What is continuous selection? I've been reading paper on ancient horse genome (Recalibrating Equus evolution using the genome sequence of an early Middle Pleistocene horse) and in abstract authors mention term continuous selection:

  We also find evidence for continuous selection on the immune system and olfaction throughout horse evolution

Can someone please explain what it means? What is continuous selection? Is it selection without interruptions, but what are those interruptions?

Continuous selection is not a term; it would not be bolded in a textbook.

When studying the history of a genome/lineage, you could have two very broad hypotheses about a given trait:

1) The trait was not present in a lineage, then appeared fairly suddenly (at least on a long time scale, it could still be hundreds, thousands, or millions of generations), and since then did not change much.

2) The trait was not present in a lineage, then the trait appeared in part of that lineage, and since then, the trait has continued to change substantially among different descendants of that lineage.

You could find evidence towards (1) if, for example, you observe a trait that is fairly constant among a diverse modern taxon but you don't see a similar trait in the cousins of that taxon.

You could find evidence towards (2) if you see a lot of diversity even among recently speciated members of a taxon.

The statement in the article is just saying in plain English, rather than using a scientific terminology, that they see evidence towards (2).


Does a severed limb/finger experience pain after its separated? If a person ends up with a severed finger will that finger, after falling off, experience any pain and start writhing? Can a limb kind of have a mind of its own for a few more seconds after separating from the body like for instance the tail of a lizard?

Pain is a signal emitted from a nervous pain receptor cell (called a nociceptor) to the central nervous system (CNS, i.e. the brain). If I hurt myself causing a small cut in my finger, nociceptors around the cut will send the pain signal to the CNS, which in turn processes it and causes the physical feeling of pain in that region.

If a finger is severed, nociceptors just above the cut will be extremely active, interacting with the CNS and causing a lot of pain. On the other hand, nociceptors in the finger itself have nowhere to "push" the pain signal to, so in this sense they cannot measure any pain - there's not a CNS connected to the finger anymore that is able to process the signal emitted by any nociceptors in the finger.


How do I read a sequence logo? I'm looking at a paper that uses several sequence logos to illustrate the consensus sequence of certain sites.

Here is the most important of the sequence logos I'm interested in:

The explanations I found about the exact meaning of this visualization were rather abstract and mathematical. I understand that the height of the letter stack is indicating in some way how strongly conserved that position is, but I have some difficulty judging the absolute values.

When are the positions considered to be significantly conserved? The paper where this data is from mentions the positions 5 and 6 as characteristic for the consensus sequence, which is not really obvious to me from this graph.

How do I interpret the absolute value on the y-axis? What does it actually mean if position 16 has around 0.6 bits of information?

I'm not so much interested in an exact mathematical treatment, but a general guide on how to read these graphs and how to interpret them in practice.

A very clear description is given in Wikipedia.

The starting point is an alignment for the region under investigation.

A. Basically, to get the height of the stack of letters for every position one has to calculate the degree of certainty about the residue (= degree of conservation) at this position in the sequences belonging to this class. I'll explain what it means:

The key parameter in this context is information. 1 bit of information can be understood as the amount "knowledge" you get when receiving an answer to one yes/no question.

Let's say we have equal proportions of all four bases at a certain position in a set of DNA sequences. To "guess" a base at this position in some sequence we have to ask two binary questions. For example: "is it Pyrimidine?" If 'yes' we'd ask "is it 'T'?" Otherwise: "is it G?". So, when the frequencies are equal we can get 2 bits of information from one observation of a base at this position in a sequence.

If the frequencies are distorted, we already have some ideas about the bases when coming to an individual observation. If we already know, say, that we have just G and A at this position with ratio of 1:1, we can just ask "is it G?", so we get clearly 1 bit. When the ratios are not even (or when the number of alternative states is not 2n), the analogy with the questions becomes much less clear and we have to resort to the very simple formula for Shannon entropy. Intuition and brief inspection of this formula would bring you the idea, that when the ratios of the residues are biased, we always have less information than for the case of equal frequencies (2 in the case of DNA).

Now to estimate the "the degree of certainty" we simply calculate the information based on the observed frequencies of different residues at this position and subtract it from the theoretical maximum (again: 2 in the case of DNA):

certainty = maximal information possible - actual information

This value defines the height of a stack of letters at each position.

The maximum value (2 bits) would be observed when we always have the same base, because "actual information" would be zero (there is no need to ask questions - we "know" the answer anycase). The minimum (0 bits) is when we have no idea about the base. One bit would be obtained if we had, say, just two equally frequent bases. And, for example, the value of 0.6 would be observed if you had, e.g. 68.5% of the time the same base A and in all other case C, G or T with equal frequencies of 10.5%.

B. As you probably already know: the proportions of all alternative bases are shown as relative heights of individual letters.


Are heterozygotes always fitter than homozygotes? Can inbreeding be beneficial? Inbreeding is mostly not very good because when there is a 'disease' in one allele, the other could/would take over the function. But when you have two of the same genes/alleles, do they, or could they have advantages? Can inbreeding be beneficial?

Certainly it is not necessarily the case that having two of the same allele is a bad thing - if there is a "bad" allele then there is a "good" allele. It can be that the heterozygote is equal, better than, or worse than either homozygote. When the heterozygote is fitter than both homozygotes it is called heterosis and, when this is the case, outbreeding/hybridisation is advantageous.

The process of inbreeding can actually improve fitness because it increases the rate at which deleterious mutations (bad mutations) are expressed, and therefore the efficacy of selection. If the population avoids fatal inbreeding depression it can have positive effects. This process of removing deleterious variants by inbreeding is called genetic purging.


What constitutes FDA's First in Class designation for New Molecular Entities? What constitutes a First in Class designation for new molecular entities? I've seen this term on FDA documents, as well as in databases (Chembl for example), but I was curious if there are any set criteria for First in Class drugs? The easy definition, in my mind, would be a drug that hits a novel target given its indication. However, if you look at antifungal drugs, you see that drugs with the same target for the same general indication (anti-fungal) treat completely different fungal infections because of their pharmacokinetics.

Are there discrete criteria for the FDA's first-in-class designation for New Molecular Entities?

"First-in-class drugs are ones that use a new and unique mechanism of action for treating a medical condition. These products are often referred to as innovative and cited as offering new treatment options for patients."
Lanthier, M. et al. (2013) "An improved approach to measuring drug innovation finds steady rates of first-in-class pharmaceuticals, 1987-2011." J.Health Aff. (Millwood) 32:1433-9;
Pharmaceutical Research and Manufacturers of America. 2015b. Innovative Oncology Medicines Have Led to Impressive Gains in Patient Survivorship. Retrieved August 26, 2015. <www.phrma.org/innovative-oncology-medicines-have-led-to-impressive-gains-in-survivorship>."
From: Lexchin, J. (2016) "How Safe and Innovative Are First-in-Class Drugs Approved by Health Canada: A Cohort Study" Healthc. Policy 12:65-7.


Results of self-administration study about pain in honeybees? There research on nih.gov about ability of bees feel pain. But I can't understand their conclusion. Could you provide necessary excerpts here from those study so it would be clear what conclusion they've got ?

And that research was granted by This research was funded by ARC Discovery Grant DP140100914. Does it mean that we shouldn't completely trust it ?

The paper shows that honeybees prefer sucrose (sugar) solution to a sucrose+morphine (pain reducing) solution. They find that injuring the bees (i.e., potentially causing pain) does not change the relative preference for sucrose vs. sucrose+morphine, but they do eat more overall when injured.

They indirectly conclude that because the bees do not seek a pain reliever they may not feel pain of the type that, for example, mammals do. This is not the same as the ability to detect noxious stimuli (nociception), which insects definitely have, it's more about the emotional/behavioral impact. They cite some evidence that morphine could potentially have similar pain-relieving effects in insects as it does in mammals due to changes in behavior caused by morphine, but of course the interpretation of their results depend very strongly on whether this is accurate or not.

ARC is the Australian govt's funding mechanism. They don't have any commercial ties to the results of research so there is no reason to have any skepticism particular to the funding source: everything has to be funded by someone.


What's keeping living species from rotting? Why do only corpses of species rot and be eaten by bacteria? What is keeping us from rotting?
Just like fruits, and foods we eat; meat and vegetables rot when left uneaten. Like food, corpses rot and get eaten by maggots. Why?
Why don't these apply to living species?

One can calculate that there are more non-human cells (mainly bacteria) inside human body than there are actual human cells. Why those bacteria don't eat us from within? Epithelium is pretty good barrier between outer world and internal systems. It is essentially one-cell thick layer that protects internal organs and infrastructure. In cases when epithelium breaks, bacteria can get into blood stream and start very bad infection, which can cause necrosis (effectively, rotting, tissue decay). Natural cell death is fought by natural cell proliferation so that there are no gaps in defense layers.

Also one should not forget about immune system that is looking for invaders or anything that should be where it is. In healthy person immune response will close gaps in epithelium and kill bacterial infections pretty quick.

Dead people, as well as dead plants, have their skin and epithelium, immune system destroyed by cell death or infection. Then bugs start to eat vessels, tasty nerve tissues, muscle and cartilages, blood cells filled with proteins and everything eatable.


Is there an example of a species wherein the female lays eggs in the male? There are of course many species which lay eggs in the bodies of another species and also many species where either the male is eaten after mating or the male dies soon thereafter. So it seems possible that a species might exist where the female lays fertilized eggs in the body of the male with whom she mated or even a different male. I could see however the problem being that there is a significant time gap between mating and the eggs being ready to be laid, so perhaps there are no cases of the former but perhaps there are cases of the latter?

Note: Looking for a form of egg-laying that is destructive to the "host" -- where the developing larvae eat the host, like in the cross-species case.

Is there an example of a species wherein the female lays eggs in the male?

Yes.

Pipefish & Seahorses to name two.

Both widely mentioned in many wildlife programs as being an example of what you've asked.


How and why did mammals go back to the oceans? If I understand evolutionary biology correctly, mammals first evolved on land as small, rodent-like creatures, in a time when reptiles were dominant on land. Eventually, they diversified into the species we know today. Some of these species, however, are aquatic - whales and dolphins readily spring to mind. Why did the ancestors of whales and dolphins leave the land to go to the oceans? How did they evolve from their original form to their superficially ichthyoid appearance today?

I'll focus on whales and dolphins (cetaceans) as you mention them by name and they are representative for other marine mammals such as seals or manatees. The evolution of cetaceans was one of the fascinating evolutionary mysteries. Clearly, they were mammals, but which mammals were their closest relatives? Clues to solve this mystery began to appear in the 1980s and 1990s.
During the 1980s and into the 1990s, paleontologists discovered several fossils that were clearly land-based mammals but shared many skeletal features with cetaceans. These fossils, including Pakicetus [(Gingerich et al. 1983)] and Rodhocetus (Gingerich et al. 1994), shared skeletal features that are unique to whales and to the Artiodactyla, commonly known as the even-toed mammals. Artiodactyls includes deer, sheep, pigs, bison, and hippopotamuses. Artiodactyls and the fossil whales share a unique skeletal feature of the ankle called an astrogalus, shown in the picture below. The astragalus is a "double pulley" structure that contributes to the ankle joint. This picture is taken from an excellent summary of whale evolution, provided by the Understanding Evolution site hosted by University of California at Berkeley. The astragalus is not present in other mammals.

The fossil whales and modern cetaceans also share unique features of the skull around the area of the ear, called a tympanic bulla. Although all mammals have bullae (plural of bulla), the bullae of cetaceans and the whale fossils is unique compared to other mammals. For more on the bulla, see this Talk Origins page. More on fossil whales can be found at the Berkeley Comparative Museum of Paleontology. The many fossils that have been found are transitional forms that link artiodactyls and modern cetaceans.

Source
Around the same time as the fossil discoveries, genetic analysis added additional evidence supporting a relationship between the artiodactyls and cetaceans (Milinkovitch et al. 1993). Although early genetic analytical techniques were not as robust as they are today, many genetic studies have since supported and refined the conclusions of Milinkovitch et al. Current evidence shows that the closest living relative of cetaceans are the hippos (see, for example Price et al. 2005 and Agnarsson and May-Collado 2008). The relationships are shown below in this figure from the Agnarsson and May-Collado paper. The dark lines are the artiodactyls and cetaceans, formally called the Cetartiodactyla.

The question remains: why? The most likely explanation is that cetaceans evolved to exploit an unfilled ecological niche or adapted to new niches that formed as a result of plate tectonics or other types of environmental changes that occurred 50-55 million years ago. The niche describes all of the living and non-living resources needed by an organism to survive. Although land-based mammals were increasing in diversity, few or none were present in the oceans. The basic hypothesis is that the early whale-like artiodactyls, like Indohyus and Pakicetus were land-based (terrestrial) mammals that spent most of their time near the water's edge. Over time, they adapted to the niches in the ocean. Fossils like Ambulcetus and Rodhocetus showed clear evidence of swimming ability, with flattened tails and the enlarged rear feet. In addition, the nostrils shifted from the front of the face to the top of the head, which we recognize as the blowhole.
The shift to the aquatic habitat allowed these species to exploit resources that were not available to land-based mammals, thereby reducing competition for the resources. Reduced competition allows more individuals to survive and reproduce.
Similar scenarios are very likely for other marine mammals, such as seals or manatees. They evolved to take advantage of ecological niches that were not filled by other organisms. This basic concept, evolving to fill available niches, is a common outcome of the evolutionary process.
The of adaptation of cetaceans and other mammals to the oceans may be similar to that of the hippopotamus. Hippos spend most of their time in the water, and they show many adaptations that allow them to live in the aquatic environment.  The eyes and nostrils of the hippo are high on the head, which allows them to remain almost entirely submerged but still see and smell, as shown below.

(Hippo photo by Johannes Lunberg, Flickr Creative Commons.)
Hippos feed underwaters, they are heavy enough to walk on the bottom of the river, and the mate and give birth underwater. The young can suckle underwater. Clearly, hippos seem to be another mammal that is "returning to water." Similar types of processes must have occurred in cetaceans for them to adapt to the marine habitat.

Citations
Agnarsson, I. and L.J. May-Collado. 2008. The phylogeny of Cetartiodactyla: The importance of dense taxon sampling, missing data, and the remarkable promise of cytochrome b to provide reliable species-level phylogenies. Molecular Phylogenetics and Evolution 48: 964-985.
Gingerich, P.D. et al. 1983. Origin of whales in epicontinental remnant seas: New evidence from the early Eocene of Pakistan. Science 220: 403-406.
Gingerich, P.D. et al. 1994. New whale from the Eocene of Pakistan and the origin of cetacean swimming. Nature 368: 844-847.
Milinkovitch, M.C. et al. 1993. Revised phylogeny of whales suggested by mitochondrial ribosomal DNA sequences. Nature 361: 346-348.
Price, S.A. 2005. A complete phylogeny of the whales, dolphins and even-toed hoofed mammals (Cetartiodactyla). Biological Reviews 80: 445-473.


Difference between bacterial chlorophylls I understand that bacterial chlorophylls are of the form a, b, c and d.
But i read in my textbook about pigments like bacterio purpurin and bacterio viridin; are they a part of the 4 types of chlorophylls and if not how are they different and what actually are they?

From A search in Pubchem database, in substances for bacterioviridin, it seems just another synonym for bacteriochlorophyll-C.

.

The incomplete page do not show any image-entry. From another entry about bacteriochlorophyll-C, I've took the following image:

Bacteriochlorophyll-C; which is being told same as Bacterioviridin

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From similar search on same website for bacteriopurpurin, it shows,

Bacteriopurpurin

is a Xanthophyll compound; with another similar entry Bacteriopurpurin

It is also being called Hydroxyspirilloxanthin

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Another search reslult, Bacteriopurpurin 18,

shows this photo:

Which is clearly a porphyrin-type compound (With smaller 4 pyrrole-type rings) with nitrogen (N) atoms.

......................................

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Though you have not mentioned in the original question, another such old term is Chlorobium-chlorophyll. When searched ;  there i could found one entry in the PubChem database, about chlorobium chlorophyll; which tells; it is same as bacteriochlorophyll-D, though the incomplete page does not display any structure.

From some other entry about bacteriochlorophyll-d; the structure given here:

Bacteriochlorophyll-D, which is being told same as chlorobium chlorophyll. Look this has a little bit different structure from bacteriochlorophyll-C (bacterioviridin according to pubchem) , because chlorophyll-D (this) is lacking a methyl group at left hand middle side of the photo.

................................................

However, I cannot ensure they are free from nomenclatural conflicts. IMO it is better to use modern terms like bacteriochlorophyll-a, b, c, d, e, f and g.

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  Reference: The PubChem Project by NCBI

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N.B. :

To quickly find differences among some main types of chlorophylls and bacteriochlorophylls; I've attached the following diagram. Most of the pictures are taken from PubChem; two I couldn't found in Pubchem, so I took them from a PMC articles. All are linked below the diagram.

Comparisons among some chlorophylls and bacteriochlorophylls.

Sources:

Chlorophyll-A : PubChem, Wikipedia .
Chlorophyll-B : PubChem, Wikipedia .
Chlorophyll-C1 : Pubchem (PubChem also tells as "Chlorophyllide C1") .
Chlorophyll-C2 : Pubchem (PubChem also tells as "Chlorophyllide C2") .
Chlorophyll-C (C1, C2, etc): Wikipedia .
Chlorophyll-D : PubChem, Wikipedia  .
Chlorophyll-E: No records seen.
Chlorophyll-F: PubChem .
Chlorophyll-F ' : PubChem .
Bacteriochlorophyll-A :  PubChem .
Bacteriochlorophyll-B : PubChem .
Bacteriochlorophyll-C : PubChem (Bacterioviridin) .
Bacteriochlorophyll-D : PubChem (Chlorobium chlorophyll) .
Bacteriochlorophyll-EF : A PMC article  * .
Bacteriochlorophyll-FF : same PMC article  * .
Bacteriochlorophyll-G : PubChem .

The PMC Article * : Bacteriochlorophyll f: properties of chlorosomes containing the “forbidden chlorophyll”, by Vogl, Tank, Orf, Blankenship, Bryant.

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What kind of parasite is this? I found this strange disease on the leaves of a pear tree. I don't know the tree's species but I found it in South Turkey, 150 km from the Mediterranean. What causes this disease?

This is pear rust (Gymnosporangium sabinae).

It is fairly widespread in the northern hemisphere:

It is a fungal infection and affects pear trees from junipers. Pruning the affected nearby junipers can help control its spread.


What is the point of Meiosis II, considering Meiosis I already produced haploid cells? Meiosis I is required so that the 2N cells become 1N, and so a 1N sperm and 1N egg can fuse to become 2N again.

But why is meiosis II required? Why does our body need to go from  2 1N cells to 4 1N cells? Can't it just use one of the 2N cells after Meiosis 1?

Source

After meiosis I, those n=23 chromosomes have two chromatides. Meiosis II just separates them into single chromatides.


Why are sequencing reads shorter than PCR products? I have desinged and tested primers for RT-PCR, then purified the PCR products from the gels and send them to sequence at GATC (SUPREMERUN) using the forward primers.

After blasting the reads to refseq, I see that they are ~30% shorter than the PCR product. Example:

PCR expected length = 182 bp
Read length = 133 bp

I must mention that in the gels the expected PCR sizes were ok.

Does anyone have an idea what is the reason for this decrease in length?

Thanks

Reliable sequencing reads start usually 50bp downstream from start of primers. Which means that 180bp-band (on the gel) sequenced with one primer will yield readable sequence in region 50-180bp (130bp length). Also I notice that sequences usually reported somewhat before reliable data, i.e. clean data starts after 52-55bp, but sequencing reports basepairs downstream from 48bp after primer start.

If you need whole-band sequence, you will have to sequence with set of two primers, each in different direction. Since you PCR this band, you already have your sequencing primers.


Why do we define anaerobic respiration as not requiring oxygen, while utilization of the Krebs cycle and electron transport chain both require oxygen? We have an electron transport chain with the final e- acceptor as SO4 2-. We say this is an anaerobic process, or specifically a case of anaerobic respiration. Elsewhere, as with fermentation and glycolysis, we have anaerobic processes that do not require oxygen. Would it be more appropriate to call these processes with the final e- acceptor as anything other than oxygen to be pseudo-anaerobic?  I say this as it seems misleading to call a process anaerobic that inherently is composed of aerobic processes.

Because oxygen is not the majority of the energy.

Krebs cycle relies on sugars. Other processes use oxygen but can do without it or primarily use carbon fuels. So they are called anaerobic.


Where to find E.coli gene expression data? I am searching E.coli whole genome expression data with different conditions, any suggestion is appreciated. Condition could be for example different growth temperature, different medias, etc.
I have tried GEO but it only gives a list and one should read all pages and samples one by one to see which conditions were used.

There are some databases in which you can search for E.coli gene expression data:

GenExpDB: E. coli Gene Expression Database
Many Microbe Microarrays Database (M3D): A resource of microbial
gene expression data
Stanford MicroArray Database (use the search tool to find relevant organisms)
Colombos (COLlection Of Microarrays for Bacterial OrganismS)
ArrayExpress

To find out about the purpose and the conditions of the experiments behind this data sets you will have to read the respective publications.


Why did humans become bipedal? Somewhere in evolutionary history homo started walking upright and became bipedal. You hear these hypotheses that, by walking upright, they could see better across the grassy savannas to escape predators, find food, find fellow humans etc. However, the most parsimonious way to accomplish looking farther across the grassy plains is by growing taller - much less adaptations necessary and hence more favorable from an evolutionary perspective. Other hypotheses say homo freed his hands to carry things. Quite fine, but some apes are known to carry around stuff. Moreover, walking on all fours increases running speed (you don't have to see far if you can escape faster) and apes climb trees better (what's a better place to hide from predators?). Hence my question: Why has bipedalism been favored in evolution?

As already pointed it out, there is no scientific consensus on the answer to this question. This is because it is hard to test proposed explanations and it's likely that several factors interacted.

All of these have been claimed to be the explanation for the evolution of bipedalism:

Freed hands for increased tool use. (Encyclopedia Britannica)
Freed hands for the use of weapons in hunting or the use of containers to transport plant foods obtained by gathering.
There are three variants: the “man the hunter” version which sees male hunting as the key stimulus (Washburn 1967 in Haraway 2013); the “woman the gatherer” version which sees women needing their hands free to carry gathered vegetable foods as the stimulus; and the “man the provisioner” version, which stresses males carrying food (either meat or plants) to provision females and offspring.
All of these explanations are probably flawed because they invoke present utility to explain the origins of bipedalism.
Bipedalism was created by female sexual selection of males with large, visible genitals.
Although unlikely, this may be correct, but it is impossible to test. (Encyclopedia Britannica)
Bipedalism evolved to aid in avoiding predators. Higher head allows you to see longer distances over the grass. (Encyclopedia Britannica)
Bipedalism evolves because it allows energy efficient locomotion between forest patches in an increasingly open environment.
“Radiator theory”: Natural selection favored bipedalism in open environments because it decreases exposure to the sun and helps keep the brain cool. (Wheeler, discussed in Haviland 2007 and Encyclopedia Britannica)
Brain is highly sensitive to heat stress.
This allowed hominins to be active in mid-day, when competing predators are less active. (Essentials of Physical Anthropology, p. 165). Since the same carnivorous animals with which hominins were in competition (both would scavenge dead game) could attack hominins, hominins were probably safer from predator attacks during midday as well.
Terrestrial bipedalism may be a continuation of an upright body posture inherent in a tree-climbing/brachiating adaptation.
Gibbons, the most arboreal of the apes and the best brachiators, walk bipedally on the rare occasions they come to the ground. (Encyclopedia Britannica)

The earliest hominin fossils appear to have been bipedal, with no clear evidence of a transition through a knuckle-walking stage, the principal mode of locomotion of modern African ape. (Kivell and Schmitt 2009, here's a secondary source, and here's a primary source that disagrees, Richmond and Strait 2000)

If this is true, then the modern African ape mode of locomotion (knuckle-walking) is a derived trait, and vertical body posture may be the ancestral trait in the African hominoid evolutionary lineages. In other words, if this is true, the ancestor of all great apes including humans was already bipedal, and modern African apes have evolved to knuckle-walk since then.
Also if this is true, the previously mentioned factors would reinforce and refine bipedal locomotion in the hominin lineage.

It is likely that explanations 4, 5, 6 and 7 all interacted to select for bipedalism. They correspond best to the paleontological and ecological data. Numbers 1 and 2 are unlikely, because bipedalism appears long before evidence of tool use.


How does the eugeroic modafinil work? How does the drug, modafinil (Provigil), exert its eugeroic (wakefulness-promoting) effects? I've read that it works by increasing dopamine and histamine concentrations in the CNS and by serving as a partial agonist at the dopamine D2 receptor. Perhaps by interfering with the function of orexin?

The exact mechanism is not known:

  Modafinil has wake-promoting actions similar to sympathomimetic agents like amphetamine and methylphenidate, although the pharmacologic profile is not identical to that of sympathomimetic amines. [...] Modafinil-induced wakefulness can be attenuated by the α1-adrenergic receptor antagonist prazosin; however, Modafinil is inactive in other in vitro assay systems known to be responsive to α-adrenergic agonists, such as the rat vas deferens preparation. [...] Modafinil is not a direct- or indirect-acting dopamine receptor agonist. However, in vitro, Modafinil binds to the dopamine transporter and inhibits dopamine reuptake. This activity has been associated in vivo with increased extracellular dopamine levels in some brain regions of animals [1].

A 2010 study has concluded that:

  Recent evidence suggests that modafinil may block the dopamine transporter (DAT) and that the dopamine D1 receptor (D1R) may contribute to modafinil effects [2].

Another one confirms modafinil's dopaminergic activity:

  These findings indicate that modafinil has a long duration of action, with alerting properties arising predominantly from dopaminergic activity [3].

It seems to be dependent on catecholaminergic signaling:

  It binds competitively to the cell-membrane dopamine (DA) transporter and is dependent on catecholaminergic (dopaminergic and adrenergic) signaling for its wake-promoting effects. [...] Modafinil is an exceptionally weak, but apparently very selective, DA transporter inhibitor. [...] The conformational constraints on the interaction of modafinil with the DA transporter - and probably, as a consequence, its effects on trace amine receptor signaling in the catecholaminergic cell - are unique among catecholaminergic agents [4].

References:

Drugs.com. Modafinil. Clinical Pharmacology. Available from http://www.drugs.com/pro/modafinil.html (accessed 29.07.2014)
Young JW, Geyer MA. Action of modafinil--increased motivation via the dopamine transporter inhibition and D1 receptors? Biol. Psychiatry. 2010 Apr 15;67(8):784-7. doi: 10.1016/j.biopsych.2009.12.015. PubMed PMID: 20132929.
Turner C, Belyavin A, Nicholson A. Duration of activity and mode of action of modafinil: Studies on sleep and wakefulness in humans. J. Psychopharmacol. (Oxford). 2013 Dec 3;28(7):643-654. doi: 10.1177/0269881113508173. PubMed PMID: 24306135.
Wisor J. Modafinil as a catecholaminergic agent: empirical evidence and unanswered questions. Front Neurol. 2013 Oct 7;4:139. doi: 10.3389/fneur.2013.00139. PubMed PMID: 24109471.


What is the process of degradation of proteins into amino acids inside living cells? Just like beta oxidation does our cells have a distinct mechanism for degradation of proteins? There are processes for degradation of amino acids but where does these amino acids come from, is it all from dietary proteins? Are they not obtained from the proteins(enzymes) that are being continuously made inside the cells?

There are two major pathways through which proteins are degraded in your generic cell: In a lysosome or in a proteasome.

The Lysosome

It's considered an organelle. It has a lipid bilayer that encloses a potent cocktail of acid hydrolases working at a low pH. The pH is maintained by a Cl-/H+ antiporter(Ref). Acid hydrolases that are being processed in the golgi are targeted to the lysosome through mannose-6-phosphate residues which are recognized by the trans golgi M6P receptors, packaged into clathrin vesicles, and targeted to acidic late endosomes which fuse, forming the lysososome (Ref).

So through endocytosis or phagocytosis, vesicles full of extracellular proteins are uptaken and may fuse with a lysosome. The hydrolases thus digest whatever they can. In a cell stress response cells may also digest their own contents with the aid of lysosomes in a process called autophagy. We can take a look here at some established lysosomal enzymes current to 2009, and if you spot a protease you can generally take a look at it's specific mechanism to see how it works. So I'll pick one out of the bunch (a lysosome has many different hydrolases remember), Dipeptidyl-peptidase I aka Cathepsin C. The mechanism of proteolysis is that of a cysteine protease which follows a bit of a generic mechanism like so:

... and so forth, you can look at a given given protease, and roughly determine how it cleaves peptides.

The proteasome

This one is a a much more directed form of protein degradation. Proteins must be tagged on lysine residues by molecules of ubiquitin, at least 4, referring to the term polyubiquitination. These are added sequentially by proteins denoted E1, E2 and E3 (see proteasome wiki). Proteins that get degraded in this manner are often damaged or come from within the cell, unlike the lysosome where the proteins probably came from outside the cell.

The catalytic domain of the proteasome is a threonine protease which follows the generic mechanism of the catalytic triad, one of the most well-studied protease mechanisms. We can view this generally through the mechanism of a serine protease, like so:

If you read through the whole thing, two notes: (1) the generic term for protein degradation is proteolysis, and (2) The mechanism depends on the protein performing the proteolysis, namely a protease.


What is a "membrane holding potential"? What is a membrane holding potential? I have come across this term but haven't been able to find a definition.
From "Voltage-gated sodium channels as therapeutic targets in epilepsy and other neurological disorders", legend to Figure 4:

Voltage-dependent and frequency-dependent inhibition of voltage-gated Na+ channels by Na+ channel blockers (A) Inhibition of Na+ currents by phenytoin is dependent on membrane holding potential. The top traces show currents evoked by depolarisation to 0 mV, with control (a standard physiological saline solution) and with 50 M phenytoin. In each of the four pairs of current traces, the larger trace is the control. The traces on the left were elicited from a holding potential of 130 mV, whereas the traces on the right were from a holding potential of 65 mV. The control current at 65 mV is smaller, due to greater inactivation induced by the more depolarised holding potential. Moreover, phenytoin is a much more effective blocker at the more depolarised holding potential. This is more evident in the bottom traces, in which the amplitudes have been scaled so that the control currents are the same size. (B) Phenytoin block builds up during repetitive channel activation. The graph shows normalised current amplitudes of whole-cell Na+ currents over the course of depolarising pulses to 0 mV, from a holding potential of 85 mV, applied at 2 Hz. Red dots indicate discrete measurements. Dashed line indicates a baseline to monitor decline in amplitude. (C) Voltage-dependent and frequency-dependent inhibition of Na+ channels by phenytoin and other antiepileptic or local anaesthetic drugs with a similar mode of action (green diamond) are qualitatively explained by a modulated receptor model. In this model, the drug binds with higher affinity to inactivated channel states than to resting channel states. Biophysical and molecular data suggest that the modulated receptor site is within the inner vestibule of the ion-conducting pore.

The membrane holding potential is the voltage level set by the experimenter in a voltage-clamp recording.


Is Black mulberry always deciduous? I have a black mulberry (Morus sp.) in my garden (or 2 actually). According to the information I could find it is a deciduous tree. The trees in my garden do indeed lose their leaves. However, as most native trees start to color yellow/brown/red in september and have lost all leaves by now, the mulberry doesn't. It remains green until the frost kicks in and only then drops its (still green) leaves. It almost looks like it doesn't want to drop its leaves, but is forced to so so. This can be seen at the picture below. Hence my question:
Is mulberry also deciduous in warm winters such as the mediterranean? And is it normal that leaves are still green when dropped?

WARNING: This answer is very tangential to the question. Confused Morus sp. with Rubus frutticosa (don't use "common name in questions"! luckily I wrote the answer using scientific names). So, as addendum: some trees tend to lose some leaves later (in my region, such trees can recover easily with broken branches).

"Always" is "always" a strong word in biology.

You describe your mulberry (Rubus sp.) as deciduous: the leaves are changed every year.

Many plants (especially trees) lose leaves in autumn/winter and they get new one in late winter/spring, few plants are marcescent, e.g. various oaks (Quercus sp.), so the leaves dry in winter and the plant lose it just when the new leaves appeaers. Some plants lose the leaves in summer.

Mulberries, like various "small plants", tend to keep the leaves until they form the new one (eventually, replacing all the shot). In my zone mulberries tend to keep old leaves until the new one are already developing.

Why this habit? Mulberries lives at borders of forests, so they try to have more energy/sun when the tallest tree lose leaves. On the other hand, being shrub and tending to radicate easily, it keeps safer in case of frosts, and it is also not a long living organism (as "plant", not as clone).

Note some decidouos young trees have also the same habits: they keep their few leaves in winter, to try to catch up. Being young also means few investment for the original plant, so it could be still a gaining habit. Look this winter on undergrowth.

Not so different to strawberries and many grasses, which replace the leaves in springs. But they are not "decidouos", just because they doesn't have a trunk or just they replace the entire shot the shots.


Are STOP codons impacted by base insertion or deletion mutation? I am learning about base insertion and deletion mutations. An example in my textbook is given below.

GUU CCA CAU AUC.

So if there is an insertion (of guanine):

GUU GCC ACA UAU C_ _ (there will be a detrimental effect on the protein created).

I'm a bit confused about how the stop codon will be read. If we have a new example with a stop codon:

GUU CCA CAU AUC UAG

When the mutation occurs (insertion of guanine) will it become:

1) GUU GCC ACA UAU CUA G

OR

2) GUU GCC ACA UAU C_ _ UAG

If mutation 1) occurs, there would be no stop codon, but mutation 2) looks strange to me. So which is the right one?

Thanks

Yes. Mutations can affect STOP codons and they do relatively commonly. These are important because they can lead to significant changes in the resulting peptide and are likely to affect protein functions or phenotype.

For a point mutation (a single base substitution), there are several possible effects:

silent mutation is a synonymous base substitution which does not change the encoded amino acids (this is neutral variation).
missense mutation is a non-synonymous bass substitution which changes only one amino acid in the protein (these can affect protein functions but do not always).
nonsense mutation is a change in a coding codon to a STOP codon (this truncates the encoded amino acid sequence prematurely resulting in a shorter peptide).
nonstop mutation is a change from a STOP codon to a coding codon (this means the amino acid sequence will continue to the next STOP codon resulting in a longer peptide).

Insertions and Deletions in DNA sequence (InDels) are important because they change all codons that follow it (not just the base substituted):

frameshift mutation adds or removes a base which resulting in a change in the reading frame: all bases following will result in new codons, including STOP codons (this commonly results in entirely new protein domains and proteins of different lengths as STOP codons will also be changed. They are encoded in the reading frame like all other codons.

As you can see, mutations which affect STOP codons are very important as they drastically change the protein sequence. This usually disrupts the protein function and causes diseases or inviable embryos. Most of these are removed from populations long-term by natural selection. However, it can rarely lead to entirely new proteins beneficial to the organism and evolutionary changes. This is more likely with duplicated genes where one can change while the other retains the original function.

As such, mutations involving STOP codons are among the most biologically important.  Another important case is splice functions. Point mutations and frameshifts can also affect intron-exon boundaries, resulting in new splice variants, skipped exons, and reading further into introns (which may contain splice junctions or STOP codons).


How are lysosome membranes protected from the attack of hydrolases? Lysosomes are a bit like the suicidal bags of cells. They help to clean cells, have an acidic pH and contain a large number of hydrolyzing enzymes.

But why don't these hydrolyzing enzymes attack and destroy lysosomes' membranes?

Early histochemical work indicated that the internal surface of the lysosomal membrane has a glycocalyx - a layer of polysaccharide, presumed to have a protective role.

  Neiss, W. F. (1984) A coat of glycoconjugates on the inner surface of the lysosomal membrane in the rat kidney. Histochemistry 80, 603–608

Subsequently it was found that major membrane proteins of the lysosomal membrane are protected from proteolysis by glycosylation:

  Kundra, R. and Kornfeld, S. (1999) Asparagine-linked oligosaccharides protect Lamp-1 and Lamp-2 from intracellular proteolysis. J. Biol. Chem. 274, 31039–31046

See this paper for a more recent study of another lysosomal membrane protein:

  Schieweck O. et al. (2009) NCU-G1 is a highly glycosylated integral membrane protein of the lysosome. Biochem. J. 422: 83-90

NCU-G1 is the mouse orthologue of the human C1orf85 protein. The NCU-G1 gene encodes a 404 amino acid protein. This is a Type 1 transmembrane protein - i.e. the N terminal domain is directed to the extracytoplasmic surface of the membrane. In vivo the protein is detected in 70 kDa and 80 kDa forms. The discrepancy between the polypeptide size and the molecular mass is shown to be due to extensive glycosylation. The protein sequence includes 9 potential glycosylation sites.


Is there a feasible way to create a large number of long random DNA strands? Suppose I want to create a large number of random DNA strands (maybe a million, or a billion, or even something close to all $4^N$ possible sequences of $N$ base pairs).  Is there an experimental way to do this?

Chemical DNA synthesis has you covered for short DNA strands.

It's possible to just use an equimolar mixture of all 4 bases when you do chemical synthesis, which results in random sequences. (This is most often used to generate barcoded primers).
The main problem with this approach is that:

chemical synthesis is not super efficient, anything above ~1-2kb will likely not be possible
If you work with a fully randomised sequence it becomes much harder to do quality control of the product (you can't sequence it).

You can also easily even calculate the probability of generating all possible sequences for a given strand length and yield.


Can anyone identify these moths? Here are two lepidopterans I collected in Oregon (USA). The wingspan of the bigger one (on the left) is ~4 cm. I spent a lot of time browsing this website hoping to find a match, but I didn't have success.

The one on the left is a Lunate Zale Moth (Zale lunata).
See Western Washington University's PNW moths page for more detailed info.

The one on the right is a Forage Looper Moth (Caenurgina erechtea).
See here for an image similar to the one in the question.
And again take a look at Western Washington University's PNW moths page for more detailed info.


Is light required for seed germination? Is light required for germination of every seed? If not, why don't some plants require it? Is there any difference in the quality and duration of light required ?

It would be interesting if someone could give both  physiological and evolutionary reasons.

Here's a partial answer, based more on common-sense then in-depth knowledge:

Physiological. One reason light is not required immediately is that many seeds are in essence bundles of stored energy (as carbohydrates, I suppose). This is what makes them attractive food for birds, squirrels, humans, etc. When they're able to escape that predation, the growing plant can use that stored energy, rather than relying only on sunlight.

Evolutionary. Seed dormancy can be a powerful tool for fitness – seeds that can remain dormant and germinate during favorable conditions could have a much higher survival rate. These conditions vary from simple: "spring" to more complex: "after having passed through the digestive system of a certain animal"; "after a forest fire"; "when there's a gap in canopy cover / less competition for solar energy". The cues that seeds "read" in order to try to break dormancy and germinate during these times therefore vary among species. Within species, there are probably often a number of cues, and as @Konrad Rudolph suggests these are probably all relatively "soft", or at least act in complex interaction with one another.


What is the term for all of the RNA in a cell at any given time? Question is asked above, simply put.

Qiagen and Life Technologies call it  RNA content, total RNA, or total cellular RNA.


Does drinking alcohol having UTI may help to kill the bacteria? It's well known that ethyl alcohol kills bacteria. And amount of alcohol in urine may be detected by EtG tests (as long as 3-4 days after intake).

Does drinking alcohol in reasonable amount by healthy individual (non alcoholic) having UTI helps to kill bacteria in the urinary tract (in order to get rid of them quicker)?

To begin answering your question,

  Does drinking alcohol in reasonable amount by healthy individual (nonalcoholic) having UTI helps to kill bacteria in the urinary tract
  (in order to get rid of them quicker)?

We have to clarify that EtG detects ethyl glucuronide which is a byproduct of ethanol and remains in the urine for several day. The presence of ethyl alcohol in urine is significantly shorter somewhere between 8-12 hours (reference).

So what does this mean? Well, in order to "kill" the bacteria causing the UTI it must be exposed to a minimal inhibitory concentration of ethyl alcohol for a certain amount of time. Depending on the bacteria causing the infection this concentration and exposure time varies.

So if the concentration of ethyl alcohol was high enough and the flow of your urination and micturition long enough, maybe, but is unlikely to have much effect.


Tracking of oxygen molecules in glucose oxidation For this reaction, found in typical biochemistry textbook:

$C_6H_{12}O_6 + 6O_2 \to 6CO_2 + 6H_2O$

I am interested in where do the oxygen atoms of $6O_2$ go. I think they go to $6H_2O$, but this is not sufficient for balance. So Does oxygen atom from $6CO_2$ also get into the carbon dioxide. Experimentally these can be confirmed by iostope labeling experiments. Reference to any such experiments will be appreciated.

I am interested in this question because the central metabolism can be understood as a electron transfer process where glucose is donor and oxygen is acceptor. We need to calculate, effectively how many electrons glucose transfers to oxygen in case of full oxidation.

I think this experiment (PDF file) will help you understand the basic concept about the fate of oxygen in aerobic respiration. Basically the result is:

The oxygen of respiratory carbon dioxide is in exchange equilibrium with body water.
Utilized molecular oxygen is converted to body water.

In respect to calculation of electrons donated to oxygen, just calculating how many NADH2 and how many FADH2 is reduced in how many steps during ETC will be able to answer your question.


What is this insect I found in northern Europe? Found this one in my bed in Northern Europe.

Around 6 mm long (5 mm body + 1 mm nozzle). Seems to have 6 legs. The back looks a bit like black-brown camouflage, the legs are red-brown, the nozzle is black.

Could this be some kind of bed bug?

Definitely not a bedbug. It is a weevil, family Curculionidae. A beetle, and not normally found indoors. It looks a bit like Baris, but I cannot tell from the picture. https://en.wikipedia.org/wiki/Baris_(weevil)


Why do diseases in the tap water of developing countries affect people from developed countries more? My siblings and I went abroad to a country that doesn't have drinkable tap water, but we did not know this at the time as the people who lived there used to drink it all the time with no issues.
One day, we all decided to drink a glass of water from the tap and we all ended up in a hospital and were really ill (I'm unsure of what we had as it was a while ago). We were told it was due to the tap water and were advised to only drink bottled water in the future as the tap water is unsafe.
My question is, why did the tap water only affect us but was fine to drink for the residents there? Is it maybe because our bodies are used to clean tap water?

You can expect that someone drinking from a water source regularly will develop immunity to the pathogens in that water source by being repeatedly exposed to them.
However, it's not quite right to say that poor quality drinking water impacts mostly tourists. It mostly impacts the people drinking that water, especially children. Immunity comes at a cost. Some example statistics from Wikipedia:

Between 2000 and 2003, 769,000 children under five years old in sub-Saharan Africa died each year from diarrheal diseases

In South Asia, 683,000 children under five years old died each year from diarrheal disease from 2000 to 2003. During the same period, in developed countries, 700 children under five years old died from diarrheal disease.

And from WHO:

Contaminated water can transmit diseases such diarrhoea, cholera, dysentery, typhoid, and polio. Contaminated drinking water is estimated to cause 485 000 diarrhoeal deaths each year.

These statistics conflict a bit, and I won't go too far into the reasons why or try to identify the correct number. I think they are all sufficient to identify this as a substantial issue in the world.
Responses to disease vary between individuals for all sorts of reasons, including genetics, overall health at the time (for example, someone well-nourished versus poorly nourished), and access to medical care and treatment. Some you could also add up as effectively "luck". In a hypothetical scenario, you could expose 100 people to a pathogen, and of those 100, many may get very sick and a few die. The survivors may then have future immunity to the same pathogen, but it would be wrong to say the population as a whole is not affected by it, you're just looking at the people who survived.


How exactly does alcohol solution kill or neutralize viruses? To reduce the risk of infection by viruses (including 2019-nCoV) the CDC suggests:

Wash your hands often with soap and water for at least 20 seconds. Use an alcohol-based hand sanitizer that contains at least 60% alcohol if soap and water are not available.
Avoid touching your eyes, nose, and mouth with unwashed hands.
Avoid close contact with people who are sick.
Stay home when you are sick.
Cover your cough or sneeze with a tissue, then throw the tissue in the trash.
Clean and disinfect frequently touched objects and surfaces.

To my knowledge most alcohol-based hand sanitizers use ethanol. In clinical settings sometimes isopropanol is also used.

Question: How exactly do alcohols, especially ethanol and isopropanol provide some disinfecting action against viruses? Are the virus particles simply dissolved? What happens?

Alcohols dissolve lipid bilayers

Many viruses have an outer lipid bilayer. Ethanol lyses cells, and in the same fashion damages membrane-bound viruses by rupturing the bilayer (which is made of ethanol-soluble lipids).

Alcohols misfold the protein coats of viruses

Additionally, alcohols denature proteins, which misfold in non-aqueous conditions. Some viral surface proteins are important for adhesion and attachment, and misfolding these renders the virus inactive. The total breakdown of viruses is essentially due to the misfolding of their protein coat (the capsid).

The same goes for bacteria

With the additional effect of dehydrating cells

Alcohols substitute the water contents of a tissue and have been as such used as fixatives. Common laboratory examples include methanol and ethanol.

Typically, 70% (140 proof) ethanol is used for bench wiping to kill or inactivate microbes. This includes viruses.

This is all standard, common, easily and readily accessible knowledge. Here's a bonus source.


What kind of larvae are these? My uncle was helping us spray the garage for ants, and he stumbled across a huge batch of some type of larvae. According to him...

  "It looked like a long, narrow clump of mud. When I broke it open, all of these larvae fell out. Whatever bugs were inside scattered pretty quickly!"

Geography: We're in Los Angeles, CA (southwestern USA)
Season: It's late summer here (early September)

Exhibit A: The pile of larvae...

Exhibit B: A similar husk of "mud" found in our garage. When it was shattered, nothing fell out...

My uncle thinks it's termites... I'm certainly hoping it isn't.

I think that it is termites larvae. For more info check this :  Termites follow the typical life cycle of insects that have a gradual life cycle: they begin as eggs, and then enter nymphal to adult stages. In termite development, newly hatched termites are sometimes referred to as “larvae,” which is not to be confused with the larvae of complete metamorphosis insects like flies.

Termite larvae typically hatch within a few weeks. They are approximately the same size as the eggs from which they hatched and are immediately tended to by worker termites. They often comprise a large part of a termite colony.

Similar to other insect young, termite larvae go through a series of molts, during which they shed their skins. From the larval stage, termite larvae may evolve into other members of the colony’s castes.

If you suspect you have termite activity in or near your home, contact a pest control professional. Termite damage can go undetected and result in significant financial loss from their damage. A termite inspector can inspect a home for signs of activity and conditions that are attractive to termites. They also can offer services to treat and protect the home from potential future damage.


How the brain is affected by Alzheimer's disease What exactly happens to the neurones in the brain?
why can't they be repaired/restored?
Why is it that there are so called 'good days'? What happens to the brain on such days?

Essentially, there's a net dysregulation of a number of genes where the additive effect of each dysregulation causes neurotoxic amyloid plaque formations, and neurofibrillary tangles of hyperphosphorylated tau protein. Not only so, these mutations induce calcium and cytokine dysregulation, and increase oxidative stress.

Specific to molecular mechanisms of amyloid beta (abeta) oligomer toxicity, a good article here makes some good descriptions. For example, abeta can reduce copper and iron ions. Oxygen reacting with these reduced metals become reactive oxygen species. They also noted that abeta reacts with many receptors, like TLR's which ended up promoting JNK-mediated apoptosis. I'd give that article a read, and I'll try to get some molecular pathology mechanisms for other facets of AD on board here.

They can't generally be repaired because the issue is with genetic mutations, and some of the mutations engage in positive feedback loops with existing conditions that make a more pronounced effect. For example, tau protein is regulated in part by O-GlcNAcylation. This is like phosphorylation, but with sugar moieties, but it becomes downregulated when glucose is low, thus increasing phosphorylation on tau (Liu et al., 2004) . Mutations that affect GSK-3, insulin resistance and/or diabetes thus can play a role in AD pathogenesis.

Some data exists to show restoration of potentially AD-causing abnormalities involving HDACs. For example, abnormal HDAC2 in AD brains hypoacetylated promoter regions for some housekeeping and plasticity genes, and they rescued the AD phenotype by knocking down HDAC2 (Gräff et al., 2012) . These are of course mouse models typically.

As for question three, I really can't say except for stochasticity. I did a review for an undergraduate course that goes over some of the recent literature involving AD genetics/pathogenesis. It might not be professional quality but it gets the message across, linked https://drive.google.com/open?id=0BwKiapIJL9T2ajc4ajhTVVRvRWc


Is there any program or website that allows me to create phylogenetic trees without having to insert an already created dataset? I asked a similar question on Quora before, but did not get any useful answers as the program the one answerer suggested turned out to have the exact same problems as all others I have found so far.

Most programs for the construction of phylogenetic trees—being made for researchers in various biological disciplines—seem to rely on the input of a dataset that is a formulation of collected genetic and/or anatomical data.

Specifically, I am looking for a program that is like this, but with a GUI that allows tree editing (i.e. you can add and remove new taxa), for example, poorly described/novel theoretical species, dubious species, and subspecies and can be used to create simplified versions of charts like these.

Have you ever tried using Mesquite?

I used it when I taught intro bio lab course as a TA.
Basically you try to come up with yes or no questions, and based on how you answer these questions it will generate a tree similar to your second link.

Can be a little bit complicated, but I am sure there are many tutorials for it on its website.


Identify this insect - genus, species (orange, black) Please help identify this insect - genus, species and anything interesting about it. Do the colors matter in the identification?

Note, this is posted separately due to comments in this other thread.

This looks like a Weevil. Specifically it looks like a red/orange-spotted lily weevil

Here is some more information on it:

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

though the information is very limited.


Cucumber on the eyes In many spas and salons I have seen people place a cold cucumber on their eyes.
 I think this might be for coolness, but why a cucumber?
And Is it actually for coolness or for something else (like lightening of dark circles, etc.)?

Cucumbers have an anti-inflammatory effect that reduces puffiness. The
  vegetable not only has a high water content, it but it's often stored
  in the refrigerator and comes out cold. This means that the water
  hydrates your skin, and the cool temperature decreases the flow of
  blood to the space around your eyes. Together, additional hydration
  and reduced blood flow can sooth the skin around your eyes and
  alleviate swelling

Source

Also it has silica.


What does this equation about DNA replication mean? Could someone help me understand this equation please? I found it in a paper which said that it was DNA replication, but why?

$\ce{dNTP + dNMP_{n} -> dNMP_{n +1} + PPi}$

I found that dNTP means deoxy nucleotide triphosphate and dNTP means deoxy nucleotide monophosphate. Deoxy nucleotide monophosphate is a monomer in DNA, but dNTP isn't.

I also would like to know if there is an equation like this in other processes in the central dogma (such as transcription and translation)?

The notation you are referring to is a way to express the elongation of a nucleotide strand (Fig. 1).

dNTP + dNMP(n) → dNMP(n+1) + PPi

means

Existing strand  +  deoxynucleotidetriphosphate  →  elongated-strand  +  pyrophospate.

Fig. 1. Elongation of DNA. Source: Concepts in Genetics.

This reaction holds for DNA replication as well as transcription.

Translation is all about protein synthesis from amino acid precursors. Each subsequent amino acid is coupled to the growing peptide by a peptide bond between the carboxyl of the growing peptide and the amino group of the new amino acid. A water molecule is eliminated during the reaction (Fig. 2).

Fig. 2. Peptide bond formation. Source: An Introduction to Molecular Biology

Hence translation can be written analogously to replication as:

amino acid + peptide(n) → peptide(n+1)

However, also in this polymerization reaction energy is needed and amino acids are activated while they are bound to the messenger RNA (mRNA) through the action of ATP. Moreover, during translation the ribosome (i.e., the protein synthesizing machinery) uses another source of energy to move across the RNA template, namely GTP. Hence, the net reaction can be written as:

amino acid + peptide(n) + ATP + GTP → peptide(n+1) + AMP + GDP + PPi + Pi

Note that this notation in itself is not a dogma as other ways are in use to denote DNA and RNA synthesis. According to Merriam-Webster a dogma is:

  A belief or set of beliefs that is accepted by the members of a group without being questioned or doubted.


Quantifying the Genetic Basis of Complex Diseases In general, there are 2 types of diseases for which we understand "causality" very well:

Infectious disease, where there is some etiological agent that causes the disease and
Monogenic genetic diseases (e.g. cystic fibrosis), where there are a set of mutations that make specific proteins that are very important non-functional.

My question is not about these diseases. Rather it's about the diseases like T2D (type two diabetes mellitus). Simply put, are complex, chronic diseases like this always traceable to genetic causes? For a given complex disease state, is there always a set of genotypes that leads to the disease? Large-scale GWA (genome-wide association) studies of course have upturned tons of disease-associated variants in complex conditions like T2D, most with tiny effect sizes.

But is it possible to get the disease with none of the disease associated variants (even assuming that you had a list of all disease associated variants; of course you don't actually have this list, but I'm just trying out an intellectual exercise)? If yes, what is the causal pathway for this way to 'get' the disease?

EDIT: To clarify my question as per comment suggestions: Do all (complex) diseases have a genetical background/causative mutation or can they arise for other reasons?

I'm not sure what you mean by "complex", but many diseases are known to arise due to exposure to toxins or to an absence of essential nutrients in the environment.
Toxic metals:
A good example of this is exposure to some metals including arsenic, lead, and mercury.  See for example this information from the US NIH and the wikipedia article on metal toxicity.
In the case of arsenic, some of this poisoning is even "natural" — i.e. due to toxic levels of this metal in ground water that hasn't been contaminated by human activity.
Diseases that have been linked to such exposures include cancer, heart disease, diabetes, and anemia.1,2
Deficiencies:
Another class of diseases that are more-or-less purely environmental are those due to nutrient deficiencies — i.e. a diet lacking in minerals or vitamins.

References:

Byrns, M. C., & Penning, T. M. (2011). Environmental toxicology: carcinogens and heavy metals. The pharmacological basis of therapeutics. McGraw Hill, New York, 1853-1878.
Tolins, M., Ruchirawat, M., & Landrigan, P. (2014). The developmental neurotoxicity of arsenic: cognitive and behavioral consequences of early life exposure. Annals of global health, 80(4), 303-314.


Finding exons in DNA problem My attempt:  I looked for the TACs because I thought this would be AUG in mRNA and ultimately Methionine (the start codon). But apparently, that's not how you do this problem.  Im confused because the answer (shown in red) doesn't have any TACs and the boxes seem to start at random places.  I am also confused as to why my professor drew a box around both strands.  I thought only one strand at a time was turned into mRNA?

UPDATE:  It has occured to me that the entire strand is transcribed and then the introns are removed.  So I know why not to look for the TACs.  But now, how can I identify the exons?

After an RNA has been transcribed, in eukaryotes it is spliced before it leaves the nucleus. This means that parts of the RNA are removed (called introns) and the ends are capped. The parts left over in the mature mRNA after removing the introns are called exons.

The mRNA does not have to start with a start codon. There can be sequences before and after the bit which actually gets translated.

Yes, only one strand of DNA is transcribed into RNA. When you look at the mature mRNA below, read the first few bases and try to find their complements in the original DNA because this is where they were transcribed from. UCAUG is transcribed from the DNA AGTAC (with TCATG on the opposite side).

Now you look for the end of the mRNA. Bear in mind that all the A's are the poly-A tail which is added during splicing and determines how long the mRNA will persist in the cytoplasm. So you look for CUAGG in the original DNA, which must be transcribed from GATCC (with CTAGG on the opposite strand).

As you can see, that's exactly where the two red boxes start and end.

Now since the mRNA you see here is mature (indicated by the poly-A tail and the 5'-cap), that means introns have already been taken out. So any bases that you can see in the DNA between the start and end that we just found but not in the mRNA must have been an intron. Or the other way round: all the bases that are in the mRNA which you can also find in the DNA must be exons.

You will notice that exactly the bit that isn't in the red boxes doesn't appear in the mRNA anymore. Or: All of the mRNA is in the red boxes. The sequence is interrupted by a short bit which you can't find in the mRNA anymore - so this must be an intron.


What are the names of these plants? I found these plants in my backyard in South Florida. What are they?

The main plant in the photo (with the larger leaves) is called Virginia creeper. The botanical name is Parthenocissus quinquefolia.   The leaves are very distinctive in leaf groups of 5 to 7 leaflets.  It is an aggressive woodland vine in the grape family Vitaceae.

Links:
https://en.wikipedia.org/wiki/Parthenocissus_quinquefolia

https://plants.usda.gov/core/profile?symbol=paqu2


Why can't we grow more teeth? A similar question but about teeth healing themselves is Do teeth have the capacity to heal?.

So I understand that teeth have the capacity to heal themselves to a certain degree. It appears to be that part of the reason they can't heal all of themselves is that they are not surrounded by cells. In that case why can't we grow teeth back?

If a tooth is grown in the gum, or somewhere else, it would be surrounded by cells and so should be able to grow back right?

It appears that sharks can grow their teeth back:

  New teeth are continually grown in a groove in the shark’s mouth and the skin acts as a “conveyor belt” to move the teeth forward into new positions.

Why can't we do this?

Unfortunately, the answer to your question isn't as well researched as other areas, I believe...let's add some complexity into this.

You're correct, teeth does "grow" in the gums. And it does start off surrounded by cells (look up: tooth bud, cap, bell stage)!

The tooth originates from an interaction between the ectomesenchyme (likely originating from the neural crest cells) and the epithelium of the mouth when it is forming while you're still an embryo in your momma's tummy.

Unlike sharks, which are homodonts (meaning, their tooth are all of one morphology), we are heterodonts (e.g. we have different shaped teeth - e.g. molars, canines, incisors, premolars). There are a couple of theories to why this occurs (look up: clone model, field model, odontogenic homeobox code - a combination of all these theories). Basically, a bunch of genes transcribe for proteins and signalling factors that create the complexity of your tooth shape and position in the mouth.

Basically, this means, our teeth are going to take longer and require more energy and effort to carve into (yes carve! lot's of the tooth shape is create by apoptosis of the regions around the "cusp" area when it is developing).

When your primary/baby teeth pop out, they serve functions such as developing speech, allowing you to eat, strengthening your jaw muscles (which in turn helps to develop your mandible and shape of the face), all this so you can have a great bite when you get older!

Luckily, sharks don't speak much underwater, so they probably don't give a poop about having properly lined up teeth. Their teeth grows everywhere. Proper bite for eating various nuts, fruits, meats and vegetables? NAH. WE JUST CHEW OFF LEGS. WE CAN ONLY SHRED STUFF. Sharks need strong ankylosed teeth (ankylosed = like an anchor? teeth are anchored into the mandible of the shark).

In contrast, humans have teeth in gomphosis (sockets), which gives our teeth some cushioning and sense of proprioception (the sense knowing how hard you're biting) when we bite on something extremely hard, to prevent us breaking our teeth - thus helping us preserve our teeth. Sharks don't have that, they just break their teeth.

Humans do finally replace their teeth, after our jaw grows enough for us to accommodate them at a genetically planned stage. This happens by tooth germs (cells) being bud off (like a flower yes :D) from the baby teeth. Note though, your 1st adult/permanent molars are already beginning to form when you're still in your momma's tummy.

I believe that the continuous creation of teeth requires more energy, but takes less time (sharks). For humans, one time creation of teeth requires less energy, but takes wayyyyy more time (and also has to be timed correctly with all our other growing bits).

TL;DR Evolutionary reasons and different functional uses of teeth between sharks and humans probably determine why we only have two sets of teeth (diphyodonts). That being said, it would be cool if we were like rats (have molars/incisors) though, which replace their teeth anytime its lost. Maybe one day we can evolve into it? Yay!

Some interesting points: You mentioned teeth "healing".

Your teeth is made up of enamel on the outside, which is NEVER replaced. It "heals" by remineralisation which is not exactly the same as growing new crystals on top of it. Kinda complex, won't go into it.

However, your teeth is always forming new dentine, which is below the enamel. In a way, your tooth really is growing back all the time. Because a new layer of dentine is deposited everyday (like...4 micrometers). This is because the dentine producing cells, called odontoblasts, are still around. In contrast, the enamel producing cells, called ameloblasts, are removed when your tooth has developed. I THINK, the reason is to make space in your enamel so it can be fully mineralised and completely filled up by hydroxyapatite. (Too much fluoride when young can block this removal of ameloblasts and its proteins like amelogenin and enamelin = forming holes, which cavitate resulting in fluorosis).

Hopefully all that answered your question. But, it was fun for me to rant anyway. Cheers.


Would chimpanzees and humans normally be in the same genus if we weren't so sensitive about it? Listening to the BBC's radio program The Why Factor particularly poignant episode What Can Chimps Teach us About Politics? hosted by Professor James Tilley, I heard Professor Frans de Waal of Emory University's Yerkes Primate Research Center, and author of Chimpanzee Politics say:

  The differences are so small; normally we would put humans and chimpanzees in the same genus, but because of sensitivities in the human species we’ve not done that.

I'm wondering if this is an opinion, or arguably correct. I understand that taxonomy is an "evolving" discipline, but are there scientific arguments or viewpoints that would suggest that chimps and humans would be in the same genus if not for public, social or individual sensitivity to the idea?

I have not seen any research that synonymizes Pan and Homo, but that doesn't mean someone hasn't tried to propose it in the literature at some point.  The proposal to synonymize the two genera of course would need to be based on accepted techniques and not emotion (such as just having a particular fondness for chimps).  And such a synonymy would necessarily synonymize all the ancestors that existed since the most recent common ancestor of humans and chimps, or a new structure for the evolutionary relationships would have to be proposed.

I think it's important to note that while there is a right answer when it comes to the structure of the evolutionary history of species, there are no right answers when it comes to naming conventions.  The names exist for our convenience.  Phylogenetic trees themselves which show evolutionary relationships are utilized for other research such as understanding the evolution of traits.  So I don't know if this researcher is thinking there is some need to re-evaluate the structure of the relationships between humans and chimps for the sake of advancing science, or if he's just trying to get his opinion across and/or cause discomfort.

Related posts

How could humans have interbred with Neanderthals if we're a different species?
Does it make sense to classify all humans in a single species?
Is there a consensus on whether or not race exists on a biological level?
Do humans have enough biological differences to be grouped into races or subspecies?


How often can you reuse coomassie stain? I usually heat to boil in the microwave, and stain for 12 minutes. How often can I reuse this buffer?

Since there's a lot of methanol in Coomassie stain, a significant amount would probably evaporate off each time you microwave it. Therefore, it'd be probably a good idea not to reuse it because (1) you're losing methanol, and (2) the concentration of everything else is thrown off.

Why do you boil the stain? I just pour mine at RT right on the gel and it works fine.


If an antiserum was raised in a buffalo by injecting it with monkey red blood cells, what would be the full name for this antiserum? Im confused, i've attempted this & what i got is buffalo anti-monkey red blood cell antiserum. I'm not sure if this answer is right

its actually Anti-Monkey RBC Buffalo Antiserum as the Ab formed is Anti-monkey RBC Buffalo Ab.


ID of a purple fungus in Virginia Could someone tell me a bit more about this fungus found growing in a nearly straight line in the lawn in a wooded area of Virginia, USA? It seems rather fragile, maybe a bit "dry"

This is not a moss, but a fungus of the family Clavariaceae. Most likely this is Clavaria zollingeri, commonly known as violet coral, but there are a few resembling species. Microscopy might be needed to be entirely sure.

The species is saprotrophic, so it grows on the woody debris in your picture.


Is it possible to make bacteria vulnerable to antibiotics it's resistant to? Since bacteria becomes resistant to antibiotics after an unfinished course, is it possible to do anything to be able to get treatment with the same antibiotic again, and reverse the resistance in the bacteria?

Or, the bacteria with the resistance will stay resistant forever (until death)?

Edit:

There are some websites that are claiming that some natural remedies might be effective, like taking "Honey", which doesn't seem to be medical facts.

Perhaps it is useful to first consider how resistance is gained:

If you treat a population of bacteria with an antibiotic, some may die and some may live.

If none die, they are obviously resistant.

If all of them die, then all of them were sensitive, meaning that the size of the population and the variation were not large enough in order for some of the bacteria to be resistant. One approach would be to try to get larger genetic variation by inducing mutations with some mutagen. In addition, you can take a larger population. This would in effect let you sample a larger part of the genetic space to see if you can find a resistant strain. Of course it is possible that this will not work.

If some die and some are resistant, the situation is slightly more complicated. One possibility is that those which lived are genetically resistant (their DNA is different). To see if this is the case, you take those which lived and treat them again with the antibiotic. If they all live, they are resistant. Another possibility is that they are scholastically resistant. This phenomenon is known as bacterial persistence. What happens is that there is a genetic switch that randomly bestows resistance in some fraction of the population, let's say 10 percent. If you now take this population and reapply the antibiotic, only 10% of the population will survive. This interesting mechanism allows the bacteria adapt more quickly, since they do not have to make modifications to their DNA.

I am guessing that if the bacteria are genetically resistant, they will stay resistant. If the bacteria are scholastically resistant, it might be possible to affect the genetic switch which causes the persistence. This, in addition to reducing the size of the population, might cause a situation where none of the bacteria in the population are resistant long enough to survive.


Why do people and animals stretch out their bodies and what is causing this behaviour? I noticed that my cat which is only 6 months old has started stretching its body from time to time. Then I thought that this motion doesn't seem very natural from another cat's viewpoint, so my cat probably didn't try to imitate some other cat all of a sudden and learned it like that. This action must have been caused by something else then. Or at least that's what I think.

Both animals and people stretch their muscles from time to time, but it doesn't seem to be caused by memory of others doing it. So how does this action originate in them?

Humans and other animals have lots of innate behaviors that are not learned from observation, i.e. behaviors that are hard-wired into our nervous system, and this is one of them. Suckling reflexes in mammals and the Moro reflex is human babies (which we grow out of) are other simple examples.

The stretching behaviours you are referring to are usually labelled pandiculation in humans (defined as involuntary stretching of the soft tissues), and yawning is often considered a special case of this. These kinds of behaviours are also normally related to transition periods between high-low activity in animals (Walusinskie, 2006). In practice, stretching functions as a way to reverse the muscular atonia during REM sleep, and is in this sense a way to restore homeostatic functions (Fraser, 1989; Walusinskie, 2006).

A paper by Rial et al (2010) deals with the evolution of sleep and wakefulness in mammals from our reptile predecessors, and indicates that stretching behaviours might have originated/evolved from post-basking activities, more specifically risk-assessment behaviours, such as:

  ...risk assessment behaviour (RAB) and consists of the suspension of current behaviour, to be replaced by head dipping movements, eye scanning, rearing and
  adopting stretch attending postures...

There is most likely much more to be said about this, and the paper cited above contains many references that can provide further clarification and evidence. A short comparative discussion of pandiculation is found in Frasier (1989).


What is C-terminal tryptic peptide? A biologist wrote to me:

... C- or N-terminus,... For example, a C-terminal tryptic peptide like AGWRGSDSHSR, would be...

I don't have any idea what that is. When I google the term ("C-terminal tryptic peptide"), nothing obvious came up. What's that? Why AGWEGSDSHSR is a "C-terminal tryptic peptide"?

Its quite simple if you look at the basics! Lets have a look at the sequence you give:

  AGWRGSDSHSR

Write that in 3-letter terms1:

  Ala-Gly-Trp-Arg-Gly-Ser-Asp-Ser-His-Ser-Arg

Pay attention to the C-terminus. The last amino acid residue in the sequence is Arginine. Now, its well established that Trypsin cleaves a polypeptide after (i.e. towards the C-terminal side of) Lysine and Arginine2.

Thus, C-terminal tryptic peptide is the peptide that remains after a polypeptide has been treated with Trypsin.


Are there ways to genetically increase mutation rate of E.coli? Are there ways to increase mutation rate of E.coli using genetic modifications? I know possible ways it can be done without genetic modifications by exposing the cells to stressful conditions like anaerobic and radiation but what are some genetic ways?

Thanks!

Mutations are caused by the insertion of the wrong bases during replication, or by chemical changes to bases, either by chemical agents or by radiation.

The rate of mutations could be increased by exchanging the E.coli polymerases with other polymerases displaying higher error rates (or with less proofreading capabilities). A lot of errors are quickly repaired via different mechanisms, knocking out all or a few of those mechanisms might result in an E.coli strain with an increased mutation rate (if they survive).
https://www.ncbi.nlm.nih.gov/books/NBK9900/

A more elaborate way would be to engineer E.coli to contain a pathway that synthesizes a mutagenic compound. The easiest way to to this would be 1 enzyme that generates reactive oxygen species, as those also cause DNA damage. You could also delete some of the catalases and other enzymes that remove reactive oxygen species instead.
https://www.ncbi.nlm.nih.gov/pubmed/16824196


Light and Dark Reaction of photosynthesis? I'm having a hard time understanding light and dark reactions because all the sites I've gone through provide different equations. Some say photolysis is H20 = H+ + O2 while some present it as H20 = H+ + OH-. Moreover some have given that NADP+ + H+ = NADPH and some have stated that NADPH+H+ = NADPH2
Could someone provide me with a better, more detailed explanation of both the light and dark phases with the equation of all the reactions that occur during the process, as well as the site of occurrence.

I can see your frustration if you meet errors such as NADPH2 but that is the price you pay for approaching as complex a subject as photosynthesis without a good biochemistry textbook. Even the on-line versions (e.g. Berg et al.) are unsatisfactory because of their layout. You will have to sit down and spend a couple of hours on the topic — all you can expect from a site like this is clarification of key points.

That said I'll offer some clarification. The first thing I'll say is that focusing on chemical equations is not the way to understand photosynthesis. It will demonstrate that the law of conservation of matter applies, but otherwise is a bit like doing a chemical analysis of a cell to try to understand how it works. This is because:

There are two quite separate reactions in photosynthesis. As the products of one are (more strictly can be) used in the second, overall equations cancel them out, and so ignore key features of the process.
Photosynthesis is concerned with the transformation of energy as much as molecular structure. Chemical equations do not really address this.
The generation of energy involves the establishment of a gradient of hydrogen ions across a biological membrane — something your chemical equation does not encompass.

So what are the key ideas to bring to the text book you are going to purchase?

The overall objective is to make sugar from carbon dioxide

This poses a problem, not particularly because of the chemical reactions, but because these reactions require energy of two kinds:

To join the carbons from the carbon dioxide into C-C bonds. This requires ATP, the free energy change of its hydrolysis to ADP being coupled to ‘drive’ the formation of a C-C bond.
To reduce the oxygen atoms of carbon dioxide to OH groups. The biochemical molecule that is used for this reduction is NADPH, so ‘energy’ is needed to reduce its oxidized form, NADP+. (I won’t go into why this can be thought of as energy — if interested you need to read about the free energy equivalents of redox couples.)

The sun provides the energy

The energy for creating the reducing NADPH and the ATP comes from the sun in a complex series of reactions (these do not involve carbon dioxide). Light of a particular wavelength is harvested and used to break a water bond so as to separate charge in a reaction that I will deliberately not balance:

(1) H2O + sunlight → O2 + H

A complex series of reactions transfer the H (more strictly an electron) between different molecules, eventually reducing NADP+ to NADPH. At the same time an equally complex process builds up a H+ concentration difference across a membrane which provides the energy to convert ADP to ATP (see also Where do the H+ ions come from in light reactions?).

This is what is called the light reaction of photosynthesis because it requires light. It occurs in the thylakoids of the chloroplast, particularly at the membrane, although the products are in the stroma.

After energy has been harvested from the sun chemical synthesis can proceed

Having harvested the energy of the sun the plant has the wherewithal to make sugar from carbon dioxide. This is referred to as the ‘dark reaction’ because it does not require light. But its name can be misleading to the neophyte as the process does not have to take place in the dark. The overall unbalanced equation is:

(2) CO2 + NADPH + ATP → C6H12O6 + NADP+ + ADP

This is actually a complex series of enzyme-catalysed reactions (known as the Calvin Cycle) and a triose is the initial product. It occurs in the stroma of the chloroplast.


Why are fatty acids consisting of even number of carbons predominant? Most of the fatty acids in animal biology consist of even number of carbons in its parent chain. What property of such fatty acids cause the biological systems to prefer them over the odd counterparts? What's so bad about fatty acids containing odd number of carbon atoms in their parent chain?

Why are fatty acids consisting of even number carbons in their parent chain predominant?

In short, it's because fatty acids are made from two-carbon blocks.

The way that most organisms make fatty acids is by the successive addition of two-carbon units (acetyl-CoA). So we usually get even-numbered fatty acids just because the building blocks are also even.

In plants and in synthetic contexts, we can have some reactions that can produce odd-numbered fatty acids (by building with two-carbon units three times to get six, and then breaking that six in half to get three, for example). Such odd fatty acids are seen in some organisms, but humans are usually thought to get them from other sources (e.g. microbiota, diet).

EDIT:

Point 1: Fatty acids are generally built two-carbons at a time.

The European Bioinformatics Institute has a really good explanation of fatty acid synthesis. The quote below is from that (https://www.ebi.ac.uk/interpro/potm/2007_6/Page2.htm):

  "Whether existing as one complex or as independent enzymes, the
  reactions catalysed by types I and II fatty acid synthases are the
  same.  Both systems are primed with acetyl-CoA, and then add 2-carbon
  units to the growing chain using malonyl-CoA as substrate."

Point 2: Odd-numbered fatty acids can be produced by various organisms, and can be linked to dysfunction in humans.

doi:10.1038/srep44845 talks about the importance of odd chain fatty acids in disease as a preface to its findings about the sources of such fatty acids. They try to narrow down where odd-chain fatty acids come from, but they definitely seem to be building their case on the pretense that odd chain fatty acids are not great in humans.

  "According to the literature, the origin of C15:0 and C17:0 has long
  been attributed to the diet, specifically from ruminant fat as the
  main contributor in a typical Western diet. This has been explained by
  the fact that these two OC-FAs are produced by the rumen microbiome
  and then incorporated into the fat deposits of the host animal
  destined for human consumption."

Point 3: Plants produce odd-chain fatty acids

An established/old paper (doi:10.1006/abbi.1994.1110) mentions this, and there's a Wikipedia article (https://en.wikipedia.org/wiki/Odd-chain_fatty_acid) that paraphrases in a nice way:

  Some plant-based fatty acids, however, have an odd number of carbon
  atoms, and Phytanic fatty acid absorbed from plant chlorophyll has
  multiple methyl branch points. As a result, it breaks down into three
  odd numbered 3C Propionyl segments as well as three even numbered 2C
  Acetyl segments and one even numbered 4C Isobutynoyl segment.


Is Circle of Willis unique to humans? I understand that Circle of Willis is a circulatory anastomotic system that provided blood to the brain.  I want to understand if this system is unique to humans or does it exist in other species or mammals to be more specific?

I found two references that talk about the circle of Willis in different kind of mammals so i think it's right to say that this particular anastomotic system of arteries is not exclusive to humans.

Here are the two references:

http://www.neuroanatomy.org/2008/054_065.pdf

http://www.ncbi.nlm.nih.gov/pubmed/14651482


Are there any known rules that neurons always follow while transmitting/receiving signals? I'm new to neurobiology so I don't know much about it. However, I have worked on artificial neural networks. Man-made AI networks all follow a handful of simple rules.
I was wondering if biological neurons also have a set of predictable rules?
E.g
What does a neuron do if it does not get stimulated/receives no signal for a long time. Will it die ... or try to find new connections that might send signals?
What does a neuron do if it is over-stimulated?
What does a neuron do if it receives a signal -> does it broadcast it to all of its connections, or only 1. Does it have a preferred output path for any incoming signals.
Can a neuron send out a new signal without having received a signal from anywhere else.
How does a neuron know if it has done his job "well". How does it get positive feedback.

Short Answer:

"Always" is always a dangerous term in biology.

Longer Answer:

  What does a neuron do if it does not get stimulated/receives no signal for a long time. Will it die ... or try to find new connections that might send signals?

What neurons do when they aren't stimulated depends on the neuron and phase of development. Typically, thresholds for spiking will decrease, but it's also normal for cells to atrophy and die: neuronal death is a critical part of development, and loss of synaptic connections and some neurons is the most obvious feature of human brain development during adolescence, rather than birthing new neurons or growing new synapses.

  What does a neuron do if it is over-stimulated?

Overstimulated neurons may die, they may also reduce the efficacy of their inputs either by increasing their thresholds or reducing synaptic weights by removing postsynaptic receptors. Calcium is an important mediator of these signals - you could read about its role in long term depression for example (this has nothing to do with 'depression' in mental health, just reduction in synaptic weight). There are also short-term effects that limit overstimulation of particular pathways, with many acts on the pre-synaptic rather than post-synaptic cell. Neurotransmitter is held in vesicles, and after release, there are fewer vesicles available for the next release event. Presynaptic terminals also often have autoreceptors that cause negative feedback and limit subsequent transmission.

  What does a neuron do if it receives a signal -> does it broadcast it to all of its connections, or only 1

Of all your questions, "does it broadcast it to all of its connections" has the simplest answer: biological neurons almost always broadcast to all of its forward connections in response to any sufficient input (just like most artificial neural networks). However, the release probability at any one synapse is typically <1. Therefore, a given cell can make much higher-fidelity (and also higher-amplitude) connections with another cell by the number of contacts. If a typical cortical neuron makes only one synaptic contact with another cell, there will be a high rate of failures of transmission between the two cells. It's common for stronger connections to involve up to hundreds of individual contacts, just between two cells.

  Can a neuron send out a new signal without having received a signal from anywhere else

Some neurons are spontaneously active. There are various types, but the most familiar are the ones thought of as intrinsically oscillating. An example are the sinoatrial node cells of the heart (although these are not really neurons, they act a lot like neurons; there are similar cells that are neurons that control respiration). There are also some CNS cells.

  How does a neuron know if it has done his job "well". How does it get positive feedback.

This question is the most complex of all the questions you asked, entire textbooks and journals are needed to answer it, and it isn't at all possible to answer here. I'll just say that many of the learning rules used in artificial networks are not biologically plausible, they are simply computationally efficient. Biological neural networks use a lot more recurrent activity than artificial ones do, and a lot of the feedback like this occurs within that recurrent network. Biological networks are also built to do a variety of computations, and learning rules that apply in one may not apply in another. For example, pattern separation versus pattern completion require completely different learning rules.

However, the very general principle of updating synaptic weights in response to errors or outcomes does hold between artificial and biological networks.


tetrads in meiosis are held together by what This is from SAT subject biology test practice question. The answer it gave me was both chiasmata and centromeres. I can understand they are held by chiasmata but why also centromeres? I looked it up, I didn't find anywhere mentioned that they are held by centromeres also, only synaptonemal complex and chiasmata.

tetrads are truly held by spindle fibers on centromeres too, but isn't the question asking what hold them together? Even without spindle fibers, they can still be held by chiasmata I guess.

A recombinase only active during meiosis - Dmc1 and a general recombinase Rad51 coat the single-stranded DNA to form nucleoprotein filaments. These filaments hold the homologs together at the chiasma, the point of attachment during crossing over.


Cancer: what does it mean "at presentation"? Unclear to me what this means:

"Objective The biological heterogeneity of hepatocellular carcinoma (HCC) makes prognosis difficult. We translate the results of a genome-wide high-throughput analysis into a tool that accurately predicts at presentation tumour growth and survival of patients with HCC."

Reference

"Presentation" is the event where the patient first visits the doctor.
For example, "the patient presented with yellowing skin and complaining of abdominal pain".
The paragraph you have doesn't make this clear, they assume you have already had your genome sequenced prior to visiting the doctor, who looks at the result, uses this tool and predicts what is likely to happen to you and your cancer based on your DNA.