is, "it depends."  The traits that will be under the strongest selective pressure will be those related to survival in the face of the most common causes of death for that species. If food is abundant but so are predators, then clearly predator evasion will be of supreme importance. If food is scarce, then perhaps metabolism-related traits will be under strong selective pressure. But it's important to remember that just because one selective pressure is stronger doesn't mean that the rest disappear. Thus, the individual's survival is dependent upon really a composite fitness that depends on a countless array of selective pressures, some of which may be larger components than others. The competition between individuals of the same species is really a complex interplay of fitness effects, then.

As for the maxim about outrunning a cheetah, what it's illustrating is that the gazelles are not competing with the cheetah for survival. They're competing with each other. If you want, you could expand it to say "...just the other gazelles and the rest of the herbivores in the environment". If a herd of gazelles and a herd of some slower animal are nearby and a cheetah attacks, one of the individuals from the slower species will probably get caught and all the gazelles will get away. The point is that the gazelles and the cheetahs fill very different niches in the environment, so they don't really compete for the same resources (as a matter of fact, one is the primary resource of the other).

When it comes to determining survival, one talks about fitness only within the context of the population (or, if you want, between species directly competing for the same niche). The less fit members of the population do not survive. Thus, the less fit ones that fail to evade the predator are simply doing a worse job evading the predator than the other members of the population. But it's not only the relative fitness that is important. Imagine that a new predator migrates into the environment, for which none of the prey has any evasive adaptation. Even though there may be a relative fitness between them regarding evading this predator, if even the best individual is not good enough to evade it, they would all have an absolute fitness that is too low to ensure survival. Then the saying breaks down, since none of the gazelles can out-run each other with respect to evading this new predator.

Of course, this idiom falls apart when you start talking about asocial species, since there aren't any other individuals around to out-run.


Veins collapse when empty Veins collapse when empty. That's because they have thin and almost inelastic walls. What has inelasticity and thinness of the walls to do with the collapsing of the veins?

Your body exists at a certain pressure, determined by your surroundings; usually, this is about 1 atmosphere of pressure, but it can go up or down (e.g. when you fly on an airplane, or when you go diving). The pressure that your surroundings put on your skin is transmitted throughout your body, and your body "pushed back" against it.

However, this means that all your blood vessels have that pressure weighing down on them along their length. Normally, when they're full of blood, the pressure of that blood will press the blood vessel outwards to counter-act this. Without the blood, however, that pressure within the blood vessel is no longer sufficient to withstand the pressure being exerted on it from the outside.

Since the walls of the blood vessels aren't thick enough to have enough structural integrity to withstand that pressure differential, they then proceed to collapse.


Can exposure to blood make pathogens resistant to the immune system? If a drop of my blood is dropped into a pool of pathogens. Does that act as "reverse-vaccination" for said pathogens?

I see this it as a potential risk for bacteria/viruses to compete or get acclimated with the weakened/dormant/key-specific of the immune system.

Please correct me if I'm wrong.

You have got the concept of vaccination a bit wrong. Pathogens have to evolve to acquire resistance to immune system (or antibiotics). Technically, the white blood cells also evolve to acquire resistance against pathogens if they don't have a strong innate immunity. Development of immunity after vaccination is also not instantaneous. The pathogen population has to "grow" in the blood for at least a few generations to become resistant. A drop of blood would probably not give the pathogen enough time to evolve. Moreover, your white blood cells will die quickly outside the body unless they are cultured in a controlled environment. Therefore, the selection pressure to evolve would also not be there.


How are DNA polymerase error rates measured? It is well known that the first DNA polymerase, Taq, is quite error prone. Newer generation commercial enzymes that have either been isolated from different thermophile species or have been improved by recombination are less error prone. How are these error rates compared? For instance, if this is done by Sanger sequencing, the average signal will dominate in reading the output and so it will be very unlikely to pick up on errors by this method.

According to their website New England Biolabs use a version of the approach pioneered by Wayne Barnes, as described in:

  Kermekchiev, M.B., Tzekov, A and Barnes, W.M. (2003) Nucl. Acids Res. 31, 6139–6147

This is basically an assay for the mutation rate in a PCR-amplified lacZ (β-galactosidase) gene, assayed by transforming E. coli, plating on the chromogenic β-galactosidase substrate Xgal, and then scoring white colonies as mutated genes. Also according to NEB, Agilent Technologies use a similar mutational assay, but based upon the lacI (lac repressor) gene.


Can anyone help me identify what type of horns these are? I picked these up at an estate sale a few years ago and now need to identify them for shipping purposes.

They are 29x18x10.5 inches in size.

A friend who works in antiques believes the are over 100 years old based on the wood they are attached to and thinks they belong to some kind of ram. That's all the information I have on them.

Any help would be appreciated.

Thank you.

Those look very much like "Catalina" goat horns. They're a popular trophy game to hunt, specifically for these sorts of displays. The goats themselves originate in Spain but are commonly found in the United States, now.


Comparative leg sizes When I was a child, my father showed me the classic essay "On Being the Right Size", J. B. S. Haldane.  It talks (among other things) about how large animals need stockier legs to support their weight.  I weigh about the same per leg as a 350 lb deer, but my legs are closer in diameter to those of a 1500 lb horse. Why?

There is an interesting relationship between the length of an animals femur, the thickness and the mass of the thickness. A point that should be taken into account is that bones can different densities and so might be able to support varying amounts. The muscle in you leg also does nothing for the support of you weight it is (basically) all in the bone. Really looking purely at the leg won't tell you much you need to strip back the tissue and get you measurements straight from that. Given the different gate strategies of various animals this can lead to differing levels of muscle surrounding the leg and could be confounding your answer.

Walter Lewin a professor of physics at MIT did a lecture series where in the first lecture he went off on one about the relative sizes and thickness of animal femurs and it is really interesting (http://www.youtube.com/watch?v=PmJV8CHIqFc - between 11 minutes and 22 minutes). The short answer was that the ratio between the thickness and the length stays similar relative to the length.


What is the cause of a protuberant belly in kwashiorkor? Kwashiorkor is a PEM (Protein–energy malnutrition) usually characterised by a pot belly. Why is there a pot belly in the case of a malnutrition? I have found contradictory reasons. This paper says that it is due to a fatty liver. This website says it is due to excess fluid accumulation in the tissues.
I noticed that these children have very skinny limbs. When I pointed that out to my teacher a few years back, she told me that the subcutaneous fat from the thighs accumulates under the belly. I can find no source confirming that, though.
So, what is the cause of the pot belly?

The Gastroenterology paper you cite doesn't mention distended bellies at all.  There is no dispute that fatty liver is a symptom of kwashiorkor.  But the Wikipedia article makes it quite clear that the cause of the distended belly is edema.

  The extreme lack of protein causes an osmotic imbalance in the gastro-intestinal system causing swelling of the gut diagnosed as an edema or retention of water.[4]

And:

  Compromised fluid recovery results in the characteristic belly distension observed in highly malnourished children.[14]

Here's another source:

  To understand the reasoning for this, it is important to know that in malnourishment, the rounded abdomen is not due to fat accumulation. Instead, the water retention and fluid buildup in the body cause the abdomen to expand. This results in a bloated, distended stomach or abdominal area.

The rest of the article goes into more detail on the phenomenon and mechanism of action.

This source seems less authoritative, but also suggests that weakened abdominal muscles (due to protein deficiency) also play a role:

  The swollen belly is the result of not only that enlarged liver, but also the loss of muscle mass, which leads to weak abdominal muscles. Together with a weakened lymphatic system that is unable to keep up with the body’s liquid wastes, when those wastes accumulate in the abdomen, the belly becomes distended.

So the author suggests that fatty liver contributes to belly distension, but is not a sole cause.  None of the sources I looked at mentioned fat accumulation as a contributor, but rather eliminated it.


What is a phospho-protein binding domain? Is this just a domain that binds proteins that have been phosphorylated? And it mediates signalling between an activated/phosphorylated protein? How is this significant with BRCA1?

This is a very large topic but I will try to partially provide an answer. Now your question has three parts as far as I understand it.

Do phospho-protein binding domains only bind to phosphorylated proteins i.e. is that their sole (observed) function.
What roles do phospho-protein binding domains mediate.
Function of BRCA1 phosphorylation/phospho-protein binding

Just to get some basics out of the way, there are three amino-acid residues in a protein that can become post-translationally modified by phosphorylation, including serine, threonine and tyrosine. Now the purpose of protein phosphorylation ranges from activation/deactivation signals to binding and changing cellular localisation i.e. recruiting a protein to different part of a cell. Now tyrosine phosphorylation, which I know by far the most about is capable of all the above. So if you think about a receptor tyrosine kinase (RTK) such as epidermal growth factor receptor (EGFR), once a ligand such as EGF binds to it, it becomes tyrosine phosphorylated (activated) through its intrinsic tyrosine kinase activity. Once tyrosine phosphorylated, many proteins are capable of binding to tyrosine-phosphorylated RTKs such as Grb2 to induce a signal downstream of RTKs. So as you can see, phosphorylation of RTK affected cellular localisation of GRB2. Excellent Ras signalling review by Karnoub & Weinberg, 2008 Nature reviews (Fig 5). Grb2 binds to phospho-RTKs through a specific domain called Src-homology 2 (SH2) domain, which provides a platform for other proteins such as Son of sevenless (SOS) which is a GEF to bind to it and induce RTK signalling through Ras. So in the above case the role of phospho-protein binding domain (SH2) is to change cellular localisation of multiple proteins and mediate signalling.

Now I'm no expert in BRCA1 but just had a quick look and it seems serine phosphorylation of BRCA1 may be responsible for its recruitment to the DNA site of damage and if serine residues in BRCA1 are mutated, the protein will no longer get phosphorylated, which may effect its recruitment to the DNA sites of damage, which may affect its DNA damage response function (Clark et al 2012 Comput Struct Biotechnol J). Now BRCA has a phospho-protein binding domain called BRCT, and that is also thought to mediate DNA binding and binds to phosphorylated and non-phosphorylated proteins. So BRCA1 phosphorylation and phospho-protein binding is though to be important in its function (Clark et al 2012 Comput Struct Biotechnol J). So to answer your question in short, phospho-protein binding domains such as BRCT do not necessarily bind to their target proteins through phosphorylation.

Hope this helps.


How to improve DNA extraction I am using the following protocol to extract chromosomal DNA from bananas:

Cut up one banana into small pieces, approximately (1 cm3)
Add ½ a cup of warm salt water and the banana pieces into the blender and set to max for 5-10 seconds
Poor into a beaker and add 1 teaspoon of detergent to the beaker
Stir for 5 mins with a spoon to break down the plasma membrane
Place the mixture into a centrifuge for 30 seconds
Pour the mixture through a gauze with a beaker catching the liquid underneath
Smoothly pour cold ethanol into the mixture at a 1:1 ratio so a clear layer of liquid will form on top of your mixture

Why is the centrifuge step (5) needed? Why would that increase the yield of DNA?

In a protocol like this, a low centrifugation is typically used to separate DNA in solution from larger, heavier components of the mixture. By lightly pelleting the banana slurry at the bottom of the tube, the DNA in solution is less likely to stick to that fraction of the mix when you pour it through the gauze. That's where your increased yield will come from.


Is the phrase "transmembrane segment" equivalent to the transmembrane domain of a protein? I am reading the Handbook of Neurochemistry and Molecular Neurobiology  and I am learning about the cell adhesion molecule NCAM2 and I have come across the following:

The overall structure of NCAM2 is similar to that of NCAM. Thus, NCAM2
consists of five Ig‐modules (supposedly of the C2‐type) followed by
two Fn3‐modules. The protein exists in a GPI‐anchored isoform and in a
transmembrane isoform that contains a 20–25 amino acid transmembrane
segment followed by a 106–119‐amino acid cytoplasmic tail (Alenius and
Bohm, 1997; Yoshihara et al., 1997).

I know that NCAM2 is located at the cell membrane and has an extracellular, transmembrane and intracellular domain. However, for the above statement: The protein exists in a GPI‐anchored isoform and in a transmembrane isoform that contains a 20–25 amino acid transmembrane segment followed by a 106–119‐amino acid cytoplasmic tail, is the term 'transmembrane segment' equivalent to the transmembrane domain? Further is the term 'cytoplasmic tail' equivalent to the intracellular domain? Any insights are appreciated.

Yes
I'll admit defeat in trying to find the section in the text you linked - if there's any one thing Google can't do, it's search.  But questions like this are better put to Uniprot, which gives quite a bit of information.  Following that link, you'll see they identify 21 AA of transmembrane topology from 698 to 718, with a cytoplasmic domain afterward.  So the cytoplasmic tail is the intracellular domain.
In a sense there is a second transmembrane domain - the signal peptide from 1-19 - but because it is cleaved little attention is paid to it.  The extracellular domain starts at 20, with an N terminus outside the cell.
To quote Wikipedia, a transmembrane domain "usually denotes a single alpha helix of a protein".  You should probably listen to them on such an issue because nobody is more fixated on semantics (it's a sort of vote).  Philosophically, you can picture that multiple transmembrane segments could operate as a functional unit - but each of these segments would be separated by some region of extracellular or intracellular sequence from the next.  A "domain" in a protein is a self-contained unit in the primary sequence, not just a series of helices that turn out to be near each other, so that wouldn't work.  And in fact if you look at a GPCR paper they speak in standard terms of seven transmembrane domains even while analyzing how they function together.


Why are restriction sites palindromic in nature? Any restriction site given in any fragment of DNA or vector molecule is a palindrome. eg restriction site for the endonuclease EcoRI is

5'...GAATTC...3'
3'...CTTAAG...5'

Clearly, this is a palindromic sequence. Why is that?

Not all restriction sites are palindromes : https://en.wikipedia.org/wiki/List_of_restriction_enzyme_cutting_sites:_E%E2%80%93F#Whole_list_navigation

EcoRI: GAATTC (note that this is not 'palindromic' in the usual sense (e.g.'anna', GAATTC read backwards actually gives CTTAAG), but only if given the G-C A-T binding)

The double strand of DNA is composed of one strand in direction 5'-3' and another into the other direction (3'-5'). Restriction enzymes tend to be homodimers, thus would bind to both sides of the double strand, expecting the same recognition sequence. But as one strand runs into the other direction, the strands need to be palindromic to form a double strand.


Hydrogen peroxide decomposition and catalase uses All google searches have simply returned more info on catalase. I'm looking for a catalyst that isn't found inside living organisms which  can break down H2O2. Looking for any resources to look at, or just examples of other catalysts.

Side question since I don't want to clutter with a new thread.
Can catalase be used for anything other than the decomposition of h2o2?

Manganese(IV)oxide can be used as a catalyst to speed up the decomposition of hydrogen peroxide


How do opportunistic infections affect an immunocompromised or AIDS patient? I mean, everyone knows that AIDS patients don't die of the HIV infection, rather the opportunistic infections. But if HIV only affects T lymphocytes, and destroys them, then that means only cell mediated immunity and humoral immunities are affected (since B cells need helper T cells to be activated).

The body should still be producing other types of leukocytes like neutrophils and macrophages, which should eliminate most bacteria. So does HIV infection render the mononucleaf phagocytic system useless as well? If yes, how so?

Clinical diagnosis of AIDS in a person infected with HIV is based on the following criteria:

A CD4+ T-cell count below 200 cells/µl (or a CD4+ T-cell percentage of total lymphocytes of less than 14%)

OR

The patients has one of the few "indicatory" diseases that strongly suggest severe immunodeficiency. See the list of this diseases here. Usually they have fatal consequences.

As we can observe, there are mostly fungal and viral infections that live inside the host cells or (in case of tuberculosis) diseases caused by intracellular bacteria. They can be overcame only with working mechanisms of cellular immunity. Other mechanisms are simply too slow, not specific or not precise enough.

Another issue is an impairment of the immunological surveillance and much higher risk of cancer in individuals diagnosed with AIDS. Precise elimination of malignant cells is fully dependent on cellular immunity.

[EDITED]
For further reading, recent paper analysing the most common causes of death in patients with AIDS in the era of anti-retroviral therapy.


Is there any evidence that soft tissue can be preserved for 65m+ years and if not what hypotheses exist to explain it? I read an article on howstuffworks.com and they mentioned how we have found soft tissue in dinosaurs. According to the article even Mummies and Mammoths have no soft tissue left. Is there any evidence that soft tissue can remain intact this long even under perfect conditions? and if not what are some hypotheses that could explain it?

Schweitzer et al. (2007) studied soft tissue preservation in a number of specimens, including an 800-1000 year old moas, 300,000 year old mammoth and mastodon, and 65 million year old *T. rex. and Triceratops. The oldest specimen was a 78 million year old Brachylophosaurus. Their goal was to try to find common environmental conditions that favor soft tissues preservation in fossils. As of this study, they have not been able to identify a single common environmental factor that seems to favor soft tissue preservation. They did note, however, that the specimens from which they could extract soft tissue (with varying success) were from fluvial sandstone environments, meaning sandy rivers. They (so far) could not extract soft tissue from terrestrial mudstone or marine environments.

Note that Schweitzer et al. did successfully extract soft tissue from the mastodon. The conditions required for mummification are probably not conducive to soft tissue preservation.  Here is a good blog article on one of Schweitzer's previous studies of soft tissue preservation.

The importance of extracting soft tissue from fossils cannot be overstated. Based on Schweitzer's work, her and her colleagues (Organ et al. 2008) were able to develop a phylogeny that incorporated both mastodon and T. rex. The used the amino acid sequence from collagen, a protein that is abundant in soft tissue. She and her colleagues repeated the analysis (Schweitzer et al. 2009) and included Brachylophosaurus, a hadrosaur. As predicted by morphological and other evidence, the mastodon was most closely related to modern elephants and the two dinosaurs were most closely related to modern birds and alligators.

Here is the phylogenetic tree derived from Schweitzer's 2009 study. Mammut is the mastodon. Brachylophosaurus and T. rex are the two dinosaurs.

Literature Cited

Organ, C.L. et al. 2008. Molecular phylogenetics of mastodon and Tyrannosaurus rex. Science 320: 499.

Schweitzer, M.H. et al. 2007. Soft tissue and cellular preservation in vertebrate skeletal elements from the Cretaceous to the present. Proceedings of the Biological Society of London B: 274: 183-197.

Schweitzer, M.H. et al. 2009. Biomolecular characterization and protein sequences of the Campanian hadrosaur, B. canadensis. Science 324: 626-631.


Pollinator mating system in orchids I came across three terms in an article on pseudocopulation. However I don't quite understand what it means.

They are:

1) solitary and haplodiploid

2) social and haplodiploid

3) diploid

These are mentioned in reference to pollinator mating systems in orchids. Could anyone please explain the above mentioned terms?

As 3cat already stated, the terms actually refer to the pollinators. While solitary and social describe the behavioural traits (see this wikipedia article), diploid and haplodiploid give information about the chromosome number of the pollinators (see here and here).

The descriptions in the article depict different combinations of both characteristics.