texts: Alternatives to CFU plating for measuring number of viable cells?

texts:
I am hoping to measure growth rates of a bacterial culture in several growth conditions. I am concerned that these growth conditions may cause cell death, which would lead to a decreased correspondence between optical density and number of live cells, so I want to independently measure the number of live cells. I understand that plating serial dilutions of a culture and counting the number of colonies to calculate the Colony Forming Units (CFU) per mL is the gold standard for measuring the number of viable cells. However, I have seven different conditions I want to test in parallel, and making 3+ plates for each condition (to do serial dilutions) and taking measurements at several points in the growth curve leads to a lot of plates. In general this method seems more labor intensive than what I need. I am mostly doing this as a sanity check, so it seems like a lot of work just for a sanity check.

My question is: are there any alternative methods to CFU plating for measuring cell viability, given that I am doing a lot of experiments in parallel? I don't have access to a FACS machine, so cell sorting won't work. I have read this question on measuring live cells in algae. I'm not sure that a hemocytometer is the right alternative for my particular high-throughput application (though you could convince me otherwise). The best answer to this question would compare from experience the precision, accuracy, sensitivity, and ease of use of this alternative method with CFU plating.

Thanks!


texts: Difference between stem cell "expansion", "repopulation", and "self-renewal"?

texts:
From this paper (link:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4130805/), I read "Thus G-CSF results in the expansion of phenotypic HSCs in the bone marrow with reduced repopulating activity and self-renewal capacity."

If expansion meant population-expansion, then would that not mean the same thing as repopulation? Likewise, self-renewal occurs through asymmetric cell-division in which a parent cell divides into two daughter cells; or it can occur through symmetric cell-division in which a parent cell divides into a progenitor cell and a daughter cell. In essence, both types of cell-division maintain or increases the population of stem cells; hence, "self-renew" or "expand". Clearly, I am missing something here with the terminologies. Please help! Lastly, I thought phenotype is a noun, then what does phenotypic even mean?


texts: What do the numbers in Photosystem I P700 and Photosystem II P680 stand for? Is it the optimum wavelenght? The maximum wavelenght?

texts: I am a bit confused about this because my teacher and english Wikipedia say it's the wavelenght the Photosystem is most reactive to; my textbook and the german Wikipedia say that it is the maximum wavelenght the Photosystem can absorb :-/


texts: How do CAM plants keep stomata closed by day and open at night?

texts:
I understand how plants open stomata, with the H+ ion removal and the resulting K+ ion influx in the guard cells to induce turgor (wikipedia article here), though not how this process relates to presence/absence of light.

However, I don't understand how CAM plants manage to keep their stomata closed during the day and how it relates to CAM photosynthesis (if at all). I know that malate ions are involved in the opening of the stomata in C3 plants, could the malic acid production in CAM photosynthesis contribute to this?

So my question is: How do CAM plants induce closing of the stomata and what signal triggers this?


texts: Which is the best model organism to implement an evolutionary study for P.falciparum?

texts:
I have to study and implement some evolutionary statistics for P.falciparum. In your opinion and by your experience, which organism should I consider in order to take the orthologs to implement this study?In general, If I wanted to extend this study to P.knowlesi, P.vivax and in general to all the parasites evolutionary related to the asian monkey plasmodia, which organism you suggest me to consider as a template? I thought about P.berghei but, since I have to consider also the Vinckeia parasites (mouse plasmodia) is there a good organism, out of the plasmodium genus, that could come in handy serving as a reference point for all these species?
Obliged


texts: this may not be on topic but I'm hoping someone here can tell me the name/manufacturer of the connectors used with the thin teflon tubing in this picture:


texts: What is the purpose of using two layers of gel in SDS- PAGE?

texts: I just made a SDS-PAGE with a top layer of stacking gel and a bottom layer of separating gel with different pH values of 0.5M Tris-HCl. The stacking was 6.8 and the separating gel was 8.8. What about this pH change makes the gels different? What effect does this have on the proteins that I ran?


texts: How does the stomach handle continuous eating?

texts:
In biology class, we learned this familiar story:  Food enters the stomach, the stomach churns it with acid and enzymes, and then, somehow, the stomach senses when the stew is ready and releases it into the small intestine.

But this simple narrative implicitly assumes that all the food of a meal comes into the stomach at about the same time, and only then does the digestion process begin.  This is often not the reality.  What happens when we eat continuously over many hours, such as at a Super Bowl party, or an all-day summer barbecue, or a long afternoon at an all-you-can-eat crab shack?

Does every new bite cause the stomach to reset its process to zero?  "Uh oh, detecting fresh, undigested food...  better start over..."  But if the stomach resets to zero with every new bite, wouldn't it eventually grow overfull?

Or does the stomach eventually get fed up with all the new introductions and just start releasing whatever it has into the small intestine, ready or not?  In that case, when and how did it decide to proceed with incomplete processing?


texts: What is the benefit of oxygen tanks to persons trappped in an enclosed space?

texts:
When people are enclosed in an air-tight space, the levels of carbon dioxide will rise to lethal levels (hypercapnia) long before the oxygen is exhausted (hypoxia).  For example, the astronauts of Apollo 13 were in danger because the carbon dioxide scrubbers in the lunar module were inadequate.  They never "ran out of oxygen", even though the oxygen tank of their service module exploded.

What would be the benefit to supplying such persons with tanks of additional oxygen?  It seems to be a futile gesture to me.

The reason I ask is a news story ongoing for several weeks.  Twelve children and one adult have been trapped by water in a cave for several weeks.  At the time this question was written, four boys were already rescued.  Officials have repeatedly expressed concerns that the "oxygen is running out" and are placing oxygen tanks in the cave.  Is there any benefit to this, or are officials simply ignorant of human physiology?


texts:
I am beginning to work in the field of human gut microbiome, and wondering how (and if) the concepts of population genetics could be applied there.

Considering the competition between the species seems straightforward, although ecological models are probably more appropriate in this case.
Considering the pan-genome of single species however seems next to impossible, as it cannot be divided into independent alleles. One could probably define a number if allels as the number of copies of a particular gene in the community. However, as it confers fitness on the whole community, it is not clear how to define selection. The notion of genetic drift also seems vague.

I will appreciate clarifications and references to relevant literature.
Update
To clarify the question:

The question is rather theoretical, motivated more by my previous work than by what I am about to do in the field of metagenomics. The latter will be analysis of shotgun sequencing data, where the focus is on identifying new species and comparing the species composition in many patients. I doubt that we will have any data permitting to study the intra-species evolution within a single patient. However, understanding how bacteria evolve to be a particular strain in a particular patient could be a plus: if members of a bacterial community with different genomes live as a group, we can't meaningfully say that some of them are more fit or less fit.
My past experience with population genetics is in the field of HIV, which for most purposes can be treated as a diploid hermaphrodite (each virion carries two copies of the genome, and the genomes are shuffled when a cell is co-infected with several virions). Thus, many basic population genetics concepts are easily applied, although the speed of evolution and the need for constant adaptation add other difficulties (motivating such approaches as fitness edge).
Finally, as was pointed in the comments, the problem is not specific to bacteria - altruism does take place in many communities, and should raise the same kinds of issues as I mentioned previously. I admit that I am not familiar with the necessary theoretical frameworks, and this can be considered a part of the question. I would guess however that most such frameworks do not account for direct gene exchange.

Update 2
A relatively recent article by Eduardo Rocha (2018) discusses the shortcomings of the neutral model (as the principal null model for modern genomics) when applied to procaryotes. This has clarified a lot for me, and I give below a short list of their points:

Mutations in bacteria cannot be treated as neutral.
Polymorphism concept is poorly defined for genomes of varying length, which requires new mathematical framework.
Promiscuity of bacteria, freely recombing and exchanging genes via the horisontal gene transfer makes it difficult to define species and apply many concepts of the traditional population genetics.
Difficulties in separating demographics and genetics (essentially, one needs a combined genetico-ecological approach).

Update 3
Inclusive fitness theory / kin theory (also here) probably fits into this context.


texts:
Like glucose, amino acids are also insulinogenic as well. So, presumably, just like glucose, the body would also like to keep amino acids levels in the blood stream below (or within) some certain concentrations as well.

This question Why is too much glucose harmful? details some of the means by which high blood sugar levels can affect various cells and body function. But, would excess blood amino acid(s) levels have similarly adverse effects?


texts: I am a newbie is DNA sequencing and BioInformatics. I am writing a school project that determines whether a DNA sequence is a gene or not using a Machine Learning Algorithm, Hidden Markov Model. After understanding the the algorithm, I now want to know when we can say this particular DNA sequence is a gene. Any help or pointers would be appreciated. Thanks


texts: Why do I have super vision in purely red light?

texts:
I installed some RGBW led strips in my apartment recently.. by some I mean everything is now lit by led strips and there isn't a single light bulb left.

One thing I've noticed over the last few days is that my eyesight is significantly sharper in pure red light. Historically I've had pretty good sight but reaching 30's I've developed some nearsightedness. I don't wear glasses since I can still see things up to ~2m from me as clear as ever but reading street signs now requires me to get closer and stuff like that.

Things that require me to squint and really try hard in daylight (or white light emitted by the led's) are really easy to look at in red light. My vision is worse in blue light and worst in green light. Is there any kind of common explanation for this?


texts:
I am trying to learn more about virology for a tentative job I could be taking soon, as a quality control person in virology.

However, I have not taken a formal virology course, nor any course work in "quality control".

Googling showed me this website for learning more QC topics, however I was curious if anyone had better suggestions.

My question is if anyone had (ideally free) resources on learning virology (in the context of preventing cell culture contamination) and quality control in industry labs they thought would be ideal?


texts:
Why does low Na+ levels cause hypotension (low blood pressure).
  Alternatively, why does excessive intake of Na+ cause
  hypertension or high blood pressure?

From what I understand, there are two different mechanisms at play. Renin secretion from kidneys occur during low salt levels in blood and hence, under low sodium concentration, high amount of Renin secretion from kidneys should actually raise the blood pressure, via the Renin-Angiotensin loop, constricting the arteries. Under high sodium concentrations, low renin secretion should be accompanied by low pressure. If the osmotic entry of water into blood raising the blood volume and thus pressure, plays a role here, will not, on increase of blood volume, decreased Vasopressin increase urinary output and thus control the blood volume, not allowing it to cause any body changes? Why isn't the first effect (renin) significant here as compared to the second (osmotic entry).


texts: Why does the clavicle ossify intramembraneously?

texts: The clavicle is the only long bone which ossifies as a membrane bone. I studied this process, but I can't find the reason why it features intramembraneous ossification?


texts: How do carbon 13:12 ratios confirm the biological origin of oldest microfossils?

texts:
I was reading this article about how Schopf and Valley’s findings in 2017 confirmed that the 3.5 billion–year-old microfossils found in the Apex chert of Western Australia are indeed remnants of living organisms, as opposed to abiotic geological structures. The most detailed part of the article’s explanation is:

Using SIMS, Valley’s team was able to tease apart the carbon-12 from the carbon-13 within each fossil and measure the ratio of the two compared to a known carbon isotope standard and a fossil-less section of the rock in which they were found.
“The differences in carbon isotope ratios correlate with their shapes,” Valley says. “If they’re not biological there is no reason for such a correlation. Their C-13-to-C-12 ratios are characteristic of biology and metabolic function.”

Can someone explain this in more detail? In particular, why should this ratio be different in biological carbon samples, compared to abiotic carbon samples?


texts: Why are successful human rock climbers so dissimilar to Hominidae primates who spend extended time periods climbing?

texts:
In rock climbing, the sport considers the Ape Index when evaluating the factors critical for success.

However, the majority of successful climbers are lithe and slim with less than 8% body fat.  As one professional described it

  “I feel very pressured to be thinner for climbing. I’m very strong, but I will likely never be thin, and I think that it holds me back…I don’t have that classic thin, long-limbed climber body…”

However, this seems completely at odds with the primates that we see on documentaries and in zoos which appear to be heavy, muscular, powerful and with considerable upper body strength.

Professional human climbers, while strong, rarely have significant quantities of muscle (Bodybuilder-esque) on their skeleton. They seek a power to weight ratio through weight-loss.

What accounts for this difference in development?  How do primates move such heavy masses through the upper canopy and why have they not evolved slimmer, smaller or more lithe frames?


texts: Why do type 1 diabetics experience hypoglycemia?

texts:
I know that type 1 diabetics do not produce enough (possibly none) insulin since beta cells of pancreas are damaged and as far as I know glucagon is produced by alpha cells (which are healthy in diabetic body, I suppose). So, my question is that since glucagon is released when the blood glucose is low, why do the diabetics experience hypoglycemia? Shouldn't the glucagon be released and increase the blood sugar?

Note that in Role of Alpha Cells in Diabetes1, the following is stated:

  Glucagon responses to hypoglycemia have been known to be blunted in
  type 1 diabetes of long duration, and this may be a result of a loss
  of alpha- and beta-cell communication secondary to insulin deficiency.

Rudy W Bilous. Role of Alpha Cells in Diabetes - Medscape - Apr 11, 2003.


texts: Are these bedbugs, or what kind of bugs?

texts: I just moved into this house a week ago and just noticed these tiny bugs around my plaster wall. I wouldn’t of noticed them but I felt them in my arm walking, I looked at my wall and saw a bunch of them in different places they’re tiny and brown.


texts: How does salinity affect the bonds of an enzyme?

texts:
According to my textbook, "Too much or too little salt can interfere with the hydrogen bonds that hold an enzyme in its three-dimensional shape". I know that NaCl is held together by an ionic bond, meaning that one atom is strongly positive (in this case sodium) and one atom is strongly negative (in this case chlorine). I would guess the polarity of salt has something to do with its effect on hydrogen bonds, which consist of a hydrogen atom which bonds weakly to a strongly electronegative atom, resulting in a similar behavior to its ionization in glass of water, since water molecules are also polar and form hydrogen bonds with one another.

My question is, how exactly does salinity affect the bonds of an enzyme?


texts: Any references contradicting Hormesis from low dose studies?

texts:
I've recently read some papers on Hormesis (the stimulatory effect of low doses of substances toxic at high doses). The papers are all published in respected peer-reviewed journals, here, here, and here for example, but they're pretty much all by one person, Edward Calabrese. I'm struggling to make sense of an issue which is clearly an acceptable enough possibility to appear in peer-reviewed journals, but which seems to have garnered absolutely no further interest beyond the one man. I naturally presumed that the concept had been dismissed by some later study, but I cannot seem to track such a study down.

To be clear, I'm not interested in policy, as the use of linear no threshold models vs Hormetic models for public policy is so highly politicized a topic with unscientific approaches on both sides (the vested interests of polluting industry vs an easily panicked population urging it's legislators). I'm just looking to fill the gap in my reading of the science. Papers showing demonstrable low dose responses which match a LNT model would be good, papers showing contrary results to Calabrese's for the same toxins would be ideal.


texts:
We have 3 color receptors in our eye, so assuming the above picture is precise we are checking for 3 wavelengths: 450nm, 540nm and 700nm.

Pink for example has an RGB value of

R (700nm): 1
G (540nm): 0
B (450nm): 1

Violet has an RGB value of

R (700nm): 0.5
G (540nm): 0
B (450nm): 1

However Violet has a wavelength of 400nm which is lower than the Blue receptor. So how can it activate the red receptor when red is clearly not active at that frequency?

Does that mean Ultraviolet appears blue to the human eye? Why is it constantly painted as violet in all frequency graphs?

The question was first duscissed here (https://physics.stackexchange.com/questions/486560/what-frequency-is-pink-color) but did not receive the answer I need.


texts: Is it possible to grow E. coli K12 with algal amino acids as the sole carbon source?

texts: Instead of glucose or glycerol, is it possible for E coli to grow on an amino acid mixture as the sole carbon source and, if so, what should the concentration be?


texts: What is the terminal electron acceptor in methanogenesis?

texts: I learnt that methanogenesis is a type of anaerobic respiration that utilizes carbon compounds such as CO2 or acetic acid as their terminal electron acceptor in their electron transport chain rather than using oxygen. However, when I went through my textbook, I found out that conversion of CO2 to CH4 is not one step reaction but many other compounds are synthesized in between and methyl-SCoM is converted to methane.In one article I read that Com-SH is the terminal acceptor When I tried searching in google for the same I came across a lot of diagrams of mechanism but some of them did not match with each other. I have no idea what's going on. It would be really helpful if you can help me out here.


texts: How can one measure the effect of a stem cell's matrix on the progeny of that stem cell?

texts:
A number of recent papers that have used hydrogels to alter the ECM of mesenchymal stem cells to quicken their development to cells used specifically for cartilage or really any other type of cell.
Here is an example of one of the articles
However, even after looking at the data sets from all of these experiments and research projects I still don't understand how this is done (i.e. what lab instruments, the actual procedure), for example of cartilage progenitors from stem cells.

I specifically want to know how this occurs in neuronal stem cells and how can we isolate those stem cells and test the effect of encapsulating them with a type of hydrogel to alter their fate? How could this be done?


texts: How does alcohol interact with sympathomimetics to affect the cardiovascular system?

texts:
There is a fair amount of information on the cardiovascular effects of alcohol, and of sympathomimetics. How do they work? And how do their mechanisms interact?

We know that similar pathologies result from each. With alcoholics often experiencing mild left ventricular hypertrophy, mild diastolic dysfunction which preceeds systolic dysfunction, resistant hypertension; and a dilated cardiomyopathy - sympathomimetics leading to cardiomegaly, sinus tachycardia, left ventricular hypertrophy, and dilated cardiomyopathy #1.

An article notes that "alcohol competes with amphetamine for the metabolizing enzymes in the liver, therefore enhancing the bioavailability of amphetamine" #2. Are any effects of alcohol mediated by sympathomimetics/catecholamines, and if so which? Et vice versa.

[1] Chemical Cardiomyopathies: The Negative Effects of Medications and Nonprescribed Drugs on the Heart https://bit.ly/2AMU6eM

[2] Myocardial Infarction Associated with Adderall XR and Alcohol Use in a Young Man https://bit.ly/2SV4wQD

[3] Cardioprotection by regular ethanol consumption: potential mechanisms and clinical application https://bit.ly/2RRVVAQ

[4] De Musset's sign https://bit.ly/2HljluG


texts: Which is more susceptible to dehydration — extracellular and intracellular fluid?

texts: I want to ask in human body, there is intracellular and extracellular fluid that makes up the total body water of our body, which is drained first when we do activities? extra or intra? if I want to do a bioimpedance measurement, does measuring only the extracellular fluid good? Thankyou


texts:
Is there term in neuroscience that describes change in neuronal circuits depending on context: low sugar/fear/... => hormones => different pathways of behavior ...?
I know that is something from Behaviorism but I search something more from "real science" like from computational biology, neuroscience etc


texts: The concept of backpropagation in neural networks actually occurs in the brain?

texts:
I am aware the Human brain has many functionally distinct components, but let us specifically consider the Human visual cortex: could Artificial Neural Networks (ANNs) be "trained" (through, e.g. backpropagation) in an analogous way to how the visual cortex "learns"?

Is the concept of backpropagation in ANNs a phenomena actually observed in the Human brain?

Related

Books on machine learning applications in Biology


texts:
I want to evaluate the level of gene expression by real-time PCR.  I have five controls that are "clinically" the same. I calculated the "fold change" of the target gene regarding each control.

What if the result of "fold change" for my target gene is different for each control? I mean it is up regulated according to three of them and down-regulated according to the rest two.

Is the intervention biased? Or should I consider the average?


texts: Does the body have a gate control for pain

texts: I understand it is not the most accurate source but I recall a House episode where he claimed the body had a control mechanism for pain in which only the most painful thing was felt. Is that true? and if so how does the body control which injury we feel and could we use this to our advantage?


texts: Why does hexokinase bond phosphate to the hydroxyl group on carbon-6 of glucose in glycolysis?

texts:
When glucose enters the cell, it is phosphorylated by the enzyme hexokinase.

Why is this phosphorylation done at carbon-6? Why not at C-1 or C-2?

In other words, why is glucose-6-phosphate being produced rather than a different isomer of phosphorylated glucose?


texts: Can someone help me identify this insect

texts: We found this insect in the basement of a friends house. It is about 1 inch in size. My friend lives in Canada


texts:
My mom was telling me that if I put the unfinished bowl of milk and cereal back to the fridge, the saliva that has been stuck to the spoon gets passed to the milk. The saliva in milk will make milk go bad faster than if there were no saliva inside. Is that true? If so, how comes? It would be great if there are scientific evidences or references to back it up.
I have found a Quora post having some people saying that it will make the food go bad faster. I was not able to find any other references


texts: At which point does a cell switch its function?

texts:
In a multi cellular organisms there are many cells of different functions. How / when does a cell change its function compared to its parent?
Is it done by influence of other cells after its has been created?


texts: If chylomicrons can not get into the capillaries, how do they supply to tissues?

texts: The transport of chylomicrons is into the lacteals mainly because they are too big to get into the capillaries and yet they later supply triglycerides in the extra hepatic tissue by traversing in the capillary bed. This seems utterly illogical and self contradicting. So something seems to have gone wrong in this line of thought.


texts: What Chemical Trigger Causes Ectomycorrhiza To Change From Asexual To Sexual?

texts: I want to know the trigger behind the change of asexual to sexual ectomycorrhiza when symbiosis with a tree root is formed. As ectomycorrhiza attaches itself to a root, it forms a relationship wherein phosphorous to the tree/plant is exchanged for glucose to the fungus. When this symbiosis occurs, the fungus, which is normally asexual, becomes sexual(male/female components) and buds form as a result. Thus I could hypothesize that if glucose is the catalyst, I could saturate the soil and cause this reaction. However, I am not sure what the actual chemical signal is, or if there is an unforeseen factor causing this change. Does anyone have any knowledge on the subject of what the aforementioned catalyst would be?


texts: DNA extraction from plants and algae don't use phenol. Why?

texts:
I don't know if here is the correct place to make this question, but I've been noticing that protocols for the extraction of photosynthetic organisms DNA don't use phenol. Only CTAB / Chloroform.

Why?

Because bacterial or animal extraction are phenol:chloroform based.

Thank you


texts: I have gone through various sites and some say there is NADPH2 and some say there is no NADPH2 there's only NADP+ ...WHich is the correct view....Please dont mark this answer as duplicates since I have asked a similar question related to photosynthesis in the past but there too I have not received any satisfactory answer bythe community .


texts: Does animal fat and meat contributes differently to our body?

texts:
Is animal fat harmful to our body or is it harmful if the amount eaten exceeds a certain amount?
I have heard fat is more concentrated than protein. If I am correct then we can get more energy from fat. Then why is fat not desirable?
Our ancestors used all the parts from their hunt, even the fat. How did it work for them?
Would eating fat be beneficial for an athlete? (May be for different purposes: power, endurance or building muscle)


texts: Why is lower case used in front of a capitalized acronym (e.g. rDNA)?

texts:
Examples: rDNA, mRNA, tRNA.

Why do we use small case for "r" in "rDNA", etc? Any particular reason?


texts: What's the mechanism behind 'losing heat through your extremities'?

texts:
I can understand how if you are not circulating enough (warm) blood, by not moving much while in a cold environment, your extremities themselves lose heat, and become cold - but I don't understand how they (the hands, feet, and head) can make the rest of your body lose heat too.

'Drawing the heat out of your body' (as people have termed it to me) doesn't make sense itself - what is the actual mechanism(s) behind the (exposed, relatively uncirculated) extremities, 'drawing' heat out of the body?

Is it that it merely draws the need to heat those (poorly insulated, circulated) extremities from the existing distribution of heating the other parts of your body, thus lowering how warm those other parts are?

If so, how does that happen? In the case above, where you're not moving the body to circulate warm blood to the hands (or using other warming stimuli like friction), how would 'heat transfer' to the hands occur then? Or does it just indeed slowly 'lose heat' and get colder and colder (which would then lead me back to my question, how would that explain the rest of your body becoming colder as a result of the extremities becoming colder)?


texts: Book recommendations for evolutionary models

texts:
I was recently working on getting a statistical model of a DNA sequence. To do this I found that understanding evolution quantitatively seems to be quite important. I would really appreciate any book recommendations on the basics of evolution.

I come from an Electrical Engineering background and have a limited knowledge of evolution and biology.


texts:
Drug interactions between properly dosed NO and other medications are not expected, but side effects may include noisy breathing, hematuria, or possibly atelectasis. (pg.no:577; Goodman and Gilman Pharmacology 13e)

What is the basis for this hematuria?  Is it because of platelet inhibiting activity of Nitric Oxide?


texts:
According to wikipedia, the active substance is nepetalactone ($\ce{C_{10}H_{14}O_{2}}$) which has weak sedative, antispasmodic, febrifuge, and antibacterial effects in humans. Why are cats so fond of it? Why do they seem to get high on it?
According to the same wikipedia page, the effect is gene-linked but it does not mention which genes, what they code for or any details whatsoever. Are all felines affected in this way or only Felis catus? What is the biochemical mechanism by which cats are attracted to catnip?


texts:
The myelination of axons has plenty of advantages. It increases signal speed in axons, and thereby reduces reaction times. This is, of course, very good for the survival of the animal in question.
Most invertebrates do not have such a myelin coating. I know, that evolution does not just evolve features, because they are useful, but it seems to me, that invertebrates are entirely outclassed by vertebrates, because of how important reaction times are to an animals survival. So if such a trait is not impossible to evolve, it would most likely have evolved multiple times in different animals. If it was as advantagious as I imagine, invertebrates without myelin would have been outcompeted by now.
So there must be a significant disadvantage to having myelin coating.
Can you explain to me, what that is exactly?
Is it just the associated energy cost?


texts: Are antibodies and hepatitis viruses of similar adaptability?

texts:
Antibodies and Hepatitis viruses both have hypervariable regions.
Is one more adaptable than the other?
Precisely how adaptable are they?
I have read that antibodies can be trained to bind to almost any antigen, is the same true for Hepatitis?

Long-Term Evolution of the Hypervariable Region of Hepatitis C Virus in a Common-Source-Infected Cohort
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC110045/

I guess the first step to answering this is to find/conduct a study in which the Hepatitus virus is mutated and selected for a particular antigen. I am not sure if this has been done, but it definately has been done for antibodies.


texts: Why is the frog genome so much larger than a fish's?

texts:
As we have heard in the summaries of the human ENCODE project, 80 per cent of junk DNA appears to have an essential function. Many fish have a genome with only one tenth the size of a usual vertebrate genome. Why can fish have 1/10th of junk DNA and be still fully functional? What has a frog more than a fish has? I'm especially interested if we can see the difference somewhere, complexity of physiology or anatomy, or such.

Jap. puffer fish genome: 390 Megabases, 47,800-49,000 genes (UniProt)

Medaka genome: 690 Megabases, 24,600 genes

Clawed frog: 1,500 Megabases, 23,500 genes


texts: why can proteolysis only occur once on a enzyme?

texts: My texbook says that proteolysis can occur once in the lifetime of the enzyme? I know that proteases must cleave the zymogen at more or more specific locations, but why can't the process take place more than once?


texts: What biochemical molecule viewer allows for changes in amino acids and resulting tertiary structure?

texts:
I am familiar with the Jmol, Rasmol and PyMoL softwares, and was recently introduced to BioBlender. However, I am completely unaware if any of these programs (or others) are capable of loading a .pdb and allowing for the change in a particular amino acid, to ultimately visualize the change in tertiary structure caused by that substitution.

Are any programs capable of performing an amino acid substitution on a molecule loaded by .pdb and showing the change in tertiary structure?


texts: Why did my isolation streak of an unknown organism on Mannitol Salt Agar turn yellow where there was no growth and magenta where there was growth?

texts: I repeated a culture twice in an entry level microbiology class for our final lab project of culturing a provided unknown organism.  One of the required tests on our dichotomous key was to culture a gram positive cocci in mannitol salt agar.  After repeating the experiment twice as instructed, and doing an isolation streak as instructed, the part of the agar with no growth was acidic while the part of the agar with growth was neutral or slightly basic.  Both cultures were incubated for around 48 hours, and the first one then refrigerated for another 48 hours while the second one was examined directly after incubation. My professor told me to disregard the results and treat it as a negative in my report, but I'm perplexed as to how this result came about.


texts: Are there examples of non-pathogenic RNA viruses?

texts:
There do seem to be some non-pathogenic DNA viruses, for example Foamy virus. Non-pathogenic viruses would be great to use for gene therapy applications, except DNA viruses incorporate themselves into the genome, which could drive oncogenesis. RNA viruses that are non-pathogenic would be great, but all RNA viruses seem to be especially pathogenic. Rabies, Ebola, Bas-Congo, Smallpox, etc.

Do there exist "gentle" RNA viruses?


texts: Are humans more aggressive during a full moon?

texts:
Is it true that we are more agressive during the night when there is a full moon?
If true, could this be a remnant from times where we needed to hunt for our food and so could see more at night when there was a full moon?

Source of question: article


texts: Why is exocrinous pancreatic cancer so lethal when compared to others?

texts:
I know it seems far fetched, but I would really like to understand why an interference with the regulation of production of pancreatic exocrine products (and which are they) is so lethal. I know that people having it generally live for one year or less (top is circa 5 years).

Why?


texts:
The formula in textbooks for $t_{\frac{1}{2}}$ of a drug following first order elimination is generally given as $$t_{\frac{1}{2}}= \frac {\ln(2).V_d}{Cl}$$where $V_d$ is the volume of distribution and $Cl$ is the clearance.

Shown below is my attempt to derive the formula but I don't know where I'm going wrong.

Assuming first order kinetics of elimination, the rate of elimination ($R$) would be proportional to the plasma concentration ($Cp$)

$$ R = Cp . k$$

Where $k$ is the rate constant.

For calculation of $t_{\frac{1}{2}}$, since this is a first order elimination, $$ t_{\frac{1}{2}} = \ln(2)/k$$
Substituting,
$$ t_{\frac{1}{2}} = \frac{\ln(2).Cp}{R}$$
Since $ Cl = R/Cp$, substituting would give,
$$ t_{\frac{1}{2}} = \ln(2)/Cl$$

Since both the formulae don't match (this one doesn't have a $V_d$ term at all!), where have I gone wrong? Also then how is $Cl$ different from $k$?

According to the correct formula, $k=Cl/V_d$. How is that so?

EDIT

Volume of distribution is the apparent volume of blood the drug takes up and is given by $$V_d = \frac {Dose}{Pc}$$

Clearance is the volume of blood that has been cleared of the drug in unit time and is given by $ Cl = R/Cp$

Correct me if the basic definitions themselves are wrong.


texts:
[

I found this little guy in my orchid on the upstairs balcony. I live at Sanctuary Point which is on the south coast NSW


texts: I have done multiple cultures of E. coli bacteria and related species over the course of my education. Almost every time, they had this revolting smell. However, other organisms used for genetics experiments (eg. Saccharomyces cerevisiae) rarely have a bad scent, if a scent whatsoever. My question is, what is it about the coliform metabolism that produces such a pungent and revolting odor? Any and all answers are appreciated.


texts: Why do we exhale after we hold our breath?

texts:
I tested this out with my friends, and I find that after they hold their breath and can't hold it anymore, they exhale air, instead of inhaling air.

Interestingly, they all try to inhale in as much air as possible before starting to hold their breath. When I told them to exhale as much air as possible before starting to hold their breath, they inhaled air after they can't hold it anymore.

It's understandable that when one exhales then holds his breath, he needs air and thus he inhales afterwards. But when one inhales then holds his breath, shouldn't he inhale again after "using up all that air he inhaled before holding hi breath"?


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


texts: Problem with joining the gene of interest into the open plasmid when their lengths are not the same

texts:
Before the recombinant plasmid is obtained in recombinant DNA, the gene of interest is inserted into a linearized plasmid by DNA ligase.

What happens if the length of the gene of interest is not the same as that of the gap in the open plasmid? (e.g. far longer) Can the gene still be connected with the gap or are other processes needed before the recombinant plasmid can be put back into the bacteria?


texts: Genome-wide association study (GWAS) search engine?

texts:
I am not a biologist and came across the term genome-wide association study or 'GWAS' for the first time today.
Now I would like to see if there is a GWAS on the particular condition I am interested in finding out about. Is there a search engine that collates all known GWAS and makes them searchable?
Note: the backup plan is to use Google, but I wonder if there's anything dedicated to this particular task.


texts: Is prion a term used to describe the normal form of the protein as well as the disease causing form?

texts:
I've been reading my textbook and it refers to prions as a normal protein with a helpful function but it can turn into a disease causing form. However, I look in my other textbook and it refers to the word prion as solely being a disease causing protein.

I'd like to know which is the correct definition. Ie. Would I be correct in saying "The prion protein is normally involved in synaptic transmission but can turn into a disease causing form"?

Thanks in advance!


texts: How can we usually "trust a fart" not to be liquid or solid?

texts:
Jack Nicholson's character Edward Cole in the movie The Bucket List said ...and never trust a fart, and a search for Al Roker leakage White House will clear up any doubts what that's all about.

How is the adult human body usually able to sense the difference between solid, liquid, and gas and enable the brain to consciously decide on the proper course of action? (e.g stay put, walk, or run!)

Per @theforestecologist's request I'll restate the question using my best "science words": How are adult humans able to determine when pressure in the rectum is the result of solid waste, liquid waste, or flatulence?

A search for answers has turned up the following:

Source: https://www.sharecare.com/health/digestive-health/how-can-i-have-normal-bowel-movements

  In a rapid "sampling reflex," these nerves inform the brain about whether the rectal contents are intestinal gas or liquid or solid stoo...

However I can't view this link further.

Searching further for "sampling reflex" I've found this

  Sensing of the arrival of stool in the rectum with activation of the recto-anal inhibitory and sampling reflexes which allow stool to enter the anal canal and to be distinguished from flatus.

This provides an opportunity for sensation to take place, but does not describe how  stool is distinguished from flatus, and doesn't even mention liquid.

At this point I'm way out of my depth.


texts: Help identifying winged, moth-like creature

texts:
I noticed this moth (?) on my sofa yesterday. It matched the color of the sofa, so it was pretty hard to see. It's about an inch long, with a yellow body and light brown wings. I think it's a T. bisselliella. I'm from Kerala, South India.

The wings:


texts:
I am curious how Gall Wasps, bacteria and other organisms induce galls to form.

Specifically, what chemicals induce gall formation?


texts: Why does absorption (at 260nm) of ssDNA increase with temperature?

texts:
In the graph below, I understand why A260 of double stranded DNA would increase with temperature increase, as more of the DNA becomes single stranded (and A260 of ssDNA is higher than that of dsDNA because the aromatic bases are more exposed, which absorb the light).

However, I do not understand why the absorbance of ssDNA also increases... I know that individual nucleotides also absorb more than ssDNA (as shown in "inequality" below), but I doubt that the covalent bonds holding the nucleotides are breaking at 80 degrees centigrade. Would this maybe be the effect of an increase in temperature increasing absorption? (I have read that increase in temperature increases collision of photons hence increases absorbance, but I am not quite sure). Thank you.

"inequality" showing which has higher A260:

  single nucleotides > ssDNA/ssRNA > dsDNA


texts: How do bats survive their own coronaviruses?

texts:
How do bats survive their own coronaviruses (without showing any symptoms)?

Or, more generically, how can viruses keep reproducing inside healthy carriers without inducing any pathogenic effect?

Are coronaviruses able to replicate themselves without harming bats, or maybe these viruses are just latent like herpesviruses in humans?

Related question: Why are bats the source of dangerous coronavirus pandemics?


texts: Sexual reproduction in organisms with 1 parent

texts: An organism that carries out sexual reproduction with itself,  for example a flower with both the anther and stigma,  does it actually contain 2 sets of genes in order to produce genetically dissimilar organisms or do it just leave the offspring to become genetically dissimilar through random crossing over during miosis?


texts: Making a hole in a tree is okay? Or does it damages the tree?

texts:
I am watching a TV series named "Treehouse Masters." What they do is make houses on trees or around it getting physical support from a big strong tree, like this:

But to make the support strong, they make a big hole in the trunk of a tree

Then they put a steel beam into it, like this:

In some cases, they make more than one hole. So, does this affect the tree in any way?

If anyone makes a hole that big or even bigger but doesn't fill it with any other thing(like the beam), will the tree heal itself?

I have heard that trunk is the most important part of a tree. So I am curious to know if this act is cruel towards the trees or not.


texts: Is Valerian extract a diuretic or an antidiuretic?

texts: I am trying to determine if valepotriates (valerian extract) is a diuretic or an antidiuretic. Some individuals take valerian as an herbal supplement for anxiety disorders. Some individuals claim that valerian extract can act as a diuretic, while others claim that it is an anti-diuretic. I am trying to determine which it is - diuretic or antidiuretic?


texts:
it was in Guatemala
it was really big like 4 inches
sorry I don't have a better photo


texts: Why do recessive lethal genetic diseases continue to exist?

texts:
I'm trying to understand, in a simplistic representation of a recessive genetic disease (e.g. Tay Sachs), why wouldn't it "disappear" over time (many generations). Please excuse the use of non-professional terminology below, I hope the point I'm trying to make will be clear.

Let's assume that, for simplicity, people marry at random and each couple has 4 children. Denote the probability of carrying the "bad" gene by p, then a couple of 2 non-carrying people will have 4 healthy children, a mixed couple will have, on average, 2 healthy and 2 carrying children, and a couple of 2 carrying people will have 1 healthy, 2 carrying, and one sick child (which we assume will not have children so we ignore it in further calculations).

Assuming large enough population and random couples and everyone gets married (for simplicity):
The probability of a couple of non-carrying: (1-p)^2
The probability of a mixed couple: 2 * p * (1-p)
The probability of a 2-carrying couple: p^2

The expected number of healthy children per couple: 4*(1-p)^2 + 2*2*p*(1-p) + p^2 = 4 - 8*p + 4*p^2 + 4*p - 4*p^2 + p^2= 4 - 4*p - p^2 = (2-p)^2
The expected number of carrying: 2*p*(1-p) + 2*p^2 = 2*p - 2*p^2 + 2*p^2 = 2p

Dividing to get the new probability for carrying the gene:
2p / (2-p)^2
Which for small enough p is clearly smaller than p (e.g. for p = 0.05 we get ~0.0263).

If I'm not mistaken this means that the number of those carrying the genes should become exponentially small (in the number of generations).

I realize this is a very simplistic model, marriages are not random, mutations occur etc. but I would expect the basic intuition to hold. What am I missing?


texts: What molecules does amylase enzyme work on?

texts:
I know that in the human body cellulose cannot be broken down by enzymes; however, I am confused as to which molecules amylase enzymes during fermentation.

I also looked at https://en.wikipedia.org/wiki/Amylase where it says that "All amylases are glycoside hydrolases and act on α-1,4-glycosidic bonds." so now I am confused.

Does amylase work to break down starch into glucose exclusively?

If not...
Does amylase enzyme break down corn cob extract which contains xylans, cellulose, lignin and some sugar for fermentation?
Does amylase enzyme break down corn stem which contains cellulose, hemicellulose and lignin for fermentation?


texts: Are cortical columns restricted to somatosensory cortical sections?

texts: From this previous question, it seems like evidence for the minicolumn organisation of the neocortex seems to be primarily based off observations around the sensory parts of the cortex, such as the primary visual cortex and the barrel cortex. Have column-like organisation been observed in non-sensory regions of the neocortex?


texts: cerebral edema and blood pressure, pulse

texts: What happens to blood pressure in cerebral edema; does systolic and diastolic rise equally? So the pulse actually slows down? Can't find anything about that, please help


texts: Can germs develop surfactant resistance in a harmful way?

texts:
Germs can develop antimicrobial resistance. It is a problem serious enough to deserve an FAQ page on the WHO website (http://www.who.int/mediacentre/factsheets/fs194/en/).

But how about surfactant resistance? We wash our body, our dishes, our clothes, and pretty much anything that is washable with soap/detergent, which means surfactants.

So can germs develop surfactant resistance in a way that is harmful to human health? If so, is there any recorded experiment about it? If not, why not?


texts: Are probabilities of mutations symmetric?

texts:
For the premise of this quiestion let's assume that there is an allele A and an allele B. The allele A has a probability P to mutate into the allele B in the given timeframe.
Is it also true that the allele B has the probability P to mutate into the allele A?


texts:
I found this cocoon outside my house and I want to know what insect might be inside it and it’s species. Please help!

I found it a day ago when it was a worm, now its a cocoon, it’s like outside the main entrance (which is like 2 metres high) and the cocoon was half way on the left, and it was out in the sun, to be honest I’m surprised little kids didn’t kill it yet.
I live in Kuwait in a town called Hadiya.

I don’t see many worms in Kuwait, I’ve only seen like 4 in my whole life.


texts: Are there any pairs of animal species that regularly prey on other?

texts: I don't mean cannibalism within a single species - I mean, are they are any pairs of species A and B such that members of species A regularly prey on members of species B, and also members of species B regularly prey on members of species A? I'm considering adults preying on other adults of the other species, not on individuals early in their life cycle.


texts: Looking for university/graduate-level texts on RNA

texts:
Although I was not a biology major in college, I took the biology introduction sequence, as well as organic chemistry and biochemistry.

I would like to learn more about RNA and ribozymes. What texts/textbooks are currently used? Perhaps it's best to begin with a genetics textbook.

The scope of the book should cover be at a undergraduate level or higher, and should cover the dynamics and purpose of ribozymes.


texts: Why is carbon dioxide produced in alcohol fermentation but not in lactic acid fermentation?

texts:
From my understanding, alcohol fermentation takes place in yeast and lactate production takes place in humans.

These two pathways take place only when there is insufficient oxygen, because the other parts of metabolism (TCA cycle, ETC) can't take place as they happen in the mitochondria, which requires O2.

For alcohol fermentation, there is production of carbon dioxide while lactic acid fermentation does not produce carbon dioxide. CO2 is produced when there is an oxidation of one carbon molecule. So my main question is: since there is a lack of O2, how does yeast produces CO2 while humans do not?

Also, how does NAD+ recycle all the time when glycolysis is happening?

Thanks!!!


texts: Is there any evidence that supports glycolysis in mitochondria or chloroplasts?

texts: Glycolysis is known to be a part of cellular metabolism undergone by both eukaryotic and prokaryotic cells, whether under aerobic or anaerobic conditions. As the endosymbiotic theory states that mitochondria and chloroplasts were once bacteria that lived apart from eukaryotic cells, do they have any enzymes or compounds suggesting that they once did glycolysis?


texts: How did the first self replicating organism come into existence?

texts:
When people try to explain evolution, they tell me that evolution is a cumulative result of mutations & natural section of the more superior individuals of a particular species. I think I'm fairly convinced with this explanation.

But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?

An answer I found on Reddit didn’t really convince me.


texts: Ciliated Epithelium & Goblet Cells Lining The Trachea

texts: My book states this - The cells produce mucus that traps particles of dirt and bacteria in the air breathed in. The cilia on these cells move this debris up the trachea and into the stomach. Isn't the stomach below the trachea? Wouldn't it move the dirt and debris up the throat so it can be removed via the mouth? My book does also state that the debris is pushed up the throat as well so does it do both?


texts: Does anxiety about weight or eating cause people to become overweight?

texts:
A while ago I saw this TED talk about the futility of dieting. The speaker suggests that a body maintains a homeostatic weight point and returns to that weight after dieting has stopped:

  Turns out the brain is an incredibly efficient regulator of body
  weight. Isn’t weight loss about how much you eat versus how much
  energy you burn? Nope, it’s not that simple an equation: it turns out
  that hunger and energy use are controlled by the brain, mostly behind
  the scenes, and this unconscious force is stronger than mere
  willpower. The brain has its own sense of what your body should weigh
  — no matter what you believe — called the set point, which has a range
  of about 15 pounds. While lifestyle changes can shift your weight
  within this range, it’s much harder to move outside of it.

The speaker suggests that once she gave up dieting, she actually lost weight. Since then I've seen a number of other anecdotal reports of people losing weight once they let go of the need to diet and started to "eat anything they wanted".

This makes me ask - does anxiety about weight and attempts to control one's eating cause people to put on weight? In other words, if there's some unresolved anxiety issue in one's life, does it cause the human body to start preparing for hard times by storing extra fat?


texts:
I have calculated the probability that any child will have a particular blood type from both the genotype level and the phenotype level assuming the human ABO Rh system is followed.

Here are the genotype probabilities:

AA+/+ 49/1764
AA+/- 98/1764
AA-/- 49/1764
AO+/+ 98/1764
AO+/- 196/1764
AO-/- 98/1764
BB+/+ 49/1764
BB+/- 98/1764
BB-/- 49/1764
BO+/+ 98/1764
BO+/- 196/1764
BO-/- 98/1764
AB+/+ 98/1764
AB+/- 196/1764
AB-/- 98/1764
OO+/+ 49/1764
OO+/- 98/1764
OO-/- 49/1764

Here are the phenotype probabilities:

A+ 441/1764
A- 147/1764
B+ 441/1764
B- 147/1764
AB+ 294/1764
AB- 98/1764
O+ 147/1764
O- 49/1764

Here is the frequency of the blood types in the 1st generation by genotype:

AA+/+ 5/101
AA+/- 5/101
AA-/- 5/101
BB+/+ 5/101
BB+/- 5/101
BB-/- 5/101
AB+/+ 5/101
AB+/- 10/101
AB-/- 5/101
OO+/+ 5/101
OO+/- 5/101
OO-/- 5/101
AO+/- 10/101
AO+/+ 5/101
AO-/- 5/101
BO+/+ 4/101
BO+/- 4/101
BO-/- 4/101

Here are the numbers and their genders; a number represents an individual from a population of 101:

Male:
0,2,5,10,11,17,20,22,23,31,34,40,41,44,46,47,50,55,59,61,62,68,71,79,80,82,85,88,89,92,94,100

Hermaphroditic(and fertile):
4,8,16,25,32,64

all the rest are female

M/F mating: 11,904 offspring in 2nd generation H/A mating(hermaphrodites can mate with other hermaphrodites, males, females, and even themselves): 3636 offspring in 2nd generation

If you divide these by 6 you will get the amount per operation. The operations I am taking into consideration are +, -, *, /, ^, nth root, and arrow arrow(tetration).

So how can I take the frequency of blood types at the genotype level, probability of blood type at genotype and phenotype levels, and total number of offspring to get a 1st order estimate of the frequency of these blood types in the 2nd generation?


texts:
Why is it that only humans commit suicide?

Many animals do 'brave' things to protect their children or family, and some male spiders sacrifice themselves so that they can impregnate the females. However, humans commit suicide without necessarily any intention to help their offspring. Why?


texts: Roughly at least, how many types of cells comprise human blood?

texts:
A long time ago there were only three kinds - red, white, and rose platelets. Advances in cell sorters and more recently in genetic techniques and differentiation studies have led to the identification of a wide variety and complex lineage of cells that comprise human blood.

Roughly at least, how many types of cells are currently identified?

I understand that "types" is a non-technical term, and I'll try to better define what I mean. For example, I do not mean to enumerate each antigen specificity separately because that would make the number fairly large and probably dependent on the individual's history.

One possible definition of a "type" would be that it has been given a name.

I don't mean to include cells that are present due to injury, clean-up, trash collection, or foreign cells including bacteria, viruses, parasites etc.

Just for an example, here is an overview of types of hematopoietic stem cells. There may be further recognized subdivisions, I don't know how far it goes. There are certainly other cells that comprise human blood. (From here.)


texts: How does use an action potential from innervation selectively modify tropomyosin over time?

texts:
Within a myofibril, the myofilaments move past one another to product muscle contraction if and only if the actin binding sites are exposed to the myosin by locally removing the tropomyosin by binding it with calcium ions

What isn't quite clear to me however is: what does a pulse from a motor neuron do to the tropomyosin in order to to excite this initial change to move the tropomyosin away and expose the actin?
Then, how does the muscle cell and/or motor neuron sustain this state of contraction, and then finally decide to end this state of contraction and return the muscle cell to its relaxed state?
Also, where exactly is the tropomyosin going after it binds with calcium ions?


texts: Are Lambic beers the product of quorum sensing?

texts:
Lambic beers are a Belgian specialty which is still made by open-air "inoculation" by airborne microbiota first, followed by additional yeasts, LAB bacteria and more joining in at the time of transferring to used wine barrels. (No yeast is "pitched" or added intentionally.)  As many as 200 organisms may play a role, and they seem to take turns, partly regulated by rising acidity and alcohol probably, but with some such as Brettanomyces seeming to simply wait their turn compared to what they will do in a single strain fermentation.

Lambic (or American Coolship Ale hereabouts) fementations can take up to 3 years.  Often a thick fluffy "pellicle" or "film" forms on the top of the barrel, like "flor" on sherry, evidently in response to and protection from oxygen. (Sure seems like a bio film.)

(There have been a few studies tracking the staggered blooms of various organisms, including one done 2 years ago at Allagash and one this year at Cantillon, but no discussion about how the sequence is orchestrated. So this is a speculative question about the evolution of these beers.)

Could interspecies quorum sensing be at work?    How could that be confirmed?


texts: Why do we age? or Do we have a theory of senescence?

texts:
There seem to be a number of ideas about why we age. Hypotheses include the gradual accumulation of cell metabolic products affecting organism function and the reduction of telomere length during cell division.
My hand-wavey idea would be "wear and tear".

Are we anywhere near a consensus theory of senescence?


texts: How can the layperson test whether a UVC light sold as "germicidal" is a fake or probably the correct wavelength?

texts:
Are there simple ways to test whether a light is likely short wave / UV-C, or at least whether it is probably a fake?
Real Example:
2 lights are allegedly germicidal and supposedly emit germicidal 254nm radiation.

Light 1 darkens transition glasses and emits the smell of chlorine / ozone.
Light 2 does neither but appears much brighter than Light 1.

Does the ozone smell of Light 1 entail that it at least emits radiation within the UVC band?
Assuming the glasses do darken outdoors and do darken in response to Light 1, given that they do not darken with Light 2, is it safe to conclude Light 2 emits no UV at all?


texts: How are latence period and duration of infectiosity defined?

texts:
I assume that infectiosity of an individual is not a binary property but a quantity that grows and decays gradually, very much like the number of infected or infectious individuals in a population.
Nevertheless, it seems to be modelled as a binary property in SEIR models where a latence period λ (where the individual is infected but not infectious) and a duration δ of infectiosity is considered, giving rise to a step function of infectiosity:

But assuming that infectiosity is a continuous variable, how are λ and δ defined? Is λ the time when the infectiosity goes above half (0.5) of its maximum, and λ+δ the time, when it goes below this value again? But isn't the factor 0.5 quite arbitrary? λ and δ – from which every SEIR model depends very sensitively – would take quite different values when factors 0.33 or 0.66 were chosen?

Is it justified to work with the factor 0.5? Or is another standard factor assumed implicitly by default? If quite another factor would be chosen, how would this have to be reflected in the
SEIR differential equations to yield the same results (solutions)?

Note, how λ and δ can be defined in terms of α (time from initial to maximal infectiosity), σ1 (left width at half maximum) and  σ2 (right width at half maximum):

λ = α - σ1

δ = σ1 + σ2

Edit: There might be a natural threshold that turns infectiosity into a binary property: when infectiosity is checked by a binary test which either tells that the person is infected (e.g. by detecting some virion or antibody) or that it is not. Only if you are able to count and distinguish the number of virions or antibodies, it will turn into a more fine-grained property.


texts:
Imagine a family pedigree.

Mathematically it is a graph, which consists of nodes and edges.
Nodes being family members, and edges - their relationships.

In a clinical setting, what is the proper term for the nodes? Would they be called 'leafs'?


texts: Do plasma B cells express the BCR or only produce soluble antibodies?

texts: Is the B cell receptor still expressed on a B cell once it has begun to produce soluble antibodies? Is there a gene change that prevents the membrane-bound form from being produced anymore?


texts:
I am wondering whether there are birds that do not vocalize at all.

I know about the distinctions between songs and calls in passeriformes.
I know that there are species that vocalize very little, like the Ruff (Philomachus pugnax).
I was curious to know whether there is a species in which vocalizations, acoustic communication, do not play any role at all.


texts: I am aware that the cytoskeleton has three structural components: actin, microtubules and intermediate filaments. I was wondering if any cell could possess a cytoskeleton made only of actin. Or made only of microtubules, for that matter. Is it possible for actin to perform the functions that microtubules ordinarily perform in a cell? Or vice versa?


texts: How does a "chromogenic mixture" produce such pronounced color differences in this Agar Art?

texts:
The Forbes.com article Bacteria Become Art Tools In Annual Agar Art Competition says:

...People’s choice winner Zita Pöstényi, a microbiologist at SYNLAB Hungary Ltd, used three agar plates and four different bacteria to create a pattern inspired by Hungarian folk art.
[...]
Pöstényi used another trick to create her colorful plates. “I used a special media for this drawing,” she says,  “It contains a chromogenic mixture which enables the detection of activities of specific enzymes.” Thanks to this special mixture, the four bacteria species she used all showed up in different colors, which allowed her to create the traditional folk art pattern.
Usually, these unique colors tells researchers something interesting about the bacteria, but for the ASM Agar Art competition, these colorful features have become the medium.

Question: How does a "chromogenic mixture" result in different bacteria showing up in different colors in such a vivid way?

American Society for Microbiology Agar Art 2019 Contest, People's Choice. "Hungarian Folk Art," Zita ... [+]ASM / ZITA PÖSTÉNYI


texts: Do goldfish really have a 5 second memory span?

texts: I heard that when people place goldfish in another tank, they just forget where they where previously? True or False ?


texts: How does evolution get around the combinatorial problem?

texts:
Imagine a combinatorial tree showing all the possible arrangements of nucleotides. Some arrangements are functional, meaning they can be plugged into a cell and create a living organism capable of reproducing. Some arrangements are nonfunctional, meaning they can't sustain any living system at all.

In evolution, new information is created as the result of what are essentially an accumulation of copying errors. My question is, would the ratio of functional to nonfunctional arrangements have to be relatively large  so that enough genetic information can arise in response to natural selection? If so, what scientific studies have led biologists to conclude that this combinatorial space is rich with functional arrangements. If it isn't necessary please explain why.


texts:
Why can't pyruvate be used directly in the Krebs cycle? Why does it have to be converted to acetyl before it enters the cycle?

Excluding the reason that the shape of pyruvate is different than acetyl and therefore it would not fit the enzymes involved in the Krebs cycle, what is the advantage of converting pyruvate to acetyl?


texts: What is the evolutionary significance of coelom formation?


texts: What kind of weird little insect is this?

texts:
What kind of insect is this?

I found it in my work room.

I live in the city of São José dos Campos, São Paulo, Brazil


texts: Could an "overactive" brain increase the chances of Alzheimer's Disease?

texts:
From  Raichle ME. 2010. Two views of brain function. Trends in cognitive sciences 14: 180–90:

  Alzheimer’s disease (AD) is the most common cause of progressive
  cognitive decline and dementia in adults. While the amyloid cascade
  hypothesis of AD posits an initiating role for the β-amyloid (Aβ)
  protein, there is limited understanding of why Aβ is deposited. A
  growing body of evidence based on in vitro, animal studies and human
  imaging work suggests that synaptic activity increases Aβ, which is
  deposited preferentially in multimodal brain regions that show
  continuous levels of heightened activation and plasticity across the
  lifespan. Imaging studies of people with genetic predispositions to AD
  are consistent with these findings, suggesting a mechanism whereby
  neural efficiency or cognitive reserve may diminish Aβ deposition. The
  aggregated findings unify observations from cellular and molecular
  studies with human cognitive neuroscience to reveal potential
  mechanisms of AD development.


texts: How quickly do bacteria lose genes after selection has been removed?

texts: If bacteria are subject to a biocide and then that biocide is removed from the population, how quickly will they lose that gene that encodes for resistance?


texts: Why isn't the biological niche occupied by whales instead occupied by fishes?

texts: As by the title. Why aren't there many more, and larger, whale shark like creatures instead of the great mammalian swimmers? I'd assume fish have a benefit in doing the whole "being under water" thing on virtue of not having to get to the surface to breathe ever so often. Seems it's not that big of a benefit, but I still assume there must be something else about mammals that makes them good at being large swimmers and divers?


texts: Known ways to modify the genetic structure of the 13 loci used in CODIS

texts:
After reading the answer to Does our DNA change during our lives?, I was wondering if and how it would be possible to change the structure of the 13 loci that are used in the CODIS database, in such a way that forensic biometrics would not be able to identify/verify you anymore.

I have read about DNA chimeras, and cases exist where a bone marrow transplantation altered the DNA, depending on the sample that was taken. However, are there any other known ways to alter DNA, such as cancer, radiation, etc?


texts: Are there neuron mediated reactions faster than reflexes?

texts:
I'm interested in how fast the human body can respond to a stimulus.  I know the fastest reflex, the blink reflex, operates around 100ms from stimulus to reaction.  I also know that the blink reflex is known as the fastest reflex in the human body.  My interest is in the fastest responses to stimuli I can find in the body.

Are there any faster responses to stimuli within the human body which use neurons but are not categorized as a reflex (due to some technicality), meaning they could be faster than the fastest reflex?  To the best of my understanding a reflex is defined by the use of neurons to convey the information, I'm just wondering if there are any grey areas which don't qualify as a reflex but may be faster.  I don't want to potentially write off an entire class of neurological behavior in my research simply because I stopped at the blink reflex.


texts:
I read that Sciomyzidae are also called snail-killing flies, which immediateley made me think: "I need those"!

Questions:

Are they really fit to control snail over-population in my garden? and
if so where do i get them?


texts: Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?

texts:
To be specific: Assume chromosomes A and B are homologous. They've both replicated into A1, A2 and B1, B2 and have formed a tetrad at the equator (synapsis). Most textbooks show either A1 and B1 OR A2 and B2 exchanging genetic material, but I've never seen an experiment/paper proving that this is actually the case, and now I've come across this figure showing both A1, B1 and A2, B2 crossing over https://web.archive.org/web/20160314020121/http://www.uic.edu/classes/bios/bios100/lecturesf04am/lect16.htm
see ("crossing over" under meiosis)

So which version is correct, or do we simply not know for sure? Thanks in advance.


texts: Incremental denaturation of protein mixtures

texts:
When a protein solution is heated above the denaturation temperature, it seems that denaturation does not happen at the time the temperature is reached, but it takes some time.

I assumed that Brownian motion degrades the protein structure more and more. But I noticed that, in practice, one has a mixture of proteins, and I wonder whether they may behave differently, causing some macroscopic effect?

As an example, taking the clear part of a chicken egg:
No doubt it contains multiple proteins. When heating it slightly above the denaturation point, it coagulates slowly.

I would like to understand in which way that is caused:

by proteins that denature at some temperature dependent rate - where all proteins behave very similar
by different proteins denaturing at different temperatures at a much higher rate than others, so that partial coagulation means some proteins are coagulated, and some are not
of course, it could be both combined, or a completely different way.


texts: Do "real" human samples tend to return fewer protein identifications in Proteomics experiments?

texts:
I'm working with bottom-up (shotgun) mass spectrometry-based proteomics and have encountered an issue. If I do a run with a HeLa digest standard, the resulting data returns many protein IDs. When I do the same experiment with cultured human cells (TCells specifically), the number of IDs drops dramatically.

We've been racking our brains trying to determine why, and it doesn't seem to be an issue with the data itself. It's as if the database search can't find sequences that fit the data.

My boss also encountered a similar issue when dealing with a previous project; the system worked well on murine samples, but there was a huge drop off in IDs when looking at human cells (with a human database, not murine of course!)

Is there some kind of known issue when looking at human cells from patients/in vitro samples? Is there a high proportion of point mutations/non-canonical sequences that upset database searches?


texts: Why are fibroblast used so commonly in cell biology?

texts: Fibroblasts are some of the most commonly used cells in cell biology. What are the properties of those cells which makes them commonly used ?


texts:
I've read that Lamarck's theory doesn't explain homologous structures.

But, what about the following hypothetical under Lamarck's theories:

A population develops an adaptation to its environment
Part of the adapted population moves away
The adaptation is passed onto the population's offspring
All offspring of the original population have the adaptation, regardless of whether or not their ancestors moved away

Isn't this adaptation a homologous structure?


texts: Where can I find a transcriptome of a normal uveal melanocyte?

texts: I am looking for a database where I could find a transcriptome (say obtained with a microarray analysis) of one (or ideally many) normal uveal melanocytes ?


texts: What are the sufficient criteria that make an entity a living homo sapiens?

texts:
When I say criteria I mean like x biological functions or y genetics.

If it were to be appearance,anatomy. A corpse completely looks like a man.
Moreover a person who has had their 4 limbs amputated, has a single largely malfunctioning kidney(they are on heamodialysis), has had every vestigial feature, like the vermiform appendix, wisdom teeth, surgically removed due to health problems. Their digestive function is almost dead. Their eyes gouged out by accident. Has severe problems in their brainstem. They can't swallow, they can't speak, they can't hear, they.....

Basically they only breathe, and have something to circulate because of artifical support. They are almost brain dead.

Even such a person that looks nothing like a man, anatomically. Is definately a homo sapiens. They are actually protected by law. They cannot have their life-support removed or be left to die. At least not in countries like Germany, Italy, Greece, France, Spain,Portugal. Legally any so.

They have every single organ system severely damaged and any more damage to a single organ system would kill them.

What makes a living homo sapiens.


texts: Experimental techniques to measure protein-protein and protein-ligand structure and dynamics

texts: We would like to compare our simulation results with experimentation. When one wants to follow experimentally the dynamics (and possibly structure) of protein-protein or protein-ligand docking (involving both small and large conformational changes for the complex), which are the most useful hydrodynamic techniques? If not hydrodynamic, which others?


texts: What is the mechanism by which quitting smoking causes increased appetite?

texts:
I guess it has something to do with  sugar regulation.

Does anyone know something more about this?


texts:
I was looking into the following problem:

Obviously, the solution lies in how much energy either can output per unit of time.
The total energy output of the sun is $3.8×10^{26} \frac{J}{s}$.
The number of lions alone pales in comparison ($10^{12}$).

However, I'm now trying to figure out how many lions it would take to have an output equal to the sun, but I seem to be having a hard time finding good data.

What's the peak energy output of a lion per second (or where/how can I find such information)?


texts: Can antibiotic resistant bacteria compete with normal one in an antibiotic free environment?

texts: The question is based on an intuition that antibiotic resistance can't come along. This mutation will probably make bacteria less tenacious. Is there any research how AR bacteria compete with normal one in an antibiotic free environment? Because if them generally lose to normal bacteria then AR bacteria is not a big threat and they can't spread to much.


texts:
I was wondering how protein denaturation works.

Are there covalent bonds, such as disulfide bridges involved, or is it based purely on non-covalent bonds such as hydrogen bonds? Why is denaturation irreversible in most cases if only non-covalent bonds are involved?
Is it possible to denature protein by rapid changes in electromagnetic field or pressure? (The articles I have read so far mention only stress factors like sudden pH, osmolarity, temperature changes...)
How can I protect a protein against denaturation? e.g. in PCR we use a heat resistant DNA polymerase, so certain amino acid sequences might protect against heat denaturation, but I need reassurance about this.


texts: Effective Mycoplasma Elimination from Primary Human Cultures

texts:
Obviously the best way to avoid mycoplasma contamination is to avoid it in the first place.  In our case, however, it is not possible to avoid.  We are culturing viruses and tissues out of human nasal swabs, washes, and biopsies.

As you can imagine, anytime you are pulling something out of someone's nose, it is quite often full of mycoplasma.  I've reviewed current examples of mycoplasma elimination, but found the section in Current Protocols in Molecular Biology to be the most helpful.

Indeed, we found that checking with a PCR based kit for common lab mycoplasma contaminants often missed detection of mycoplasma, because it did not include "clinically relevant" strains. Kits which did include these species clearly detected mycoplasma, in addition to Hoechst stain confirming their presence.

Now the question is there a good way to remove them?  We've tried serial dilutions, elimination kits (also MycoZap), titrated doxycycline and enrofloxacin doses, and even mouse passage.

Of these mouse passage was probably the most effective, but not desirable because it might induce additional confounding factors.  The kits had fair results, but 5 passages post treatment mycoplasma were again detectable via Hoechst stain (PCR detection persisted through out).

The dox and enrofloxacin may have produced better results at higher concentrations, but cell toxicity became a serious issue.  I was wondering if anyone had examples of combination methods for cleaning primary cells and/or virus stocks (been grown on more standard immortalized cell lines) for a more complete treatment method.

Just as note on our hands, we regularly check our cell lines, and are in fact maintaining a mycoplasma free tissue culture system.  Further, as proof of concept, we were able to clean a culture that was known to be infected with M. hominis with kits.

It doesn't seem worth the effort, but is there any evidence to suggest typing down to the species would be worth it in the eradication effort?  Each donor could conceivably be providing a different contaminate.


texts: Once the genetic material for Dengue Fever is inserted into the human DNA, would the Dengue Fever molecular material be in the form of its own isolated DNA fragment or will it be inserted directly into some existing piece of our DNA?


texts: Why don't individuals with sickle cell trait suffer from sickle cell anemia?

texts:
Ostensibly, in people with sickle cell trait, half of the hemoglobin in their body would be defective.

Is it actually the case that sickle cell hemoglobin is produced in equal amounts?
If not, how is that regulated? If so, how does that still not cause anemia?


texts: What triggers programmed cell death in humans (from outside the cell)?

texts:
What triggers programmed cell death in humans? Is it decided by the brain (for the entire body)? Or is it a local decision of a cell by its environment? Something else?

I realize that there might be different cases. But I'd like to get a general idea of where (and why, actually) does this happen.

EDIT

As linked to by a comment below - one type of cell-death (Necrosis) just "happens" to a cell. And perhaps there are other types that are decided by the cell.
What I'm asking about (and trying to understand more) is about the idea that cell-death might be initiated externally to the cell because it would be beneficial to the whole organism. Such as "the separation of fingers and toes" mentioned in Wikipedia  .   "Who" would initiate it? Are there examples of the CNS initiating it? Notifying the cell by nerves? By hormones? Are they initiated by neighboring cells? (And if so - what cells have the "clout" to send such signals?)

What I'm trying to understand is who decides when a cell dies in those cases where it's not the cell itself.


texts: Why do dendritic cells have CD4/CD8 on their surface?

texts: Why do dendritic cells have CD4 or CD8 antigens on their surface? What is their function without the presence of a T-cell receptor?


texts: Studying changes in DNA for causes of cancer

texts:
First of all let me say that I'm not into Biology myself... but I have a question for those of you who are.

From what I've read, cancer is caused by 'faulty' DNA that behaves abnormally. Mutations can occur for various reasons, ranging from simple 'copying errors' to environmental factors.

I was just wondering whether current research has dealt with storing DNA of people or animals (e.g. rodents) and observing how it changed, especially for cases where it eventually resulted in cancer. Something along the lines of this, but I'd like to know what research has actually been done so far.


texts: What is the predominant purpose of Alkaline Phosphatase in skeletal muscle fibers and liver cells. I know that it is a hydrolase enzyme that speeds up the degredation of proteins, lipids, starch and other biomolecules. But what does it does it specifically do in muscle and liver cells. And why is it in higher concentration in the liver ? Is it because of the livers purpose as an organ (cleanse and detoxification) ? Therefore pino/or endocytosis occur in higher rates ? I appreciate anyone with any intelligent insight.


texts: What are polytene bands, and why are they there?

texts:
Drosophila polytene chromosomes have been particularly useful in genetic research, as it made cytogenetic gene mapping possible with very little effort. This was primarily accomplished due to polytene bands, which are naturally-occuring (no stain) fixed bands seen along the chromosomes via microscopy.

We have been exploiting these bands for decades, but it seems as though their function isn't quite clear.

What is the cause of the visible polytene bands, and what function do they serve?


texts: Why is competence useful for a starving cell?

texts:
I know that some bacteria become competent when there is not much food available in their environment.

I don't really understand why this is useful for the cell. I've seen some other organisms form a biofilm or get together to become a slime when starved and I understand the utility of this mechanisms (reducing energy consumption and being able to move around easily to look for nutrients).

The only plausible explanation that I see is that being competent might be useful to take advantage of the DNA of dead cells. Am I right?


texts: I have investigated some of the links to known microarray databases, such as arrayTrack, omnibus (NCBI), TCGA. I find that when trying to get microarray images I either get an exotic file format (such as .sdf or .cel) or text base information. Does anybody know of publicly available microarray images (preferable with metadata too) in .svg, .png, .jpg or another well known image file format?


texts: What is the developmental basis of the placental sac?

texts:
The placental sac is the organ that provides nutrients to the embryo from the mother.

My question is that, since this obviously involves a lot of complexity, where does the sac originate from  (maternal / embryonic) ?

Also, what is the genetic basis of the above? do the genes intercommunicate between the embryo and the mother ?


texts: are the spontaneous generation and evolution the same idea but in a different time scale?

texts:
I was in my biology class, learning the history of spontaneous generation and how this idea was discarded. I told my teacher that is the same as evolution but in a different timeline. I Argue that evolution does not explain how life formed, but complemented by abiogenesis. Ultimately it is almost the same thing. Therefore it could not rule out spontaneous generation.

I got an F.

My appreciation is so wrong?


texts: How to determine the height/bits in a sequence logo?

texts:
I am trying to create a sequence logo, and I am completely confused by how to determine the height/bits for each column. So, for example I understand how to create the flat sequence logo: (add up all the letters, the letters should represent their ratio for that position) but not the normal sequence logo:.

I have been reading this paper "WebLogo: A Sequence Logo Generator" again and again and I can't figure out how to determine the bits/height for each given position.


texts: Pneumonia in children after abdominal operations

texts:
This textbook says:

  Consequently,  young  children are prone to  suffer from pneumonia after abdominal operations, because they resist breathing (being abdominal) due to  pain.  As a result the secretions in the lungs tend to  accumulate,  which may become infected and cause  pneumonia.

Iam unable to find which secretions are they and how breathing removes them from lungs?

I thought it could be pleural effusion but unable to figure out the mechanism involved and how it gets infected if it remains there for long.


texts: Where do methyl groups in the human body come from?

texts: Where do methyl groups in the human body or other mammals come from? Do we synthesize them (where?) Do we get them from our diets (in what? anything beside methionine?) Do our gut microbes produce them for us (and are we dependent on them for that?)


texts:
Whether couple is White male and colored female or White Female and colored Male
but they always give birth to colored one.

Why Interracial couples always give birth to colored one?


texts: How is centriole number maintained during meiosis?

texts:
I've found a website (Pearson's BioCoach) that claims centrioles duplicate in Prophase II. Is this accurate? Does it depend on the species in question?

Looking at three textbook illustrations of meiosis, none of their illustrations are consistent. All depict the movement and number of centrioles through Telophase I the same way: centrioles replicate in S of Interphase, then do their thing through Meiosis I. We end up at Telophase I with 2 centrosomes, each with 2 centrioles. There is one centrosome at either pole of the cell.

After that, the diagrams are unclear:

One text (general biology) seems to indicate either centrioles or entire centrosomes replicate after Telophase I, because Prophase II is shows both cells with 2 centrosomes, each with 2 centrioles.

Another (basic genetics) illustrates 2 daughter cells of Meiosis I inherit one centrosome each following Telophase I. In Prophase I, the centrioles in this centrosome splits, with one centriole going to either pole. Cytokinesis after Meiosis II results in 4 daughter cells, each with one centriole.

A third (more thorough genetics) stops depicting centrioles after Telophase I, instead showing the spindles growing in an aster formation from an empty space, the space where there were 2 centrioles up until Telophase I.


texts: Do epigenetics determine the proteins a cell produces and therefore it's function?

texts:
I'm having trouble understanding what epigenetics is in a simple sense.

How I imagine it is that if we had 2 twins with identical DNA and we let them live we will see that they'll develop differently. Their DNA will stay the same (unless the DNA gains mutations, which could lead to cancer...) but their epigenetic tags will differ. These epigenetics tags determine the execution of parts of the DNA and the way the twins live their lives determine how the tags will be distributed. It's hard for me to find an example.

Another way I think of epigenetics is for example the cells in the muscles have a specific epigenetic tags to produce the specific proteins needed to create the muscle and the cells in the skin for example have different tags, produce different proteins which produce the skin.

Is my understanding of epigenetics anywhere close to the truth?


texts:
Food goes in, excrement come out. This seems obvious.
But it seems like the mass of the excrement is less than the one of the food.

Most people I asked answered: "There's a difference because it's transformed into energy, like heat...". I think that's bull-excrement.
There's still the law of conservation of mass: our body does no nuclear reactions, or does it?

Example:
Someone's on a "high protein / low carb" diet, he may ingest like 1kg of food, he isn't really productive on the toilet (it's difficult to find any fibers in those diets), he loses 500g in a day... My question is: where does the 1.5kg of matter go?


texts: Evolution - The ability to control ear muscles

texts: Among animals the ability to control ear muscles is pretty common, but only a few humans have the ability. Is it because we in general lost this ability ?


texts: Why is this oxoglutarate dehydrogenase and not oxoglutarate decarboxylase?

texts:
I was looking at the oxoglutarate dehydrogenase complex and saw the reaction mechanism for its E1-TPP mechanism, which results in the formation of a stabilized carbanion intermediate.
The mechanism begins with a protonation, but since the "goal" of the enzyme is to form the carbanion intermediate, it seems to me that the decarboxylation is the key part of the reaction. So why is this a dehydrogenase-catalyzed reaction and not a decarboxylase-catalyzed one?


texts:
I would have some related questions about the mating types of fungi.

Does a single spore generate a mycelium possessing only one mating type? If it does not in general, do Ascomycota and Basidiomycota possess only one mating type per individual mycelium?
Are homothallism and heterothallism properties of the individual mycelium or of the species? The definitions that I find in my book and on line confuse me. I understand that homothallism is the property of a mycelium (possessing only one mating type or can it possess many mating types in a similar way to hermaphrodite animals? cfr. question 1) that can mate with itself (if it can possess many mating types and it can mate with itself only by using gametes of different mating types, is it still homothallic?) and heterothallism is the property of a mycelium that is not homothallic, but I am not sure I understand, because I read of homothallic and heterothallic species too: is a homothallic species a species where at least some individual is homothallic, where all individuals are homothallic or something else?
I am sure that mating type is a property characterising at least gametes, but is it a property of indiviual cells too? As an example, I know that it is necessary, among many species of fungi, for two gametes to belong to two different mating types in order to produce a zygote. Some fungi, as it is the rule among Basidiomycota, reproduce by somatogamy, i.e. the nuclei generating the zygote are from somatic cells, other than gametes. In such cases, are there species where it is necessary for the somatic cells of a homothallic mycelium to belong to a different type than the type with which they are undergoing plasmogamy? Thank you very much for any answer!


texts: How come large herbivores have such thin legs?

texts:
Edit:
This question is very similar to this and related to this one (though the latter focuses on homology instead of scaling laws). However, the answer to this question is far more comprehensive, in particular it offers a plausible explanation why horse legs evolved as they did (vs human or even rhino legs).

Large grazing mammals such as horses, moose, and cows tend to have relatively thin legs despite being up to ~1000kg. For example, this rider's and her horse's legs appear to have about the same cross-sectional area both for below and above the "knee":

If this horse is 500 kg (a mid-range mass for horses), each leg would have to support 125 kg, compared to only 37.5 kg for a 75 kg adult. Why don't we see a corresponding difference in cross-section?


texts: Why does an autoclave need to pressurize steam?

texts:
I've looked this up on other sites and they say that an autoclave needs high pressure in order to raise the boiling point of water so that you can achieve steam of a higher temperature.

If you look at this diagram though, it seems to me as if it would be much simpler to further heat the steam at the ambient pressure of the autoclave room. Does the pressure of the chamber play some role that I am unaware of? Thanks in advance for clearing this up!


texts: Electrically facilitated active transport across a membrane

texts:
I'm trying to go back to school to do a PhD in control theory, specifically concerned with control of glucose. The glucose system can be controlled using two chemicals: insulin and glucagon. I was wondering if there was any precedent for controlling the active transport of a chemical across a membrane using a tiny electric current. Has this ever been done?

The reason I ask is that I want to avoid relying on mechanical systems that are prone to being bogged down by attacks from the native immune system.

Any knowledge on the subject/recommendations for attacking this problem/alternative subreddits or websites would be greatly welcomed.


texts: What would be a single elegant-sounding word denoting controlled increase or decrease?

texts:
I am a biologist and frequently encounter the words 'upregulated' and 'downregulated' in the literature. Appropriately, these words are flagged by my browser spell-checker; they don't seem to be very widely recognized outside of the biology community, and I find them quite ugly.
I would appreciate any and all suggestions for (ideally) single words or concise phrases that convey the same meaning: increased or decreased in a controlled or causative manner by the action of some external factor.
A general use case: "In experiment A, we determined that gene B was upregulated upon exposure to toxin C, while genes D, E, and F were downregulated."
Of course I could say that 'expression of gene B was increased by/in response to...' but 'B was upregulated' is so much shorter. Surely, though, there must be some way to convey this concisely without using such an annoying construction as 'upregulated'.


texts: Why do we blow when we're out of breath?

texts:
When people are out of breath from exercising, instead of breathing normally they partially obstruct their expirations by blowing out instead of breathing out.

Why is this?

EDIT: This photo illustrates what I'm referring to.


texts:
I took the following picture of this spider in northern Switzerland (alt: ~700m) with macro flash (then it is not so big: probably around 2-3 cm, including the legs)

This spider made its web on the house and it goes out only during night.

In this region we have many Araneus diadematus, but this one looks totally different.

Is it the same family or another? Does anybody have a clue for the real name?

UPDATE: I saw it this afternoon (gave a fly to the web to make it go out), the body is probably around 7-8 mm wide and 9-11 mm long). And now I am sure the colors are more or less right.


texts: Link between pornography abstinence and hormone levels

texts:
I have a question regarding abstinence from pornography, and also possibly celibacy, and how these two lifestyle choices affect hormone levels.

Trends such as No Fap have been emerging recently. An excerpt from their website states :

  No Fap held you to sharply increase your testosterone levels.

Is this true? From my research, I see no evidence to suggest this. Links to any studies would be appreciated. It is clear that people participating in No Fap have experienced psychological changes, but whether these changes are present on a hormonal level is an interesting proposition. If there is no hormonal change, what does this infer about what has happened to the minds of participants?


texts: HPV. How do viruses persist outside the body?

texts:
The main route of transmission of human papillomavirus (HPV) is generally believed to be sexual. While fomites have been postulated for inexplicable infections, sexual health professionals regularly counter that lying respondents are the more likely explanation.
Research into HPV seems to have mostly stalled and there are few in depth in-vitro studies into viability of the virus outside the body, the infectivity of fomites or their infective dose that I could find.
There are some footnotes and references to animal models, with claims that HPV can remain infective at least 7 days after desiccation but no upper limits. There is some more precise research but understanding the significance is difficult for layman.
For example research published in Nature stated HPV-16 "can remain viable and capable of transducing the reporter construct upon stimulation of cell cycle re-entry for at least 2 weeks, but most likely for no longer than 4 weeks."
How can one understand the viability and limits of viruses, and HPV in particular, outside the body?
To clarify: Despite the fanciful language of the bounty I'm not looking for certainty, but general principles of environmental virology and an overview of statistical observations in regards to HPV in particular.
Note: The various aspects which influence the persistence of viruses in the environment spoken of below are summarized with some additional detail in a literature review published in 2010 in Food and Environmental Virology.