What is the name of this plant (see pic)? This plant was found growing in Colombia.

That looks like a member of genus Lupinus, flowering plants native to North and South America:

I couldn't find a good resource for species of Lupinus in Columbia so I can't help you with the species, unfortunately.


What are the different, high-level programs along which a eukaryotic animal cell can follow? What are the different, high-level, disjunct (mutually exclusive at one particular point in time) programs or pathways along which a eukaryotic animal cell can follow? Examples of programs would include growth, cell division, senescence and quiescence. Are there programs that differ between cell types?

Any I'm missing? If so, references much appreciated.

To see the width of your question, have a look at what the Gene Ontology considers a cellular process:

http://www.ebi.ac.uk/QuickGO/GTerm?id=GO:0009987#term=children

I don't think you can agree on what's high-level, so it's better to see them all, I think. Also, for completeness, there is a list with cell types which is admirably maintained:

http://en.wikipedia.org/wiki/List_of_distinct_cell_types_in_the_adult_human_body


Why are there no endoparasitic mammals or reptiles or birds? I am curious why there aren’t any endoparasitic mammals, reptiles or birds

Endoparasite being a parasite that live In the host whereas ectoparasite lives On the host

I hope this clears up confusion

Short answer size.

endo/ectoparasites need to be small to go unnoticed, and be hard to eliminate. The smallest mammals and birds are still much larger than a flea, fluke or other endoparasite. That's why larger parasites leave after feeding, if a vampire bat hung on the cow indefinitely the cow would eventually notice and do something, something as simple as rolling over could kill them quite effectively. While an animals infested with fleas can not do much to get rid of the fleas. The few large endoparasites either evolved from much smaller parasites (tapeworms) or exploit some strange insensitivity in the host(cymothoa) This means there is no path to ectoparasite which could lead to endoparasite.

Why there are endoparasites evolved by other means in vertebrates what exactly would they evolve from, there are no birds or mammals that would survive being cut off from outside oxygen or passing through a digestive system. It is like asking why no flying trees have evolved there just is no path to get there or from where they are now, or if there is a path it is so unlikely that it has not occured.


Why is it necessary to have both cone and rod cells in the eye? Our eyes have both cone and rod cells. Rod cells measure the intensity of light whereas cone cells identify the colour of the image formed in the eyes. So cone cells must also be able to identify white, black and grey and also their shades.

So it wouldn't have been that much trouble to just have cone cells cells as identifying black and white would have been the same as measuring the intensity of light. Wouldn't it?

First off - both the rod and cone system measure light intensity; both sensory cells increase their responses when excited by more photons (Purves et al., 2001). Hence, your introductory sentence that rod detect luminescence and cones color is incorrect. They are both sensitive to luminescence.

You are correct that rods detect gray scales, while cones perform color coding. Both systems can detect gray shades; while rods are limited to that, cones are not. Rods are very sensitive to light and in a dark-adapted state are capable of detecting a single photon. Hence, they operate under conditions of low-lighting at night and as such they mediate night (scotopic) vision. Cones are photon-hungry and need more light to operate (photopic conditions).

Why have cones? Because color vision helps to detect and differentiate stuff.
Why have rods? Because night vision is helpful.
Why have both? To be successfully equipped to thrive in both light and dark environments.
Do we need them both? No - even nocturnal hunters that don't have rods have been shown to be able to hunt at night. Not only that, these geckos have been shown to be able to detect color in starlight (Röll, 2000). Under these lighting conditions, human retinae rely on the rod system and are unable to detect color.

References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates
- Röll, J Neurocytol (2000), 29(7): 471-84


Is spliceosomal RNA called snRNP or snRNA? I have been reading articles by various sources, and they seem to interchangeably call the U1/U2/U4/U6 compounds involved in RNA splicing snRNPs as well as snRNAs.

This confuses me deeply. They must only be one or the other, no?
Thank you in advance!

snRNA: small nuclear ribonucleic acid

snRNP: small nuclear ribonucleoprotein

snRNA refers to the RNA itself. snRNP refers to snRNA complexed with some protein(s). You could call spliceosomal RNA either depending on the context.


How many cells does the smallest animal have? Note: question rewritten to prevent misunderstanding and make it more answerable

I know that some small animals like C. elegans display surprising sophistication with a very small number of cells. But I wonder, among the animals with known/estimated cell count, which has the fewest cells?

To make the question answerable, please note these constraints:

I'm only asking about members of the kingdom Animalia, so single cell organisms and colonials like Vovox are excluded. If there are single cell organisms which are classified under Animalia (I think there aren't, but not 100% sure), I still want to know about the smallest multicellular animal.
I'm only asking about species where we can distinguish individuals. If some kind of polyp or sponge is just a bunch of cells which can merge with or separate from other cells and remain a viable organism, it's not interesting.
Please only consider species where the adult form reaches some size and stops growing. (Macroscopic) examples like the tapeworm, which continues building more proglottides throughout life, or fish which continue getting larger as they age, are excluded.
If the species consists of distinctive, stable "subgroups" of different sizes, the smallest size subgroup counts. For dogs, the size of the average chihuahua counts. For C. elegans, the size of the hermaphrodite (959 cells vs 1031 in the male) counts.
What counts is the number of cells in a healthy adult of the species or the relevant subgroup. For non-eutelic animals, make that the average healthy adult. Not the smallest ever observed exemplar, and also not amputated or stunted exemplars.
I am aware that we haven't discovered all microscopic animals yet, and haven't counted the cells of all discovered ones. Still, I'd like info on the current level of knowledge, including current known cell count, evidence that something has less than the current lowest known-for-sure count, and other relevant information.

Rotifers are microscopic protostomes with around 1000 cells apiece.  This website claims the smallest rotifers have less than 100 cells, but I couldn't confirm this.  Most rotifers are eutelic — within a given species, each adult individual has the same number of cells (Encyclopeia of Life: Rotifers).

(Source)

Edit: Myxozoans might be even smaller.  These are microcsopic parasites that have been classified as cnidarians based on molecular studies.  They have complicated life cycles including a single-celled stage.

(Source)


What happens when you take a deciduous tree and place it in a climate controlled greenhouse? The greenhouse would have stable level of light, (matched with day/night wavelength brightness changes like outside the greenhouse), humidity and temperature.

Do certain processes in the tree not trigger?
Does this harm the organism, and are there changes in life expectancy?

It harms the trees, seasonal chemistry in the plant is reduced and weakened they have tried growing apples and decidious fruit trees at the equator and they have to treat them chemically to help them stay stronger:
http://www.actahort.org/books/49/49_14.htm
the tropics have seasonal queues, and in a greenhouse with no temp and light change, the plant would be very disoriented, the critical glucose and leaf cycling would be very degraded, because plants have most of their queues from temps, water and sun.
http://www.madsci.org/posts/archives/2001-02/981072513.Bt.r.html
more infos


How does a decrease in free Ca2+ result in nerve/muscle overexcitability? I have in my notes that a decrease in free Ca2+ increases membrane permeability to Na+ so that it is brought closer to threshold, but no further details. So how does this work?

The thing is that the Voltage Gated Channels,they are closed in resting state because Ca2+ is bound to it.So,in the resting stage,Ca2+ somewhat blocks the Na+ - K+ channel.But since there is low Ca2+ so there won't be much Ca2+ for guarding of channels and so it will lead to an increase in permeability.See the photo and imagine the gate being guarded by a Ca2+.I hope this helps.


Cat purring: What are some possible underlying mechanisms behind purring and bone remodeling and formation? http://www.scientificamerican.com/article.cfm?id=why-do-cats-purr

The article above says that cats purr mostly when they're wounded or under duress. They hypothesis that cats purring leads to increases in bone density and bone healing. How is this possible? What are some physiological possibilities for something like this to occur?

I don't see any journal articles backing up any of these claims. Is it similar to how ultrasound in clinical trials works?

Is the cat purring affect formation of osteoblasts? What is possibly happening microscopically?

The author is likely referring to the mechanosensory behavior of bone (reviewed in Huang and Ogawa, 2010; lots of Google Scholar citations). Bone loading produces very tiny mechanical deflections (strain) which are translated into biochemical signals that promote bone growth through the action of osteoblasts. Burger and Klein-Nuland (1999) review possible mechanisms.

The low frequency soundwaves produced during purring overlap the frequencies that have been shown experimentally to induce bone formation (1-50Hz; e.g., Castillo et al., 2006; Xie at al. 2006). Although an interesting hypothesis, I don't think that osteogenesis in response to purring has ever been experimentally shown in cats.

Huang C, Ogawa R. 2010 FASEB J. 2010 Mechanotransduction in bone repair and regeneration. 24(10):3625-3632.

Burger EH, Klein-Nulend. 1999. Mechanotransduction in bone--role of the lacuno-canalicular network. FASEB J 13(Suppl):S101-S112.

Castillo AB, et al. 2006 Low-amplitude, broad-frequency vibration effects on cortical bone formation in mice. Bone 39:1087-1096.

Xie L, et al. 2006. Low-level mechanical vibrations can influence bone resorption and bone formation in the growing skeleton. Bone 39:1059-1066.


Why severely increased Ligand (eg Hormones) concentration downregulates the Receptor? As an example continuous high blood level of GnRH in humans causes a suppression of LH and FSH. This is due to the fact that increased GnRH downregulates GnRH-Receptors . My question is how this is done and why? What are the probable molecular mechanisms underlying this effect?

Kumar P, Sharma A. Gonadotropin-releasing hormone analogs:
Understanding advantages and limitations. J Hum Reprod Sci.
2014;7(3):170-174. doi:10.4103/0974-1208.142476
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229791/

Gonadotropins are hormones synthesized and released by the anterior pituitary gland, which act on the testes and ovaries to increase the production of sex hormones and stimulate production of either sperm or ova.
The hypothalamus contains Gonadotropin-releasing hormone (GnRH). Intermittent released of GnRH is responsible for the biosynthesis and secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary gland.
LH stimulates interstitial cells to release testosterone, which triggers spermatogenesis. The rising level of testosterone exerts negative feedback control on the hypothalamus and pituitary glands.
GnRH has been shown here in a negative feedback loop
This feedback loop has great interplay with the number receptor levels as you suggest.
(From a quick search) I found one paper (behind a paywall) that states the following information when studying rats:

We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection [of GnRH agonist (triptorelin)] (about 38% of control).

Transcription does not equal translation, but it seems that acute increased levels of GnRH cause a reduction and mRNA of GnRH and GnRH-R and therefore potential reduction (down-regulation) of protein levels of GnRH-R.


What are the differences between how glucagon and cortisol work to increase blood sugar? As I understand, both cortisol and glucagon cause an increase in blood sugar concentrations. However I don't understand how they work differently or why they work separately. I would be very grateful if someone could explain the seperate roles and functions of these two hormones and also the different effects that they have (I believe cortisol also has something to do with promoting lypogenesis in adipose tissue at the trunk of the body and lypolysis at the extremities).

Glucagon and cortisol are VERY different types of hormones, though each of them can affect glucose metabolism and effectively can increase glucose concentrations in the blood (albeit through different mechanisms).

Glucagon, pictured above, is a 31 amino acid peptide hormone (i.e. PROTEIN) that is released from the alpha-cells within the pancreatic islets. Glucagon travels through the blood and acts predominately in the liver on glucagon receptors. The glucagon peptide binds to the glucagon receptor on the OUTSIDE of the cell and transmits a signal to the INSIDE of the cell. This occurs when the glucagon binds to the receptor, changing its conformation or "shape" on the inside of the cell, which then causes binding and activation of a G-protein inside the cell ($G_S$). This $G_S$ protein activates an enzyme within the cell (adenylyl cyclase) to increase the concentration of a substance called cyclic AMP (aka cAMP) that activates a number of enzymes that ultimately increase the amount of glucose released by the liver. These effects are IMMEDIATE effects, which is why we sometimes give glucagon injections to treat patients with hypoglycemia (i.e. dangerously low blood sugar concentration). However, sustained glucagon signaling likely has effects on the expression of the enzymes that cause the glucose to be released from the liver as well (though that is a discussion for another question).

Cortisol, pictured above, is a steroid hormone (i.e. LIPID) that is released from the adrenal glands, specifically the zona fasciulata, which is the middle of the three 'layers' of the adrenal gland. Cortisol is referred to as a glucocorticoid and exerts its major effects through changing gene transcription in a variety of cell types. The way that cortisol does this is by binding its cortisol receptor, which is generally thought to be in the cytoplasm inside the cell. Upon binding of cortisol to the cortisol receptor, that complex is then transported into the nucleus of the cell where it binds DNA and can increase or decrease the transcription or expression of target genes. In the case of cortisol, these genes are for the enzymes that increase glucose production of the liver, and thus increase the body's capacity to maintain or elevate blood glucose. There is also some evidence that cortisol has additional effects independent of gene transcription, but that is outside the scope of this question. Regardless, the effects of cortisol on glucose metabolism are not immediate, but rather they take >30 minutes to several hours to begin to take effect.

As mentioned in the question, both glucagon and cortisol affect glucose metabolism. Cortisol also affects the transcription of a number of genes involved in adipose tissue and lipid metabolism, as well as genes that are involved in protein metabolism and inflammation. Cortisol can be injected into a patient with an autoimmune "flare-up" in order to quell the inflammation, but those are different mechanisms of cortisol than its effects on glucose metabolism. A description of those effects is also outside the scope of this question, but could easily be read about in recent reviews on cortisol available on PubMed, e.g. Recent Cortisol and Fatty Liver Review.


How are collagen fibers in skin aligned with respect to skin surface? I read in one paper that collagen fibers in dermis are randomly oriented in direction with respect to the skin surface. I can't locate that paper now. However, I came across this paper that indicates that collagen is always aligned parallel to the skin surface (page 3). Which one is correct?

Collagen underneath the epidermis is not completely randomly oriented, in fact mostly they are directed along the muscle fibres beneath them.

This was first observed by Karl Langer and hence was given the name as langer's lines( of skin tension). This peculiar arrangement of collagen is responsible for maintaining integrity of skin at times of stretching force developed on them by the muscles. Had they perpendicular, then skin would tear easily.

This also has clinical relevance because during surgery if an incision is made along these lines the scar would be minimum.

Source: https://en.m.wikipedia.org/wiki/Langer%27s_lines


How does hypocalcaemia have an effect on the excitability of cell Hypocalcemia increases sodium influx by leak channels. Why does this elevate the resting membrane potential and increase excitability?

Assuming the question is in respect to neurons..in a nutshell...resting membrane potential & excitability both depend upon sodium permeability which in turn depends on potential difference of the excitable cell....now as the sodium influx is increased the minimum voltage required to increase the conductance of sodium decreases far below its normal value...so for a small increase in membrane potential from the normal very negative level the sodium channel becomes activated elevating the resting membrane potential...

In fact, the calcium ion concentration needs to fall only 50% below normal level before spontaneous discharge of peripheral nerves occur giving rise to "tetany"...

Reference- Adapted from Guyton & Hall- Textbook of medical physiology (12E)

You can also refer to Berne & Levy's & Ganong's physiology book for further details


Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA? A search following a recent news item led me to a CDC Morbidity and Mortality Weekly Report for 23 March 2020 which says in part:

  SARS-CoV-2 RNA was identified on a variety of
  surfaces in cabins of both symptomatic and asymptomatic
  infected passengers up to 17 days after cabins were vacated
  on the Diamond Princess but before disinfection procedures
  had been conducted (Takuya Yamagishi, National Institute of
  Infectious Diseases, personal communication, 2020). Although
  these data cannot be used to determine whether transmission
  occurred from contaminated surfaces, further study of fomite
  transmission of SARS-CoV-2 aboard cruise ships is warranted.

Identifying bits of RNA does not imply a surface is infectious and that's not what I am asking about here.

This reminded me of answer(s) to Was 14,000+ year old DNA “laying around in cave dirt” protected from degradation, or is it just naturally this robust? which explain that small fragments of DNA can be quite stable in some environments; in some places on Earth the DNA in the soil can be ten thousand years old.

Question: Roughly speaking how stable are short sections of single-stranded RNA in exposed environments compared to double-stranded DNA?

The answer is likely to contain "It depends on..." as did the answer to the DNA stability question, I'm primarily interested in the differential stability between the two.

The main difference in stability is due to the very high amounts of RNase in pretty much all fresh biological materials. Naked RNA is easily degraded by just touching it with skin. The first step in most RNA extractions is often to add an RNase inhibitor.

For example, from Wikipedia's Ribonuclease; RNase contamination during RNA  extraction:

  The extraction of RNA in molecular biology experiments is greatly complicated by the presence of ubiquitous and hardy ribonucleases that degrade RNA samples. Certain RNases can be extremely hardy and inactivating them is difficult compared to neutralizing DNases. In addition to the cellular RNases that are released, there are several RNases that are present in the environment. RNases have evolved to have many extracellular functions in various organisms.


Is every decision we make already "pre-programmed" because of DNA? DNA has information about our cells and how every cell should act.

Since I am made entirely of cells, including things that make my mind, aren't decisions coded for by DNA by proxy of our cells.

Even asking this question is a decision that has already been made because that's what my DNA told my cells to do?

"Do we have free will?" It's a big question.
DNA (among other epigenetic factors) code for proteins, so ultimately it determine our cells, which in turn are responsible for our neurology, although how this translates to behavior is variable depending on factors beyond DNA@Remi.b's answer. De facto you're asking about the extent that our brain structure and neural activity determines our conscious stream. This boils down to "Do we have free will?". That question historically was only accessible to philosophers. It is now accessible (but not completely answerable) to biologists, more specifically neuroscientists. It's a great question, but is still open to a lot of subjectivity.
An evolutionary explanation.
Anil Seth, professor of cognitive and computational neuroscience at the Sackler Centre at the University of Sussex, gives a very good answer to the question at 25:44 in this BBC Life Scientific interview.

We are determined to have it in both senses of the word...
Yes, we do have free will because we can behave the way we wish to behave. We cannot decide what to will.

Paraphrasing the guts of the answer: it's very important for the brain to differentiate between internalized experience, and reflex.
Reflex, such as placing your hand on a hot stove, never reach the "conscious stream". These have an obvious correct choice; in this case, removing the hand from a hot stove is clearly the right choice, every time.
Then there is internalized experience. Complex problems have many potential losses and gains. To cope with this, the brain needs to internalize, reflect, and is taking note and making a plan; the sensation of free will. By taking note of that situation within it's context and the plan, we can perhaps change our actions the next time we encounter a similar event so that we can optimize our choices to attempt to cause the least damage to ourselves and/or maximize the benefit.
How is learning achieved.
We have established that there is a need for new memories to form in order to solve complex problems. Long term memories are the result of new physical synaptic connections in the brain. This connection endures whether it’s being used or not.
Psychologists put these into two broad types are two kinds, implicit (akin to reflex; how to read, how to play your favorite song on an instrument etc.) and explicit (the things we are consciously aware of). Explicit memory comes in two forms: episodic and semantic (Tulving, 1972). (i) Episodic memory includes experience. For example, that time you planted some seeds and a potato grew. (ii) Semantic memory is abstract to your own experience. Something more like "Primordial potatoes originated in southern Peru".

To bring this back to the original question "Is every decision we make already pre-programmed because of DNA?" It's long winded. Our choices are built upon the results of our past choices in a given environment. We are able to make these choices, to an extent depending also on other variables, because of the products and machinery encoded in our DNA.
The philosophers answer
If this answer is a bit scary or makes your choices seem futile, you can simply sit around and do nothing instead of doing whatever you normally would do; it's your choice.
See a similar question answered from a different perspective over at Philosophy.SE.


Are antibodies removed before blood transfusion I am an O blood group person meaning, I can donate my blood to all as I don't have any Antigen A and B. But my body does contain antibodies A and B right?
If they were along with the donor blood, wouldn't they cause clotting with the recipients blood?
We spent a whole period over this. My teacher said they probably remove the antibody before transfusion, but I couldn't find much info on that. I postulated that these antibodies can not work outside the donor body for some reason.
Thanks for the help

I quote from the below.
Groups and Red Cell Antigens
by
Laura Dean (page 7). Available at:
http://www.ncbi.nlm.nih.gov/books/NBK2265/
"Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation."
I dont think the antibodies are removed, but in countries with a good medical system I believe the matching blood type is always used.
http://en.wikipedia.org/wiki/Acute_hemolytic_transfusion_reaction


ATP required for cell processes I haven't been able to find anything that tells me how much ATP is needed for DNA replication, transcription, and translation in humans, just papers that mention ATP used in those processes.

I need to know how much ATP is needed for these processes because once my cell from scratch is alive I feed each cell 50 nanograms of glucose which yields 5 trillion ATP. If I use these numbers plus the numbers for other metabolic processes I get roughly the amount of ATP needed per cell before mitosis. If I know this then I will know if I need to feed my cells more glucose or if 50 nanograms is enough.

So how much ATP is needed for DNA replication, transcription, and translation? I want it in terms of per nucleotide and per amino acid so that I can multiply that by the amount of DNA total, amount of DNA in any given gene, and amount of amino acids in any given protein.

For DNA replication and transcription you need NTPs. In a dsDNA purine content will be same as pyrimidine content. I am considering that all nucleotides are synthesized de novo which would consume more ATP than getting nucleotides from the salvage pathway.

  Fig 1: Pyrimidine synthesis. Taken from Wikipedia.

  Fig 2: Purine synthesis. Taken from Wikipedia.

CTP synthesis requires one extra ATP:

UTP + Glutamine + ATP + H2O → CTP + ADP + Pi

UTP synthesis requires 2 (Step 1; Fig 1) + 1 (Step 5; Fig 1: PRPP requires 1 ATP to form) +  2 (UMP → UTP) = 5 ATPs

CTP requires 6 ATPs

GTP requires 8 ATPs (Fig 2) (ATP synthesis would also require 8 ATPs but for simplicity let us assume that ATP is already present).

Conversion of dNTP from NTP requires thioredoxin which in turn requires NADP but let us forget that.

Assuming a 50% GC content one base pair of DNA would require in an average 10 ATPs (assume a stretch of 4nt — ACTG, this would require 1+6+5+8 ATPs; i.e. 5 ATPs per nt; 10 ATP per bp)

For RNA the ATP consumption would be 5 ATPs per nt.

For protein synthesis, for every codon, the elongation factor requires one molecule of GTP and aminoacyl-tRNA synthetase requires 1 molecule of ATP. So the net consumption per amino acid would be 9 ATPs.

I am ignoring the initiation reaction that also requires ATP to phosphorylate the initiation factor. Also, I assume that amino acids are obtained from diet and are not synthesized by the organism.


Why do we have wrinkly fingers after swimming? I found an explanation for my question here http://www.pitara.com/science-for-kids/5ws-and-h/why-do-we-have-wrinkly-fingers-after-swimming/, which suggests that water washes out sebum (special oil, which covers our skin) and water gets into outer layer of now unprotected skin by osmosis. This article also suggests that fingers are not really shriveled - they are water-logged. But is this right? I think I observed many times my wrinkly fingers after swimming, but I never felt that they are water-logged. Any thought on this matter would be highly appreciated.

Great question, for which still no definite answer is known despite ~100 years of research.

A simple physical basis for the wrinkling however seems unlikely as glabrous skin without sweat glands does not wrinkle, and as wrinkling requires the activity of specific nerves.

Moreover plausible evolutionary ideas, which used to be popular, such an anticipated improved ability to grab, don't appear that clear in newer experiments.

For the information above, and an even more detailed answer, please see Haseleu, Omerbasic et al. 2014 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0084949


Loss of taste and smell during a SARS-CoV-2 infection In France the loss of taste and smell (la perte du goût et de l'odorat) is considered as one of the key symptoms of a SARS-CoV-2 infection (although googling shows that it is considered less definitive elsewhere). What causes such a loss of taste and smell?
More specifically, an infection by SARS-CoV-2 is rarely associated with nasal congestion, so one cannot blame mechanical obstruction (and it would not apply for the loss of taste). One can then think of the virus attacking the relevant sensor cells or a less direct effect via disrupting the relevant metabolic chains. I will appreciate clarifications/explanations/references.

This is not completely clear to say the least, but there are some hints. Please keep in mind that there was not much time for extensive research, since this disease is still quite new. What seems clear (at least at the moment) is that most like the nerve cells (in the olfactory bulb as well as in the taste bud) are not directly affected, since they do not express the ACE2 receptor on their surface which is needed by the virus to enter a cell.
In the nose, there are two studies, which link the loss of smelling to massive damage of the epithelial cells surrounding the nerve cells. These cells have a lot of ACE2 receptors and are thus susceptible for an infection with SARS-CoV-2. An infection leads to the death of these cells, which disturbs the balance of ions for the nerve cells leading to loss of smell. Specifically this seems to affect sustentacular cells. Since the epithelial cells recover over time, smelling comes back. This also fits the description of affected people, who describe the loss of smell as a sudden event, while the recovery happens gradually.
For the tasting it is less clear, but it also seems that supporting cells (which carry ACE2 receptors) are affected. For sensing of sharp (for example Chili), which is not chemical sensing but via pain sensing, it seems that at least a part of the cells are also susceptible to the virus as they express ACE2.
Taken together this seems to indicate that important cells in the vicinity of the nerve cells are hit by the virus, causing anosmia and ageusia. It is also important to note that not all people who lose their sense of smell also lose the sense of taste.
For furter reading have a look at the references, the first one is a nice article in the scientific american, the second goes deep into the topic with a lot of nice images.
I will have a deeper look into the topic later and probably update the answer.
References:

Mysteries of COVID Smell Loss Finally Yield Some Answers
COVID-19 and the Chemical Senses: Supporting Players Take Center
Stage
Massive transient damage of the olfactory epithelium associated with
infection of sustentacular cells by SARS-CoV-2 in golden Syrian
hamsters
SARS-CoV-2 Receptor ACE2 Is Enriched in a Subpopulation of Mouse
Tongue Epithelial Cells in Nongustatory Papillae but Not in Taste
Buds or Embryonic Oral Epithelium
Real-time tracking of self-reported symptoms to predict potential
COVID-19


How does HCl not burn our stomach? How does the digestive acid (HCl) not burn the surrounding membrane of our stomach? It digests the majority of raw food we eat but how does it stay safely in our stomach?

Also, how does the stomach maintain the ability for a human body to retain HCl for all lifetime?

Mucous-producing cells at the neck of the gastric pits create a layer of protective mucous covering the stomach lining. This mucous layer includes bicarbonate ions which act as a chemical barrier against the protons in gastric juice.  See here for some evidence.

The stomach lining stays protected because the mucous layer is continuously replenished.


Naming convention of miRNAs I'm trying to understand naming convention of miRNAs. I've found the wikipedia article about it nomenclature Based on it, I try to figure out what is hsa-let-7a. As far as I understood, hsa refers to human but I expected a "mir" or "miR" after hsa but there is a word "let" .So my question is that hsa-let-7a is a name for a single mature miRNA or is it a name of a miRNA family(if there exists such a thing) ?

Some general aspects about miRNA nomenclature in addition to canadianer's answer:

mir refers to the pre-miRNA whereas miR refers to the mature form
mir-x-y mir-x-z for example mir-1-1 and mir-1-2 refer to different precursors that give rise to same mature miRNA (i.e. miR-1). These different precursors can be regulated differently.
The mature miRNA resulting from the 5' arm of the precursor hairpin has a suffix of -5p; similarly the product from the 3' arm has the suffix of -3p. Previously, the lesser expressed/abundant (or unexpressed) of the two products was designated with an asterisk. For e.g. miR-124*. This convention is obsolete now. Any miRNA by default has the -5p/3p suffix. This is useful especially in case of let-7 because there is no uppercase notation to differentiate precursor from the mature miRNA. For example, the mature form is always denoted as hsa-let-7b-5p even though the -3p is never expressed.
A "family" consists of miRNAs with the same seed sequence (usually 2nd-9th residue). Sometimes it can be observed that one of the arms is less conserved than the other between different precursors. For example in the case of let-7 the -3p(s) do not have a conserved seed sequence, however, all -5p(s) have the same seed sequence.

And as mentioned in the other answer, the name let-7 just sticks around because of historical reasons.


Why don't chromosomes double in S-phase? DNA doubles in S-phase, but chromosomes don't double in S-phase, in spite of the fact that chromosomes are formed by the condensation of DNA. Why is this so?

First, chromosomes are composed of an original and a replicated chromatid, called sister chromatids. Chromatids are composed of tightly packed DNA.

DNA is replicated after the end of the S-phase, or in other words, the material composing the two sister chromatids is there. The catch is that chromosomes and chromatids aren't actually condensed yet, the DNA is still completely unpacked at this stage. So in fact, while you do not see actual chromosomes, the material composing them has been duplicated during the S-phase.

DNA condensation occurs two steps later during the prophase, where distinct sister chromatids/chromosomes are then formed from the packing of DNA that was duplicated during the S-phase.


Found Skull(?) in Ontario Canada, help identifying please skull?...now maybe thinking its a bird pelvis?...(I don't know thats why I'm here!)on the beach in Northern Ontario Canada, have been wondering what it is. Any ideas? As you can see it is very small, fits in the palm of my friends hand.

Thanks so much!

Kimberley,

Yes, this is a synsacrum, a part of a bird's pelvis. I would say it's from a cormorant, as I have found this comparison of different synsacra online (third from left):

No idea about the exact species, though.

Image source:

https://hiveminer.com/Tags/cormorant,skeleton


Why can we use mouse-produced antibodies on mice tissues? I have seen biologists use mouse grown primary antibodies in mouse tissue, and they've told me that if the blood is perfused well then there is no problem with this method. How does the secondary antibody (anti mouse) not stick everywhere on all the mouse antigens in the tissue?

Clarification: I  understand that the secondary antibody is very specific to all mouse "class" primary antibodies. Can I ask then why using a secondary mouse antibody does not recognize background antibodies in the tissue, the ones that the mouse produced for itself naturally before I added any of my primary antibody? Are the existing primary antibody levels already present in the mouse much lower than the levels of the primary antibody I am adding?

The reason why the secondary antibody only recognizes the primary antibody is relatively simple: It is directed against the Fc-part of the primary antibody. As this part is species specific (but constant between all antibodies from one species, hence the name constant) a secondary anti-mouse antibody is directed against all mouse antibodies.

The general principle can be seen in the figure (although this is from immunolabelling, the principle stays the same, Image from the Wikipedia):

The anti-mouse secondary does recognize the antibodies which are present in the tissue. These are usually present at low levels (unless you work with immune tissues as spleens) and only cause a relatively low background. If it causes a problem, you can treat your sample before you add the primary with an Fc block which blocks the antibodies present in the tissue so that the secondary antibody will not recognize anymore later.


Is there a way to determine how many times a given cell divided? Do cells divide into exact duplicates? If not, is there a way to determine how many times a given cell divided?

Yes, its called the HayFlick limit. A cell will divide until their telomeres reach a critical length,which is usually around 40 to 60 cell divisions. The cells then enter cellular senescence and cease to divide. However, cells may also stop dividing due to (ROS) or reactive oxygen species, cell to cell fusions, or activation of oncogenes, the latter of which is a gene that has the potential to cause cancer.


Can swarming locusts act as a vector for any human pathogens? What human pathogens can the locusts currently swarming in Africa act as a vector for?

E.g. can the locust swarm 'become a reservoir for' SARS-CoV-2? Measles? Ebola?

I have not heard of locusts being a vector for any pathogen. For immunocompromised people, they can on rare occasions be infected by bacteria carried in the guts of insects. For desert locusts, their main gut bacteria is Pantoea agglomerans (Enterococcus agglomerans). This species has been listed as a pathogen of immunocompromised patients.


Specificity of Protein Kinases in Signaling Pathways..? In most of the signaling pathways the activated receptor when activates Protein Kinase through the action of secondary messenger, then these protein kinases almost always phosphorylate on the specific Serine, Threonine, or Tyrosine amino acid residues? what is the reason of phosphorylating specifically these amino acid residues. why not other than these amino acid residues are choosen for phosphorylation ?

Phosphorylation requires a nucleophile and hydroxyl oxygen acts like one. Serine, theronine and tyrosine get phosphorylated on the free OH group in their side chains.

Nitrogen, in some cases also can act as a nucleophile. In case of histidine, the imidazole nitrogen is phosphorylated during bacterial chemotaxis signaling. As far as I know eukaryotes do not have an enzyme for histidine phosphorylation.

Carboxylic groups in glutamate and aspartate can technically be phosphorylated as it happens in case of phosphoglycerate. Glutamate is phosphorylatyed by the enzyme glutamine synthase during the synthesis of glutamine. Same happens in the case of aspartate during aspargine synthesis. However, this is a reactive intermediate and the phosphorylation is not stable like that of hydroxyls.

Other amino acids do not have such nucleophilic groups to render an attack on the phosphorous atom in phosphate- so they are not phosphorylated.


How are cell death like apoptosis and entropy related? In Perspectives on Statistical Thermodynamics, Yoshitsugu Oono, it is written that

  Do not conclude, however, that since the second law is invincible,
  information thermodynamics is unimportant. It is possible for a system
  we are interested in to perform something that ordinary thermodynamics
  does not allow, and to pay the price somewhere else. For example, it
  may be possible to go beyond the limit of thermodynamics for the time
  being by shifting the average value of fluctuations, although the
  price must be paid (dearly) later. There must be such cases in
  molecular machines. It is argued that cell senescence is due to the
  accumulation of defects and wastes, but cell death could have a more
  active implication of carrying away the debt caused by utilizing
  information. Thus, entropic apoptosis and entropic altruism are
  conceivable.

but I don't understand the following two points.

Why is cell death associated with "debt caused by utilizing information"? Do cells die for increasing entropy to compensate the entropy decrease which caused by their using information (but what kind of information)?
Why can we conclude "Thus, entropic apoptosis and entropic altruism are conceivable."? Does this mean, to let other cells decrease the entropy by consuming information, some cells kill themselves to increase entropy?

Unless you have a closed system, don't bother with the second law. These sound like some poetic descriptions but they won't tell you much about biology.

  It is argued that cell senescence is due to the accumulation of defects and wastes, but cell death could have a more active implication of carrying away the debt caused by utilizing information.

The first part of sentence which I italicized here is sufficient to understand the biology: cells age and die off because they accumulate defects. Organisms, whether single-celled or multi-celled, ultimately get around this by making lots of copies of themselves and expecting some to fail.

The second part of that sentence says "could" and is poetry to describe the first half, as well as the sentence that follows. It doesn't add any more science, unless you care about the existence of "entropic altruism" in the universe, which sounds to me like a religious rather than scientific approach. It's just stating that cell death (and perhaps, to an extension, death of multicellular organisms) can be useful to organisms/species rather than merely destructive. There is nothing wrong with finding beauty in physics and mathematics, but beauty in itself says nothing about how things work or how things should be.

In the context of a multicellular organism, cells kill themselves to not kill/harm the whole organism (e.g., to not develop into cancer, or as a planned event during development). The biological reason they do this is because multicellular organisms that have evolved genetic mechanisms to identify potentially harmful cells and have those cells die are more likely to reproduce and produce more multicellular organisms like themselves. If you want to interpret this as "entropic altruism" because cell death increases entropy, that's fine, but no thermodynamic argument is needed or even all that helpful in explaining the biology.

Note also that the book you cite doesn't seem to be in common use; it has no reviews on Amazon or Google books, and a previous book by the same author only has 1 review. I don't have anything against the author and they could be an excellent statistical physicist, but language like this makes me think they are not a biologist.


Identify this insect - beetle (?) Please help identify this insect - genus, species and anything interesting about it. (Species of beetle?)

Old link - please vote to un-delete it https://biology.stackexchange.com/questions/64042/can-you-identify-these-insects?

That's a red rhinoceros beetle. Although, "red rhinoceros beetle" is not the correct name. I'm simply observing that it is red, and that it is a rhinoceros beetle. So, according to wikipedia: suborder Dynastinae. Do an image search for "red rhinoceros beetle" and you'll stuff that looks quite similar. Searching google for that specific image show's that it is a 3d printed model. The list of bugs in list of 3d printed models includes something called "Rozenkever". Which is remarkably similar to "Red Beetle" in German.

Golofa porteri perhaps


Understanding the use of English tenses in biological journal articles My colleague and I (second language speakers) got in an argument in understanding the sentence:  " however, how this complexity and diversification have been achieved remains rather poorly understood.” in the context of the below Abstract’s report.
In short, the question is:
Does this sentence valid till the end of this report? i.e. the complexity problem continued and not solved in this study?
His understanding that this sentence stated in this report as a past context or past story, i.e. the abstract is telling us how our knowledge was? and this study solved and answered how this complexity happens and achieved.
Reference:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1852327/
I know these questions are mostly about understanding English rather than biology!
I appreciate your help.

I regard this is more of a question for SE English Language and Usage under the tag “technical”, and will vote to move it there. However, as the answer relates to reading papers in molecular biology, I provide an answer here.
Linguistic interpretation without context
The tense used in the phrase “X remains poorly understood”, taken in isolation, suggests that this is the situation now. Hence, it is the situation at the end of the study.
However…
Interpretation in context
This is the Introduction section of the paper. In the Introduction to papers reporting experimental biological research, it is usual (and helpful to the reader) to explain the background to the study and why it was undertaken. In this case to explain that the incomplete understanding of the subject justified further studies such as the one to be described.
This is made clear at the end  of the Introduction, where one often indicates in a sentence what the work to be described adds to knowledge: “Our results show that flagellum originated very early, before the diversification of contemporary bacterial phyla…”.
So the minimal implication is that as a result of the work described “X is now better understood”. And that is clearly the case here.
This is borne out by the final paragraph of the Results section in which the authors emphasize the contribution to knowledge that their work has made. You don’t get published in PNAS by saying that you have left the field still in the dark!
Why not use a different tense and say that you the problem has been solved?
An alternative would have been to write:
“Before this work was undertaken X was poorly understood”
The reason for not doing this could either be “scientific modesty” (also known as don’t antagonize the referees by appearing arrogant) or acknowledgement that, despite the significance of the work presented, there are still aspects of the problem that are not understood.


Why is hydrogen sulphide being generated on Caribbean beaches? Once again, there has been a massive influx of Sargassum weed in the Caribbean. It is coming ashore on Atlantic facing beaches and forming piles up to 3m deep. As it dries and decays, hydrogen sulphide is being emitted. Why?

It would seem from a quick perusal of the literature that this is caused by sulphate-reducing micro-organisms. To quote from the eponymous Wikipedia article:

  Sulfate occurs widely in seawater, sediment, or water rich in decaying organic material. Sulfate-reducing microorganisms are common in anaerobic environments where they aid in the degradation of organic materials.

which is consistent with the situation described.

In biochemical terms, these anaerobic bacteria are using sulphate rather than oxygen as the final electron acceptor (oxidizing agent) in the elctron transport chain which generates ATP through the chemiosmotic mechanism. The reaction for the reduction of the sulphate to hydrogen sulphide (dissimilatory sulphate reduction), according to the Wikipedia article already quoted, is:

A simple way of thinking about this is that in both aerobic and anaerobic respiration the oxidizing agent itself becomes reduced. Whereas oxygen is reduced to H2O, sulphate is reduced to H2S.


Transcriptionally-mediated DNA damage I'm researching the genetics of brain cancer, and finding a huge number of mutations in voltage-gated channels.  It stands to reason that some of this DNA damage is due to the DNA being transcribed heavily, or in an open chromatin conformation more often, leading to more breakage and damage due to environmental stress.

Of course, those are just guesses.  Does anyone know of any research papers in the area?

There seems to be some solid evidence that transcription promotes mutation because the untranscribed strand is able to form secondary structures which expose bases to chemical mutagenesis.

Here is a recent paper about transcription-associated mutagenesis:

Kim H et al.(2010) Transcription-associated mutagenesis increases protein sequence diversity more effectively than does random mutagenesis in Escherichia coli. PLoS One 5(5):e10567. doi: 10.1371/journal.pone.0010567.

From the abstract:

  During transcription, the nontranscribed DNA strand becomes single-stranded DNA (ssDNA), which can form secondary structures. Unpaired bases in the ssDNA are less protected from mutagens and hence experience more mutations than do paired bases. These mutations are called transcription-associated mutations. Transcription-associated mutagenesis is increased under stress and depends on the DNA sequence. Therefore, selection might significantly influence protein-coding sequences in terms of the transcription-associated mutability per transcription event under stress to improve the survival of Escherichia coli.

The authors cite a number of papers in their introduction which document the phenomenon that you could follow up. Just in case the focus on a bacterial system puts you off, the Kim et al. paper has in turn been cited in:

Wright et al. (2011) The roles of transcription and genotoxins underlying p53 mutagenesis in vivo. CARCINOGENESIS 32:1559-1567

Abstract in full:

  Transcription drives supercoiling which forms and stabilizes single-stranded (ss) DNA secondary structures with loops exposing G and C bases that are intrinsically mutable and vulnerable to non-enzymatic hydrolytic reactions. Since many studies in prokaryotes have shown direct correlations between the frequencies of transcription and mutation, we conducted in silico analyses using the computer program, mfg, which simulates transcription and predicts the location of known mutable bases in loops of high-stability secondary structures. Mfg analyses of the p53 tumor suppressor gene predicted the location of mutable bases and mutation frequencies correlated with the extent to which these mutable bases were exposed in secondary structures. In vitro analyses have now confirmed that the 12 most mutable bases in p53 are in fact located in predicted ssDNA loops of these structures. Data show that genotoxins have two independent effects on mutagenesis and the incidence of cancer: Firstly, they activate p53 transcription, which increases the number of exposed mutable bases and also increases mutation frequency. Secondly, genotoxins increase the frequency of G-to-T transversions resulting in a decrease in G-to-A and C mutations. This precise compensatory shift in the 'fate' of G mutations has no impact on mutation frequency. Moreover, it is consistent with our proposed mechanism of mutagenesis in which the frequency of G exposure in ssDNA via transcription is rate limiting for mutation frequency in vivo.


How standardized is lab-grade skim milk? I was surprised to learn in the answers to this question that in many cases the preferred cryoprotectant for many organisms is skim milk, rather than something more simple and well-defined like glycerol. And indeed, Sigma will happily sell you lab-grade dried non-fat cow's milk for lab-grade prices.
It seems to me that this could potentially cause significant variability and reproducibility issues. Milk is pretty sensitive to the condition of the producing animal, and when dealing with a cow we're talking about a very large and complex source that's not hyper-standardized like lab-grade rodents.
I don't seem to be able to find anything much about specification on Sigma's site, however (the spec sheet for milk has only the obvious like "opaque white fluid").
Does anybody know to what degree lab-grade milk is actually standardized, and if this should be a concern for protocols like cryoprotection?

There is a degree of variability in milk, and in some cases this cause problems in protein work. Despite being a standard for ELISAs, it's not known to be the most reliable blocking buffer. As far as cryoprotection goes, variability doesn't seem to be a major concern.
Standardization varies depending on manufacturer. The Sigma link you included reports a quality level of MQ 200. The MQ level is something Sigma created in an attempt to increase clarity about quality controls. Products rated MQ 200 are for non-regulated applications. For this level they will provide a site-quality self-assessment, a certificate of quality/analysis, and specifications. They also have a notification system that customers can opt-in to for updates on quality control features. There's information on what each quality level meansand a breakdown of what they will notify you about on the Sigma website.


Are alpha-ketoglutarate and glutamate involved in all transamination reactions? Is it true that for all biochemical transamination reactions, that alpha-ketoglutarate and glutamate serve as the amino group acceptor and donor, respectively?

If this is true, then is it safe to assume that alpha-ketoglutarate is necessary for every transamination reaction?

The major transaminases such as the aspartate transaminase and alanine transaminase involve the glutamate α-ketoglutarate interconversion. Even the GABA aminotransferase employs glutamate/α-ketoglutarate. It seems that all transaminases use glutamate/α-ketoglutarate; in fact most of them do.

These are a few that don't:

Beta-alanine--pyruvate transaminase.
Tryptophan--phenylpyruvate transaminase.
Pyridoxamine--pyruvate transaminase.
Aminolevulinate aminotransferase.
Serine--pyruvate transaminase.
Aspartate--prephenate aminotransferase.

And a few more (see here). Most of these are present in plants.


Do all proteins start with methionine? Start codon AUG also codes for methionine and without start codon translation does not happen. And even the ambiguous codon GUG codes for methionine when it is first. So does this mean that all proteins start with methionine as the first amino acid.

You are correct in thinking that since the translation of mRNA begins with AUG, which codes for methionine, then all proteins should contain a methionine at their N-terminus (aka start site). But, it is indeed not so. First of all, I want to mention about variations in start codon. As you say, AUG is not the only, but actually the most common, start codon, and it codes for methionine in eukaryotes, or formylmethionine in prokaryotes but only at the start site. But, this start codon can also vary and become GUG or even UUG, coding for valine and leucine respectively. And the twist is, it still codes for methionine or formylmethionine1. In rare cases, such as heat shock, other codons like CUG, ACG, AUA and AUU, are also used for initiation 2. It is so because start codon itself is not sufficient to begin translation, other nearby factors, like the Shine-Dalgarno sequence, or initiation factors, also play a role. One such factor is the initiation tRNA. At the beginning of translation, tRNAMet or tRNAfMet binds to the small subunit of ribosome. So, whatever be the start codon, the first amino acid will be methionine3.

Now, coming back to the main question, N-terminal methionine, although being the first amino acid, is not present at N-terminus of all proteins. This is because of a process that is known as post-translational modification. After a polypeptide is completely translated from mRNA, it is modified at different places by different enzymes, which are regulated by different (internal or external) factors. There are more than a hundred post-translational modifications known4, one of which is the removal of methionine from the N-terminus of a polypeptide. N-terminal methionine is removed from a polypeptide by the enzyme methionine aminopeptidase5.

The question which immediately comes to mind is Why are proteins modified after translation? Well, there can be various different causes of it. First of all, post-translational modifications are regulated by many factors, and this process is called post-translational regulation6. Another point is cell targeting. Attaching different groups to polypeptides makes them more stable at their target location. For example, by attaching lipid molecules to polypeptides (in a process called lipidation) makes the polypeptide more stable and suitable for cell membranes4. A yet another factor is increasing stability. Yes, you read it right, in some cases, N-terminal methionine can destabilize a protein! For example, an extra N-terminal methionine not only destabilizes but also disrupts the native folding configuration of $\alpha$-lactalbumin7. There can be numerous other factors too, which promote removal of N-terminal methionine from polypeptides.

Thus, in short, No, not all proteins contain a methionine at their N-terminus. I hope this helps!

References:

 1. Touriol, C., Bornes, S., Bonnal, S., Audigier, S., Prats, H., Prats, A.-C. and Vagner, S. (2003), Generation of protein isoform diversity by alternative initiation of translation at non-AUG codons. Biology of the Cell, 95: 169–178. doi:10.1016/S0248-4900(03)00033-9

 2. Ivanov IP, Firth AE, Michel AM, Atkins JF, Baranov PV. Identification of evolutionarily conserved non-AUG-initiated N-terminal extensions in human coding sequences. Nucleic Acids Research. 2011;39(10):4220-4234. doi:10.1093/nar/gkr007.

 3. Sherman, F., Stewart, J. W. and Tsunasawa, S. (1985), Methionine or not methionine at the beginning of a protein. Bioessays, 3: 27–31. doi:10.1002/bies.950030108

 4. Post-translational modification - Wikipedia

 5. Liao, Y.-D., Jeng, J.-C., Wang, C.-F., Wang, S.-C. and Chang, S.-T. (2004), Removal of N-terminal methionine from recombinant proteins by engineered E. coli methionine aminopeptidase. Protein Science, 13: 1802–1810. doi:10.1110/ps.04679104

 6. Wolfgang Schumann; Wolfgang Schumann (Prof. Dr. rer. nat.) (2006). Dynamics of the bacterial chromosome: structure and function. Wiley-VCH

 7. Chaudhuri, T. K., Horii, K., Yoda, T., Arai, M., Nagata, S., Terada, T. P., & Kumagai, I. (1999). Effect of the extra N-terminal methionine residue on the stability and folding of recombinant alpha-lactalbumin expressed in Escherichia coli. Journal of Molecular Biology, 285(3), 1179–1194. doi:10.1006/jmbi.1998.2362


For how long can a raven stay airborne (a week or more)? I'm wondering for how long a raven can stay continuously airborne, if strained to do so? If it makes a difference, I'm mostly interested in the Common raven, Corvus corax. Are there for instance any information on long-distance dispersal (wind-blown individuals over sea?) that can be used to roughly estimate this? Information on other corvid species could also be interesting, as a rough proxy.

If you are wondering, my motivation for asking is the biblical story in Genesis 6–8 (the deluge of Noah). Here, Noah sends out a raven and a dove to look for land. From the story it appears as if the raven can stay airborne for a longer time than the dove, which returns to the ark to rest. Is there any realism in the claim that a raven can stay airborne for one or maybe even two weeks?

Some background from Genesis 8 (this translation):

  After forty days, Noah opened the window he had made in the ark. He sent out the raven, and it departed. It went back and forth until the water had dried up from the land's surface. He then sent out the dove to see if the water had subsided from the land's surface. The dove could not find any place to rest its feet, and it returned to him, to the ark. There was still water over all the earth's surface. [Noah] stretched out his hand, and brought it to him in the ark. He waited another seven days, and once again sent the dove out from the ark. The dove returned to him toward evening, and there was a freshly-plucked olive leaf in its beak. Noah then knew that the water had subsided from the earth. He waited yet another seven days and sent out the dove [again]. This time it did not return to him any more.

So the raven couldn't find a place to land, and it flew around until it could do so. A week later, the dove still couldn't find a place to land, but a week later it could. Thus, either (a) the raven was flying around for more than a week (as much as two weeks) or (b) the raven could more readily land in a wet area than the dove. Can either of these be true?

Can't be very sure about ravens but the maximum recorded flight duration is of Common Swift — 10 months.
Alpine swifts also remain airborne for up to 6 months.

Pigeons can fly up to 1800km in a long flight. From this article (pubmed):

  In the United States, the longest pigeon races involve flights of 1800
  km and, because substantial financial rewards accrue to the owner of
  the fastest pigeon, there is severe selection for those pigeons that
  home the fastest.

Wikipedia article on pigeons says that they can fly at 80km/h but I suspect because the other wikipedia page on flight speeds says that average flight speed of peregrine falcon is 65-90km/h. So assuming that average speed of pigeon is 60km/h it should be able to fly for 30h. According to this paper, the speed with minimum power consumption is 8-9m/s (~30km/h). At this speed they should be able to fly for 60 hours. In the same paper it is estimated that the maximum continuous power output is ~10.5 W; if a pigeon has 11g of stored fat (per 400g body weight — assumptions from the same paper), and given the calorific value of fat — 38kJ/g, it can fly upto 38 × 11 ÷ 10.5 = ~40h. This means that the best trained ones can perhaps manage to fly for 2.5 days straight.

Now ravens are heavier (~3 times heavier) but are more aerodynamic and can fly faster. However, I guess they cannot perhaps fly 7 days straight.


Use of progesterone in preventing ovulation? I have heard that progesterone in contraceptive pills or interuterine devices have been known to prevent ovulation. How is this possible since the LH and FSH are only affected by oestrogen not progesterone (am i wrong?)  Also,  my textbook says hormonal intrauterine devices contain progesterone to lessen uterine lining but doesnt the uterine get maintained by progesterone ?

Edit : I have yet to receive a satisfactory answer... Help anyone?

When progesterone alone is used as a contraceptive it is assumed that the oestrogen level is endogenously maintained by the follicular cells.

Yes mainly oestrogen and only little does progesterone inhibits LH or FSH secretion.

LH surge is the principle stimulator of ovulation.

  However,experimental work has suggested that immediately before the LH surge occurs, there is probably a sudden depression of estrogen...and this might be ...that leads to LH surge
  [source: Textbook of medical physiology A South Asian Edition- Guyton & Hall]

If progesterone or progesterone-oestrogen combinations be given before ovulation then feed back inhibition of LH surge occurs.This would lead to contraception by anovulation.

Progesterone is only known to proliferate the endometrial lining.

However, administration of progesterone or oestrogen -progesterone combinations after ovulatory phase helps to achieve high concentration of these hormones ,much before the normal time required to attain peak levels due to endogenous secretions alone.

This helps to depress the FSH -LH secretion by feedback inhibition very quickly causing involution of the corpus luteum and early shedding of the endometrium termed as breakthrough bleeding

REFERENCE:

reference site
Textbook of Medical Physiology A South Asian Edition-Guyton & Hall


Why does yawning impair hearing? When I yawn I can't hear anything happening around me. I also feel some kind of muscles inside my head contract and hear a faint hum, but it is not loud enough to explain not hearing other sounds. I can force those muscles to contract even without yawning and it produces the same effect of humming and no other sound, so I suppose they cause this effect, but how?

What really happens? What muscles do I feel?

It is related to Eustachian tube. It links the back of throat and the middle ear and allows air pressure to equalize in the middle ear. When you yawn air pressure goes up in this and it bends the ear drum and causes impair hearing (notice, just impair and not stop).
Yawning also helps to open Eustachian tube.


Volley theory and sound amplitude/power Assume a pure tone (single frequency) is listen, lets say 2 kHz. If I understand correctly the temporal theory (aka timing theory), in a cochlea neuron the action potentials create a signal that will have one spike for each single tone cycle with the exception of some gaps due to the minimal interval between neuron triggers.

Volley theory extends previous model to a set of neurons. The union of triggers in all neurons of the set will have at least one spike per cycle (with few exceptions). In other words, the base frequency of the signal composed as the union of triggers of all neurons in the set will be the same frequency than the one of the incoming sound.

My question is, if in this model the trigger intervals is used to encode the sound frequency, and taken into account that usual models for neuron activity only take into account intervals between action potentials (all-or-none), how sound amplitude (power) of the sound is translated to the nerve signals. That is, the differences in the nerve activity caused by two tones of same frequency but different amplitudes/powers, assuming frequency/volley model.

It's complicated.

The simplest explanation is that sound amplitude/level/loudness is encoded by the number of participating units, including off-best frequency cells that get recruited when amplitudes are high (the concept of 'tuning width' is helpful to understand). Loud sounds will recruit cells of a wider best-frequency range with high coincidence, for example (see Carney, 1994).

In some experimental paradigms, this hypothesis holds; in others, it does not. It is most likely that the perception of loudness is quite context-dependent and also depends on background, the presence of energy in other frequencies, and adaptation.

Similar to how absolute brightness is not all that perceptually useful (and therefore humans display incredible invariance over very wide brightness ranges), loudness is probably perceptually most useful in terms of relative loudness: sounds that are getting louder may be approaching, for example.

References

Carney, L. H. (1994). Spatiotemporal encoding of sound level: Models for normal encoding and recruitment of loudness. Hearing research, 76(1-2), 31-44.

Heinz, M. G., Issa, J. B., & Young, E. D. (2005). Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment. Journal of the Association for Research in Otolaryngology, 6(2), 91-105.

Neuhoff, J. G., McBeath, M. K., & Wanzie, W. C. (1999). Dynamic frequency change influences loudness perception: A central, analytic process. Journal of Experimental Psychology: Human Perception and Performance, 25(4), 1050.

Relkin, E. M., & Doucet, J. R. (1997). Is loudness simply proportional to the auditory nerve spike count?. The Journal of the Acoustical Society of America, 101(5), 2735-2740.


Defining: Evolutionary (quantitative) Genetics and Population Genetics How do we define the fields that are Evolutionary (quantitative) genetics and population genetics. What set these two fields apart? Can you try to provide definitions?

To my intuitive understanding, I'd tend to think that population genetics is a subfield of evolutionary genetics.

According to Hartl & Clark on population genetics:

  "Population genetics deals with Mendel's laws and other genetic
  principles as they apply to entire populations of organisms.... also
  includes the study of the various forces that result in evolutionary
  changes in species through time."

According to Conner & Hartl also on population genetics:

  "Population genetics is the study of naturally occurring genetic
  differences between organisms; these differences are called genetic
  variation. Genetic variation is important because it is the raw
  material for evolution... to understand the purview of population
  genetics, we need to have a better understanding of populations and
  genetic variation"

According to Conner & Hartl on quantitative genetics:

  "Most phenotypic traits do not fall in to distinct categories, but
  rather are continuously distributed... These traits are called
  quantitative or metric traits because they need to be measured not
  just scored."

According to Falconer & Mackay on quantitative genetics (my personal favourite book on quant gen, which spends the first 5 chapters going through population genetics):

  "Quantitative genetics is concerned with the inheritance of those
  differences between individuals that of degree rather than of kind,
  quantitative rather than qualitative.... It is nevertheless a basic
  premise of quantitative genetics that the inheritance of quantitative
  differences depends on genes subject to the same laws of transmission
  and having the same general properties as the genes whose transmission
  and properties are displayed by qualitative differences.
  Quantitative genetics is therefore an extension of Mendelian genetics, resting squarely on Mendelian principles as its
  foundation."

Personally I would say that evolution is inescapably a population genetics process and (virtually) no study of it can be done without some understanding of population genetic principles. Many evolutionary genetics problems can be best dealt with using quantitative methods, and quantitative genetics is an extension of population genetic principles. Population genetics relies on selection, drift, mutation and gene flow - these are all key quantitative genetics.

Population genetics study focuses then on the four basic principles above from a (simplified) Mendelian view, while quantitative genetics deals with more realistic evolutionary genetic phenomena by allowing for, and assessing, genetic variance from many loci influenced by additivity, dominance, and environmental factors. Both fields are studies of evolutionary genetics, population genetics can be studied whilst ignoring quantitative genetics, but quantitative genetics relies on population genetics principles so I would call it an extension of - but not sub-field - of population genetics.


is it possible to completely reconstruct a family tree by DNA comparison alone? Having DNA samples of all or almost all members of a population of, say, a few hundred or thousand individuals, is it possible to draw the entire family tree of those individuals? (Let's not assume monogamy or any other facilitation).

This may be a sum of two different questions:

does comparison of two DNA samples give any information other than topographical distance between individuals? In other words, is it possible to tell two sisters from a mother and a daughter by DNA alone?
(more a mathematical question than a biological one, maybe) having the relative topographical distance of all members of a group, can their full graph be drawn?

No, it is not possible to determine ancestry with just two DNA samples, but it is possible with three: http://www.nature.com/nature/journal/v487/n7407/full/nature11251.html.

Essentially, each sequence region in the progeny can be traced to either the mother or the father, but you really need both sequences to have any confidence.  That would get you one node on your tree.  You would need additional samples from higher generations to rebuild an entire ancestry.

However, it might be possible with hundreds of samples from laterally related individuals.  In fact, I think this is the fundamental hypothesis of the 1000 genome project, http://en.wikipedia.org/wiki/1000_Genomes_Project, and it pretty much worked.  Isolated populations can be discriminated by broad DNA sequence analysis.

To reconstruct your tree for a single ancestry, you would just want to use more closely related individuals (many, many of them), and then generate a phylogenetic tree, which should roughly correspond to the family tree you are investigating.


Which came first: The Chicken or the Egg? Has there been any serious scientific inquiries into answering this age old question?

Most theories about origin of life say that unicellular organisms were first and multicellularity (like chicken) evolved much later, so in that meaning egg (single cell)* was first. Also, almost all chicken ancestors lay eggs (primitive birds, non-avian reptiles, amphibians, fishes and so on...) so eggs existed much earlier than chickens.

*in the meaning of zygote. The development of chicken embryo starts in hen's oviducts, so it's not a single cell at the moment when hen lays it (Gilbert, 2000).


How is the effective dose calculated when only part of the body is irradiated? For calculating the effective radiation dose in Sv, the equivalent dose absorbed by each body part is averaged according to tissue-specific weighting factors, which sum up to 1.

If not the whole body is irradiated, how are these factors used?

Not sure that I understood your question correctly.

The concept of "effective dose" was specially introduced to provide a mechanism for assessing the radiation detriment from partial body irradiations in terms of data derived from whole body irradiations. The effective dose is the mean absorbed dose from a uniform whole-body irradiation that results in the same total radiation detriment as from the nonuniform, partial-body irradiation in question.

What is probably misleading you is the sum of the weighting factors to be 1. This is because we try to liken the partial body irradiation and the whole-body irradiation and the weighting factors represent the relative tissue sensitivity and susceptibility to the radiation. Your radiation should not go over all possible tissues and organs, you just assume the irradiation to be zero at them that cancels their summands so that they can be ignored in the final calculation. In other words, it is absolutely fine (and it is even so "by design") to have only some of the WT*HT factors in your formula.


Different flowers have same colour I notice that certain (wild) flowers have the same colour, although they are not closely related. For example, the yellows of the dandelion (Taraxacum) and the buttercup (Ranunculus) are, at least to my eyes, identical (my observations are in the Netherlands).

I know that the colour is intended to attract insects; is this parallel evolution or are there certain biochemicals which provide colour and are easy for the plant to synthesize? Or something else?
Edit: I used the buttercup and dandelion because that was the first pair I found physically close enough for a photo; the cowslip, celandine and charlock mustard are all (to my eyes) the same yellow. I have also seen similar blues, reds and violets, and shall try to collect examples next time I go cycling on the dyke.
When I look at colour tables like https://en.wikipedia.org/wiki/Web_colors#Extended_colors I see numerous colours which I do not recall ever seeing in wild flowers.
Edit2: I retract my remarks about blues, reds and violets; it's hard to judge colours when cycling past and when I pluck the flowers and compare directly there's a definite difference, for example:

However I still find the yellows very similar; here the charlock (left) is lighter but the buttercup, celandine and dandelion look identical to my eyes.

Comments seem to suggest a biochemical cause; can anyone confirm (or disprove) it?

I think parallel evolution is likely due to the cost to produce the pigments in plants.
Xanthophylls and carotenes are made from only carbon, oxygen and hydrogen. This provides most of the yellow colours without using up nutrients.
Anthocyanins and betalains also need nitrogen, which can be a limiting nutrient for plants.
Wikipedia has a section on plant pigments at:
http://en.wikipedia.org/wiki/Biological_pigment


Is Aspergillus clavatus an unicellular organism? I could not find the piece of information form Burton Human Parasitology -book and not by Google.
Yeast is divided to two phylums: one of them is Ascomycota.
Aspergillus clavatus belong to the given phylum.
Yeast is unicellular.
So it is possible that Aspergillus clavatus is unicellular.

Can you tell whether the Aspergillus clavatus is an unicellular orgarism or not from the following picture?

I need to find unicellular parasites that cause damage of brain. The fungus causes patulin so hemorrhaging of brain, but should still be unicellular to meet the criteria.

You're right in saying that yeast is single celled.

However, moulds are described to be filamentous fungi that are multicellular. The filaments of the mould give colonies "a woolly, fluffy, or velvety appearance, sometimes punctuated with a granular or powdery aspect that is produced by the formation of asexual reproductive structures"(1).

Aspergillus is such a species. The filaments are called hyphae. In Aspergillus, hyphae have divisions or walls which separate it into multiple cells. This is called septate hyphae.

McPherson, et al. Henry's Clinical Diagnosis and Management by Laboratory Methods. 22nd ed. 2011. Saunders.


What does it mean to say that the sympathetic nervous system is organized for diffuse activity? "Sympathetic activities generally serve to mobilize the energy stores of the body, to increase the blood flow through certain regions (e.g., the heart) at the expense of other areas (e.g., the abdominal viscerae), and to exhibit the outward signs of alarm and excitement.

Because the sympathetically innervated effectors generally have a wide distribution, even when the sympathetic supply to only one type of effector (e.g., the vasomotor fibers to the cutaneous blood vessels) is stimulated, the bodily response is diffuse."

1-By 'mobilize the energy stores' they mean metabolize or use up ?

2-'The bodily response is diffuse' - does that mean several parts of the body participate in the response but with no major effect individually ?

"Mobilize" in this context means to:

  to release (something stored in the organism) for bodily use

Merriam-Webster

"Diffuse" means "spread out": it doesn't say anything about whether the effect is "major" or "minor" and I don't think it's useful to think in those terms. Instead you should just appreciate that there is no specific target affected by sympathetic activation, rather it is a whole body response: almost every organ system is involved.

Sympathetic nervous system activation occurs when an organism needs to be ready to act immediately (such as in a 'flight or fight' response), which includes more metabolism in the muscles and increased sensory sensitivity. It also includes compensating by reducing metabolism in the gut: even though digestion is a source of energy, it is slow rather than immediate and costs a lot of energy in the short term through the processes of digestion.


Is it possible in modern biology to make any person's identical twin (or genetical clone) using his DNA? I was told by a Biotech professor (who came in our college for a guest lecture) that Bio Technology has now become so advanced that if we want to make an identical twin (or Genetical DNA Twin) of a person then we can now be able to it using his DNA. I am a Mathematics Student so I don't know much about it. I just attended the lecture because I found it interesting. I am sorry, I know I should have asked this very simple question in Quora but, I wanted a precise answer which could be believed. So I asked here, where I will get answers only from the very experts. I apologize again Thank You So Much in advance

Edit 1 :- I am satisfied with @Remi.b 's answer, @Bryan 's explanation and @anongoodnurse ' references. I should also have mentioned genetical DNA Clone in the place of identical twin. Now I've added.

I will assume that by "identical twin", you refer to "clones". Individuals who share the same genetics but of course do not necessarily share the same womb. I won't pay much attention in detail epigenetic modification nor in the length of telomeres.

While it has never been done for ethical reasons, we would probably be quite able to make a clone of a human being. We can take a cell from an individual, make it totipotent again, like a zygote and then, insert this zygote into a woman's uterus. The resulting individual is a clone and therefore have identical genetics, just like two identical twins. Similar technics have been used to clone Dolly the sheep.

We cannot, however, modify the DNA in all cells of a living individual to make this individual a perfect cone of another one.


What specific markers does a Covid-19 PCR test look for? I've done a search and can't find anything as to what specifically makes a Covid-19 positive that identifies it as unique. I would expect to see something like this:
https://madridge.org/journals-admin/uploads/fulltext/MJV/images/mjv-118-t002a.gif
or
https://i.stack.imgur.com/423Ay.jpg
Instead I find this:
https://communitymedicine4asses.files.wordpress.com/2020/05/2020-05-07-17_38_07-covid-19-testing-what-you-should-know.png?w=624
and
https://myrepublica.nagariknetwork.com/uploads/media/PCR_20200513092900.jpg

The SARS-CoV-2 diagnostic tests that are currently in use, both serological and nasal swab, are binary tests - they either are positive or negative, like a pregnancy test. They do not (yet) report viral titre, like the first image you linked, or look at restriction enzyme "gene fingerprinting" patterns, like the second. They simply tell you if either a part of the virus is in the sample (RNA or capsid protein in the two nasal swab tests) or if your immune system has seen enough of the virus to mount an antibody-mediated immune response (the IgM/IgG blood tests).
It's worth pointing out that all of the current tests in the US are available under emergency use authorizations from the FDA, meaning they haven't gone through the usual (and time-consuming) process of full qualification and validation. That type of work needs to be done in order to develop quantitative testing ("You have a viral titre of X, compared to an average range of Y through Z."), which will likely appear in the coming months and years as the proper development work is done to support their validity.


Can someone identify this odd looking spider? I found this spider crawling on my tile floor. We live in rural central Virginia.  I’ve found spider species with similar looks but nothing exactly like this. Its size was less than 1 inch. Can anyone identify it?

I agree with JulPal's comment from August.  It looks very much like a male Thiodina (now renamed Colonus) sylvanus.  As with many Salticids, the females look rather different, and it turns out that there is apparently a similar species of Colonus in the area, which can be distinguished in the field by the fact that the white mark on the carapace is not a block so much as a thick longitudinal line.
I attach an image from Tree of Life, with the link below:

http://www.tolweb.org/Thiodina_sylvana/5911


Why are red blood cells not attacked by NK cells? All cells containing a nucleus present MHC-I, while some specialized cells present MHC-II in addition to that. Since erythrocytes lack any MHC why do natural killer cells not attack them?

It is my understanding that any cell which starts presenting foreign peptides on MHC-I will undergo apoptosis after Th finds them, or if they stop presenting anything at all, they will be eliminated by the NKs.

So what mechanism prevents erythrocytes from being destroyed by the immune system?

The question states, not quite correctly, that "if they stop presenting anything at all, they will be eliminated by the NKs".  In fact, simply not having MHC is not enough to trigger destruction by NK cells.

NKs have a two-part trigger. Part 1 is an activator; part 2 is a suppressor. When the activator is present, and the suppressor is not present, then NK cells will destroy the target.

The suppressor is typically MHC class I, which is present on almost all normal cells. That means that NK cells will not destroy normal cells. There are many different activators, but most normal cells have at least one of the activators also present. That means that NKs are normally primed to destroy, but refrain from destruction because they also sense the suppressor.

With that explanation, it should be clear why RBC are not destroyed by NK cells. Even though they lack the suppressor, they also lack any activators. Since there are no activating signals, the NKs don't need to be also suppressed, so the lack of MHC doesn't lead to an attack.

Sample references:

Two-signal requirement for activation and effector function of natural killer cell response to allogeneic tumor cells
Controlling NK Cell Responses: Integration of Signals for Activation and Inhibition

It's also possible that RBC further protect themselves by showing a "marker of self" on their surface (Role of CD47 as a Marker of
Self on Red Blood Cells) but that doesn't change the important point about NKs mode of activation.


Why is there Turner syndrome if one of the X chrosomes is inactivated anyway? In females one of the two X chromosomes will condensate and turn into Barr bodies. So chromosome abnormality-free women will only have a single transcriptionally-active chromosome. Then why can abnormalities like Turner's syndrome still occur in the  presence of a single active X chromosome?

Pseudoautosomal region in mammals

On sexual chromosomes, we have a so-called PseudoAutosomal Region (PAR). The PAR is the region which still recombine with the Y chromosome (in males only) and is though to be important to allow separation of chromosomes during meiosis.

Pseudoautosomal region and dosage compensation

Because the PAR is diploid in males too, there is no need for a mechanism of dosage compensation and hence, in females, the PAR of the inactivated X-chromosome remain active.

Turner Syndrome

Turner syndrome is caused by an issue of dosage of functional elements found in the PAR. In people having Turner syndrome the PAR is haploid, while it remains diploid in both healthy males and healthy females.

Here is a small review paragraph from Sybert and McCauley (2004) that report the evidences suggesting that Down syndrome is caused by haploidy in the PAR. Please see the linked paper directly for further references.

  Loss of interstitial or terminal long-arm material of the X chromosome (Xq) can result in short stature and primary or secondary ovarian failure.15 Deletions distal to Xq21 appear to have no effect on stature. In general, loss of the short arm (Xp) results in the full phenotype. Very distal Xp deletions are compatible with, but do not ensure, normal ovarian function. Loss of this region usually confers short stature and the typical skeletal changes, in part as a result of haploinsufficiency of the short stature–homeobox (SHOX) gene, located in the pseudoautosomal region of Y and Xp. The SHOX gene is probably not the only gene responsible for the skeletal features. Aneuploidy itself may contribute to growth failure. Loss of a region at Xp22.3 appears to be associated with the neurocognitive problems in Turner's syndrome. Loss of the testis-determining factor (SRY) gene locus on the short arm of the Y chromosome (e.g., 46,X,del(Yp)) also leads to the phenotype of Turner's syndrome, even without a 45,X cell population. A region on Xp11.4 has been proposed as critical for the development of lymphedema.


Constantly wiggling moth pupa - will it emerge soon? Today I found a moth pupa in the soil in my garden in western Sweden. It's about 15 mm long.
I have found similar ones before, but this one is wiggling a lot more, even after I put it down and put a bit of dirt over it. It's been moving for more than an hour now, but less now than in the beginning.

I was hoping to see it emerge, but if it will take more than a day or so, I will probably put it back. So, what I'm wondering is if this wiggling is any indication of how soon it will emerge. Or if there are other ways to tell.

Update: an hour later it has stopped moving. Maybe it was just very disturbed by my presence. I'm keeping it in a jar with soil and a stick for climbing up on, and I'll decide what to do with it tomorrow.

Update: 12 hours later and it seems very still. But I'm letting the question remain since I really want to know if there are any signs to look for.

Final update: After 16 days it had turned almost black, and was still very active when handled.

And after 17 days this moth came out:

I posted the same question on tumblr and got an answer:

  It depends on the species. This one looks like a Noctuid. I’d give it
  two weeks to a month or so. You may be able to see its wings showing
  through the darkening pupal case when the time draws near! Just make
  sure you give it somewhere to climb up and expand its wings when it
  ecloses.

After keeping it until the moth emerged, I now know that wiggliness is not an indication of maturity, but turning dark is.


Are there anatomical differences between male and female mammal brains before action of hormones? is there any evidences of these differences during development stages prior to hormone driven sexual differentiation? mice studies ?

Yes. Dewing et al. (20030 found that gene expression in mouse brains differs between male and female mice about 10.5 days after the mice had sex. This occurs before hormonal contributions to brain development. They identified about 35 genes that were appeared to show preferential expression in the female brain and another 16 that appeared to be show preferential expression in the male brain. Most of the genes identified were transcriptional regulators, signaling molecules, or involved with cellular differentiation. Of these 51, three were verified as showing female bias, and two of these were located on the X chromosome. Four genes were verified showing male bias, and two of these were located on the Y chromosome.
Similar results were found by Xu et al. (2002). They identified several of the same genes as Dewing et al., plus others that were linked to the sex chromosomes. They identified a total of six genes on the X chromosome that showed strong female expression bias during brain development. At least three of the genes were homologous between the X and Y chromosomes but showed different expression patterns between male and female brains at different stages of development.
The differences in genetic expression may cause some microscopic anatomical differences during brain development that is not explained by hormones (Bocklandt and Vilain 2007). They reviewed several studies that found differences in neuron growth, and density of vasopressin fibers in the lateral septum were more likely to be due to genetic expression than to hormonal expression. Bocklandt and Vilain did not identify the specific ages of the mice that showed these apparently gene-regulated differences but it is reasonable to speculate that these differences begin to appear in association with the differential gene expression.  Bocklandt and Vilain did not identify macroscopic differences between male and female brains prior to hormonal expression.

Citations
Bockland, S. and E. Vilain. 2007. Sex differences in brain and behavior: Hormones versus genes. pgs 245-266. In: Genetics of sexual differentiation and sexually dimorphic behaviors (D. Yamamoto, ed.). Academic Press.
Dewing, P. et al. 2003. Sexually dimorphic gene expression in mouse brain precedes gonadal differentiation. Molecular Brain Research 118: 82-90.
Xu, J. et al. 2002. Sex differences in sex chromosome gene expression in mouse brain. Human Molecular Genetics 11: 1409-1419.


How does the Pectoralis Major work when doing a bench press? Disclaimer, I'm not a biology undergrad and I only know the basics about muscle movement.

I know that doing a bench press works the chest, and specifically the Pectoralis Major because, well, I feel muscle soreness. However, it is not obvious to me what the Pectoralis Major has to do with extending the arm.

Thinking about muscle contraction, I see clearly how, for example, the Bicep flexes the elbow when it contracts. In a similar way, when the Pectoralis Major contracts you get horizontal shoulder adduction.

But what about the bench press? The majority of the movement consists of raising the arms upwards from a tucked position, and the is little shoulder adduction.

Thanks!

The pectoralis muscle attaches to the top to the inner half of the clavicle, just underneath the biceps on the inner part of your arm and the breastbone (a.k.a the sternum) which is found in the middle of your ribs. See below:

So taking that in account the pectoralis muscle helps bring your arm closer to your body (adducts your arm), pulling it forward in front of you (flexes the humerus) to push up like you would when you bench press. This action can be seen below.


A basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism Could someone help me out with a basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism? Based on empirical research OR on a theoretical model.

An example of 2 or more non-identical alleles cooperating across replication iterations/generations between individual organisms would be even beter. I somehow find this more spectacular :)

Please let me know if I'm not mentioning enough elements to answer the question. It's a very broad question and I accept very broad answers - semantically and across scientific branches.

All the best,

Flo

Personal background: I am new to the scientific field of biology. I think I caught up on some of the basic principles of genetics, allellomorphs, loci and DNA replication and I've gotten interested in the workings of alleles.

Reading your updated question, I think you are interested about epistasis. Let me know if I am mistaken.

The concept of epistasis might be confused with the one of pleyotropy, so I will define both terms.

Pleyotropy occurs when one gene influences multiple phenotypic traits. Note: the phenotype, to make it simply is what a living things look like (its cells, proteins, shape of the face, size of the leaves, etc…). It is often thought in duality with the genotype which is the total genetic information contained in an individual that codes for the phenotype (Be careful, the environment is also an important factor influencing the phenotype, if you make sports you will have big muscles!)

Epistasis is when the effect on the phenotype of one gene depends on the presence of several (or only one) other genes. Wikipedia gives this (simplistic) example:

Here, two bi-allelic genes are involved. One gene that determines the hair color. The two alleles influence the phenotype such: one allele gives red hair and the other allele gives blond hair. Now There's another bi-allelic gene coding for baldness. One allele causes the bearer to be hairy and the other one causes the bearer to be bald. Therefore, if an individual carries the allele "Bald" in the "Baldness" loci, what this individual carries on the other loci is not important because it will result into the same phenotype anyway, he is bald. Now if in the baldness loci, the allele is "Hairy", then the expression of the other gene "Hair color" matters and therefore if the allele is "blond", the bearer has blond hair and if the allele is "red" the bearer has red hair.

The "Baldness" gene is called a modifier. One can also say that the expression the "Hair color" gene depends on the genetic background of the individual.

Now cases of epistasis are not always that easy and if they influence the fitness, this kind of epistatic interaction might have implications for their evolution.


Did any warm blooded animals evolve back into cold blooded? Pretty much as title says - wondering if evolution can go from mammal back to reptile - either in theory or practice.

Secondary ectothermy has been suggested in living crocodylians by Seymour et al. (2004). Their rationale is based on:

Presence of a 4 chambered heart (otherwise only found in endotherms)
Post-cardiac shunting via the foramen of Panizza and "cog-tooth" valve, which develop secondarily in crocodylians
Lung structure and ventilation during locomotion

Thus ectothermy in extant crocodylians is associated with being aquatic or semiaquatic. These authors suggest that endothermy may have been ancestral for dinosaurs as well.

Seymour RS, Bennett-Stamper CL, Johnston SD, Carrier DR, Grigg GC. 2004. Evidence for endothermic ancestors of crocodiles at the stem of archosaur evolution. Physiol Biochem Zool 77:1051–1067.