Why some neurons are tetraploid Why are some neurons tetraploid, and how does this result from it's ancestor cell ?

Neurons are tetraploid in pathological situations like Alzheimer disease:

Neurons that duplicate their DNA are rarely observed to undergo mitosis, and they remain for long time as tetraploid cells, in accordance with the chronic course of the disease. We have recently shown that cell cycle re-entry and somatic tetraploidization occurs during normal development in a subpopulation of RGCs (retinal ganglion cells), giving rise to enlarged neurons with extensive dendritic trees. Tetraploization in these neurons occurs in response to the activation of the neurotrophin receptor p75NTR by an endogenous source of NGF (nerve growth factor).

Source: Frade JM, López-Sánchez N. A novel hypothesis for Alzheimer disease based on neuronal tetraploidy induced by p75NTR. Cell Cycle 2010; 9:1934 - 1941; PMID: 20436277; http://dx.doi.org/10.4161/cc.9.10.11582

These neurons are generated in response to nerve growth factor (NGF) acting through the neurotrophin receptor p75 (p75NTR), which induces E2F1 activity and cell cycle re-entry in migrating RGC neuroblasts lacking retinoblastoma (Rb) protein. We have also showed that brain-derived neurotrophic factor (BDNF) prevents G2/M transition in the tetraploid RGCs, thus being crucial for the maintenance of the tetraploid status as well as the survival of these neurons. The realization that tetraploid neurons can be readily observed in the vertebrate nervous system has important physiological consequences.
Several eukaryotes are known to undergo endoreduplicative cycles leading to somatic polyploidy, thus increasing cell size in specific tissues. Examples of polyploidy in neurons are known in some invertebrates.

Source: José María Frade. Somatic tetraploidy in vertebrate neurons - Implications in physiology and pathology. Commun Integr Biol. 2010 Mar-Apr; 3(2): 201–203. PMCID: PMC2889987


Digestion Enzymes in Carbohydrate Metabolism? Digestion of carbohydrates is ending in small intestine with mainly disaccharidases. Isomaltose is broken down to 2 molecules of glucose by the enzyme called alpha dextrinase(oligo-1,6 glucosidase or isomaltase) which hydrloyze 1,6 linkage of isomaltose. In the case of glycogen metabolism there is debranching enzymes that are transferase and alpha 1,6 glucosidase. According to this informations can we say that alpha dextrinase (isomaltase) and alpha 1,6glucosidase are the same enzyme ?

1,6-glucosidases are a class of enzymes and not just one enzyme. It does not mean that all the members of this class are the same enzymes. They catalyse the same kind of reactions but their properties and substrate specificities differ. Check BRENDA for details.

BTW, dextrin-1,6-glucosidase is a synonym for amylo-alpha-1,6-glucosidase. Other 1,6-glucosidases are different enzymes with different EC numbers.


What does it mean to "cure" microscope slides? I am reading a journal paper and I have come across the following statement in the materials and methods section regarding the preparation of microscope slides:

Coverslips were washed once more with PBS, inversely mounted on
microscope slides with ProLongTM Diamond antifade mountant containing
DAPI (Invitrogen). Slides were cured for 24 hours at room temperature
before observation.

I am not sure what exactly is meant by the statement the "slides were cured". I have searched on Google for some answers but I have not found anything useful. Any insights are appreciated.

In this context, "cure" is a chemical term. Definition from Wikipedia :

Curing is a chemical process employed in polymer chemistry and process engineering that produces the toughening or hardening of a polymer material by cross-linking of polymer chains. Even if it is strongly associated with the production of thermosetting polymers, the term curing can be used for all the processes where starting from a liquid solution, a solid product is obtained.

So here it means that the slides were incubated at room temperature for 24 hours to let the mounting media harden. Of note, not all mounting media harden, some may require specific conditions to cure like UV light (example), and the curing step changes the properties of the mounting media like the refraction index. From the ThermoFisher website :

Formulations of mounting media that can add favorable properties such as optimizing the refractive index to match that of glass, preventing photobleaching, or preserving samples for long-term storage are widely available. Keep in mind that some require time to “cure” or harden. For mounting media that need time to cure, it’s important to let the sample fully harden before imaging so that you don’t inadvertently damage or destroy your sample by moving it around on the slide or cause photobleaching of your stained cells. Typically, the refractive index of the mounting medium will not reach its specified value until after it has fully cured, and its photoprotective properties will increase during the curing process. The degree of hardness after the mounting medium has fully cured will also vary; some will set like jelly while others will set like hard plastic


What is the role pyruvate carboxylase in lipogenesis? I just know that Acetyl-CoA is a positive allosteric modulator for pyruvate carboxylase, but I cannot find anything else.

Okay so pyruvate carboxylase is a ligase-class enzyme, meaning it forms covalent bonds. What we see is that pyruvate is carboxylated into oxaloacetate by pyruvate carboxylase, here's our proposed reaction,

What this does is replenish mitochondrial oxaloacetate levels, because when we switch into lipogenesis, TCA intermediates must be shuttled into the cytoplasm for forming triglycerides, like so,

Also here, page 2, they go into how the production of NADPH is coupled to acetyl group export and how PC must perform the aforementioned function to keep substantial flow maintained. Block quoted them for ease of access,

  As shown in Scheme 1, the
  generation of NADPH is coupled to the transport of mitochondrial
  acetyl groups into the cytosol for fatty acid synthesis.
  Acetyl-CoA is generated in the mitochondria by the oxidative
  decarboxylation of pyruvate, and, after condensation with oxaloacetate,
  acetyl groups are transported to the cytoplasm as citrate,
  which undergoes ATP-dependent cleavage to yield acetyl-CoA
  and oxaloacetate. This pathway requires a continuous supply of
  oxaloacetate, which is produced by the activity of PC. AcetylCoA,
  a building block for the synthesis of long-chain fatty acids,
  is then converted into malonyl-CoA by acetyl-CoA carboxylase
  (ACC). Meanwhile, the oxaloacetate generated in the cytosol
  from citrate is reduced with NADH to malate, which in turn is
  oxidatively decarboxylated in a reaction catalysed by NADP+-
  dependent malate dehydrogenase (‘malic enzyme’; EC 1.1.1.40).
  The pyruvate thereby produced is taken up by the mitochondria
  and carboxylated to give oxaloacetate, while the NADPH
  generated is used in the pathway of fatty acid synthesis.


How many humans have been in my lineage? Is it almost the same for every human currently living? If I were to count my father, my grandfather, my great-grandfather, and so on up till, say chimps, or the most common ancestor, or whatever that suits the more accurate answer, how many humans would there have been in my direct lineage?

And would it be almost the same for every human being currently living?

A quick back-of-the-envelope answer to the number of generations that have passed since the estimated human-chimp split would be to divide the the split, approximately 7 million years ago (Langergraber et al. 2012), by the human generation time. The human generation time can be tricky to estimate, but 20 years is often used. However, the average number is likely to be higher. Research has shown that the great apes (chimps, gorilla, orangutan) have generation times comparatble to humans, in the range of 18-29 years (Langergraber et al. 2012).

Using 7 million years and 20 years yields an estimated 350000 ancestral generations for each living human. A more conservative estimate, using an average generation time of 28, would result in 250000 generations. However, some have argued that the human-chimp split is closer to 13 million years old, which would mean that approximately 650000 generations have passed (using a generation time of 20 years).

The exact number of ancestral generations for each human will naturally differ a bit, and some populations might have higher or lower numbers on average due to chance events or historical reasons (colonizations patterns etc). However, due to the law of large numbers my guess would be that discrepancies are likely to have averaged out. In any case, the current estimates of the human-chimp split and average historical generation times are so uncertain, so that they will swamp any other effects when trying to calculate the number of ancestoral generations.

However, this is only answering the number of ancestral generations. The number of ancestors in your full pedigree is something completely different. Since every ancestor has 2 parents, the number of ancestors will grow exponentially. Theoretically, the full pedigree of ancestors can be calculated using:

$$N_\text{ancestors} = \sum_{i=1}^t 2^i \hspace{1em} \text{or} \hspace{1em} 2^{t+1}-2$$

where t is the number of generations. However, this will yield an unreasonably large number of ancestors (~$2.3*10^{105}$ over just 350 generations), since it assumes that all of your ancestors are unrelated. Basically, you run into something called pedigree collapse, which means that your pedigree will have many overlaps (due to inbreeding, overlapping generations etc), so all of your ancestors cannot be seen as unrelated. In practice, this means that the number of ancestors in successive generations will stop doubling for each generation you go back, and will eventually start shrinking, which will drastically reduce the number of unique ancestors. For more on this, see answers to the question Initial population when i count backwards?. That question is basically asking about the same issue, but less specifically. There might be studies that have tried to calculate the average number of ancestors to living humans, but I haven't seen any. Therefore, I cannot say anything more specific about the average number of unique ancestors for a living human individual.


ID Sunbird in Oman - White, Dark Grey, Yellow Some extensive web searching has not helped me find this bird I discovered in my travels. They were flitting too fast to get a decent picture, but here is the best description I can obtain from memory:

Dark Grey from their head to their back. Their wings looked black but, as I said, they were flying about. Throat and breast were pale, probably white. Belly and vent were bright yellow. Their beak was a similar shape to the Purple Sunbird. They were taking nectar from bushes bordering a house which had small white flowers.

There are 4 species of Sunbirds in Oman.
https://en.wikipedia.org/wiki/List_of_birds_of_Oman

Based on your description and how common are the different species I think they were most likely mainly Purple Sunbird (Cinnyris asiaticus) https://en.wikipedia.org/wiki/Purple_sunbird
At the moment, in fact, they are not purple at all. They are moulting their feathers and also the male have extensive yellow on breast and belly. Among the species of Oman's Sunbirds it is the only one that shows black wings (in males) contrasting with the brownish/grey upper parts precisely as you observed.

MOULTING MALE

FEMALE (left)


Can one talk about deacetylation of a promoter rather than associated histone? I am confused on a detail in a paper I am reading and am not sure whether I am misunderstanding the wording or misunderstanding the concept.  I am including the whole abstract of this paper for background:

Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes.
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, Keeney GL, Daftary GS.
Abstract:
Endocrine regulation of uterine biology is critical for embryo
receptivity and human reproduction. Uterine endometrium depends on
extrinsic sex steroid input and hence likely has mechanisms that
enable adaptation to hormonal variation. Emerging evidence suggests
that sex steroid bioavailability in the endometrium is determined by
adjusting their metabolic rate and fate via regulation of cytochrome
(CYP) p450 enzymes. The CYP enzymes are targeted by ubiquitously
expressed Sp/Krüppel-like (Sp/KLF) transcription factors.
Specifically, KLF11 is highly expressed in reproductive tissues,
regulates an array of endocrine/metabolic pathways via epigenetic
histone-based mechanisms and, when aberrantly expressed, is associated
with diabetes and reproductive tract diseases, such as leiomyoma and
endometriosis. Using KLF11 as a model to investigate epigenetic
regulation of endometrial first-pass metabolism, we evaluated the
expression of a comprehensive array of metabolic enzymes in Ishikawa
cells. KLF11 repressed most endometrial CYP enzymes. To characterize
KLF11-recruited epigenetic regulatory mechanisms, we focused on the
estrogen-metabolizing enzyme CYP3A4. KLF11 expression declined in
secretory phase endometrial epithelium associated with increased
CYP3A4 expression. Additionally, KLF11 bound to CYP3A4 promoter GC
elements and thereby repressed promoter, message, protein as well as
enzymatic function. This repression was epigenetically mediated,
because KLF11 colocalized with and recruited the corepressor
SIN3A/histone deacetylase resulting in selective deacetylation of the
CYP3A4 promoter. Repression was reversed by a mutation in KLF11 that
abrogated cofactor recruitment and binding. This repression was also
pharmacologically reversible with an histone deacetylase inhibitor.
Pharmacological alteration of endometrial metabolism could have
long-term translational implications on human reproduction and uterine
disease.
Citation:
Zheng Y, Tabbaa ZM, Khan Z, Schoolmeester JK, El-Nashar S, Famuyide A, et al. Epigenetic regulation of uterine biology by transcription factor KLF11 via posttranslational histone deacetylation of cytochrome p450 metabolic enzymes. Endocrinology. 2014;155:4507–20.

My question is on the fourth-to-last sentence of this abstract specifically:
"This repression was epigenetically mediated, because KLF11 colocalized with and recruited the corepressor SIN3A/histone deacetylase resulting in selective deacetylation of the CYP3A4 promoter."
This sentence seems to say that SIN3A/histone deacetylase is deacetylating the CYP3A4 promoter itself (i.e. it is deacetylating a region of DNA directly).  However, shouldn't a histone deacetylase be deacetylating a histone, not a region of DNA?  Am I misunderstanding the mechanism?  Or is "deacetylation of the CYP3A4 promoter" really a short-hand way of saying "deacetylation of a histone that is associated with the CYP3A4 promoter"?
Thanks in advance for your help!

The authors obviously meant to write that the histones associated with the promoter become deacetylated. They cannot mean the promoter itself as that is DNA.

What they wrote is not shorthand or acceptable alternative usage, but just a mistake — published papers often contain typos and mistakes of this sort. Probably the authors meant to write the technically correct form of words but lost a phrase. Or perhaps they had exceeded the limit to the number of words allowed in the summary, and so they went through trimming, but trimmed too much.

Why didn’t the referees pick this up? Of course they should have, but they were probably more concerned with the contents of the paper and whether the experiments described by the authors justified their conclusions. They are busy scientists and probably doing the job voluntarily.

In conclusion, scientists are human, scientific writing is difficult, and everyone makes mistakes. But we should still try to convey our ideas as clearly as possible, and certainly not copy something that is technically incorrect or ambiguous, just because it has made it into print.


Where do i find microbes like tardigrades in winter Just bought a microscope and i want to see microbes like tardigrades.  Where should i look? I have found many bacteria and what seems to be motionless single celled organism.  I want to see movement and feeding.  Ps snow on the ground and frozen ground

Tardigrades are best found by soaking moss in water. Even in the winter, under the snow, that is the best place to look. Let tap water sit overnight, uncovered before you add it to the moss to let the chlorine come out. And then strain the water with fine-mesh cloth to see what was in the moss. I would not call tardigrades "microbes" though. Even though "microbes" is not a scientific term, I think of microbes as bacteria, while tardigrades are microscopic animals.


Why is there symmetry in animals? If cut a cut down the middle, both halves are symmetrical.

Why is it that most animals are symmetrical?

Is there an energetic reason for this? (as in, it is energetically favorable to create the same thing twice instead of making something new)

Intuitively, symmetry is useful for balance. A weight-nonsymmetric animal would have to expend additional energy to keep itself balanced (and this would also increase neural complexity for maintaining balance).

Mirror-image pieces only have to be coded once in the genome as a rule-of-thumb, allowing reuse of (mostly) the same genetic pieces with a few orientation and growth-origin markers thrown in. If you put vastly different parts on each side, you have to encode them (making the genome larger with more opportunity for mistakes and harmful mutation)


Why has life evolved around oxygen? Why has life evolved around oxygen? Many lifeforms require oxygen to breakdown bio-molecules and release energy. I think there are two possibilities:

Reactions with oxygen tend to release more energy, so it is profitable to use oxygen for metabolic activities.
It is chance that it got to be oxygen; it could have been anything.

Which is right? Or is there some other possibility?

Edit: Yes, it is true that there are organisms to which oxygen is toxic. But you can't ignore the large numbers of organisms to which it is absolutely necessary for living. Why could it not have been some other molecule? Which property of oxygen drives it to become the most useful in bio-processes?

I think you need to consider that oxygen is toxic to large groups of microorganisms, because it poisons their electron transport chains.

Strict anaerobes does not tolerate the presence of oxygen at all and as such I would argue that life can survive and thrive without O2.

Also life on earth evolved under conditions were O2 levels were extremely low, in fact when some organisms started to release oxygen into the atmosphere it caused an extinction event (Great Oxygenation Event).

So I think you need to change your question to why did life adapt to the presence of oxygen?


What will happen if one keeps the photosynthesis plant active 24x7? While reading this article online something said on it made me wonder.

Also, there have been suggestions and a Dawn / Dusk type of ramp up and down to simulate the slow changes in the sun have value, but we have not seen solid universal data in this regard to date...

It made me wonder if we are simulating the sun in a dark room for growing the plants with the help of red, blue, and a little bit of far-red light, what will happen to the plants if we keep the ideal conditions for which the plants carry out photosynthesis whole day? Does it affect its yield or the plants die out quick?
I am an engineering student working on indoor farming, my knowledge of botany is the same as a high school student. So if I am wrong please tell me.

Ideal conditions for photosynthesis
You mention ideal conditions to carry out photosynthesis, I would just like to point out that this includes carbondioxide levels, temperature, and nutrients as well as light.
Flowering
As anongoodnurse mentions performance might be measured by blooming which, in most flowering plants, has a day-light related component. However, for general growth increasing daylight over the 'natural' day length can often increase yield.
Daylight Cycles
The important point to note is that plants do 'ramp up' at dawn getting ready to start photosynthesizing (for some plants with temporal photosynthesis mechanisms (see CAM photosynthesis) this can be even more important). The reason plants do this is because plants can suffer from 'photobleaching' which can be considered similar to sunburn in humans, if they are not ready for sunlight. Getting 'ready' can involve lots of things including opening stomata (pores) to let CO2 in, changing which metabolic pathways are active,  and moving about chloroplasts inside cells. Plants 'figure out' how and when to ramp up based on circadian rhythms which work well on 24 hour clocks and slight changes over time. Thus 12 hrs to 16 hrs can be a big change, particularly if the change happens by lights coming on earlier. Additionally, the 24 hour 'clock' means that plants will do better with 18hr light then 6hrs dark cycles than 36hrs light 6 hrs dark, because the total cycle length should be about 24hrs.
Photosynthesis Side Effects
Finally, constant photosynthesis does take its toll on plants as photorespiration accompanies photosynthesis. In C3 plants (most crops) this can reduce photosynthetic output by 25% whilst creating ammonia as a byproduct. The ammonia needs to be detoxified as a build up in the cell can cause cell death. Thus plants need enough 'respite' from photosynthesis to deal with photorespiration byproducts or they will suffer.


Can we disambiguate competing molecular mechanisms of learning and plasticity by measuring electrical activity of neurons? I have been reading with fascination about the several molecular- and cellular-scale mechanisms and structural changes that underlie what we refer to as long-term plasticity. For instance, [1], [2], [3].

In particular, there seem to be at least: synaptic scaling, synaptic pruning, synaptogenesis, spinogenesis, neurogenesis.

My questions:

How do each of the above mechanisms/ events affect the classical extracellular single/ multi-unit spikes, postsynaptic potentials (LFPs), and local electric fields? Does a mechanistic forward model exist, which specifies the biophysical transformation from synapse-level changes to spikes and LFPs? Are there spike simulators out there that model these properties?
Using such a forward model, can we solve a statistical inverse problem to infer anything at all about these LTP/LTD-induced small-scale structural and functional changes?
For instance, one metric of analysis could be: post-spike-time filters (self-terms and cross-terms) inferred using statistical point-process models. Another could be the shape of the action potential itself, which is typically used only for spike sorting, and then discarded.
Has something along these lines been done? Or is it infeasible? If so, why?
Finally, If anyone could give a brief overview of the gamut of synapse-scale physiological/ imaging techniques used to characterize these mechanisms, I would be very grateful!

Just adding a little bit here. Estimating changes in connectivity based on STDP is hard
http://klab.smpp.northwestern.edu/wiki/images/2/2b/Stevenson_Inferring_Plasticity_2011.pdf

but yes - these questions are enough to keep a big field busy for a long time.


Debug Fresno; why are the released mosquitos said to be sterile? I saw in the news that Verily Life Sciences will participate in an experimental release of sterile male aedes aegypti mosquitos in Fresno, California. Aedes aegypti is considered an invasive species in California, and can be a vector for human disease including dengue fever, zika, and chikungunya (according to the video). See the Verily blog Debug Fresno, our first U.S. field study and/or the attached YouTube video Introducing Debug Fresno.
The released male mosquitos will carry a bacterium called wolbachia, which when transferred to the female during mating will prevent eggs laid by the female from hatching. Wobachia presence, parasitism and mutualism with insects is widespread, and Wikipedia's article on it even includes a section on applications to human-related infections.
Question: Are the males said to be sterile because of the bacteria which results in nonviable eggs, or are they also incidentally sterile in addition to being vectors for the wolbachia bacteria (and eggs were presumably fertilized by other matings)?

Males are effective sterilization vectors
You can think of male mosquitos as fertile only in theory. Any mating of these mosquitos will generate no offspring whatsoever, so they are effective sterile and they spread this characteristic to females.
The bacteria makes they sterile in the end, the same way any disease in others cases.


What does the thalamus consist of? There is a long list of thalamic nuclei which are somehow embedded in the thalamus, a "large mass of gray matter located in the dorsal part of the diencephalon", according to Wikipedia.

I wonder what the nuclei are embedded in:

In a pool of glia cells or of other more or less unspecific "thalamic
neurons"?
Does the thalamus consist mainly of nucleic or of non-nucleic
neurons?
How are the non-nucleic neurons of the thalamus classified?

Edit: In the Scholarpedia article on the thalamus one learns, that thalamic nuclei essentially are relays, and that there are relay neurons and interneurons in the thalamus. Might it be the case, that relay neurons can but interneurons can not be assigned to a specific nucleus (= relay), that means: interneurons build a somehow separate neuronal structure that is somehow interwoven with the nuclei?

This is an interesting question with good comments. I did medical school, and I am here on unix.se, so let me give some thoughts:

The central nervous system consists of "gray" and "white" matter. In the spinal chord you have this gray butterfly shape, in the neocortex it is "gray matter" (neuron's cell body) and "white matter" (neuron's myelinated axons).

There is no room for a "pool of glia cells" - from tip to tail all the neurons and their axons are highly organised.

Now the brain is already complicated. It is divided into 5 segments, and the Thalamus is quite in the center of everything. Some other nuclei (e.g. the ones connected with the 12 head nerves) have a well defined function, but the Thalamus is hard to define.

The famous "limbic system" is close by, and is also complex.

A high resolution MRI should give a good estimate of neuron/myelin distribution, to the millimeter.  But I am afraid it is not an easy gray-or-white question, but some complicated arrangement, with e.g. short unmyelinated axons.

(The MRIs can look very different)

It is even worse than I thought: this histologic picture shows how hard you have to look to even define a nucleus.

Thalamus Nissl stained

"thalamus histology" give very nice results in google. In the MRIs you can mostly just see that it is something a bit in between gray and white.

First I checked Nissl stain: this really colors neurons (body and dendrites), but not axons.

The stain is labeled "myelin-nissl", and it is blue and magenta, so this must be a combination. But -- I can't even tell which is which!

Well it must be pink is neurons, and thus blue is myelin. This makes sense with the Cn A = cornu ammonis = hippocampus region bottom right, the pink-white spiral, and with the outlining of nuclei. But very counter-intuitive...I trust them it is the appropriate stain.

Keep in mind this is a section to show the nuclei (at their max?), so other parts/sections will look quite different.


Approximately how thick is a single strand of cat (domestic housecat) hair? I did a little research to lead me to finding the general range of width for human hair, which is anywhere from around 30µm to 180µm... approximately.

I'm trying to compare this to the width of cat hair, since I have been told (and it does seem a bit evident) that cat hair is much thinner than human hair in general.

I can't seem to find any information on this.  Does anybody have any answers?

Note:  I apologize if this isn't the right Stack Exchange forum for this question.  I wasn't sure where to put it, so I did an SE site search for 'cat' and this one seemed to be the most appropriate.

There are a few different types of hair on a cat.  But I think you are referring to the down hair on the cat.  It will also vary on the breed of domestic cat.  As a general statement, you can find a lot of quirky characteristics of mammals by looking at early genetics papers where people where trying to find genetic elements to obvious phenotypes.

For the down hairs, you can see "The ‘rex’ type of coat in the domestic cat."
Journal of Genetics [0022-1333] Searle, A G and Jude, A C yr:1956 vol:54 iss:3 pg:506

Table 3. Thickness in µ of normal and rex down-hairs

[Type of Cat][Diameter in um][SE of Mean]

Normal          25.8;   1·32;

English rex     16·2;   0·54;

German rex      17·0;   0·50;


How can alcohol cause blindness? Strong alcoholic beverages (e.g. moonshine) are reported to have caused blindness amongst some people.

How exactly can alcohol make someone go blind?

Is that because different forms of "rubbing" and homemade alcohol: ethanol, methanol, isopropyl and moonshine cause damage to the optic nerve?

Disclaimer: I am interested in what exactly is the biological process of certain alcohols on the optic nerves and what in particular triggers the blindness.

Methanol is rapidly absorbed not only after oral ingestion but by inhalation or after cutaneous exposure and becomes oxidised in the liver to formaldehyde and to formic acid, metabolites which are more toxic than methanol itself and which inhibit mitochondrial ATP production.

  Histopathologically, circumscribed myelin damage behind the lamina cribrosa of the optic nerve has been reported. The electrophysiological changes following acute methanol ingestion suggest that methanol affects photoreceptors, Muller cells, and the retrolaminar portion of the optic nerve.

Source : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771266/

Several years ago there were numerous cases of blindness and death due to Methanol in Estonia.

If you ask : What exactly happened?

Waste from wood (sawdust, shavings), and other cellulose-containing materials (paper, rags, etc.) can be processed by applying excessive heat and acids, resulting in degraded cellulose into sugar (glucose). Sugar obtained is fermented to get ethanol. However as a side-effect, some methanol is produced as well. This compound is not safe to drink. Basically, someone sold it (illegally) as an ethanol drink (I am not sure if they stole it and tried to monetize it this way.).

There was a (stupid) joke that somewhat popularized knowing about this problem:

  (roughly translates to) "Guys, let's drink faster, it is getting dark."

Other impurities in the alcohol could have similar effect, but I can confirm at least the methanol part.


How does Cro protein expressed by lambda phage kill its host? I read that the DNA segment of lambda phage integrated in host DNA could switch between lysogenic state where cI represses the expression of Cro and lytic state where Cro expression takes over and self produces more.

But how exactly does the high production of Cro kill its host?
The virus has a DNA segment shielded with a protein coat. While entering host it gets attached to host membrane and releases DNA inside without damaging host. Then how does host get killed when virus goes outside it which happens during lytic phase and doesn't happen when it got inside?
And if the virus has to go outside host, it needs protein coating. How is that produced? Is it produced only during lytic phase or also during lysogenic phase?

Have a look at the wikipedia page on lambda-phage (it is nicely illustrated and referenced).

See this map of the lambda-phage genome (Source).

Cro (Controller of Repressor's Operator) does not kill the host. It is a transcription factor that represses cI. cI, in turn, represses Cro and other pro-lytic genes (expressed from the PL promoter), thereby forming a positive feedback loop with Cro (some people also use the term "double-negative" feedback loop which in my opinion is incorrect).
During infection the virus just injects its linear DNA into the host via a porin protein (a sort of membrane channel). But at the peak of the lytic cycle many virus particles are formed inside the host cell (not just DNA but fully packed viruses). The viral proteins R and S cause breakdown of the cell membrane and the cell wall, which facilitates cell lysis.
As mentioned in the previous point, the virus is fully packaged while inside the host. This happens only during the lytic phase. During lysogeny, the viral DNA gets integrated with the host genome and remains dormant until triggered by some kind of stress such as UV (which actually leads to activation of SOS response protein RecA which by degrading cI tilts the balance towards the lytic cycle).


Species Identification: Liberian "kiss-meat" snail Before my wife immigrated to the US from Liberia as a kid, she loved eating "kiss meat". It's a freshwater snail they collect from the swamp during the rainy season and eat as a delicacy, so called because you suck the meat out with a kiss.
Here's a YouTube video of this process, so you can get a good look at the snail and see its habitat (mangroves).
This is the best image from the video that I could find. They've been washed and the rear of their shell has been broken off. I can't get Stack Exchange to let me add a second picture );

I have not been able to find any other references to these snails, except under the name "kiss meat". Would anyone be able to identify these?
(Note: There seems to be a similar looking brackish snail commonly called "African Periwinkle". I don't think this is the same thing.)

It's Tympanotonos fuscatus from West Africa. They harbor near the roots of mangrove at low tide. Due to their tendency to bioaccumulate heavy metals, they have been used in studies of environmental presence of heavy metals, and the samples taken from markets have been found to be excessively high in cobalt and manganese.


Colonial Cells Demonstrating Cell Specialization Are there any living examples of cellular colonies demonstrating very primitive cellular specialization?  If so, what do we know about how they assimilate?  How independent are the individual cells and what do we know about their behavior (for example, do they, perhaps, migrate to different colonies in certain proximities)?

Probably not what you are looking for but the protozoan slime mold Dictyostelium discoideum lives as free amoebae which can coalesce into a multicellular migratory slug that eventually forms a fruiting body in which some cells form the stalk while others form spores.

Slug formation is by chemotactic signalling with cyclic AMP as the signal. I seem to remember that there is a predatory species of slime mold which uses cAMP to attract D. discoideum as prey, but I can't bring the name to mind and have failed to find it online.


Sheep vs. Furry animals Why can't we take the fur of a fox without killing or skinning it just like the sheep , what's the biological or chemical structure or even the trait which is on a sheep's body that separates wool from its skin
Why can't we apply the bioclip technology on furry animals too ?

Fur, wool, and hair are all made of keratins.

To the best of my knowledge wool and fur are separated arbitrarily, based on the properties of the fibres. This arbitrary division allows rabbits to have fur but selective breeding has produced angora rabbits, which have wool. The opposite should be possible, with time you could breed a sheep that has fur.

Length; Wool grows continuously and animals are clipped when the fibres are long. Fur often has a maximum length.

Structure: The structure of the keratin in the wool makes the fibres kinked (crimped). These kinks aid the production of fabrics. I believe the cuticular scales also aid in the production of fabrics.

Fur doesn't have kinks, so even if it's long enough to weave the fabric is likely to lack durability.

Some furs are used in textiles rather than pelts. Possum fur is 'plucked' and woven into fabrics with wool. The resulting fabric is slightly less durable. However, possum fur is hollow and smooth so possum fur fabrics are very soft and warm. The clothing is very good to to wear.

However, fur is generally inferior to wool for textiles and it took a couple of decades to develop techniques to produce textiles from possum fur. This happened because of odd ecological and economic drivers. Possums are are a major pest species in New Zealand where they contribute to the decline of native birds and insects. Millions of possums are killed every year in New Zealand. The market for possum skins is very small. This is why so much effort was put into producing a fabric from possum fur.

So you could shear a fox and produce a fabric but the fabric would likely be poor and there's no reason to do so.


Is RGB diode lighting okay for the eyes? Is a light source giving off light composed of red, green and blue lights harmful to the eyes? Does it lack any important qualities that other artificial light sources, such incandescent lamps or white LEDs may have?

Is it alright to use RGB light panels in a room instead of the usual lighting?

At a fundamental level, no, we're fine with LED lighting.  The absorption spectra of our cones are quite broad, and RGB LEDs are chosen to match our color sensitivity reasonably well.  That red+green looks the same to us as light that is actually yellow is because our eyes can't tell the difference since we don't have good enough spectral resolution in our vision.

There could be more subtle emotional or other complex effects, but to a good approximation, if it looks right it is right, and there aren't magical frequencies that we need to avoid e.g. retinal degeneration or something else awful.  (Well, large amounts of UV are bad, but RGB LEDs don't produce a significant amount of UV.)


Which range are the Therapeutic Indices of Currently-Prescribed Benzodiazepines in? A compound's therapeutic index is defined as:

$$TI = \frac{LD_{50}}{ED_{50}}$$

What range are the therapeutic indices of benzodiazepines in? For the method of administration I would prefer intravenous as with it one can estimate the therapeutic indices via other routes. Of course for humans it is difficult to find LD50's but a rat/mice LD50 will suffice provided the ED50 is for the same respective species. Such benzodiazepines I am interested in are (Although I will accept your answer if you just give me an estimate of the therapeutic indices of the drugs in bold, the others are just icing on the cake):

Alprazolam
Brotizolam
Clonazepam
Clorazepate
Diazepam
Estazolam
Flurazepam
Lorazepam
Lormetazepam
Midazolam
Nitrazepam
Temazepam

Wikipedia quoted this article as a reference for its statement about alprazolam having a therapeutic index of 100:1, although I can't confirm that, since I can only read what's immediately available in that link. There's a figure saying less than 100:1 for diazepam though.


Can cancer cells in the same person, organ, and origin have different DNA? Is it possible for cells from the same tumor to have different genetic material, and if so, to what degree is it possible (how fast do they mutate) ?

Cancer cells and normal cells differ on the genetic basis but they share the same genetic background, so they have not different DNA in the sense of two different people. They have to be different, since cancer cells have to accumulate mutations on a number of genes to become a cancer cell, which can survive and will not be directed into apoptosis. These are genes which control the cell cycle, certain growth factors, tumor suppressor genes, cell signalling and so on. In all these genes there need to be either activating or deactivating mutations present. Most of these mutations are point mutations (single nucleotide polymorphisms, SNP), where only one base is altered to achieve a mutation. An example for such a mutation would be the mutation in the B-RAF kinase, which is involved in signaling and activating genes, where a point mutation exchanges Valine 600 to glutamic acid (V600E, for reference see here). These are relatively small differences between these two cells. The Cancer Genome Project aims to sequence cells from a cancer and also normal cells from the same individual and then do a comparison. Later stages tumors often tend to genetic instabilities where complete regions of the genome are duplicated, inverted or deleted, see here for a review.
A more basic overview is given by the Ebook "Essentials of Cell Biology" by the Nature Group, which has an overview of cancer cells.

Regarding the mutation rate, this is hard to estimate. There are a few papers available here, but they focus on the mutation rate in germ cells, so these are mutations that are transmitted to the next generation. The estimates there are between 70 and 100 mutations per generation per individual, depending on the research method. You can find a nicely explained blog article here, which gives a number of original references, too.

The mutation rate in cancer is a different thing, since this depends on which genes are mutated. The mutation rate for cancer has to be higher for the cancer cells to allow to collect the necessary transformations into a cancer cell, but these mutations seem to occur only in a few hotspot regions of the genome (Further references can be found in this article called "The causes and consequences of genetic heterogeneity in cancer evolution" and in this called "Emerging patterns of somatic mutations in cancer"). There are two article called "The mutation rate and cancer" which are interesting in this context. They can be found here and here. As always, if you have problems with getting the articles, let me know, I can help there.


Is there a biological explanation for a 0.5 difference in allele size with PCR product? CONTEXT

I am currently working on a set of diversity, this diversity in interspecific (within the same genus). I am using SSR markers, the primers were designed on one species and are working really well within the species (lot of diversity and difference between allele of 1 at least).
When trying them on the other species, I observe the normal non-amplification which could be due to mutation in the primer DNA sequence. But, for some genotypes I have been observing a new allele just between the two older ones (like the new one is 185.5 and the olders were 185 and 186.

QUESTIONS

Is that kind of observation frequent when using primers designed on other species?
I understand how a 1 pb difference could occur CACACA ==> CACCACA, but what could the biological explanations be for a 0.5 pb difference between alleles?

In my experience, working with a similar approach in Campylobacter jejuni, the base pair measurements from these techniques are imprecise and need to be carefully calibrated. I am unsurprised to see 0.5 base pair differences, this can be seen been runs and even, in the worse case situation, between even and odd wells in the same plate(!).

I would use Sanger sequencing to determine the sequence you are getting in one of your isolates, and then use this as a calibration control included in every run.


Endogenous retroviral insertions as evidence for evolutionary relationships among primates A synopsis of a 2005 paper in PlosBiology by Yohn et al. states that:

  Searching the genomes of a subset of apes and monkeys revealed that
  the retrovirus had integrated into the germline of African great apes
  and Old World monkeys—but did not infect humans and Asian apes
  (orangutan, siamang, and gibbon). This undermines the notion that an
  ancient infection invaded an ancestral primate lineage, since great
  apes (including humans) share a common ancestor with Old World
  monkeys.

Also, Micheal Lynch writes :

  "Remarkably, we have found many cases of parallel intron gains at
  essentially the same sites in independent genotypes," Lynch said.
  "This strongly argues against the common assumption that when two
  species share introns at the same site, it is always due to
  inheritance from a common ancestor."

Since shared ERVs in humans and chimps is touted as one of the proofs of humans and chimps sharing ancestry (like by Ken Miller here), does the above paper (and quote) undermine this line of reasoning?

Is there any good (recent) source which discusses proof of common descent using ERVs?

The Yohn et. al. (2005) paper (from Evan Eichler's lab) is describing a single type of endogenous retroviral element (loosely think of it as a 'species'), called PTERV1. They show that there were multiple independent infection events that resulted in permanent integrations in the ancestors of modern species (~3-4 MYA in the ancestors of gorillas and chimps, ~1.5 MYA in the ancestors of baboons and macaques). This in no way contradicts the notion of common ancestors among the apes/monkeys; indeed, they state this as a given in their analysis (emphasis mine):

  A total of 275 of the insertion sites mapped unambiguously to
  non-orthologous locations (Table 2), indicating that the vast majority
  of elements were lineage-specific (i.e., they emerged after the
  divergence of gorilla/chimpanzee and macaque/baboon from their common
  ancestor).

The presence of an ERV (or intron, or any general genomic synteny), can be used as evidence to support a particular model of common decent. Changes in genomic architecture are stochastic processes, and the work you cite by Li et. al. (Lynch lab) is showing us that ERV placement can occur at a similar, or nearly identical, location at a much higher rate than previously thought. We therefore need to take this into account then calculating how strongly a shared ERV increases our confidence in a given phylogenetic model.

The video you linked to uses a completely random (i.e., very simple) model of ERV integration, setting the chance of an insertion at a given location at 3.3e-10. The findings by Li tell us that this is incorrect. In daphnia, at least, ‘hotspots’ may account for nearly 25% of new intron gain. The video also failed to include all of the instances of ERVs that are not shared between humans and chimp (back-of-napkin, this could account for differences of ~0.3% between their genomes, see Mun et al. 2014). This will increase the probability of an exact match occurring by chance (e.g., put two people in a room, what’s the chance of them having the same birthday? Put 100 people in a room, what’s the chance of any of them having the same birthday?).

So, let’s be extremely conservative and say that the chance of the same insertion at a given location in both chimps and humans is one in one thousand (1e-3, seven orders of magnitude more probable than in the original model). Sixteen shared ERVs are identified in the video; if each is considered an independent event because of no shared decent, we are still looking at odds around 1e-48 (1e-3 ^ 16). An alternative could be that they are derived from insertions that predate the split from a common ancestor. Given Li et. al., maybe each event should be given a probability of only 0.75 instead of 1.0 (as per the video) because up to 25% of them could be from hotspots. In this scenario, the probability is 0.01 (0.75 ^ 16). Therefore, the second hypothesis is 46 orders of magnitude more probable than the first. In my mind, this is extremely compelling evidence that humans and chimps share a common ancestor, using only ERV data.

I want to be clear, I am fudging these numbers extensively towards not supporting common descent. The real odds will be much higher in favour of common descent.

For further reading, Welkin Johnson wrote a comprehensive review on ERVs in 2015 (paywalled, so you may need to search for Alexandra Elbakyan's scientific literature retrieval method if you don't have institutional access).

References

Johnson WE. (2015). Endogenous Retroviruses in the Genomics Era. Ann. Rev. Virology. doi: 10.1146/annurev-virology-100114-054945

Li W. et al. (2009) Extensive, Recent Intron Gains in Daphnia Populations. Science. doi: 10.1126/science.1179302

Mun S. et at. (2014) Chimpanzee-Specific Endogenous Retrovirus Generates Genomic Variations in the Chimpanzee Genome. PLoS One. doi:  10.1371/journal.pone.0101195

Yohn et. al. (2005). Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans. PLoS Biol. doi: 10.1371/journal.pbio.0030110


Tree of Life in Text Format Wondering if there is a tree of life in Text format for open data sharing.

Perhaps not though the tree of life website, but the Open Tree of Life exists to fulfil this need. You can export newicks of nodes which you are interested in.


What is MHC haplotype? What is MHC haplotype? I did check out the wiki article, but did not understand.

(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

A haplotype is commonly defined as

  ...a group of genes within an organism that was inherited together from a single parent. -- Nature Scitable

This definition of haplotype applies whether it is just a few genes or all of the genes on an entire chromosome$^1$. In the case of the major histocompatibility complex, it is a group of more than 200 genes on chromosome 6 (Janeway et al. 2001). The set of alleles$^1$ inherited together from one parent form the MHC haplotype. Thus, one offspring will inherit two different MHC haplotypes, one from each parent. The different haplotypes with so many genes helps keep genetic variation in the overall complex, which improves the immune response ability of the organism.

The term is derived from haploid, which means half of the normal set of chromosomes. Humans for example are diploid, meaning it has two copies of each chromosome, one inherited from the mother (maternal) and one inherited from the father (paternal). So, when you inherit just one half of the crhomosome pair, you are inheriting a haplotype.

For general reference, it's important to note that haplotype was not always used to reference a group of two or more genes inherited together. It was commonly used to as a term to represent a sequence of nucleotides together on the same chromosome, even if only part of a single gene. For example, Bowen et al. (1995) used mitochondrial haplotypes to study the migration of loggerhead turtles across the Pacific Ocean. They used 350 nucleotides of the mitochondrial control region. The control region is over 1000 nucleotides in size but Bowen and colleagues only used 350 nucleotides from part of the control region.  This use was very common in the 1990s and early 2000s before it became easier and less expensive to sequence entire genomes, or at least many genes.

Citaton

Bowen, B.W. et al. 1995. Trans-Pacific migrations of the loggerhead turtle (*Caretta caretta) demonstrated with mitochondrial DNA markers. Proceedings of the National Academy of Sciences USA 92: 3731-3734.

Janeway, Jr., C.A. et al. 2001. Immunobiology, 5th edition. Garland Science, New York.

Footnote

More accurately, it would be the set of alleles at each gene locus (gene location) inherited together. The same genes are inherited from either parent, but the alleles (variations of the gene) may be different between the two parents.


Exact definition of 'convergent' and 'divergence' in cell signalling? From what I understand, we refer to 'signal convergence' as being when two different ligands/stimuli lead to the same (at least in part) responses inside a single cell. This may or may not be due to activation of the same pathway, so for example we can refer to the response of a muscle cell to adrenaline and to stimulation by the nervous system via acetylcholine as convergent because they both lead to the release of calcium. We can also refer to the activation of the phosphoinositide pathway by both activation of beta phospholipase C via a heterotrimeric Gq protein, and activation of gamma phospholipase c via the tyrosine kinase pathway, as signal convergence.

So it seems to me that 'convergence' is defined on the level of the cell with it being, in a nutshell, different stimuli resulting in the same effect regardless of at which point in some internal signalling pathway the two responses 'converge' (at least in part).

Now with divergence I am getting slightly more stuck, and I have not seen a single, clearly stated, definition. Firstly, does divergence refer only to the level of the cell, or also for the whole organism? In particular, I am thinking of cases where a single ligand has different responses in different cells, such as adrenaline leading to increased contraction in muscle cells and glycogen breakdown in the liver (I know this isn't the best example because adrenaline technically leads to glycogen breakdown in both cell types).

Perhaps instead divergence is only referred to on the level of the cell, as with convergence? So for example generally tyrosine kinase stimulation activates several different proteins, which trigger different responses: ras, gamma phospholipase C etc. Even the phospholipase C pathway produces DAG and IP3, which have different responses. But then it seems to me like practically all pathways are divergent if this is the case, because generally pathways lead to several responses inside the cell. So with the case of phospholipase C which cleases PIP2 to DAG and IP3, the DAG can regulate metabolism and transcription etc via protein kinase C and the IP3 leads to calcium ion release that causes muscle contraction. Would this be referred to as divergence?

I would greatly appreciate if someone could just state what exactly convergence and (especially) divergence refer to. I am relatively new to cellular and molecular biology.

In my experience those terms are primarily used intracellularly, but I wouldn't argue that it is wrong to use them more broadly, it's just that essentially everything released extracellularly is going to have some level of divergence, so it makes more sense to use a separate classification scheme (i.e., endocrine/paracrine). Between cells, the terms are also used in other contexts such as the nervous system to refer to inputs from multiple neurons synapsing on one neuron (convergence), and outputs from one neuron synapsing on many targets (divergence).

Convergence just means multiple signalling pathways converging on the same target: like multiple pathways that can activate phospholipase C.

Divergence just means that one effector, which could be a protein such as a kinase or a second messenger like IP3, has multiple targets.

You are quite likely to get both convergence and divergence within any given signalling pathway. In my opinion, this is one of the ways that biology is not taught well in schools: textbooks might make it seem like convergence and divergence are these concrete, specific classifications, but they are really just descriptive terms. Phospholipase C pathways are a great example that displays both. If you are talking from the perspective of activation of phospholipase C, you are probably talking about convergence because there are so many ways to activate phospholipase C, but at the same time, if you talk from the perspective of the G protein subunit that is activating phospholipase C, that G protein probably has other targets as well, so that's divergence. And downstream of phospholipse C you have divergent effects of DAG and IP3.


What are "anchor regions" in the human genome? I've been reading this paper entitled "A high-resolution map of the three-dimensional chromatin interactome in human cells", about interactome in 3D chromatin.

  We next applied the above algorithm to the 518,032 anchor regions in
  the human genome, with each containing one or a few HindIII
  restriction fragments (fragments shorter than 2 kilobases (kb) are
  merged) (Fig. 2a), and uncovered a total of 1,116,312 chromatin
  interactions with a false discovery rate (FDR) of 0.1

Simple questions: what are these anchor regions in the human genome?

How could I group them into types/categories?

Thanks

Good question. Anchor regions are regions that connect to the nuclear matrix. More specifically, in eukaryotic organisms, chromatin is anchored to the nuclear matrix by short DNA sequences of about 100-2,000 bp called matrix attachment regions or MAR. To answer the second part of your question, there are many categories (and opinions about those categories) of anchor regions. The most comprehensive way of categorizing these regions however I believe is by whether they are constitutively (always) or transiently (sometimes) bound to the nuclear structure.


How many times did photosynthesis evolve? Was it a 1 and done thing? Plants seem to have developed photosynthesis by the endosymbiosis of cyanobacteria. Is the latter the one time in Earth's history that the process independently came about?
Any answers would be greatly appreciated

The emergence of photosynthesis has occurred rather independently in multiple organisms. One way of looking at this is to look at the taxonomic distribution of photosynthesis reaction centers, which points to 5-10 origins according to current data (mostly in bacteria). That number has some big error bars as we are talking about very deep, old branches of the tree of life.
There are other criteria that we could use- for example the evolution of carbon fixation. However, that includes also chemoautotrophy, and is thus a bit more expansive.
Note that by some definitions the acquisition of cyanobacteria in plants may not even represent an independent emergence of photosynthesis, as the cyanobacteria already did photosynthesis!
If your question is more narrowly "how many times did photosynthesis evolve in eukaryotes" (not bacteria or archaea), then you would also need to include animals that do photosynthesis in a way similar to (though I believe less efficiently than) plants. They seem to similarly use endocytosis to acquire photosynthetic machinery from photosynthetic cells that they eat.
Update
In response to comment from @shigeta, I'll add that the review that I link focuses on the reaction centers (RC) genes. They note that the RC genes probably had a single emergence, but that horizontal gene transfer is probably responsible for the current distribution of the organismal trait of photosynthesis:

Significant evidence indicates that the current distribution of photosynthesis in bacteria is the result of substantial amounts of horizontal gene transfer, which has shuffled the genetic information that codes for various parts of the photosynthetic apparatus, so that no one simple branching diagram can accurately represent the evolution of photosynthesis (Raymond et al., 2002).


Please help to identify this insect It is approx 1.5 inch (3 cm to 4.5 cm) long

The insect's back and wings.

Insect from its forward side

Just few hours ago (around night 10 to 10.30 pm local time), this insect entered into our home, flying in high-speed and hitting to wall, objects, and to us. To keep it calm we turned the room-light off. Then it became steady on my father's shirt even after the light again turned on, and it was a beautiful moth-like insect. After taking photo it gently freed out of the room.

Here in India, it is rainy season (after summer).

P.S. I've very very little-experience in practical-zoology, however after few hours google search it seems to match with those moths tagged as "hawk-moths", and another notable feature when it was flying it looked like a hummingbird or a small bird, that was written in the description of some "hawk-moths" in different sites. Initially we're taking time to decide whether it is an insect or a bird.

As MattDMo suggested, this is a hawk moth.  Given your location and season, this is why I thought it was either the Impatiens hawkmoth (Theretra oldenlandiae) or the  White-edged hunter hawkmoth (Theretra lycetus).  And finally, why I now think it is the Brown-Banded Hunter (Theretra silhetensis).
Brown-Banded Hunter Hawkmoth
The Theretra silhetensis exhibits a solid white line along the upperside of its abdomen, and more of a faded banding pattern on the forethat corresponds with your picture.  These moths are also common in India.

It is differs from T. oldenlandiae in being very much paler in color
and with white line down center of abdomen.

When it comes down to it, that solid single white line is the biggest indicator it is a T. silhetensis over a T. oldenlandiae or T. lycetus.

While my final answer is the brown-banded hunter hawkmoth, below are the original two species I suspected it was and why.  I've included them below simply for reference / alternative comparisons.
Impatiens Hawkmoth
Theretra oldenlandiae was my original instinct, since it is a more common in your area and the banding/stripe pattern matches to a T.

But, upon closer inspection, there are two things that don't quite align:

Your Specimen exhibits pink suffusion, especially on the back edge of the fore wing.
Your specimen has a single dorsal line, not two.

For these two reasons I think it is not the Impatiens Hawkmoth and thought it was more likely the...
White-edged hunter hawkmoth
Theretra lycetus is not as common on the T. oldenlandiae for your location, but the pink suffusion supports this idea.  See below for a picture:

This still doesn't explain the double vs. single white stripe along the upper abdomen.  Which is why I know believe it is the...

As an aside, this could be an example of polymorphism vs. identifying characters. Welcome to the world of taxonomic lumpers and splitters...


Balanced vs Maximized Codon Optimization I have worked with the optimization of several viral proteins, from different viruses/families, with different results.

When Menzella, 2011 was published I tried that method.  I found quite the contrary result, in that randomization did far poorer than straight maximization of codon usage.  I chucked this up to working within the context of viral infection (though it was also true in transient expression from plasmid transfection under CMV promotion).

I was quite excited by Pechmann and Frydman's Nature article which highlighted the importance of the location of the codon within the protein when regarding optimal vs suboptimal codon selection. Oddly enough we were able to deploy this information most successfully with the purposeful deoptimization of a protein.

Pairing a locational awareness, screening for secondary structure, and then maximizing codon optimization has had the best results for more than a year.  By maximization, I mean choosing the most optimal codon in every instance that doesn't violate:

Needed restriction sites
Predicated Secondary Structure
Location gradient to a lesser extent (ibid.)

This is all well and good, but we've been having problems with my institutions preferred vendor for gene synthesis.  A post-doc that just joined my lab recommended a company I had never heard of before, and they posed an optimization strategy I had never considered before.  Instead of maximizing codon optimization, they propose a "balanced" codon optimization that matches the normal distribution of codons in the target organism.

For example, the codon bias for alanine in humans breaks down (roughly) as follows:

GCC 65%
GCT 20%
GCA 11%
GCG 4%

As opposed to a maximization strategy which would seek to use "GCC" when ever possible and only when there was an issue switch to "GCT," the balanced stratgy would seek to replicate the above distribution as closely as possible.

Has anyone tried a balanced codon approach, especially when compared to a maximization technique?  My overall goal is to maximize expression of naturally poorly expressing protein.  I know that straight maximization can occasionally lead to poor expression for a variety of reasons (often fatal secondary structure), but this seems like it would hardly increase expression at all.

I would be further interested if anyone else had experience within a viral context.

I know that there have been a few related questions, mostly in the context of E. Coli.  I don't think this is a duplicate, but would be willing to remove if it is seen as such.  If I run into some extra funds I may test this empirically, but often when I'm trying such a test it's only in relation to 2-3 proteins, which might not be representative.

Codon usage optimization is still pretty much heurestic. The most common factor we think are important in E. Coli are:

optimization to highly expressed genes, i.e. maximization of codon adaptation index http://www.ncbi.nlm.nih.gov/pubmed/19359587/
keeping the optimal GC content http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0107319
not introducing motifs that are somehow detrimental, e.g. restriction enzymes, or some dinucleotides http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0056642
adapting to available tRNA http://www.plosone.org/article/info:doi/10.1371/journal.pone.0007002
minimizing folding energy (in the first ca. 30 codons) and minimizing the amount of hairpins at the 5' end http://www.sciencedirect.com/science/article/pii/S0014579305010719
optimization of 'codon context' e.g. dicodons but also using nonoptimal codons between secondary structure for more accurate folding http://www.ncbi.nlm.nih.gov/pubmed/15772378
optimization of codon balance and also maybe the introduction of a 'ramp of slow codons' in the beginning of a gene to avoid 'traffic jams' of ribosomes later on. http://www.ncbi.nlm.nih.gov/pubmed/20403329

Most probably it's a mixture of all of those.

Disclaimer: We are working on a codon optimization strategy for e.coli/yeast/hela and it works in e. coli but is yet untested in human cells. If you want to take a long shot just shoot me a message and we could try it. Apart from this, I would also offer you to have a look at your sequence and see if there is anything 'strange' from the codon usage point of view and what I think what be the best optimization strategy.


Why is nitrogen isotopic labelling required for protein NMR? Why is labelling required for Nitrogen (by 15N) for studying structure of a protein using NMR?

It is not strictly required. Isotope labelling is required when the usual isotope does not have a magnetic spin (for example 12C). 14N has a spin of 1 and exhibits 3 spin states: -1, 0 and 1. The isotope, 15N has a 1/2 spin. As noted in this book, analytical methods exist for both nitrogen isotopes.

However, 15N is preferred for NMR studies because the chemical shifts produced by 14N can be too broad to be detected by high resolution NMR spectrometer.

From wikipedia:

  Nitrogen-15 is frequently used in nuclear magnetic resonance spectroscopy (NMR), because unlike the more abundant nitrogen-14, that has an integer nuclear spin and thus a quadrupole moment, 15N has a fractional nuclear spin of one-half, which offers advantages for NMR like narrower line width.

From http://chem.ch.huji.ac.il/nmr/techniques/1d/row2/n.html:

  The 1D 14Nitrogen NMR experiment is much less sensitive than Proton (1H) but has a much larger chemical shift range. Its signals are broadened by quadrupolar interactions. The larger the molecule and the more asymmetric the nitrogen's environment, the broader the signal. Hence, the small and highly symmetric aqueous ammonium ion gives a very sharp line (fig. 3), less than one Hertz wide. Liquid ammonia, being less symmetric, is 16 Hz wide (on a 400 MHz spectrometer at room temperature). Urea is larger and asymmetric so the line-width is approximately 1 KHz. Molecules that are significantly larger than urea yield signals too broad to be observed with a high-resolution NMR spectrometer. However, the nitrogen chemical shift range is wide and so may be readily used for distinguishing nitrogen species for very small molecules.


What would be the shortest and optimal method of extracting human cells for PCR? Is there a colony PCR like protocol for human cells? I am trying to devise a quick method to extract genomic DNA from human cells for a PCR.

I first collected cells by centrifuging  saline mouthwash (0.9% NaCl) and extracted genomic DNA using kit followed by a PCR protocol which works fine but is a rather lengthy process.

I tried to cut short the method and removed the DNA extraction steps by using pelleted spit samples as templates for PCR and increased the initial denaturing step from 3 minutes to 5 minutes. However this method was not reliable as some of my samples were amplified and some were not.

Can anyone suggest me a reliable protocol here?

Thanks!

I am not confident in my reply, but the article linked below has methods for DNA extraction of various human sample types( blood, hair, urine, Cheek)

For what its worth, my professors always told me DNA extraction was more of an art than a science, and one has to tinker to get it just right.

Maybe for something really quick, you could try a protienase K "squishing buffer" and then boil it for like 10 mins in the buffer and then try running PCR.  I am just an undergraduate though so take my words with a heavy grain of salt.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792701/

Here is how they gathered the buccal samples:
buccal swabs:

  five healthy adult volunteers were recruited (age range, 22–35 years),
  and demographic information, including age, health condition, sex,
  population ancestry, hair color, and hair treatments, was collected.
  The volunteers recruited were asked to rinse their mouth with tap
  water, 30 s before sampling of buccal swabs, to avoid the
  contamination as a result of food particles. For each individual, both
  sides of buccal mucosa were wiped with a cotton swab for 15 s, and a
  total of five samples was collected in 500 μl 10 M Tris-HCl, 10 mM
  EDTA, 2% SDS, containing 1.5-ml microcentrifuge tubes. Isolation of
  DNA from cotton swabs was performed.

Here is a copy paste, hyphens are mine.

DNA Extration:

  Buccal swabs:

  -samples were suspended in 500 μl lysis buffer [10 mM Tris (pH 8.0), 10 mM EDTA, and 2.0% SDS], and 50 μl 10% SDS, followed by 5–10 μl 20
  mg/ml proteinase K

  -incubated 1–3 h at 56°C until the tissue was totally dissolved

  -The DNA was then extracted from each sample with an equal volume of phenol:chloroform: isoamyl alcohol solution (25:24:1) and mixed gently
  by inverting the tubes for 3 min.

  -samples were then centrifuged (Eppendorf 5415R; Hamburg, Germany) for 10 min with 10,000 g (4°C),

  -upper aqueous layer was transferred to a fresh, sterilized microcentrifuge tube.

  -RNase A (10 μl of 10 mg/ml; Fermentas, Thermo Scientific, Germany) was added, and the solution was incubated at 37°C for 30 min.

  -Equal volumes of chloroform:isoamyl alcohol solution were added and centrifuged (Eppendorf 5415R), again with 10,000 g (4°C) for 10 min.

  -The upper aqueous layer was transferred to a sterilized microcentrifuge tube, and double the volume of chilled isopropanol
  (Merck, Whitehouse Station, NJ, USA) was added, along with one-tenth
  volume of 3 M sodium acetate, and chilled at −20°C for 1 h for
  precipitation.

  -After 1 h, the sample was centrifuged (Eppendorf 5415R) at 10,000 g (4°C) for 10 min.

  -After decanting the supernatant, 250 μl 70% ethanol (Merck) was added, and the pellet was dissolved; the mixture was centrifuged at
  10,000 rpm for 10 min, and the supernatant was decanted gently.

  -The pellet was air-dried under laminar air flow, and the dried pellet was resuspended in 50 μl nuclease-free water or 1× 10 mM Tris-HCl, 1
  mM EDTA, pH 7.6 (TE), buffer and frozen at −20°C or at −80°C for
  storage.


Why is the resting potential of a neuron so close to the equilibrium potential of K⁺? I know this has something to do with the K+ leak channel. I just don't understand how.

I know that 3 Na+ are pumped out for every 2 K+ pumped in. This makes the cell interior net negative.

I know that K+ is allowed to leak out slowly via K+ leak channels.

How does this place the resting potential of the cell so much closer to the equilibrium potential of K+ than Na+?

Lets just go with the basic Hodgkin-Huxley equation:

$$C_M \frac{\text{d}V}{\text{d}t}=-g_{Na}(V-E_{Na}) -g_K(V-E_K) -g_L(V-E_L)$$

At rest ${\large\frac{\text{d}V}{\text{d}t}}=0$ and therefore $V$ is dependent on the conductances ($g_X$) of different ions. Since $g_K \sim 30\times g_{Na}$, the resting potential is closer to $E_K$ (Nernst equilibrium potential of K+).

What it basically means is that since potassium has higher membrane conductance, it diffuses faster thereby attaining equilibrium faster than sodium (in isolated cases assuming only one ion at a time). When both ions are present the resting potential is because of both the ions but since K+ diffuses faster, it has a major contribution to the resting potential compared to Na+. Leak current that is described in the above equation is a general leak (non-specific). Other channels like rectifiers and voltage gated channels are important when talking about action potential and all these channels contribute to the conductance; however you can group all that into a single metric called membrane conductance. Voltage gated channels can be considered separately when studying the dynamics (in this case the conductances themselves become a function of voltage).


Is "tonic activity" common for neurons firing in the brain? I've been reading about Dorsal Raphe Nucleus, a serotonin- rich part of the brain. I noticed mentioning of "tonic activity" - regular pulsing that releases neurotransmitters. On top of this "tone" the nucleus can fire bursts of spikes(action potentials?) that further increase neurotransmitter concentrations for a short time.

Is this kind of tonic firing common throughout the brain, or is it DRN specific?

Most neurons that have been studied have spontaneous activity. Tonic firing is common in sensory neurons as well as cortical neurons. However, this could be very biased since it is difficult to study neurons that are silent in vivo. In vivo studies are blind, meaning that we usually do not see which neurons we are recording from. This is known as the "dark matter" problem (ref 1).

Also, it is known that there are homeostatic mechanism for maintaining average firing rate. Basically, if a neuron doesn't fire much, then the input sensitivity of the neuron increases to produce more activity (ref 2). But we don't know how widely this can be applied.

References:

Shy Shoham, Daniel O’Connor, Ronen Segev. How silent is the brain: is there a "dark matter" problem in neuroscience? Journal of Comparative Physiology A: Neuroethology, Sensory, Neural, and Behavioral Physiology, Vol. 192, No. 8. (1 August 2006), pp. 777-784  doi:10.1007/s00359-006-0117-6
Gina G. Turrigiano. Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same. Trends in Neurosciences, Vol. 22, No. 5. (1 May 1999), pp. 221-227, doi:10.1016/S0166-2236 (98)01341-1


What determines excrement's caliber? Often, pieces of feces have a clearly-defined shape and size — both length and width (that is, cross-sectional diameter, or caliber). But that width seems to vary quite a bit, even among pieces of feces from the same person. Why? What determines the width? Why is it wide when it's wide, and why is it narrow when it's narrow?

With the help of Bristol Stool Chart (BSC) and full explanation of conditions related to different stool sizes from this link you could have a full understanding over stool size.

  » Type 1: Separate hard lumps, like nuts Typical for acute
  disbacteriosis. These stools lack a normal amorphous quality, because
  bacteria are missing and there is nothing to retain water. The lumps
  are hard and abrasive, the typical diameter ranges from 1 to 2 cm
  (0.4–0.8”), and they're painful to pass, because the lumps are hard
  and scratchy. There is a high likelihood of anorectal bleeding from
  mechanical laceration of the anal canal. Typical for post-antibiotic
  treatments and for people attempting fiber-free (low-carb) diets.
  Flatulence isn't likely, because fermentation of fiber isn't taking
  place.

  » Type 2: Sausage-like but lumpy Represents a combination of Type 1
  stools impacted into a single mass and lumped together by fiber
  components and some bacteria. Typical for organic constipation. The
  diameter is 3 to 4 cm (1.2–1.6”). This type is the most destructive by
  far because its size is near or exceeds the maximum opening of the
  anal canal‘s aperture (3.5 cm). It‘s bound to cause extreme straining
  during elimination, and most likely to cause anal canal laceration,
  hemorrhoidal prolapse, or diverticulosis. To attain this form, the
  stools must be in the colon for at least several weeks instead of the
  normal 72 hours. Anorectal pain, hemorrhoidal disease, anal fissures,
  withholding or delaying of defecation, and a history of chronic
  constipation are the most likely causes. Minor flatulence is probable.
  A person experiencing these stools is most likely to suffer from
  irritable bowel syndrome because of continuous pressure of large
  stools on the intestinal walls. The possibility of obstruction of the
  small intestine is high, because the large intestine is filled to
  capacity with stools. Adding supplemental fiber to expel these stools
  is dangerous, because the expanded fiber has no place to go, and may
  cause hernia, obstruction, or perforation of the small and large
  intestine alike.

  » Type 3: Like a sausage but with cracks in the surface This form has
  all of the characteristics of Type 2 stools, but the transit time is
  faster, between one and two weeks. Typical for latent constipation.
  The diameter is 2 to 3.5 cm (0.8–1.4”). Irritable bowel syndrome is
  likely. Flatulence is minor, because of disbacteriosis. The fact that
  it hasn't became as enlarged as Type 2 suggests that the defecations
  are regular. Straining is required. All of the adverse effects typical
  for Type 2 stools are likely for type 3, especially the rapid
  deterioration of hemorrhoidal disease.

  » Type 4: Like a sausage or snake, smooth and soft This form is normal
  for someone defecating once daily. The diameter is 1 to 2 cm
  (0.4–0.8”). The larger diameter suggests a longer transit time or a
  large amount of dietary fiber in the diet.

  » Type 5: Soft blobs with clear-cut edges I consider this form ideal.
  It is typical for a person who has stools twice or three times daily,
  after major meals. The diameter is 1 to 1.5 cm (0.4–0.6”).

  » Type 6: Fluffy pieces with ragged edges, a mushy stool This form is
  close to the margins of comfort in several respects. First, it may be
  difficult to control the urge, especially when you don‘t have
  immediate access to a bathroom. Second, it is a rather messy affair to
  manage with toilet paper alone, unless you have access to a flexible
  shower or bidet. Otherwise, I consider it borderline normal. These
  kind of stools may suggest a slightly hyperactive colon (fast
  motility), excess dietary potassium, or sudden dehydration or spike in
  blood pressure related to stress (both cause the rapid release of
  water and potassium from blood plasma into the intestinal cavity). It
  can also indicate a hypersensitive personality prone to stress, too
  many spices, drinking water with a high mineral content, or the use of
  osmotic (mineral salts) laxatives.

  » Type 7: Watery, no solid pieces This, of course, is diarrhea, a
  subject outside the scope of this chapter with just one important and
  notable exception—so-called paradoxical diarrhea. It‘s typical for
  people (especially young children and infirm or convalescing adults)
  affected by fecal impaction—a condition that follows or accompanies
  type 1 stools. During paradoxical diarrhea the liquid contents of the
  small intestine (up to 1.5–2 liters/quarts daily) have no place to go
  but down, because the large intestine is stuffed with impacted stools
  throughout its entire length. Some water gets absorbed, the rest
  accumulates in the rectum. The reason this type of diarrhea is called
  paradoxical is not because its nature isn‘t known or understood, but
  because being severely constipated and experiencing diarrhea all at
  once, is, indeed, a paradoxical situation. Unfortunately, it‘s all too
  common.

  Interestingly, the interpretations and explanations of the BSF scale
  that accompany the original chart differ from my analysis. To this I
  can only say: thanks for great pictures, but, no thanks for the
  rest...

  Excerpted from Fiber Menace, page 117-120; BSF Chart: wikipedia.org

But to make it more clear:

Reasons behind thicker and harder stool:

Lower fiber food
Lower liquid intake
Lower physical activity
Lack or lower amount of bacteria related to retaining water inside rectum and colon
Medication:

  Many medications have constipation as a side effect. Some include (but
  are not limited to) opioids also known as narcotics, diuretics,
  antidepressants, antihistamines, antispasmodics, anticonvulsants, and
  aluminum antacids. Certain calcium channel blockers such as nifedipine
  and verapamil can cause severe constipation due to dysfunction of
  motility in the rectosigmoid colon.

Metabolic and muscular

  Metabolic and endocrine problems which may lead to constipation
  include: hypercalcemia, hypothyroidism, diabetes mellitus, cystic
  fibrosis, and celiac disease. Constipation is also common in
  individuals with muscular and myotonic dystrophy.

Structural and functional abnormalities

Any physical digestive tract line problem which cause interference of stool movement. Like cancer or some kind of inflammation that could ban the canal

  Constipation has a number of structural (mechanical, morphological,
  anatomical) causes, including: spinal cord lesions, Parkinson, colon
  cancer, anal fissures, proctitis, and pelvic floor dysfunction.

  Constipation also has functional (neurological) causes, including anismus, descending perineum syndrome, and Hirschsprung's disease. In
  infants, Hirschsprung's disease is the most common medical disorder
  associated with constipation. Anismus occurs in a small minority of
  persons with chronic constipation or obstructed defecation.

Psychological

  Voluntary withholding of the stool is a common cause of
  constipation.The choice to withhold can be due to factors such as fear
  of pain, fear of public restrooms, or laziness. When a child holds in
  the stool a combination of encouragement, fluids, fiber, and laxatives
  may be useful to overcome the problem.

Edit:

In the second provided link you could get how cross-sectional diameter changes based on what you eat or how you behave with your body mentally or physically if you are a healthy person.

But as you are interested more on cross-sectional size of stool and reason behind it, consider the fact that colons and rectum are water absorber. The more stool stays there the more thick and dry it gets. So if you ate more fiber you will probably have softer stool and thinner caliber as the result of pressure of the rectum canal. Because some bacteria which are active in the fibers of stool are water absorbers too and the reason behind why doctors insist on eating more probiotic products is to keep these bacteria present and stable and also to get vitamins from their activities. So you could change your caliber only by eating more fiber more water and having more physical activities and also for consistent thick and dry stool (constipation) individual must share the problem with doctor because it could bring more dangerous problems in future or maybe it's a sign of some other serious disease that person's body is already dealing with. Most of the time it's nothing but our diet and hours we are sitting for variety of reasons or maybe focusing on another activitys (work, computer games, disabilities, watching tv and so on and so forth).

https://en.wikipedia.org/wiki/Constipation
https://www.gutsense.org/constipation/normal_stools.html


NADP and NADPH in in vitro metabolisme test I did an in vitro metabolism test using chicken liver S9 as the source of the enzyme. I did two different of method experiment. one was using NADP and second was using NADPH as the co-factor. my compound was fipronil, and I expect it to be metabolised become Fipronil sulfone (through oxidation reaction). The results, when I use NADP, fipronil sulfone formed was very low concentration, but in contrast, when using NADPH, I got high amount of fipronil sulfone.
what is the different using NADP and NADPH in this experiment?
Thank you for sharing the informatio.
Kind regards

Alex

Are you sure your question is accurate?

NADP in solution does not exist... it can either be NADPH which is the reduced form (has gained an electron in the form of a H atom and now has the potential to give that electron to another molecule in the solution) or NADP+ which is the oxidised form (has lost an electron in the form of H atom and now has the potential to gain an electron from the solution).

In your experiment, Fiprinol to Fiprinol Sulfone is an oxidation reaction, so the enzyme catalyses the removal of an electron from Fipronol, and it does that with the help of NADP+, which is missing an electron itself and therefore takes it from Fiprinol (oxidises it) to give a high Fiprinol Sulfone yield.


Is it possible to remove one strand of double stranded DNA in vivo? Assume we do have a double stranded DNA sequence in human cells, say

...ATCGATATCGATATTGCAGAGCATAGCTATAA...
...TAGCTATAGCTATAAGCTCTCGTATCGATATT...

Now I want to cleave one strand, such that I do have

...ATC..........................TAA...
...TAGCTATAGCTATAAGCTCTCGTATCGATATT...

The distance is not so important to me, so it can be 20 bp I remove or 1000s. Hence, if I need some PAM or so and it is not nearby the target deletion site, I will simply move in 5' resp. 3' direction until I find it and cleave there, as long it is ensured that I have the target site single stranded then.

I would be very grateful I you could help me here!

Both TALEN and ZFN gene editing technologies use a pair of single-strand endonucleases that ultimately lead to a double strand break. Cas9 in CRISPR-Cas technology, however, cuts both the DNA strands (there are some Cas enzymes in certain bacterial species that cut only a single strand [ref]).

  Image courtesy: http://www.xenbase.org/other/static/CRISPr.jsp

So, if you use a single unit of the pair, you can cut one strand of the DNA. You can use another nuclease to impart a cut at another site in the same strand. This will still not lead to the removal of the DNA sequence between the two cut sites. There is no available technology that can do this in-vivo. Possibly (a wild guess), you can use a modified oligonucleotide (or even an IVT synthesized RNA) that can bind to this stretch of sequence and break its interaction with the other DNA strand. In any case, a stretch of ssDNA would not be stable and be repaired quickly by polymerase.


What Software could I use to create Diagrams of Biochemical Processes like these? Cross-posted at GraphicDesign.SE here

Is there any software software that I could use to (closely) create pathways as depicted in these diagrams?

Or does anyone happen to know what software was used for these diagrams specifically? [Sourced from Harper's Illustrated Biochemistry (31e) and Murray's Medical Microbiology (8e) respectively]

I would like to be able make alterations such as adding extra steps, changing color, including newer pieces of data and such-like for the purpose of making my own notes.
I assume that knowing which software was (or can be) used to create these, I'd have greater versatility making the edits I need, or creating something in similar from scratch for other processes/pathways.

By posting to this forum, I presume the question is whether the illustrators of this and other biochemistry books used software specifically designed for the purpose of drawing reaction pathways, or, if not, whether such software exists. From my experience of using such illustrations in my own teaching over the years, I believe that the answer is probably no (although there are a couple of what I would consider ‘almosts’ mentioned below.) The main reason I would not expect this is that it would not seem commercially viable (biochemistry teachers and book illustrators are hardly a huge market) and you can get by with more generic pre-existing applications.

The class of application I consider best for this is termed a vector graphics application (popularly known as a ‘drawing’ application), as opposed to a bitmap or raster graphics application (popularly known as a ‘paint’ application). Although today there are applications that combine both functions, vector graphics applications have the advantage that they are more easily editable and they scale to any print resolution. The professional applications in this area can be very expensive and have a steeper learning curve than bitmap graphics applications (such as Adobe Photoshop). Moreover, they may lack features needed for biochemical use. It is therefore be worth exploring cheaper offerings, or investigating specialist vector graphics applications more focused on engineering or computing diagrams.

For biochemical work I personally would require software to be able to provide the following:

Controllable geometric lines (Bezier curves)
Customizable arrowheads
Text control that at least allows subscripts and
superscripts, and ideally both simultaneously, e.g. for a charged
phosphate species.
Rotatable text (as in the upper example)
Basic graphic primitives (as in the lower example)
Export to vector formats accepted by other applications (PostScript or PDF) to allow output in formats and at resolutions required for print publication.

How do different applications satisfy these criteria? They all support basic graphic primitives, and most allow export at least as PDF, if not the more flexible PostScript.

Surprisingly the creation of a line with an arrowhead is not straightforward as one is dealing with a combination of two separate objects. Although all applications tend to provide straight lines with arrowheads, curved lines with arrowheads tend to be absent from the general applications (even the most sophisticated) because a curved line is not really a line as such, but is generated as an oval segment with a stroke (visualization of its drawn edge) but no fill (the body is transparent). I have tended to use this sort of application (going back to MacDraw II of the Classic Mac) and fudge the arrows on them by combining them with straight lines of the same length as the arrowhead. However they are provided by more specialized diagramming software like OmniGraffle (mentioned in another answer) or the dedicated ChemDraw (which I find too limiting to use other than for export).

Text handling is the other problem. Placing a superscript directly above a subscript is a page layout operation that only dedicated mathematical software (e.g. MathType) is likely to support. Microsoft Word’s equation editor will do this, but export is only as PDF, and import into other applications varies in effectiveness. If you work in a generic application you will have to fudge it yourself with separate text boxes.

What are the choices for generic vector drawing applications? Adobe Illustrator is the most sophisticated, is used by most professional illustrators, but is very expensive (it is now subscription only). Other vector drawing applications that I am aware of but have not used include the commercial Corel Draw (cheaper than Illustrator) and the even cheaper Affinity Designer. As mentioned in a comment, there is also the free application, Inkscape. Free trials are available with most applications, so I would recommend seeing what is the best solution for your personal situation.

Addendum

I have just had a quick look at BioRender, which was mentioned in another answer. It has many different modules, including ones for biochemistry (including a Glycolysis pathway template) and seems quite attractive. However if you want to use the results for publications you need a $35 per month personal academic subscription (or your institution to buy a site license). I guess you tend to get what you pay for.


Help identifying this bird from Southern Brazil I've seen a few of these birds at my university located in the extreme south of Brazil.

I noticed they usually stay on wet areas and like to eat small critters, such as worms and young tadpoles (I'm not completely sure about the last one).

I also noticed they usually stay alone in a particular area or, at maximum, two in the same location.

Also, here we also have many Southern Lapwings, which are in the breeding season, and one of them sometimes attacks the bird in the picture (for apparently no reason). When attacked by the Lapwing, this bird bristles the feathers of his neck and just dodges the Lapwing's attacks.

Does someone know what bird is this?

P.S.: Sorry for the bad picture. I couldn't get closer to it.

That is Syrigma sibilatrix, the whistling heron. In Brazil we call it "maria-faceira".

Here is Syrigma sibilatrix page in Wiki Aves ("aves" is birds in Portuguese): http://www.wikiaves.com.br/maria-faceira

Wiki Aves is by far the best source for birds in Brazil. It is a very well documented and reliable source, maintained by great ornithologists.

PS: Regarding the Southern lapwings: they are not really attacking, they are just trying to drive off the intruder. And there is a reason: the lapwings nest on the ground. I was "attacked" by them several times (I'm from the Southern Brazil), when I inadvertently approached their nest.


What determines the shape of the center-surround receptive fields of retinal ganglion cells? The wikipedia article about receptive fields of visual system tells us the following:

  The receptive field is often identified as the region of the retina where the action of light alters the firing of the neuron. In retinal ganglion cells (see below), this area of the retina would encompass all the photoreceptors, i.e., all the rods and cones in the retina.

Then it shows some pictures

I understand the part where it says that the neurons firing increases as we put light on the center of the receptive field (for ON center type) and etc.

What I'm not sure about is the location of this circle; where is this circle that we put light on?

What I think might be the answer is that, as the quote says, the circle is the area of retina where we have the rod/cone shaped photoreceptors.

So this means that, for every ganglion cell, the photoreceptors connected to it are always shaped like a circle?

The center-surround structure is created by the horizontal connectivity of the horizontal cells (Periman et al., 2012)  that receive input from multiple photoreceptors (Fig. 1).

Fig. 1. Retinal patch showing the connectivity between a horizontal cell and photoreceptors. Source: Harvey Mudd College

The horizontal cell passes on the congregate output to the bipolar cell, which in turn drives the retinal ganglion cells (RGCs) that send their axons to the optic nerve and send the signal on its way to the brain.

The photoreceptors are connected in two concentric circles to the horizontal cell. When light stimulation of the inner patch (center) evokes an excitatory response in the RGC, and the outer circle (surround) inhibits this response, the receptive field is said to have an ON-center configuration. In the reverse scenario, it is OFF-center (Fig. 1). This center-surround configuration is one of the first visual processing steps in the visual system and enhances contrast in the perceived image.

Fig. 2. ON and OFF center-surround receptive fields. Source: Brain Connection

Reference
- Periman et al., Webvision. The Organization of the Retina and Visual System. Utah


Has anyone yet figured out how sensory signals for eyes and ears are encoded by our organ into electrical signals? The most obvious way to give sight to blind and hearing to deaf is to give them a replacement organ for these. In order to do that we would need to understand how our eyes and ears encode sensory information into electrical signals which then go into the brain. My question is, how close are to understand this mechanism at this time?

I think the encoding is quite well understood, and in fact there are artifical cochleas available for deaf people: https://en.wikipedia.org/wiki/Cochlear_implant
For retina replacements, I think the hurdle is establishing the connections from any device to the nerve.  There are roughly 120 million rods and 6 million cones in the human eye. (Per Wikipedia: https://en.wikipedia.org/wiki/Photoreceptor_cell )  These connect to about 1.2 million optic nerves, so making the proper connections would seem to be a non-trivial matter.


What does (deaths / (resolved + deaths)) describe in an emerging epidemic? It would seem in a emerging epidemic, where the time to resolve a disease is long, an evaluation might be used such as:

(predictive mortality rate) =  (deaths) / (deaths + resolved)

Is this a standard metric?  And if so what is it called?

It would seem that this kind of metric would be a predictor as to the ultimate mortality rate, unadjusted for treatment advances. The intent is to describe the demonstrated mortality of those who have acquired the disease, without influencing of the number of people who have acquired the disease.  This would be helpful where R0 is large and/or Specific Interval is small. However I cannot find references to a metric similar to this.  Pointers appreciated.

The problems with the measure you've proposed have been addressed on MedicalSciences.SE:

https://medicalsciences.stackexchange.com/q/20970/8728

The short version is that this measure isn't very informative while there are unresolved cases, because it ignores what is known or expected about those unresolved cases, and it is not a standard measure.

In the long run (when almost all cases are either recovered or dead) it approaches the case fatality rate because the denominator of (resolved + deaths) becomes equal to the total number of cases. Until then, it doesn't tell you much at all.

You could track the case fatality rate over time based on time of initial diagnosis to look at effects of new treatments.