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Have there ever been "half-twins" who were halfway between siblings and twins?
Have there ever been two human siblings who were 75% or more genetically related?

Yes.
A case of semi-identical twins was reported in 2006. These twins share 100% of their maternal alleles and 50% for their paternal alleles. It's hypothesized this arose from a double fertilization of the egg, followed by the formation of two 46XX/46XY twins.
Another hypothesized mechanism of twinning involves the fertilization of a polar body (essentially when the egg divides prior to fertilization; polar bodies are a normal part of meiosis, but aren't usually able to b fertilized). This would give the twins the same maternal chromosomes, but different paternal chromosomes. However, this type of twinning has not yet been observed.

Though your question doesn't make sense to me, I believe the answer is Yes. See the following paper about "sesquizygotic" twins:
Gabbett, M.T., Laporte, J., Sekar, R., et al. 2019. Molecular support for heterogonesis resulting in sesquizygotic twinning. New England Journal of Medicine, 380(9):842-849.

Sesquizygotic multiple pregnancy is an exceptional intermediate between monozygotic and dizygotic twinning. We report a monochorionic twin pregnancy with fetal sex discordance. Genotyping of amniotic fluid from each sac showed that the twins were maternally identical but chimerically shared 78% of their paternal genome, which makes them genetically in between monozygotic and dizygotic; they are sesquizygotic. We observed no evidence of sesquizygosis in 968 dizygotic twin pairs whom we screened by means of pangenome single-nucleotide polymorphism genotyping. Data from published repositories also show that sesquizygosis is a rare event. Detailed genotyping implicates chimerism arising at the juncture of zygotic division, termed heterogonesis. opens in new tab, as the likely initial step in the causation of sesquizygosis.

It's possible this could have resulted from two sperms fertilizing one egg!

Probably, yes.
According to this paper, siblings have a mean of 0.50146 relatedness with a standard deviation of 0.03761. This means that this is an event which is 0.25/0.03761 = 6.6471683063 standard deviations above the mean, a near-7-sigma event. This occurs once in 66,937,665,852 (67 billion) events. However, there have been around 100 billion human births. This means that yes, there have probably been humans siblings who are closer to twins than normal siblings.
(This assumes there is no kurtosis causing platykurtic behavior.)
There is a 78% chance that this has happened at least once for every 100 billion human siblings pairs, or about about 1.5 times in human history assuming there have been about 100 billion unique sibling pairings.

Your source belongs in the question, as evidence of an attempt to answer your question is required on this site.

@anongoodnurse Where is that rule written for this site? (Genuine question, I can't find it.)

https://biology.stackexchange.com/help/how-to-ask

There's also this: https://biology.stackexchange.com/help/self-answer

I think the logic needs to be expanded here. The one-in-67-billion event is between two siblings, not between all humans. You'd need to account for the distribution of sibling counts (e.g. an only child doesn't count, two siblings only count as one pair, but four siblings create six pairs).

@Darlingtonia Yes, exactly. I don't expect great data to exist on this for early humans, but I would imagine the average number of children to be above 3.


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Why is the expected time to coalesce the same as the ploidy times inbreeding effective population size?
The expected time to coalesce, in generations, is the same as the ploidy (e.g., 2 for humans) times Nef, the inbreeding effective population size, under coalescent
theory. Why?
Both ploidy * Nef and the expected time to coalesce are equal to the summation from generation $t=1$ to infinity of (t(1-((1/(ploidy * Nef)^(t-1) * (1/(ploidy * Nef)))))), or written more prettily:
$$\sum_{t=1}^{\infty} t\left(1-\left(\frac{1}{\text{ploidy} \cdot N_{ef}}\right)^{t-1} \cdot \left(\frac{1}{\text{ploidy} \cdot N_{ef}}\right)\right).$$
Why, and what does it mean to have an "infinite" generation (in the summation)?
The time to the last coalescent (of two gene copies) is ploidy * Nef.
If you multiply this whole summation by the number of pairs of genes, the result is a new summation which represents the sum over generations of the probability that coalescence occurs in the t-th generation, or the probability of the first coalescence occuring within t generations.

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How does symbiogenesis explain reproduction of organelles along with the cell?
Symbiogenesis is an evolutionary theory that says that prokaryotes eventually evolved into eukaryotes (having multiple organelles and better structure) by forming symbiotic relationships with other bacteria that have been absorbed, or have entered the cell in an initially parasitic way.
My question is that when the individual bacteria have become organelles, what happens when the cell reproduces? The bacteria were individual entities with their own reproduction mechanisms before they became organelles. Do they still divide in their own way inside a cell (and are subsequently present in both halves of the cell when it is dividing itself), or does their division somehow get incorporated into the cell's own DNA?

I'm not sure about all organelles but mitochondria and chloroplasts are commonly used examples of independent devision in eukaryotic cells. They have independent DNA that forms separate mitotic spindles during division. Similar mechanisms likely existed for other organelles originally but the genetic material may have eventually been combined with the nuclear DNA for simplicity. This is a very simplified explanation but I think addresses the basic question.

Welcome to Bio and thanks for your answer. Could you cite references or other sources to allow users for background reading?

My impression is that other organelles like golgi and ER that are essentially contiguous lipid membranes split by fission in association with cytoskeletal components, independent of DNA. I'm looking and it appears that it mayalso occur by different mechanisms in different organisms.

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Are non-lytic viruses reproducing themselves in the host cell?
Non lytic viruses can cause cancers like the HPV. But aren't they reproducing themselves as they don't ruptures the cell. Or are they just not reproduced in enough numbers so that the cell keeps working. But if they stays in the cell and/or not reproducing how are other cells infected to cause a tumor? Just by normal division or within a stem cell?

You are conflating production of infective viral particles with lysis of the host cell. While true for some well-characterized bacterial viruses, like lambda, or T4, there are other bacterial viruses that can produce infective particles without lysing their host cell (e.g., M13, and related viruses).
Likewise, in mammalian cells there are plenty of examples where either an RNA virus (like the RNA-tumour viruses, also called retroviruses) where the viral genome integrates into the host genome, but can also produce infective viral particles. These viruses have external coats that include both proteins and lipid bilayer membranes (the viruses pinch-off, or bud, from the host cells' surface).
Many DNA viruses also integrate a copy of their genome into the host cells' genome following infection (e.g., Epstein-Barr Virus (it can cause mononucleosis), and members of the Herpes Simplex virus family that infect neurons and can cause chicken pox, or genital herpes).  Once you are infected with these DNA viruses your body is never rid of them, rather your immune system and cellular defence mechanisms "fight" the infection such that the titre of infectious viruses drops to nil, but you still have a reservoir of circulating antibodies that can be detected--and used if you are exposed again.

Do you think a tumor is growing due to viruses are replicated and leaves the host cell and infects another cell, or is it more likely that that hostcell creates a tumor by dividing himself again and again?

@Marijn it depends on the tumor, but frequently tumors grow clonally (although there may be multiple "starting" clones), wherein the initially-transformed cell multiplies and makes copies of itself. Remember, cancer is almost never caused by a single event - multiple things need to happen inside a cell for it to become cancerous. See the Knudson hypothesis.

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What kind of cell has the most different receptors?
All hormones and neurotransmittors has their own receptor. Now some of the cells has a few different receptors but others has many sorts of receptors. So what are the most receptive cells? Are that the some braincells?

I think this is difficult to answer. What is meant by "most receptive" ?  The number of receptors on a cell's surface is known only for a few well studied cases, and many cell surface receptors are not characterized at all, or have not even been discovered. And more receptors does not necessarily translate to a more "sensitive" cell, as receptor sensitivity can be modulated in other ways too.


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When touch and pain are caused by heat/cold or pressure how are the nerve cells triggered?
I suppose that when your skin is smoothly touched by any cold/heat or pressure we feel that because our AB cells notice this due to a kind of change in the nerve cell.
But when you touch something hot but not noxious how is that registered different from something what is cold or puts pressure on the skin. How works their mechanisms differently?
A step further is when due to heat/cold or pressure inflammation is started. I read that there are for each stimuly different receptors available. But what is the difference between an inflammation caused by heat/cold and pressure. How can heat create a different cascade of enzymes compare to pressure while both are inflammations and not adding any chemicals of themselves?

The receptors (and the sensory neurons) for different stimuli are different.


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How does the hypothalamus get the information out of the blood?
The hypothalamus is a very important nervecentre which checks continuously how many hormones neurotransmittors and other molecules and information (like temperature) are there present, so it can keep a kind of balance in our body. But how does the hypothalamus do this? Does he has so much different receptors on his membrane for each type of molecule one or does it do that in a different way?

First of all, there is not such a thing as "the" hypothalamic membrane. The hypothalamus consists of multiple nuclei, and each nucleus contains numerous cells (neurons and glia cells).
The mechanisms by which the hypothalamus senses hormone concentrations in the peripheral blood are rather complex. In recent years, considerable research has been done to elucidate the central mechanisms underlying thyroid homeostasis [6], which involve the regulation of TRH release from the hypothalamic paraventricular nucleus [1, 2]. Therefore, my following explanations are focussed on the control of TRH secretion, but similar considerations apply to other hormonal systems [7-9].
First, hormones have to be conveyed by special transport proteins across the blood brain barrier (BBB). In case of thyroid hormones, this is accomplished by tanycytes in the circumventricular organs [3]. They control the transition of hormones from the blood to the cerebrospinal fluid (CSF), and partly directly to glia cells via the transport protein OATP1C1. In glia cells thyroxine (T4) is deiodinated to form the more active hormone triiodothyronine (T3). T3 is then transferred to neuronal target cells via the transporter MCT8 [4, 5], where it exerts its homeostatic effects by inhibiting TRH release. Hypothalamic TRH secreting cells have, however, multiple afferent signals. In addition to thyroid hormones they include clucocorticoids, leptin, alpha-MSH, norepinephrine, cocaine and amphetamine-related transcript (CART), endocannabinoids, agouti-related peptide, neuropeptide Y (NPY), GABA, galanin and probably multiple additional signalling substances. This enables the TRH neuron to act as an integrator of energy homeostasis [1, 2, 6].
Of course, the TRH-secreting cells in the respective hypothalamic nuclei have receptors for all afferent hormones and neurotransmitters. Some of them (e.g. for catecholamines) are located on the cell membrane, others (e.g. for thyroid hormones or steroids) in the nucleus.
As mentioned, similar considerations apply to other hormonal systems [7-9]. Recent research suggested e.g. the existence of a receptor-mediated transport system, which conveys insulin trough the blood-brain barrier [9].
1: Joseph-Bravo P. Hypophysiotropic thyrotropin-releasing hormone neurons as transducers of energy homeostasis. Endocrinology. 2004 Nov;145(11):4813-5. PMID: 15489313. http://www.ncbi.nlm.nih.gov/pubmed/15489313
2: Joseph-Bravo P, Jaimes-Hoy L, Charli JL. Regulation of TRH neurons and energy homeostasis-related signals under stress. J Endocrinol. 2015 Dec;227(3):X1. doi: 10.1530/JOE-14-0593e. PMID 26527565. http://www.ncbi.nlm.nih.gov/pubmed/26527565
3: Rodríguez EM, Blázquez JL, Pastor FE, Peláez B, Peña P, Peruzzo B, Amat P. Hypothalamic tanycytes: a key component of brain-endocrine interaction. Int Rev Cytol. 2005;247:89-164. Review. PMID 16344112.
https://www.ncbi.nlm.nih.gov/pubmed/16344112
4: Kersseboom S, Visser TJ. Tissue-specific effects of mutations in the thyroid hormone transporter MCT8. Arq Bras Endocrinol Metabol. 2011 Feb;55(1):1-5. PMID 21468514.
http://www.ncbi.nlm.nih.gov/pubmed/21468514
5: Bernal J, Guadaño-Ferraz A, Morte B. Thyroid hormone transporters—functions and clinical implications. Nat Rev Endocrinol. 2015 Jul;11(7):406-17. doi: 10.1038/nrendo.2015.66. Nat Rev Endocrinol. 2015 Sep;11(9):506. PMID 25942657.
http://www.ncbi.nlm.nih.gov/pubmed/25942657
6: Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front Endocrinol (Lausanne). 2015 Nov 20;6:177. doi: 10.3389/fendo.2015.00177.  PMID 26635726.
http://www.ncbi.nlm.nih.gov/pubmed/26635726
7: Thon M, Hosoi T, Ozawa K. Possible Integrative Actions of Leptin and Insulin Signaling in the Hypothalamus Targeting Energy Homeostasis. Front Endocrinol (Lausanne). 2016 Oct 20;7:138. PMID 27812350.
http://www.ncbi.nlm.nih.gov/pubmed/27812350
8: Herman JP, Tasker JG. Paraventricular Hypothalamic Mechanisms of Chronic Stress Adaptation. Front Endocrinol (Lausanne). 2016 Oct 31;7:137. PMID 27843437.
http://www.ncbi.nlm.nih.gov/pubmed/27843437
9: Blázquez E, Velázquez E, Hurtado-Carneiro V, Ruiz-Albusac JM. Insulin in the
brain: its pathophysiological implications for States related with central
insulin resistance, type 2 diabetes and Alzheimer's disease. Front Endocrinol
(Lausanne). 2014 Oct 9;5:161. doi: 10.3389/fendo.2014.00161. PMID
25346723,
http://www.ncbi.nlm.nih.gov/pubmed/25346723/


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How to get white bioluminescence?
So I was wondering if it is possible to get white bioluminescence. Actually, I have heard dinoflagellates that produce blue light when there is some disturbance in the water. So I was wondering how to make this blue as white. If it works inside a flask, that is also fine because it should officially work.
So there are a few certain species of dinoflagellates that produce blue light when there is a disturbance in the oceans they live in. It is something like this:

Now, they regularly live in calm seas, and when there are small disturbances like waves or a person walking through them, they start glowing. This is one of the most stunning examples of bioluminescence.
I was planning to make use of these dinoflagellates. I was planning to put them in a black box, with a glass pane at the bottom. In the black box, there would be a tiny and slow motor to simulate the disturbances. Now, my only question is how to make these dinoflagellates glow white instead of blue. Are there any certain species of dinoflagellates that glow white that I am not aware of, or do I have to add any certain chemicals to the water to make them glow white (Please give a chemical that won't hurt the dinoflagellates), or is there any certain food to make them glow white, or should I add any changes to the glass pane to make the blue light look like white light?
BTW here is an image of the model I am talking about:

It's not perfect but is just a base model. Thanks in advance. If you need any other information, please comment.

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Identification of a spider — South India
I found this spider jumping around in my garden , to describe it is blue and black . I noticed that it has strong front legs and a pointed posterior , it has blue designs on a black body . I live in South India ,ie , a tropical region . It is approximately 1cm in length .

was that two-three mm?

This looks to me like Thiania bhamoensis (Metallic Blue Jumper), whose species distribution includes India. It has a notably pointy abdomen, as you noted, and the listed size range appears to be consistent as well.
I do not believe this is Phidippus audax due to the colour inconsistency (only the chelicerae are blue) as well as the fact that the known species distribution lies entirely within North and South America.

Yes , seems like a female since , it's greenish .The body design patterns and habitat all checks out .


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To which ungulate species does this tooth remainder belong?
Found on the beach in Çanakkale, Turkey.

I have found a lot of these, but this is the first one that has parts like long teeth. My other findings have sometimes 4, sometimes 6 tubes. Very solid, stone-like objects. Is this from a marine animal or is it a non-living formation, I wonder.
Below image is for scale in centimeters.

View from top and bottom

Other similar findings without teeth-like parts

Additional images:

Thanks. As I thought from just the side photo in your original post, it looks like a molar of some ungulate. I don't know anything definitive but I'll try to look into it a bit more for you. (you will find other similar photos on our site -- so do a search if you haven't already)

Thank you. Interesting, I always find these things on the beach. I did not figure out the reason. I'm waiting for your further explanations.

Whales, dolphins, seals, etc. are marine ungulates. When they die, they are fed upon and what's not edible/eaten/disintegrated sometimes makes it to shore. Your specimens are lovely. The best I ever found was a seal molar. One.

I have 30 - 40 items like these, but I am still not sure that there is marine remnants in them. I checked seal and dolphin molar after your comment, but they are very different than mine. You are lucky.

@anongoodnurse right you are about the marine ungulates. However, just cetaceans (e.g., whales and dolphins) are of the Ungulata clade. Seals are order Carnivora and are not considered part of Ungulata. However, all ungulates and the extant members of Carnivora are lumped together in the larger Ferungulata clade.

@turin I'm in the throes of final exam season at my university with much grading to do -- I'm unlikely to explore this topic further for the time being. I hope someone else can help you narrow further!

@theforestecologist no problem. Good luck with your exams.

Its definitely not a marine mammal, just based on size and general configuration.
those convoluted ever growing teeth are pretty diagnostic of non-cetacean ungulates.
Just based on the pattern I would say bovidae, but that does not narrow it down much in turkey, the H shaped central portion is fairly diagnostic of bovidae. However you have several antelope species not to mention domesticated animals that each would fit that category.
I suggest changing the title to ask for ungulate tooth identification. You need someone specialized in mammalian teeth to narrow it down to species. if you can add more shots of the tooth crown (the complex ends like those below) that is the part most useful for identification. See the examples below. The more you have the better.

Source

Thank you @John. I will change the title as you suggested and add more tooth crown images.

I have added new images. Just for your information.

Sheep or goats teeth.
As it was found at the edge of water and may be from drowning, I would predict that it is much more likely to be from a sheep, as goats are so very much safer around water.

Image from:
"Enamel hypoplasia in molars of sheep and goats, and its relationship to the pattern of tooth crown growth"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403278/
But really I know because I was a farmboy.

A pic from the top is better than one from the side, a side shot is not very diagnostic in mammals.

I think he's basically right, because: which animal has been cooked in 20,000 BBQ's over the years on beaches in Turkey? sheep an goats. statistically, its 20 times more likely to be a sheep than another common ungulid because of the meshoui type tradition.


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How many times is a single strand of mRNA translated into a protein?
In other words, is the mRNA damaged or somehow "marked completed" in the translation process? Or does it pop out the other side of a ribosome ready to be translated again? If the latter, how many copies of a protein result from a single strand of mRNA?
Thank you in advance!

A relevant question, but the topic is covered in general textbooks in the section on translation. On the web try searching for polysomes and then think about what their existence implies. A search for mRNA half-life will reveal the answer: “It depends on the mRNA and the organism.”

Thank you for the pointer, @David. With your assistance, I think I was able to answer the question.

I'm answering my own question for the benefit of anyone else who might be wondering about this. (Please note that I'm just a programmer, not a biologist, but thanks to David's comment, I was able to come to what I think are some correct conclusions.)
A single mRNA strand can be translated more than once, even more than once at the same time. The polysome that David references is a group of two or more ribosomes all attached to the same mRNA strand, all working on translating it simultaneously.
I believe that it may be possible for a single mRNA strand to be translated hundreds or even thousands of times. My reasoning for this is that a virus injects one copy of its RNA into a cell, and from this one copy, new viruses are replicated until the cell bursts. This "burst size" varies by host cell and virus, but it can range from hundreds to tens of thousands or more. While there are still a lot of things I don't understand about the specific steps the RNA goes through (are there intermediary copies made from which multiple mRNA strands are produced?, etc.), it still seems to suggest that a single strand of mRNA can be translated a lot.

Note that for translation and transcription are two different things. Transcription is copying the RNA into new RNA. Translation "reads" the RNA and makes protein. Your third paragraph confuses the two. In the case of SARS-CoV-2, the RNA genome (+ sense single stranded (+ss) for this virus) is the same as a mRNA in a cell, but it is copied into a double stranded RNA and then made into a new +ss for packaging and translation. see here

Thanks for the comment, @bob1. What I meant by that remark was that I didn't know if the viral RNA was the actual thing being translated or not. Conceivably (at least to my naive mind), the "master" RNA could first be transcribed into intermediary copies which are then translated. I reasoned that this might allow thousands of copies of a virus to be replicated even though a single mRNA strand can only be translated a smaller number of times. I was trying to acknowledge the holes in my knowledge that would invalidate my earlier, simpler logic.

See the diagram in the paper that I linked. It shows that the incoming COV-2 is partially translated to produce a replication and transcription protein which forms a complex with the RNA, which then produces dsRNA and goes on to produce ssRNA for both translation and viral progeny.

@bob1, Wow, there is a lot to unpack there. Thank you for the help and pointers!

The  question asks about mRNA, but your answer seems focused on one particular viral RNA. It fails to address the differences in mRNA half-lives between species (eukaryotes v. prokaryotes) and within species. Nor does it address the mechanism of mRNA degradation. I suggest you need to do more reading if you really wish to understand the answer to the question you have asked. Have you searched this site to see if the topic has been covered previously?

@David, yes, I came to this site specifically hoping to find and answer to that question, and when I did not, I asked it myself. I am unsure what you mean when you say my answer is focused on one particular viral RNA. I refer to viral RNA only to show that it must be possible for RNA in general to be translated many times, though clearly there are many holes in my knowledge, including that I do not yet know what differences there are between viral RNA and mRNA. I have not marked this as the answer for that reason. Perhaps someone more qualified than I will be so kind as to write an answer.


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Trying to identify a Spider found in rural Missouri, USA
I am trying to identify this spider found indoors in a rural area near Kansas City, Missouri. I cannot recall seeing one like it in my 14 years of living here but I have now found 3 inside in the past week. The one in the attached photo I found in my bed when I woke up. I would estimate that it is 2-3cm, legs included.

Sorry to be so long; I just came across this question.
There are a couple of clues as to the identity of your spider - the two-toned color pattern, with mahogany legs and cephalothorax, and grayer abdomen being the most important one.  The other is that you found it in your house.  It's been my experience that these spiders are commonly found in houses at two times of year - the adult males in the spring, and the adult females in the fall.
The most important clue is hard to see in your original photograph, but I took the step of lightening it with the Photo app, to let me see the front of its cephalothorax (see below)

What you can see is that the eyes are arranged in a fairly straight line across the fairly flat face.
The other locally common two-toned (red-and-white or red-and-grey) spider, Dysdera crocata, has a very different face.  Dysdera is a streamlined, 1950s style racing spider, with forward projecting chelicerae and a pointed-looking front end (see below)

You'll notice the pointy front end, and the way the eyes are arranged in a tighter, almost clustered, curved line.
Your spider is one of the Flat-faced Sac Spiders in the genus Trachelas.  I'd say it was probably T. tranquillis, but there are a number of western species, and I'm not sure where the ranges go to.
Here's a reference photo of a male Trachelas species to compare with yours:

Here's the Bug Guide link to Trachelas:
https://bugguide.net/node/view/26206
Note that colors and light/dark shades are not necessarily going to be the same in photographs as in real life, even above that Trachelas (like Dysdera) shows a range of color from white to grey abdomen and from red to almost brown cephalothorax and legs.

Excellent answer.

It might be this one:Dysdera crocata
(Woodlouse Hunter)
https://spiderid.com/spider/dysderidae/dysdera/crocata/
more pictures of this spider from different places in the link below.
 https://spiderid.com/spider/dysderidae/dysdera/crocata/pictures/
I know this is a bit thin as an answer but i know very little about spiders in the US,if anybody has knowledge about this spider please feel free to add the information.

I think it’s Metaltella simoni. Check it.

Image from Wikipedia

We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.

Hi @Mistake, I've added an image to your answer. If you can find a better image, and perhaps a reference that would be nice.


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Aren't tortoise bones fused with the shell? How did this tortoise (in the post) survive without it?
I've just read this story about a tortoise that lost a good portion of its shell in a forest fire here in Brazil and got a 3D-printed prostheses.
Here's the picture of it:

The way it looks like, it seems there were no bones fused with the shell, and that the shell was just a thin layer hovering over its body below, like the bones were entirely contained inside the body and you could just remove the shell.
What really happened here?
Were all the bones burned until they all fell off?
Wasn't the spine supposed to be there to?
How could this be even survivable?
Or maybe in this species the shell is not fused with the bones?
Thanks!

The shell has several layers. I believe this specimen has lost the kreatin scutes (very painful!) and the inner layer that has become visible is the bone layer.


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How do scientists create an environment that favors the selection of a microbe with higher production of a certain enzyme?
Let's say you want to create a strain of bacteria that is resistant to heat. You expose all bacteria to high heat and those who have mutated to survive this heat will be the survivors. Then you allow this group to reproduce and continue to gradually raise the heat until you are left with a population of highly heat-resistant bacteria.
Let's say you wanted to do the same but instead of selecting heat resistance you want to select for the production of a certain enzyme, for example amylase. How do you manipulate the environment so that only those with higher production would survive?
One thing that comes to my mind would be introducing all the microbes to an environment where the substrate they need to break down to survive is scarce. So the specimens that would create the most enzymes to break it down would survive. But then all of the other specimens would benefit too because the enzyme from the high-producing specimen would also give them the substrate they need to survive - so it would not be isolated but rather would 'carry the entire population on its back' (I have no idea whether this is how it would work, this is an idea)

Interesting, has there been a case where the enzymes did change shape to adapt? Also, wouldn't the poor enzyme producers also use up the product of the enzymatic reaction and therefore the high-producers won't be isolated?

No. Most substrates for growth have to be taken up by the cell before being metabolized. The lac operon mentioned by @user338907 contains a permease gene for this purpose.

@user338997 ? Lac permease doesn’t transport lactose into the cell?

@David Are you saying enzymes are working within the the cells? I'm pretty sure some enzymes are excreted to the environment where they break down their substrate. To clarify what i meant in the above comment i'll give an example: let's say 1 High-Amylase  producing microbe is put in an environment of scarce starch - and survives thanks to its ability to make the most out of the scarce nutrients around it - the problem is the glucose it will produce will also be available to the Low-Amylase producing microbes - who didn't contribute to survival whatsoever but still get to live on

I suggest you do a little reading on this yourself. Some substrates like proteins or polysaccharides are too large to be taken up by cells so they do excrete extracellular proteases and glycosidases to break them down into smaller molecules that can be taken up and metabolized internally. Ok, starch will not be permeable, but I was considering the general situation. If you need a group of enzymes to metabolize starch, other bacteria can only hitch a ride on the extracellular ones, which is no use if they lack the intracellular ones.

But if we take glucose for example, isn't glucose the final form of sugar needed for cellular respiration? And if there is a secretion of enzymes to the extracellular environment, and the activity of these enzymes results in free glucose in the extracellular fluid environment, then it seems these bacteria could soak it up and hitch a ride., preventing natural selection (they weren't the fittest but they were always around the fittest)

@Anonymir, It's really going to depend on your organism, the phenotypes you're selecting for, and on the goals of your experiment. I don't think there's one methodology that will work in all circumstances. As for the amylase example, I would first ask why you want to select for this? Are you planning to harvest an enzyme for specific applications downstream? Is maximizing yield important? Or are you doing simply interested in experimental evolution via positive selection?

I am interested. In the fermentation industry they use mold to make many foods taste sweet (thanks to amylase) and savory (thanks to protease) and in japan where mold-fermentation is common, they specially select spores for genetic qualities such as amylase production - in order to create the best taste of the final product. This interests me and i wonder if the process can be automated or made more efficient.


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Why Can't the passage of acquired behavior be considered acquired inheritance?
While reading about a cross-fostering experiment conducted on Male California mice and Peromyscus californicus, I came across the fact that the behavior acquired by a generation of mice due to foster-parents is transferred to the next generation as the next generation also gets the same amount of parental-care and attention as the first.
As we can say that behavior is also a character in a way (and is influenced by genes as well as environment), wouldn't the transfer of such behavior over time (if the mice bred by foster parents were positively selected for) be considered 'inheritance of acquired characters?'

Yes, a behaviour is definitely a phenotypic trait.
Some acquired trait (typically behavioural traits but not only) can indeed be transmitted to a few future generations. But make sure to understand the mechanism. I can think of 3 different mechanisms:

epigenetics
covariance between parent fitness and offspring fitness (within one genotype and one environment) typically due to to parental care.
Transmission of tradition (in the broad sense). A tradition is also sometimes called a meme.

One will need a link to the specific paper you are reading to know what mechanism is in play in the study you are reading.


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Why Isn't mineral transport in xylem multi-directional?
According to our textbook, Xylem transport is only unidirectional while transport through phloem is multi-directional.
But minerals are taken up by xylem from the surrounding tissues actively, and even though they flow along with the water column, they are actively unloaded near 'sink' sites. Sometimes, minerals are also taken up from aging parts and transported to growing areas of the plant. Then shouldn't mineral transport through xylem be multi directional?
Please Explain

Physics: movement from high concentration (soil/roots) to low concentration (air/stomata) + surface tension properties of water and capillary action...

Movement through the xylem is powered by transpiration of water through stomata in leaves and a sustained tension in the xylem itself due to water's cohesive properties.  See: https://en.wikipedia.org/wiki/Xylem#Cohesion-tension_theory
The "multi-directional" transport you are talking about does not actually occur in the xylem.  Minerals have to be transported OUT of the xylem before they can move other ways.  Transport THROUGH the xylem is uni-directional; transport OUTSIDE of the xylem can be multi-directional.

Movement of water through the xylem is caused by root pressure, capillary action and mainly via transpirational pull. All these factors results in a net upward movement of water molecules through the xylem vessel.
In the phloem, movement is multidirectional because of the presence of companion cells. These companion cells have many mitochondria that can carry out aerobic respiration to provide sufficient energy for active transport of substances in the desired direction.
The xylem vessel has no protoplasm, hence water cannot move due to active transport — hence it can only go upwards.

the movement is not multi-directional because the minerals that are transported in the xylem vessel do not need to go anywhere else apart from going up the plant for the leaves to use them this includes the water carried by them.All the leaves are in one direction (which is up the plant)therefore there is no need for the vessels to have a lot of directions which would slow down the plants processes are rather avoided.

Welcome to the site!  Would you ind adding some references for this, please?


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Why guard cells need to turn malate into postassium malate to become turgid?
According to the Active Potassium Transport Ion concept given by Levitt et.al, stomata open due to turgidity in guard cells. It seems that guard cells turn the starch produced by photosynthesis into malate (which is a stable solute and should increase the osmotic pressure of the cell) but then go on to invest energy to exchange the hydrogen ions of malate with potassium ions.
Thus guard cells basically invest energy to turn malate into lots of potassium malate (so that water will enter due to increase in osmotic pressure), but why should such a process evolve if they can become turgid by just producing lots of malate?


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What is the difference between the glycolate pathway and photorespiration?
I came across the definition of photorespiration as a process that forms CO2 from O2 in the presence of light. However, the CO2 is released only when the plant cell undergoes the conversion of glycolate to PGA, i.e in the glycolate pathway.
Most textbooks seem to use the term photorespiration and glycolate pathway interchangeably, but then they seem to say that the glycolate pathway evolved to regain the energy lost in the formation of glycolate, whereas photorespiration is wasteful. How is this possible?
Shouldn't photorespiration be a conservation pathway as well? It is trying to regain lost energy from glycolate, isn't it? or Have I got the two terms completely confused?
Please Explain

I don't even think that photorespiration is wasteful. It seems to me like plants generate CO2 for photosynthesis when amount of CO2 in environment is less.

Can you actually describe what process according to you is photorespiration?

As per what I have studied, I can define photorespiration as the process in which RuBisCO uses O2 and produces CO2 when amount of Oxygen in environment is higher than that of CO2. But, though it uses more ATP and also produces ammonia,  it seems to me like plant is generating CO2 for its own benifit i.e. photosynthesis. So it does not seem totally wasteful.

That would actually make some sense as the feedback for that would be less photorespiration and more photsynthesis due to increase in CO2 concentration. So in those terms glycolate pathway is just a pathway for photorespiration, right?

From http://plantsinaction.science.uq.edu.au/book/export/html/64 "Wang and Waygood (1962) had described the ‘glycolate pathway’, namely a series of reactions in which glycolate is oxidised to glyoxylate and aminated, first to form glycine and subsequently the three-carbon amino acid serine." So, it says that glycolate pathway is just a part of photorespiration in which glycolate is metabolized.

I appreciate the attraction of the idea that Nature is too smart to allow wasteful processes, but the suggestion made by @another 'Homo sapiens' just won't wash. I know of no evidence that the concentration of CO2 in the atmosphere varies appreciably, and if it did I can't see that the production of CO2 by plants would affect it significantly. And I imagine there have been many previous attempts to rationalize this inconvenient truth.

@David Amount of CO2 doesn't vary appreciably, but that of O2 does. Because RuBisCO cannot choose O2 instead of CO2 just because % of O2 has risen by 0.001% or something. By photorespiration, plant not only produces CO2, but also consumes O2 i.e. it increases amount of CO2 two-fold, which might affect it significantly. Also, when it comes to smartness of nature, there can be a long debate about why evolution gave rise to photorespiration and why plants still use C3 cycle.

The simple answer to the question posed in the title of the question is as follows. The glycolate pathway is the series of reactions converting phosphogycolate to reusable carbon intermediates + CO2. Photorespiration is the combination of two processes:

The oxidation of the enodiolate intermediate on Rubisco to phosphoglycoate + 3-phosphoglycerate.
The processing of the phosphoglycolate produced by the glycolate pathway.

You cannot use the two interchangeably as there is no respiration (use of oxygen) in the glycolate pathway. The glycolate pathway is just the latter part of photorespiration. I'm not sure what the text books are that confuse the two, but Stryer presents this quite clearly in Figure 20.6 and 20.7 at http://www.ncbi.nlm.nih.gov/books/NBK22344/#A2795.
I am not familiar with the term "conservation pathway" in your final question. I would call the glycolate pathway a "salvage pathway" (although this term is more commonly used for recycling the skeletons of the products of macromolecular, esp. DNA, degradation). It does not salvage all of the carbon skeleton of phosphoglycolate as some carbon is lost to the atmosphere as CO2.


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What is the speed of human immune reactions?
It's easy to find general lists of immune systems: innate/adaptive, complement, phagocytes, B/T cells, and so on. Annoyingly, they are very skimpy on quantitative information regarding the speed of these reactions and that matters a lot.
I'm wondering how long after for example bacteria entering the body, do immune systems kick into action? I'm guessing the complement, clotting, and local phagocytes are the fastest but I could not find actual times required.
I found speeds for some immune systems but not for most. This recent recent study on the immune reaction against SARS-CoV2 has a rough time course with dendritic cells early and antibodies from activated B cells in weeks. This more detailed time course, also for Covid, shows the IgM peak at around 2 weeks ("The majority of patients appeared to have seroconverted by day 14").
Ok, but what about all the other processes? How fast can an innate immune cell hone in via chemotaxis, how fast are T killer cells on the scene upon viral infection, how fast is the complement or clotting cascade really, how does antibody production vary in speed between triggers and individuals? I hope you can point me towards any data that might shed light on this. I appreciate any leads.

As a possible lead: hit-and-run viruses, such as those related common cold, give up before the the adaptive immune system kicks in. This is how they avoid forming immunity in the hosts. And this is about a week time.

Don't forget allergic reactions.

Thanks, Roger. That's very interesting.
@DK: I guess immune overreactions = allergies often come in after the real defense work is done, don't they?

I just point that out because your post was talking in terms of weeks, whereas allergic reactions take minutes

Although it's focusing on mechanical injuries, Time Course of Immune Response and Immunomodulation During Normal and Delayed Healing of Musculoskeletal Wounds provides a number of time points for specific immune responses along with references. That should get you started.
This article is looking specifically at musculoskeletal injury situations rather than infections, and suggests that both the types of cells/responses involved and their timing can vary in other situations or infections. For the injury situations, they summarize:

Such injuries are associated with local inflammation and typically
heal in the following order of events: inflammatory phase [0–7 days
post-injury (dpi)]; regeneration phase (4–14 dpi); and remodeling and
repair phase (14–>28 dpi).

Answers shouldn't entirely depend on outside resources. You certainly don't need to recapitulate the whole reference, but can you include enough content so your answer would stand alone?

I see your point, but in this case the OP seems to be asking for so much detail that a partial recap or summary would be insufficient. The article is a review, so is already digested/summarized.  I'll try to add some more to the answer.


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In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis?
Ketogenesis pathway maps show acetoacetyl-CoA converted to HMG-CoA and only then to the first ketone body acetoacetate. Why this detour instead of directly hydrolyzing off the CoA to get there in a single step? Is it possible that some ketone bodies are made by direct conversion? The enzyme acetoacetyl-CoA hydrolase to do this job exists and can be found in rats.

I've been Googling this a bit and the trail seems to run dry for the acetoacetylCoA hydrolase after about 1980. I suspect that there is something fishy about it. I notice that the acetyCoA hydrolase turned out to be an alternative activity of the thiolase, and wonder if it is something similar and is not active under the appropriate physiological conditions. There aren’t many biochemists around these days that know about this stuff, and I don’t rate your chances of finding one on this list, but I hope I am proved wrong. Fair question, though.

Thanks David for researching this. Too bad we both came up short so far. A future research project hopefully.

The answer I would give here is because HMG-CoA is a key intermediate not only in ketogenesis but also in cholesterol (isoprenoid) biosynthesis. The 'starting intermediate' may be considered to be  HMG-CoA for both pathways. (An example of what Lehninger called 'the molecular logic of living organisms' perhaps)

After further checking, I found that HMG-CoA synthase rather than HMG-CoA lyase is the enzyme which is regulated. This enzyme also plays a vital role in cholesterol synthesis. HMG so produced can either form mevalonate, which leads to cholesterol synthesis, or form acetoacetate. Therefore if acetoacetyl CoA were directly hydrolyzed, it would short circuit the cholesterol pathway.
The enzyme can be regulated by succinylation. Its synthesis can be regulated by several transcription factors. Evidence suggests that hormones play a role in each of these processes. References: Harris, et al., Journal of Investigative Dermatology 114(1) 83-87 (2001); F.G. Haggart, Biochem. J. Mar. 5, 338 (pt. 3) 569-582 (1999); Quant, P.A. et al. Eur. J. Biochem. 187, 169-174 (1987)
Most Biochemistry texts today list HMG-CoA as the source of acetoacetate with no mention of direct hydrolysis of acetoacetyl-CoA. This suggests that if direct hydrolysis of acetoacetyl-CoA does occur, it probably plays a very minor role.

If you wish to post a second answer to a question it should stand alone and not refer to a first one you have (or should have) reservations about. You are able to edit or delete any answer you post, so I would suggest you do this to consolidate them into a single answer, comprehensible in itself. (And as one of the few people who answer questions on biochemical metabolism I’ll have a look at it when I have a moment.)

Since you now seem to be posting using two separate accounts, you may find this information on merging accounts to be of interest ...

I believe it is related to the fact that the enzyme HMG-CoA lyase is regulated by glucagon (activates) and insulin (inactivates). It appears that this extra step was added so the pathway can be hormonally regulated.

Welcome to Biology.SE! I could see this as a mechanism for maintaining a step, but I don't see how adding an extra step to an existing pathway could be selected for especially to allow future regulation. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion.  ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and [edit] your answer accordingly. Thank you!

This is a good example of how to format references.


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Does food really give our bodies the energies that we have determined by burning them in the lab?
You are likely to have come across numbers like sugars 17kJ/g (4kcal/g) as the energy supposedly available to our bodies after eating. Yet these values have been determined using very artificial means, typically lighting up food with a red hot iron in a steel chamber at high oxygen pressure.
Many historic energy values have been proven wrong in the past. For example, salad leaves had zero calories in many historic energy tables before we realized that bacteria in our gut can break them down and we in turn can break down bacterial products, gaining back part of the chemical energy of the plant.
Are you aware of any research that has determined the energy value of different foods in more natural conditions, ideally in humans? I expect some calorie values to change from those determined by the bomb calorimeter, don't you?

I think there are two different things you are asking about.
The first is the standard enthalpy of combustion, which is indeed measured more or less as you describe. There's absolutely no problem with that, because the total energy released by the metabolism of glucose to CO2 is exactly the same as released by combustion. On the way down the energy slope you might even use some of it to make ATP and actually do some "work". There might be some small corrections needed (you run at 37C and not at 25C for example) but no matter which way you take, turning glucose and oxygen in carbon dioxide and water will release the same amount of energy. And remember, we need a lot of this energy just to keep warm, so the waste heat in metabolism is not really a waste.
The second part is a bit more complex, when you're talking about food. Here the bomb calorimeter part is a bit misplaced, because most foodstuffs will be analyzed using other techniques to determine the amount of carbohydrate, fat and protein. Then they'll do a calculation to get the number of calories in your food. This should get you quite close to the real number of calories, as stuff that's not digestable by humans is not counted. Regarding the salad bacteria: I'm not sure if they put it on the labels, but we know whether or not certain fibers will be metabolized, and you could take those into account as well if you wanted. It wouldn't make much of a difference though, almost all of the fiber we consume is coming out the other end.
If you want to know more, you're getting into a swamp of definitions and standards. For example you could skim this FAO report:
http://www.fao.org/docrep/006/y5022e/y5022e03.htm#TopOfPage (chapter 2 METHODS OF FOOD ANALYSIS)
http://www.fao.org/docrep/006/y5022e/y5022e04.htm#TopOfPage (chapter 3 CALCULATION OF THE ENERGY CONTENT OF FOODS - ENERGY CONVERSION FACTORS)
This shows that people are working hard on the problem you're posing, using a wide variety of approaches. It shows that every method has its problems, but also that all the values are quite close to eachother.

Hi VonBeche, sure the enthalpy of combustion of glucose is per definition constant, but it's of course more interesting to know what fraction of that potential can be captured by our bodies for its own purposes as in ATP, NADP, and the like. It also probably varies between individuals how efficient this capture is. And it probably even varies in the same person over time. I'd venture a guess that we recover more from food if we are fasting than if we have just had too far much to eat. I'll check out your links. Thanks.

That's the 40% of the other answer, and also that will be roughly constant (there are only so many pathways). You might just "burn up" the ATP in some cases (in brown fat for example), but the glucose isn't going anywhere without your body getting all the products from glycolysis (or whatever pathway is used).

The device you refer to is a bomb calorimeter. Inside one of these, a sample of material is completely combusted. Typically, the heat from the combustion warms a measured mass of water and the rise in temperature is used to calculate the Calories/Joules in the material.
Of course our cells don't ignite food and burn it to completion. Even if they did, some of the heat from the process would escape collection. Cells use the process of cellular respiration to harvest the energy. The basic version of cellular respiration describes the utilization of glucose to create ATP, by far the most used substance to power the energy needs of the cell. Here's just one source that takes you through the calculations of how efficient this process is: http://www.tiem.utk.edu/~gross/bioed/webmodules/ATPEfficiency.htm
So, at least for the very common sugar glucose, only about 40% of the total Joules, as measured in the calorimeter, end up as ATP. Most other food substances we use for energy share much of the same chemical pathway as glucose. I haven't seen calculations of their efficiency but suspect it would be roughly similar.
One of the most basic and important lays of physics is that no transfer of energy is 100% efficient. (Read more here: https://en.wikipedia.org/wiki/Energy_conversion_efficiency ). The remaining energy in the glucose that was not converted to energy in ATP is "lost" as heat. By lost, it is meant that it's not avaible to do any useful work other than heat us up. Of course, being homeothermic ("warm blooded") animals, that's useful too.

The U of Tennessee link you sent is great. They propose a very simple calculation that gives a good first approximation. Energy captured in ATP divided by theoretically available energy from glucose combustion ~ 50% after correcting for concentrations.

But that's does not yet take into account the energy required to metabolize glucose. Most of us get our glucose from polymers, so we need to make enzymes to break them down. Then we need to import and ship it to the cells that do the chopping; more energy required. Then in the cell that gets that molecule of glucose, the glycolytic enzymes don't come for free, right? What would be left of the 50% efficiency estimate when all these expenses are taken into account? 25%, 10%,..?

It's true there are a few steps in glycolysis that require energy but, in subsequent steps, this investment is returned. The calculations include this, they are a net value of the process.  As to parsing out the energy required to produce the enzymes involved, and to manufacture mitochondria to govern most of this energy harvesting, I've never heard of anyone attempting to calculate this. All of that is generally included under the category of "what we need the energy for".


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What is the share of body energy that the brain consumes? Is 20% reliable?
"20% of the energy at only 2% of the weight" is a frequently regurgitated factoid. More precisely, it should read: 20% of oxygen consumption.
The problem starts when one looks into the source experiment. The Wikipedia article on the brain offers Mink et al. 1981. Unfortunately, that paper merely summarizes the data of others and itself references the ancient 1957 paper by Kety, The general metabolism of the brain in vivo (reference 50). Alas, Kety again only summarizes the data of yet others from the 40s and 50s (see table 1). So, we have a horrible case of he said, she said.
Does anybody know of a more recent and more reliable study that estimates the % of energy consumed by the brain?


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What is the thinking behind the naming of arachidonic acid?
Arachidonic acid, the double bonded fatty acid, is occasionally misrepresented as having to do with spiders (arachnids). The Wikipedia entry explains that it's instead elated to "arachis" = peanut in New Latin. Alas, peanut oil does not contain any of it. Bizarre! What went through the mind of the person who named this lipid and caused all the confusion and mispronunciation by learners? Is there any good reason for the name?

I’m voting to close this question because it is not about a problem in biology, but about the trivial name given to a compound over 100 years ago. It is little more than a rant, disguised as a question, the answer which can not possibly be known "what went through the mind…".

There are finitely many letters and possible combinations of them making words, and many many things to be named. Inevitably, some of the words will be similar or even homonyms. To me, having some really limited and basic knowledge of Latin and (Ancient) Greek, there is no real confusion here. All terms related to spiders have a different stem containing an n, namely arachnophobia arachnologist, Arachnida ...
Regarding the naming, it was suggested in 19131 based on its similarity to arachidic acid, which is indeed a (minor) constituent of peanut oil.

1 Martin, S. A. et al. The discovery and early structural studies of arachidonic acid. J Lipid Res. 2016

Thanks Domen. That's just the paper I was looking for. I'm citing here to document the answer for readers here: "The name, arachidonic, was suggested in 1913 based on its relationship to the well-known arachidic acid (C20:0). It took until 1940 before the positions of the four double bonds were defined at 5,8,11,14 of the 20-carbon chain." Arachidic acid seems to a minor constituent of peanut oil at around 1%.


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What is the Specific Nature of Observable Micro-evolution
I am wondering what the proven mechanisms of micro-evolution are. For instance, in the case of bacteria, when a strain evolves that is resistant to antibiotics
1) Is the genetic combination that enables the bacteria to resist the antibiotics present the entire time and only made prevalent by the environment through natural selection, or do mutations occur to the DNA that change the organism so that it can then survive?
2) With the antibiotics removed, is the evolved strain generally more resilient in a normal environment or weaker?

A good answer would require writing a whole introduction to evolutionary biology which is way too broad. You should have a look at a very introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

In short, (1) No, mutations do not occur strategically in order to adapt. They just occur, their effect on the phenotype is random but sometimes such random effect is beneficial and it then gets selected for. (2) A priori we would think there is a trade-off and evolving defense against an antibiotic would come at a cost which makes this antibiotic-resistent strain less competitive in an environment without antibiotic. However, this prediction might well fail in many cases where such trade-off do not exist or are negligible

I agree with remi.b that the question suggests some misconception about evolution. The question could be refined to asking about the relative importance/contribution, to the process of adaptation, made by standing and novel genetic variation which is an important topic in evolutionary biology.

Please note that, to biologists, there is no such thing as "microevolution" or "macroevolution" - there is just evolution.

@MattDMo - Remi. b notes in one of his answers that it was microbiologists themselves who invented the term macro/micro evolution (http://biology.stackexchange.com/questions/39711/have-there-been-any-macro-evolution-experiements?rq=1). If this terminology is unacceptable then what terms are used to draw distinctions between evolutionary behavior observed in a lab vs. that which is inferred from fossil records and theory? I would think that this is a useful distinction.

@Ian please read the rest of what Remi wrote in that answer. The term was never properly defined, it has been heavily criticized in the intervening 90 years, and today has been appropriated by creationists and proponents of intelligent design, two hypotheses which have no place in scientific discussion. As I implied in my previous comment, there is no distinction between evolution observed in a lab vs. that observed from fossils, etc. - why should there be? Is there something about a lab experiment on human timescales that makes it less scientific or something?

@MattDMo - Yeah, I read the whole thing. But as a layperson I find the terms helpful even if they have baggage. The difference is that the precise mechanisms and characteristics of evolution observed in the fossil record are currently unknowable, right? When evolution occurs in a lab or within a generation it can be analyzed and understood, which makes it quite a bit more interesting (at least to me).

@Ian evolution works the same way regardless of whether you're in a lab or the Badlands of the Dakotas digging up dinosaur bones. I strongly suggest reading Understanding Evolution from the University of California, Berkeley to learn more. It's not just that the terms have baggage, it's that they're meaningless. You insist on creating a dichotomy when there is none. The only difference is in the number of genes that are affected, and that's a continuum, not a discrete separation into "micro" and "macro".

@MattDMo - Well I actually do plan on reading that page cuz I'm interested, but right off the bat I notice that they too use the term microevolution (evolution on a small scale) :) (http://evolution.berkeley.edu/evolibrary/article/evo_36).

There are several mechanisms through which a bacteria can evolve antibiotic resistance.
One way is by acquiring an already-existing gene from another bacteria or virus by what is called horizontal gene transfer. In this case, there is no requirement for any mutation to occur although the new gene can be integrated into the host genome and so, in a sense, the genome itself is mutated since it now contains a new gene but the gene itself is not.
Another way of acquiring resistance is indeed by genetic mutations. One beautiful example of this is the resistance acquired toward some aminoglycoside antibiotics. This class of antibiotics interferes with the ribosome assembly by binding to a specific site of it. In some cases, a simple point mutation of the aminoglycoside-binding-site is enough to acquire resistance. Some strains of bacteria exhibit aminoglycoside resistance due to a transport defect (mutation of a channel for example) or membrane impermeabilization (mutation of a pump), acquired by other mutations. Others use specific enzymes to digest the antibiotic, different variants (mutants) of such enzymes broaden the spectrum of resistance.
There are many other different cases in which a simple mutation is enough to acquire resistance.
Here some references:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC182597/
http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/aminoglycosideresistance.htm
http://www.antibioresistance.be/aminoglycosides.html
https://www.ncbi.nlm.nih.gov/pubmed/27690121
https://www.ncbi.nlm.nih.gov/pubmed/27651364
https://www.ncbi.nlm.nih.gov/pubmed/27699821
With the antibiotics removed, is the evolved strain generally more resilient in a normal environment or weaker? No, in general, there is no extra advantage in being resistant to an antibiotic if the antibiotic is not present.


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Spider Identification: Is this an Arizona Recluse?
I found this spider in my toilet bowl. It was after dark. We live in Prescott Valley, AZ at around 5100' elevation at the edge of a development fairly close to the mountains in grass land.
I'm concerned its an Arizona Recluse (or Desert Recluse). We saw a few of these around the house during the warmer months; this is the first I've seen in a while since its gotten cold, but my wife just did some extra cleaning.
I don't see a violin shape, but this article points out that desert recluse's don't have a noticeable violin. It also looks like it has 3 sets of eyes, but the 4th may just be hidden due to the angle since it looks like the 3 I see in the pics aren't centered quite right. Anyways, if anyone has some insight I would be happy to know. The leg span was a bit bigger than a penny.

Hmmm. I had one like this on the bathroom counter. It was huge by comparison, 3 inches leg span, and a dark green fuzzy abdomen. I am in the northern Sonoran Desert. I am trying to find my spider. It ran up the mirror to get away from me. Definitely non-aggressive.

I don't think it's an Arizona recluse. Characteristic of all recluse spiders (including the five varieties found in Arizona):

Long thin legs
Oval shaped abdomen
6 eyes in dyads (pairs)
Uniformly colored abdoment with fine hairs
No spines on legs
Legs are uniformly colored
Light tan to dark brown in color
Distinct violin-shaped mark on on the back points to the posterior of the spider (less obvious on Arizona recluses)
Body not more that 3/8" in length

Your spider has spiny legs. That, plus the fact that Arizona recluses are even less likely to live where humans do (as your article states), and are attracted to dry places, makes your spider an unlikely candidate, but I could be wrong.
Loxascelidae, Loxosceles reclusa

That makes me feel a bit better, although it doesn't look like a wolf spider either, because of its more uniform color. So I'd be curious to know if anyone has a positive ID. Maybe Southern House Spider?

@Ian Probably a huntsman, I'd say, based on the eye arrangement.

@augurar - Wouldn't a huntsman have crab shaped front legs? These look vertically jointed.

@Ian Based off of this site and this one a huntsman seems the most likely.  You can see the sideways leg orientation is not always obvious, depending on posture.

@augurar, Yeah I guess the first photo on your second link looks similar, especially the eye pattern (assuming the fourth top eye is hidden in my photos).

The key for this spider is the set of four 'tailpipe' spinnerets.  That's characteristic of the Ground Spiders in the family Gnaphosidae.  Recluses don't have that - the bulbous Recluse abdomen has the spinnerets oriented underneath like most spiders.  The recurved upper row of similar-sized eyes on this spider is also consistent with that group.  Not being familiar with western spiders, I'll just leave it at that.
Ah!  I finally realized that I need to add further details in the answer itself!  So, for sources, I refer you to Kaston, BJ, 1972 How to Know the Spiders; Cushing and Ubick 2009, Spiders of North America; and Bradley 2012, Common Spiders of North America.  An invaluable site is also Bug Guide, from which the following photos come: https://bugguide.net/node/view/1970/bgpage .
Note particularly the 4-pipe spinnerets.  I'm not suggesting any of these as yours; just that yours is most probably also a Gnaphosid of some kind.  Also, I now realize that I can only add 1 photo to this.  Well, this will do.


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Differences among competent cells?
What are the differences among the following competent cells DH5 alpha, Nove blue, and BL21? Why some of them are for cloning and others are for protein expression?
Any references where I could find the answer?

There are a lot of differences, you can check the companies that sell competent cells for guides on how to choose (NEB, Sigma Aldrich). But there are only a few things that matter for the really common uses of competent cells.
The most important part of selecting your cells is choosing cells suitable for protein expression or for plasmid preparation.
The cells meant for plasmid prep carry certain mutations like endA that inactivate nucleases that would otherwise degrade DNA. Typical choices here would be DH5$\alpha$ or XL1-Blue.
Cells meant for protein expression have some proteases mutated, and can often use different promotors like T7. A typical example are BL21 cells, and BL21(DE3) which can use the T7 promotor.


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What is the definition for vitamins?
I have found the following definition on Wikipedia:

An organic chemical compound (or related set of compounds) is called a
  vitamin when the organism cannot synthesize the compound in sufficient
  quantities, and it must be obtained through the diet;

That doesn't seem to exclude essential amino acids and essential fatty acids though, and those are also organic chemical compounds that by definition can't be synthesized in sufficient amounts.
So is the definition incomplete?

Generally speaking, bulk essential nutrients (e.g. amino acids, fatty acids) are used stoichiometrically to form macro cellular structures and are 'baked in' to the structures or compounds they are used to make. Once those structures are destined for degradation, sometimes the bulk essential nutrients can be recovered and reused in the synthesis of other structures or compounds, but catabolic elimination from the organism is always an option that yields useful energy.
Vitamins, on the other hand, are usually used catalytically. Vitamins are not 'baked into' the compounds they help make or process; vitamins transiently participate in the reactions required to make or regulate a compound or structure, but don't ultimately get 'used up' by that process.
Ultimately, vitamins don't have a bulk energetic value to a cell. For instance, once vitamin E (α-tocopherol) is oxidized, its only fate is to be excreted as waste. Fatty acids and amino acids, once destined for degradation, have their remaining chemical energy extracted prior to excretion of their downstream waste products.
It is philosophically interesting to remark on the diversity of bulk biomolecular building blocks that are still necessary for some organisms to obtain from their environment. Not all of them get called vitamins.

It's just naming convention. We recognize, officially, the 13 vitamins based on activity, but we intentionally classify amino acids, etc. as such instead of as vitamins. It's just one of those things that people stick to so that it's standard, such as beverages as a blanket term for certain drinks but not for every type of fluid. (maybe that's a bad example, but hopefully you get the idea)


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At any given moment, how much energy is stored in the human body as ATP?
At any given moment, approximately how much energy is stored in the human body as ATP in the ADP-P-bond?
This of course depends on what type of cell it is and the activity of the individual in question. The calculation should be fairly simple, as we know that ATP hydrolysis release about 30 kJ/mol. Hence, the question could actually be re-phrased to $"$At any given moment, how much ATP does the human body have?$"$

how much googling have you done? I'd start with "how many ATP molecules in human body" and then multiply that estimate by 30kJ/mol

All I can find is how much ATP the human body uses per time unit. I'm not seeking that but rather how much present ATP there is at a given time.

that is generally expected that you'll add what you;ve found to your question. Is makes it much better

what do you think of following approximation: ATP is not a long-term storage hence every day you consume all ATP you produced from food/fat. That means that on average day-to-day you have X mol ATP/min * 24 hr? where X is the number of ATP/min body burns.

I'm not looking for that either. If you froze time and started to count all ATP molecules in a human body, that's the number.

then you will have to specify when exactly you freeze time: 1 hour before breakfast, right after dinner? Numbers will vary greatly, I suppose

ATP burned per minute is not a useful number because the turnover is so high. 2000 kcal/day is dozens of kilograms of ATP so obviously ATP is turned over more than once a day, but there's probably more than one molecule of ATP being passed around between all the ATP synthases.
This blog claims 250 grams. Taking the estimate of ATP concentrations(1-10 mM) from wikipedia and multiplying by a 60 kg person pops out 150 grams (for 5 mM). The ATP/ADP ratio is about 5 to 1 under physiological conditions, so I'm comfortable leaving out that source of error.
So: Probably a few hundred grams, depending on a lot of things. Which is about .2-.7 moles, for reference. 6-20 kJ is not a lot, in fact even at the upper end of estimates you're looking at maybe 8 dietary calories, and probably more like 3.

Each of us burns approximately twice our body weight in ATP every day. So double your body weight and divide that number by the number of seconds in one day; that will give you the average mass of ATP. N.B. a person with a higher mass will have a higher answer.

Is there a reference for that?

My memory may not be what it used to be, but I thought I read a quotation by Paul D. Boyer (Nobel Prize recipient in 1997 for his work on ATP synthesis) where he cited that figure, but I may be off by a factor of 2 according to this slightly more well-known source which says "equivalent to your body weight": https://en.m.wikipedia.org/wiki/Adenosine_triphosphate


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How do baby birds get fed when they are only a day or two old?
The eggs belonging to the robin on my porch hatched. The baby birds are very tiny, just lumps. They are not opening their mouth and cannot even seem to lift their heads. How do they get fed when they are so helpless?

The hatchling's neck muscles are stronger than you think, because hatching from the egg requires strong neck muscles. Newly hatched songbirds and others do indeed open their mouths after they have had sufficient rest following hatching, though you don't seem to have witnessed this. They have little neck control and their heads wobble initially, but feeding is so important that they are born with this ability.

Songbirds and most seabirds have altricial young, meaning that the newly hatched birds are blind, featherless, and helpless. Immediately after hatching, altricial birds can do little more than open their mouths to beg for food. They remain in the nest where the parents can feed and protect them while they continue to develop. For the first week of life, most altricial birds cannot control their own body temperature and must be constantly brooded (kept warm) by their parents.

This makes sense, as most altrical birds only spend about two to three weeks before flying off to start their own separate lives.
Newly hatched poultry chicks (precocial birds, which also include ducks and sea birds) can live for 48 hours on the last of the egg yolk that they take in just before the strenuous work of hatching out of the egg.

Incubation periods are longer for precocial birds than altricial birds, allowing for increased embryonic development in the egg, and therefore they have relatively advanced motor and sensory functions at hatching.

Feeding poultry is actually not necessary during that time. The chicks are strong enough to stand, drink, and peck for food soon after birth, but it's not necessary for life. What they cannot do is regulate their body temperatures well.
Nesting Cycle


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How do racing pigeons know the way back to their roost?
I have read that a standard way to do pigeon racing is that the male and female are separated and the pigeon races to its mate.
My understanding that in these cases the roost is several miles away from the release point. How does the pigeon know how to find the roost?
I have heard that sometimes they will hold up the mate in the air, but at several miles away, how would that help.


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Why is there a low rate of kidney disease related deaths in the Baltic countries?
A noticeable feature of the map of kidney disease related deaths is that the Baltic countries, Norway, Finland, Estonia, Latvia, Lithuania, etc have lower rates:

Why is this?

The poor separation between the color scale makes it really hard to tell what the rates are, except for the high countries. I'm not convinced that the Baltic countries have lower rates. Are there actual numeric data anywhere?

would be really useful to have a link to the source.

To me, the best correlate of cancer rate here looks like population. I wonder if this is a similar effect to Gelman's US kidney cancer example.

Affluent countries have higher rates of diabetes which is the major cause of renal disease.

Baltic countries include only Estonia, Latvia, and Lithuania. And if you meant baltic region, then what countries are included is a little bit up to everyone's defintion but you would definitely include Russia (which rate of Kidney disease is quite high). So what countries did you mean exactly?

Looking at this map I can't see any obvious difference with the baltic states (or states of the baltic region of whatever you meant). Mongolia, central Africa or central America does not seem to have a lower rate of kidney diseases.


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Are clones less likely to be fertile?
I know that hybrid animals like mules are infertile. What about clones? Do cloned animals show the same fertility as their original?

Do you know why hybrid animals are infertile?

@Cell Have you ever noticed that some people have a tendency to answer a question with another question?

@ImprisonedRhesus Answering questions with other questions can be a good pedagogical technique, since those questions are meant to guide your logical thinking while allowing you some creativity (i.e., without giving away the answer too directly).

Also as a curiosity - mules are typically infertile, but there are dozens of well-documented cases of mules and hinnies that have successfully reproduced, so it's not an all-or-nothing thing.

@iayork You should be more cautious before calling other people snarky and a bully. The original poster was implying that clones may be infertile for the same reasons that hybrids are otherwise why even bring it up? I know that the topics are completely unrelated hence I wanted to gauge how much the original poster knows before answering. Unlike your verbose, jargon filled, one-size-fits-all answer, I like to answer with the knowledge and expertise of the asker in mind.

@Cell and yet you clearly did annoy the original poster, so your claimed goal failed completely. Since evidence shows you don't understand how people read your comments, you should reconsider your approach. Data trumps theory every day.

Cloned animals, at least in the first generation, are often subfertile and have lower viability than their progenitors. The reasons for this are complicated but often are related to epigenetic changes that lead to altered gene regulation.
Further reading:

Although the technology of SCNT has been applied successfully by many research teams, some SCNT animals have abnormal or lethal phenotypes, including facial abnormalities, pulmonary hypertension [3], contracted tendons [9], low birth weight [10, 11], as well as distinct depigmentation of the skin and hair ... Based on previous studies, insufficient epigenetic reprogramming of somatic donor cells may result in phenotypic abnormalities in the offspring ...

--Dysregulation of genome-wide gene expression and DNA methylation in abnormal cloned piglets

The epigenetic state of the ES cell genome was found to be extremely unstable. Similarly, variation in imprinted gene expression was observed in most cloned mice, even in those derived from ES cells of the same subclone. Many of the animals survived to adulthood despite widespread gene dysregulation, indicating that mammalian development may be rather tolerant to epigenetic aberrations of the genome.

--Epigenetic instability in ES cells and cloned mice.

Because few clones survive to birth, the question remains whether survivors are normal or merely the least severely affected animals, making it to adulthood despite harboring subtle abnormalities originating from inadequate nuclear reprogramming ...  Our results suggest that many expression abnormalities are common to the NT procedure whereas some reflect the particular donor nucleus. These results further emphasize the severity of placental dysfunction and illustrate abnormalities in clones surviving to birth.

--Abnormal gene expression in cloned mice derived from embryonic stem cell and cumulus cell nuclei

Although clone D had a poorer libido and entered puberty later than those of the other cloned male cats, he produced gonadal hormones within the average range. Four of the cloned male cats had normal fertility.

--Reproductive fertility of cloned male cats derived from adult somatic cell nuclear transfer.
(Note that this paper concluded that the cloned male cats had "normal fertility", but one of four (25%) had reproductive abnormalities (reduced libido and delayed puberty); the numbers are too small for anything definite but I would say this is evidence for abnormal fertility, not the reverse)
Some early papers do claim normal fertility of cloned mice, but those are simply based on the fact that the cloned mice could have offspring (i.e. were not completely infertile) and didn't actually compare fertility of cloned vs. "normal" laboratory mice.

Wakayama, T., Perry, A.C.F., Zuccotti, M., Johnson, K.R. & Yanagimachi, R. Full-term development of mice from enucleated oocytes injected with cumulus cell nuclei. Nature 394, 369–374 (1998).
Wakayama, T. & Yanagimachi, R. Cloning of male mice from adult tail-tip cells. Nature Genet. 22, 127–128 (1999).


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How plausible is it that pesticides and mosquito spraying is affecting insect populations?
I live in Massachusetts and I notice that there are a lot fewer bugs than when I was a child. 40 years ago if you drove around for 4 or 5 hours in the summer the grill of your car would collect a noticeable amount of bugs. Nowadays, I can drive for the whole summer and there is not a single bug on my car. I rarely see a butterfly of any kind. I have not seen a monarch butterfly in years. When I was kid butterflies were omnipresent in any meadow or field. Even 20 years ago I remember cursing all those annoying Japanese beetles flying around. Haven't seen one in years. There used to be huge gypsy moth infestations. Even in off years, you would see the caterpillars plastered all over the sidewalks. Nowadays, sidewalks are all clean, not a single squashed bug.
I thought maybe this was because of mosquito spraying. In Massachusetts for many years we have had these huge mosquito spraying programs that cover every square inch of the state. The method used is what they called ultra low volume spraying or something like that. Even so, I can't see how it would be possible. For example, I saw a schedule for spraying in my county on an each day they would have 5 different towns listed. I don't see how a few trucks could possibly spray anywhere enough insecticide to depopulate 5 towns worth of bugs. I mean in my town alone there are probably a couple hundred roads and many areas that have no road access. How many roads can they possibly drive in one night? It doesn't seem possible, yet there no bugs.
Is there some kind of cumulative effect, or are these poisons so incredibly powerful that they just wipe everything out with even tiny amounts being released? How plausible is it that pesticides and mosquito spraying is affecting insect populations?


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Why do some viruses have only one serotype, but others have many?
Some viruses, like the virus that causes mumps, have only a single serotype, meaning that variants of the disease are immunologically identical. However, other viruses, like the influenza virus family, has many different serotypes. Why is this?


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This graph about logarithmic and arithmetic plots. Shoudn't it be the other way around?

From the textbook 'Brock biology of microorganisms, 15th edition'
The black lines points to the linear graph with the caption 'Logarithmic' and to the curved graph with the caption 'Arithmetic'. Isn't this the reversal of what they are?

No it's correct. The arithmetic plot uses the left side of the graph and if you take the log of the values on the arithmetic plot (log10) it'll plot out a straight line; the red one which use the right side as the y-axis.

To add to @m4rio's comment: As someone once said "biochemists worship at the alter of the straight line" (It is the logarithmic plot that is linear, as is the Lineweaver-Burk plot, the Eadie-Hofstee plot, the Hanes plot, and quite a few others: they are all linear transformations of non-linear 'primary' plots)

It's always a good idea to carefully examine the numbers on the axes and draw your own conclusions before looking at the labels.

The image is correct, although the presentation is confusing because the association of the lines with the axes is not indicated clearly.
Plotting on an arithmetic scale (the "normal" sort of axis we all first learn about), an exponentially growing number of cells will result in a line that starts out looking pretty flat and then suddenly shoots up.
If you're interested in knowing the rate of growth, this sort of line isn't very useful, because the same rate will have different slopes, while the same slope indicates different rates, depending on the number.
If you instead plot the growth curve against a logarithmic axis, then you get a graph that focuses clearly on growth rate, with the same slope always indicating the same rate, no matter how many cells are present. Thus, if the growth rate is consistent, you'll see a straight line, as in the example presented.


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Do mutations occur while growing virus for preparing inactivated viral vaccine?
The development of mutations in virus is reported to happen during replication, especially for an mRNA type virus like SARS-COV-2

Viruses that encode their genome in RNA, such as SARS-CoV-2, HIV and
influenza, tend to pick up mutations quickly as they are copied inside
their hosts, because enzymes that copy RNA are prone to making errors

My question is do mutations occur while mass manufacturing inactivated viral vaccines?
Simply because the process of manufacturing inactivated vaccines replicate the virus in large quantities, there might be large number of mutations occurring. Will this make each batch different from one another? Or do they control the replication process to limit the mutations?
Veritaisum did a recent video on the study on mutations in long term evolution experiment of E.Coli. It is clear that mutations do occur even in standard controlled environment.

I already asked in medical sciences stackexchage https://medicalsciences.stackexchange.com/q/27469/22302. Reposting here for visibility

"inactivated viral vaccines" - note that the major Covid vaccines are not of this type. Moderna and Pfizer are mRNA vaccines. Astra-Zeneca and Janssen uses harmless non-Corona viruses.

Please don't repost questions. For this one, this site is more appropriate than Medical Sciences.

@MSalters there is a significant portion of covid vaccines manufactured using inactivated viruses. And mRNA vaccine is not a viable in many parts of the world. Hence asked this question

@MattDMo I was tempted to repost the question here as I did not get answers in the other portal. No harm intended; just opening up to wider audience and seeing if I can find answers. I could not get a solid result while googling too.

@karthikeyan I'm sure there was no harm intended, but it's against the Stack Exchange rules. If you didn't get a result elsewhere after a few days, just delete the question and then repost it here. We just don't want multiple parallel discussions going on at different sites.

Very simply, mutations do occur, as they do for any cultured organism. This is a well recognized problem in many fields of biology where organisms are cultured and remains in particular a problem for cultured mammalian cell research.
As far as I know there is no method for slowing or altering the rate of mutation as this is an inherent part of the RNA-dependent RNA polymerase. This happens irrespective of the environment the virus is grown in and is one of the ways that viruses of this sort combat the immune system and ecosystem changes - they produce so many mutations over the generations of viral replication that some of the progeny will be more fit in the environment in which they are replicating.
In fact, they produce so many mutations at each replication cycle that these viruses can not be called a single "species" they are actually what is referred to as a quasispecies.
It is part of the difficulty of producing vaccines against things like influenza and related viruses as they can change from the phenotype seen in the wild. However, we have methods of checking that the viruses are the same or similar enough antigenically that it makes no difference for the immune response to the vaccine.

IIRC, you can change the rate of mutation by changing codons. There are 64 codons for 20 amino acids, so not all mutations will change the resulting virus. For example, "CUA"  and "UUA"  both encode for Leukin, but "CUA" is more stable. That's because an A->U mutation would produce "CUU" and "UUU", but only CUU encodes for Leukin.

@MSalters - yes, this potentially outputs stable functional viruses, however in a normal infection (in the lab) defective particles outweigh the functional by some orders of magnitude. The error rate of the RdRP is constant for the virus, so even if you have the CUA codon, it doesn't mean it will change the rate at which it is mutated, just that functional virions will more likely have this codon.

@bob1 I haven't looked at this in years, but I believe the codon can actually affect the mutation rate and certain codons are more prone to slippage and are more likely to be read by the wrong tRNA than others. Take this with a huge grain of salt, I am vaguely remembering conversations with colleagues from several years ago, but I do think there is something along those lines.

@terdon - in what systems? We are talking about an RdRP in viruses here.

@bob1 huh, good point. If (big if) my memory serves me and there are indeed different rates of error for different codons, I would expect that to also be the case for viral RdRP. But I'm really just making wild guesses and assumptions based on vague recollections so I certainly won't press the point.


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Does baking soda interfere with digestion when cooked into food?
Baking soda is useful for tenderizing meats and leavening baked goods. In the case of meats, it allegedly breaks down proteins/amino acids.
However, does this usage pose a risk to digestion? Could the baking soda continue to neutralize the stomach acids? Or does its effect "wear off" after some time marinating? Or does it "decompose" sufficiently by the cooking?

The relationship between acid and bicarbonate is that 1 H+ neutralizes 1 bicarbonate (HCO3) molecule as represented in the following equation:
HCl + NaHCO3 --> NaCl + H2CO3
So assuming that the stomach has a pH of 3 and a volume of 100 ml (see table 1, HS = Health Subject, mean vol = 133 ml). A pH of 3 means a concentration of H+ ions of 0.001 mol/l (conc = negative log10 of the pH...10-3 mol/l). Now, assuming all the bicarbonate added makes it to the stomach, we can work out empirically how much bicarbonate it would IN THEORY take to neutralize all the acid in the stomach
The above means that for 100 ml (0.1 l) of stomach acid there is enough hydrogen ions to neutralize 0.0001 mol (n = C * V; 0.001 mol/l * 0.1 l) of HCO3. NaHCO3 has a molar mass of 84.007 g/mol. Using our very best chemistry:
Mass = number of mole * molar mass
Mass = 0.0001 mol * 84.007 g/mol
Mass = 0.0084007 grams.
Now, there's a about 5 g of baking soda in 1 teaspoon. This is a massive amount more than you see in the equation above.
So what happens to the rest?
Well, in real life, some reacts with the food during preparation, some (a lot) is lost to decomposition from heat, some isn't consumed, and last, but certainly not least; the stomach adds more acid to maintain its pH, which is essential for function of the proteolytic enzymes in the stomach.

Wow that's awesome. I never got to take a chemistry class, so this is super enlightening. Thanks!

Sodium bicarbonate is alkaline in nature and it breaks down in presence of an acid.
When you eat it it gets neutralized by the acid in your stomach,this will increase the PH a bit but it will normally not interfere with your digestion.
When sodium bicarbonate breaks down it splits into CO2,water and sodium,so it will add sodium to your body and it might have a negative effect on your blood pressure and kidneys.

So it depends on quantity and time, assuming the baking soda begins breaking down as it comes in contact with the raw meat (acidic)

sodium bicarbonate does not break down in contact with meat or it breaks down very slowly,it increases the alcalinity of the meat and act as a salt.you can read about  sodium bicarbonate here https://en.wikipedia.org/wiki/Sodium_bicarbonate

@trondhansen Can confirm. A glass full of baking soda water tastes a lot like a glass full of salt water.

it had been dangerous if it had a massive reaction in contact with meat or the human body.


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Help identifying snake? (Southern California)
I just got home after a brief, surprise thunderstorm ... to find a pretty good size snake lounging in the breezeway at the garage side door.  (Presumably, it was seeking shelter from the rain?)

Could anyone please identify this type of snake?
Is it poisonous?
And in any case, is it likely to bite if it felt disturbed or provoked?

Thank you very much in advance!
Diameter: ~~4cm (~~1.5")
Length: ~~1m (~2-3'+) [though hard to say, since it's only been seen curled up]
Location: Southern California, mountainous desert region (~3K' altitude)

EDIT (~11pm PT):  It's still there. :O

Welcome to Biology.SE. Please upload your pictures rather than just providing links (posts should be self contained and not require anyone to follow links). In addition, please  give an estimate of the size of the snake. For more information on how to use this site please take the [tour] and then see the [help] starting with [ask] questions effectively on this site. Thanks!

Hi, @tyersome --
I appreciate the welcome, and the tips.  (I'd tried to upload the photos, but wasn't familiar with the resulting syntax.)
I've updated the question accordingly, and hope this helps.
Any insights appreciated.  Thank you!

Almost certainly the Western Rattlesnake (Crotalus viridis, which is probably the most common rattlesnake in California. It has the characteristic fat body and stripes of a Rattlesnake.
Western rattlesnakes are very common in much of the western part of the USA from southern Canada south into Mexico and across the Great Plains.
See second link for photos with similar colouration to yours.
Like all rattlesnakes, it is venomous and will bite and envenomate when threatened. Get a professional to deal with it.

Thank you VERY much.  The snake eventually left on its own, though we've since been in contact with Animal Control, in case it returns.
They say rattlesnakes are considered "emergency" service calls -- so your identification was VERY important info in that regard.


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underwater bug identification
There is a small pond outside my work (more like a run-off ditch from a parking lot). Once a year it gets swarmed by this tiny bug. I am having some trouble identifying it. The biggest ones were about 1mm in size. I found these in Indiana. They are tan/light brown and the bigger ones had small 1-2 small black marks on their backs. Sorry for the blurry images, They were kinda quick and hard to capture from the camera on my stereomicroscope.
Here is a macroscale video:
https://photos.app.goo.gl/1BEN7NP8okWqGKVh9
Here are some microscope photos:

Please update with 1) location, 2) more details (e.g. size, coloration, notable features), and better photo(s). Thanks!

It is very hard to tell from the photographs, but from them having a small "beak-like" structure (3rd photo), I think this is likely to be a Water Flea (Daphnia species), which is a common, cosmopolitan genus of small zoo-plankton.
They are typically about 1-5 mm (0.039–0.197 in) long and actively swim through the water, collecting algae to feed on.

If you look at the macroscale video, they seem to move smoothly and in the direction that the oval points. If you look at this youtube video, daphnia seem to move sideways and in jumps like a jellyfish: https://youtu.be/sD9Tg0Qw-Yg?t=48

@user1402154 is could be that you have more than 1 organism type in your sample - the 3rd photo could easily be a different species from the other photos, given differences in shape and gut position. Have you looked at pages on common microorganisms in pond water? there might be something that rings a bell for you.

Ive googled it a bunch. Is there a particular resource you recommend?

@user1402154 These guys seem OK: https://www.microscopyu.com/galleries/dic-phase-contrast/pond-life

it was bigger than most of those. I am starting to wonder if they're amphipod or amphipod larvae. They appear in the spring during the flooding and then disappear for the rest of the year. Maybe theyre terrestial amphipods with a water/larva stage?
they could totally be sandhopper larvae