text:
Why is the current Ebola outbreak different from previous outbreaks?
I don't know if this question has an answer at this time, but I would like to know if there is some biological reason why the current Ebola outbreak is so much more complicated and widespread than in the past. Traditionally it has been initially very virulent and has then has rapidly waned. I hope what I am saying is accurate, and if so why dont we see the same pattern now ?

Can you provide some references/proof for your statements (e.g. fatality rates over time of the current outbreak), and also explain more accurately what you mean (e.g. complicated in what way)?

This is too long for a comment, so I put this in here: The main reasons are sociological. From the data I have read so far, this outbreak (actually these are two independent outbreaks, one in West-Africa and another one -not connected- in the Democratic Republic of Congo) is not exceptionally deadly in terms of Ebola. The death rate is about 60% which is extremely high compared to other diseases, but Ebola had reached up to 90%...
I think the main differences are that this outbreak struck in a much more populated area which has a very poor health care system (if you can call it like this at all). Then it happened in a border region, I recall reports about a traditional funeral of a Ebola victim which infected visitors, some of them crossed the border afterwards.
Then it was completely underestimated in the beginning, because a lot of cases stayed unknown. This led to a wider spreading as people who got sick infected relatives and medical personnel subsequently. And although the reaction has been powered up a lot since then, it is still not adequate to contain the outbreak.
Former outbreaks happened in rural areas which where easier to contain with a smaller number of personal, which is not possible this time. If you want to read further about this, I recommend the blog of Tara C. Smith which has been doing research about Ebola for some time and also worked in crisis response teams.
Especially interesting are these two:

A historical perspective on Ebola response and prevention
Addressing more Ebola myths

You are correct that this seems to be two separate outbreaks, see http://www.who.int/mediacentre/news/ebola/2-september-2014/en/

For some background, it is essential to know that Ebola is actually a group (genus) of ebolaviruses, each with different fatality rates. There are five known species of Ebola, and four are known to cause disease humans (WHO: Ebola virus disease; wikipedia).
The known species of Ebola includes:

Zaire ebolavirus (or just ebolavirus)
Sudan ebolavirus
Bundibugyo ebolavirus
Tai ebolavirus (only one known human case)
Reston ebolavirus (can infect but does not seem to cause disease in humans)

Zaire ebolavirus is the deadliest strain (with Sudan second), and also the one that is causing the current outbreak. A table of all known ebola outbreaks can be found in the WHO report (WHO: Ebola virus disease), which shows that the historical fatality of the Zaire strain has been between 44% and above 90%.
From my limited understanding, when dealing with ebola it is essential for infected individuals to be identified early so that they can get intensive care (most importantly intravenous fluids because of dehydration), but also to prevent further spread. This is probably what has failed during this outbreak, but another problem is also that the size of the outbreak has put tremendous strain on an already weak healthcare system. These outbreaks have also occurred in well populated areas in countries with very weak governments, that also lacked experience in dealing with ebola (both in the administration and among the population).
In many former outbreaks, the initial death rate is very high since early victims are found at late stages of the disease, but when the outbreak is more controlled the death rate drops due to supporting care of infected individuals. I don't know to what extent this has been the case during the current west african outbreak. However, the overall fatality rate of the current outbreak is 52% (tabulated Aug. 28 2014), with 44% in Sierra Leone and 66% in Guinnea (WHO: Ebola virus disease update - west Africa), and this lies well within the normal fatality rate of the Zaire ebolavirus.


text:
Attaching suspension cells to coverslip during mycoplasma contamination detection
I am planing to screen my cell cultures for mycoplasma contamination using the Hoechst 33258 DNA staining method.
This method is suitable for adherent cultures. Is this method suitable for suspension cultures?
If yes, what is the procedure to attach my suspension culture on coverslip and prevent washout of cells during staining.

microscopic methods require some experience in cell culture (to see and identify things). You can use other techniques too such as PCR based methods.

Related: How to convince suspension cells to adhere more tightly?

If you are working with suspension cells, it's always easier to use Flow cytometry but if you want to use microscopy then I would suggest using chamber slides. You just have to put your cell suspension inside the chamber and then stick the cells to the microscope slide. After that you can do whatever treatment you want just by putting in the chamber the proper solution and wash afterwards. The more the steps the more cells you'll lose mostly because of pipetting so try to pipette always at the same corner and be gentle. To stick the cells to the slide your best option is to centrifuge the slide. Unfortunately in my lab that wasn't an option so I just fixed the cells with methanol while there were suspended in PBS and it worked very well. Most of the cells were attached to the slide and the staining was perfect.
Hope I helped. Good luck!

Contamination detection in suspension cells
For contamination detection in suspension cells, use the culture media of these cells: (with no antibiotic)
NRK, 3T6, A549, VERO Cells
These cells are good hosts, especially for Mycoplasma then contamination is easily detectable using optical microscopy after staining. check host cell culture for contamination before transferring suspension cells.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
If two definitive ovums are fused will they form an organism?
Pretend that somehow in a laboratory two definitive ovums (finished 2nd miotic divisions) are
are fused together. Will they form a new species?

Are you thinking about fusing ovums from different species?

no the same species (humans)

No, it is not possible. The reason is the genetic imprinting, which takes place on the parental DNA in the egg and the sperm. Here small modifications are added to the DNA which marks them as silenced. So some genes are expressed from the mother (while the fathers copy is not expressed) and vice versa.
There are even genetic diseases which are caused by imprinting. One example is the loss of a gene region on chromosome 15. Depending in which copy its lost, either the Prader-Willi Syndrome or the Angelman Syndrome occur. PWS is inherited via the father, Angelman via the mother. Another interesting article on imprinting can be found here.
If you combine two eggs, some genes, which are not imprinted in the father, will not be expressed in the developing embryo which will finally lead to death of it. However, researcher deleted the maternal imprinting in mice and mimicked the from the father and made off-springs from two mothers possible. This is something which is ethically very problematic in humans. The article can be found here:

Birth of parthenogenetic mice that can develop to adulthood

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Standard Classification of Disease
I am working on a project for health center. It involves the creation of a database of all diseases. Currently I want to classify disease on the base of their category based on international standard.
Did anyone know where i can find one, I did a lot of research but was only able to come across this which seem not very useful to me: ICD

The two I know of off the top of my head are

OMIM : Online Mendelian Inheritance in Man. This is very good and very well organized but only deals with inheritable diseases, no infections etc.

Human disease ontology. From their webpage:

The Disease Ontology has been developed as a standardized ontology for human disease with the purpose of providing the biomedical community with consistent, reusable and sustainable descriptions of human disease terms, phenotype characteristics and related medical vocabulary disease concepts through collaborative efforts of researchers at Northwestern University, Center for Genetic Medicine and the University of Maryland School of Medicine, Institute for Genome Sciences.

The DO is probably perfect for your needs.

I don't know if you're also interested in mental health issues, but the DSM (Diagnostic and Statistical Manual of Mental Disorders) is the standard typology for that subject area.
edit: I see that the Disease Ontology that @terdon lists also has mental health as a category.


text:
Why does sulfonamid not inhibit the growth of Rickettsia?
Sulfonamid is an antimicrobial agent, why has it no effect on the growth of Rickettsia?

Sulfonamides competitively inhibit the enzyme dihydropteroate synthase, which is involved in the tetrahydrofolate synthesis pathway in most bacteria. Rickettsia lack this enzyme target, and thus possess a natural resistance to the antibiotic. As tetrahydrofolate is an essential compound, it is believed that Rickettsia possess an alternative enzymatic process which is not susceptible to sulfonamides, or the bacteria simply acquire the compound (or its immediate precursors) from their environment.

richettsiae lacks folP gene which encodes for dihydropteroate synthase and folA which encodes dihydrofolate reductase enzymes. This shows that richettsiae lacks the target of sulfonilamides. therefore sulfonilamides are ineffective to inhibit its growth and thus if given may lead to increased mortility and morbildity.
reference:http:escholarship.org


text:
In biosynthesis of cysteine and methionine, where does the sulfur come from?
Methionine and Cysteine are the two amino acids containing sulfur. According to wikipedia, cysteine is built from methionine. However, the wikipedia also claims that methionine is synthesized from cysteine.
So, a chicken and egg problem (esp. since eggs are a rich source for those proteins). Where do living things get their sulfur to build these amino acids in the first place, in what forms is sulfur available biologically?

Microorganisms (and plants) make cysteine from serine using H2S as the sulphur source. Condensation of these two directly gives cysteine in some bacteria, but most often the reaction sequence is:

serine + acetyl-CoA >>> O-acetylserine + CoA-SH
O-acetylserine + H2S >>> cysteine + acetate + H2O

As you say, in terms of the sulphur, cysteine and methionine are interconvertible.
Animals rely upon their diet for methionine, and can make cysteine from that methionine.

+1 and accept: the key info was that H2S is a sulfur source.

Which plants use H$_2$S? I only found sources about microorganisms doing this and plants using soluble forms sulphur.

Apparently, a number of them can take up H$_2$S. http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0062048&representation=PDF.

First of all, the wikipedia article you quote states that methionine is synthesized from cysteine in plants and microorganisms, not in humans. In humans, both cysteine and methionine are essential amino acids which means that they cannot be produced by the human body but need to be acquired elsewhere.
Now, this is mostly done by eating proteins that contain these amino acids. The proteins are broken down and the amino acids (or their constituents, such as sulfur) are reused. In mammals, cysteine is produced from serine but the sulfur comes from methionine via homocysteine:

So, methionine comes from the diet and it is then used to produce cysteine.


text:
Results of a complete DNA sequencing - are they 100% reusable?
Is that correct that a complete DNA sequencing (the whole genome) need only to be done once (per person)?
After that is done, it the complete genome can be stored and once the new genes (and their purposes are confirmed) are discovered, the scientist can simply go back to a previously sequenced data and to find it this particular person has this new gene or not.

A single run of sequencing won't cover the entire genome, in most cases. That's why they do multiple rounds in order to increase horizontal (covering more regions of genome) and vertical (a.k.a depth; more reads per locus so that you can be more confident) coverage.
Edit by dd3:
In the cases where "a new gene is discovered", i.e. genome reannotation, it is possible to go back and look at previously stored sequence data to find out what alleles a person has (everyone has every gene, unless they have a deletion that spans the full length of the gene). This is a bioinformatics project, and if you are interested in learning more, I would recommend searching for recent publications on genome reannotation and remapping of sequence reads.
Whole genome sequencing is generally not recommended for prognosis of a specific disease like breast cancer. The common approach is to do a PCR of the biomarker loci and if necessary do a Sanger sequencing. However, if you have the money you can get your whole genome sequencing done :P
The number of runs required to increase the depth varies for different genomic regions. This article says that CpG islands require more runs. According to this article, the depth should be >3 per genotype marker.

@WYSIWIG... Thank you. But how does it work in practice. Let's say someone wants to be tested for probalility of occuring a breast cancer. In that case - will only a particular region of genome be sequenced to find if a BRCA1 gene is ok? Please excusing me for a naive questions - but how many runs (approximately) are required to sequence the whole human genome?

edited the answer.. the comment was getting too long.. :)

for many of the technologies in use today, 30x coverage can still be problematic.  Should mention that the sequencers have biases which systematically give hard to interpret or easily misinterpretable data.  but given this, the data could and should be reused if its a whole genome sequence.

excuse me @shigeta, what is a "30x coverage"?  Thank you.

coverage is an estimate of the number of times each individual base in the target sequence has been sequenced.  so 30x coverage means you would have produced an assembled sequence where 30 sequencer outputs would contain an average base.  the coverage needs to be so deep because the short sequences from the sequencer (a few hundred bases) there is some uncertainty in each sequence, errors in sequencing, and  the resulting difficulty placing any given sequence. this paper might help:http://www.ncbi.nlm.nih.gov/pubmed/23393025

@Mitten: Coverage (vertical coverage) as I mentioned previously, is number of reads that map to a region of the genome. We generally look at the average coverage throughout the genome.

To your point, fast forward to today, whole genome sequencing is more affordable  costing about $900 (without compromising on privacy) for the following 130x coverage for the Exome, 30x for the rest of the Genome. The cost of Genome Long Reads is still very expensive.

Is that correct that a complete DNA sequencing (the whole genome) need
  only to be done once (per person)?

Likely, yes.  But I think you vastly overestimate how often this is done.  If someone gets their DNA "sequenced" at 23andMe, for example, they are not getting their whole genome sequenced.  They are getting individual bits believed to be possibly clinically relevant sequenced.  It's a different technology than you would use to get the whole genome.  A whole mammalian genome is really big, therefore kind of expensive to sequence, and is mostly non-coding DNA of questionable relevance.  Therefore you can just genotype the exact bases of interest, or maybe do exome capture, which gets you full sequence for the 1% or so of the genome that is currently annotated to be coding.  Obviously either of those approaches would no be all-inclusive, so one might wish to redo them at a later date with new targeted regions of interest.
Even if you did get a whole genome done with current technology, right now it has limitations, namely read length, that make it hard to work out certain details.  I could easily see someone needing to redo a genome using a longer read technology, when that technology arrives.
Also, we aren't really discovering that many new genes. Certainly not protein-coding ones.  What is more likely is that we discover that variants in this or that gene might be clinically relevant to some health parameter.

Apart from what WYSIWYG said.
It might also be the case that you need to re-sequence because you're interested in seeing the changes that might have occurred since the last sequencing. Remember that cells keep dividing and therefore changing, so the DNA is slightly different from one cell to another (and from one population of cells or tissues to another). Single-cell sequencing is almost here.
The obvious example here is a tumour. It helps knowing what happened and if possible detect the driver (or drivers) mutation (cancer cells tend to increase their mutation rate).


text:
Spider identification please

Can someone tell me which spider this is please? I've found a few of them in my home in North-London, are they poisonous?

Can you please add where you actually live?

Im North London. Also this one is yellow/brownish with black markings but I have found others with a darker purple back..

I have taken to color correct your image so the spider can be identified easier.

@Chris your color correct makes the spider look green on both of my screens. I'd suggest having at it again :p

It think this spider is a Tegenaria domestica also known as the barn funnel weaver in North America and the domestic house spider in Europe. See here or here (picture taken from the first link):

They are not poisonous and usually avoid confrontations, but can bite.

That's really informative, thank you for your help.

Does this species ever have a greenish hue to it, or are you putting that down to the OP's lighting?

@rotaredom I think this is due to the image. I have corrected the color already, have a look into the edit history to see the original version.

Ah, gotcha. Looks like you've got it nailed, then.

I'm not convinced this is the same species, actually.

Its my fault with the colour, i captured it in a red plastic pot but tried to get a bit of white paper inside for the pic.  It was a yellowish/brown with dark black markings

Hi, I'm afraid this definitely is not a Tegenaria and definitely is a Scytodes.  Look at the long, spindly, almost delicate legs, and the very odd carapace.  The 'Rohrschach Blot' markings on the carapace are quite different from the wavy lines on the Tegenaria carapace as well.  Scytodes are slow-moving spiders of closets and quiet areas, rather like their distant cousins the Recluses.  Quite harmless, though, as far as I know.

Very nice, indeed!  This is a Spitting Spider (one of the Scytodes species, but I'm not sure which is most likely over in the UK).  That's a good photo, by the way.  This spider is easily told in the wild by its odd-shaped, domed carapace, with the 'Rohrschach-blot' design around the edge, and the spindly, banded legs.  It's a slow-moving, very mild-mannered spider, with one of the more fascinating methods of catching prey:  basically it spits a sticky saliva in zigzags that restrains the potential food, then rambles up and bites it.
I include a photo and a couple of links for your enjoyment - using a familiar species from the US, Scytodes thoracica.
https://bugguide.net/node/view/3347
https://www.youtube.com/watch?v=LaP52uKg2pU


text:
How do people digest fat after gall bladder removal surgery?
How do people digest fat after gallbladder removal surgery?
How can they tolerate a high fat diet?

This is not a problem, since the gall bladder "only" stores bile, but the production itself happens in the liver. There are some cases described which can get problems digesting very fatty food, but for most people this is not a problem. Additionally eating low-fat food in the first few weeks after the removal is recommended. See here for some more details.
The picture below shows the location of the gall bladder and also the bile ducts (picture from here)


text:
Fabric melting spider juice
I live in the southern rocky mountains of Canada. I was in bed the other night when I saw a small scurrying shadow out of the corner of my eye. The source of the shadow was a small spider (95% sure it was a barn funnel weaver), approx 2cm in diameter. I killed the spider.
Interestingly, what intrigues me is that the place on my bed where I killed the spider the jus of the spider had melted to the sheet (!). How could that happen?

I tried to cut out the extraneous wording from your question - what do you mean by the spider jus had "melted" to the sheet? Can you clarify?

I think what he's saying is he smashed the spider and left it overnight on the sheet and it broke down the sheet fibers or left a hole.

Please look at sheet label and state cotton/linen/other fiber.

Some spiders are known to eat their own silk when breaking down a web and reconstructing it (https://en.wikipedia.org/wiki/Spider_web#:~:text=It%20is%20common%20for%20spiders) or even stealing the web of other spiders and eating it (https://frank.itlab.us/photo_essays/papers/Argyrodes_kleptoparasite_spider.pdf). It may very well be that some types are able to digest various silks or other fibres. I'm not aware of any studies that test whether a spider could digest - say - wool or other natural fibres.
If your sheets were silk or other natural fibres, it's feasible that their digestive juices were strong enough to break down your fibres. Who knows, maybe their digestive juices are even strong enough to break down synthetic fibres (unlikely, but I don't know any study that has looked at that).


text:
Is 8 hours of sleep necessary?
Many studies claim that humans need 8 hours of sleep. During sleep there are several different stages, from stage 1 to 4 as well as REM sleep. However, are all these stages actually necessary? If yes, what are the importance of each stage, if no, which stage(s) are/is insignificant?

Can you give some examples of sources that others can read supporting your claim that we need "8 hours"? It would definitely help strengthen your question.

It's controversial, but there are some indications for the role of different sleep stages by selective restricting these stages on volunteers of sleep studies and looking at the effects the next day. There found many different roles but broadly speaking, the best evidence is that nonREM (stage 1-4) sleep plays a role in memory consolidation (storing of new memories from the previous day) and creating "space" for new memories the following day, while REM sleep has a role in problem solving and mood calibration. The work of Matthew Walker (Berkeley) and Robert Stickgold (Harvard) is particularly

Please add references!

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review


text:
Mechanistically, how does calcium chloride aid in bacterial transformation?
I am looking to get more information about the mechanism of the $CaCl_2$ in the bacterial transformation. I read online about the topic but I didn't found any reverent information on the topic, I don't have access to most of the scientific publications. However, I found this website. According to this website, there is a lot of theory about the mechanism of calcium chloride in the bacterial transformation. Would it be possible to get a short scientific referenced explanation about the topic and I can or cannot be related to heat shocks?

Frankly, the mechanism is not known even now.

Duplicate of http://biology.stackexchange.com/q/50591/3340 but the other question is also unanswered.


text:
Can you replace glucose with glycerol in cell media?
In order to feed an animal cell in process called Respiration, can I replace Glucose with Glycerol?
The Equation bellow:
Glycerol + Oxygen -> Water + Carbon Oxide

Experiments have already been carried out regarding the utilization of glycerol by yeast cells. Maybe this is what you were asking?
http://onlinelibrary.wiley.com/doi/10.1111/j.1432-1033.1968.tb00353.x/pdf

In most cases, it's not a good idea to replace glucose with glycerol in animal cell media. Animals do possess the ability to metabolize glycerol, via a pathway starting with the enzyme glycerol kinase. However, glycerol kinase is only expressed in certain cell types, such as liver cells and kidney cells.
References:
http://www.brenda-enzymes.org/enzyme.php?ecno=2.7.1.30
http://www.ncbi.nlm.nih.gov/books/NBK22591/


text:
What are the binding sites (or receptors) of cortisol?
I am in the process of a OCR GCSE Case Study, and my question is "Do the benefits of anabolic steroids outweigh the risks, which has an obvious conclusion.
I need to know the scientific name, or a scientific analysis of why it causes an increase in protein synthesis,  for the binding of cortisol to understand this quote:"Anabolic steroids may block the binding of cortisol to its receptor sites, which would prevent muscle breakdown and enhances recovery.". For without enough understanding i can't explain it.

might be nice to know what OCR GCSE - would be a good change/update to question

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. What research have you done so far to answer this on your own? What have you found out, and where exactly are you stuck? This is not a forum or tutorial site, we expect you to have done previous research on your own. Google searches and Wikipedia are excellent places to start, as is PubMed.

The intracellular receptor for cortisol is called NR3C1.
http://www.uniprot.org/uniprot/P04150
To my knowledge, a direct (competitive) effect of anabolic steroids on the binding of cortisol to NR3C1 has never been proven. The anabolic effects can easily be explained by other targets. A good starting point for further reading might be this review:
https://www.ncbi.nlm.nih.gov/pubmed/22101547


text:
How are muscle fibre size and oxygen consumption related?
Does anyone know of a paper which correlates the muscle fibre size to oxygen consumption in mammals? I am trying to find a correlation between muscle fibre type, size and (absolute and specific) oxygen consumption.

How much googling have you done? It seems there was some research: http://www.ncbi.nlm.nih.gov/pubmed/8904581 http://www.sciencedirect.com/science/article/pii/0026286268900022 Is it relevant?


text:
What is/are the effect(s) of altering the Tris concentration on polyacrylamide gels?
Why do we use two different concentrations of Tris (i.e. 1.5M Tris in resolving gel and 1.0M Tris in stacking gel)? For the gel to run properly there needs to be a different pH, but that can be done with with same Tris concentration and altering the HCl concentration.


text:
I found these in my bathroom and WC
Are they somehow dangerous? What are they and how can I get rid of them?

These are silver fish (Lepisma saccharina) and harmless. Wikipedia says (image taken from the article):

Silverfish are nocturnal insects typically 13–25 mm (0.5–1.0 in)
  long. Their abdomens taper at the end, giving them a fish-like
  appearance. The newly hatched are whitish, but develop a greyish
  hue and metallic shine as they get older. They have two long cerci
  and one terminal filament at the tips of their abdomens; the filament
  projects directly off of the end of their body, between the left and
  right cerci. They also have two small compound eyes, despite other
  members of Zygentoma being completely eyeless, such as the family
  Nicoletiidae.
Like other species in Apterygota, silverfish are completely
  wingless. They have long antennae, and move in a wiggling motion
  that resembles the movement of a fish. This, coupled with their
  appearance and silvery scales, inspires their common name. Silverfish
  typically live for two to eight years. Silverfish are agile runners
  and can outrun most of their predators (including wandering spiders
  and centipedes). However, such running is possible only on horizontal
  surfaces, as they lack any additional appendages, and therefore are
  not fast enough to climb walls at the same speed.[citation needed]
  They also avoid light.

disgusting. They look like cockroaches with their antennas.....

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Significance of Nissl bodies
What is the significance of Nissl bodies? How are Nissl bodies different from any other RER seen in any other cell of the body?

Hi there, I think this is a homework question. Please add a refference and try to solve it on you own first. Otherwise you may not get answer.

https://en.wikipedia.org/wiki/Nissl_body this might be a good start.

I am going to try answer this question.
The origine of this name came from article writen by Franz Niessl (18660-1919) and published in 1894. HE found this substance after he visualized it by nissl stainning method invented by him.
This basophilic substance was just only find in dendrites of neurons, not axones. It is composed by RNA polyribosomes.
Basicly i am tring to tell you that Niessle body is just older name from old ages of histology.
Niessel body is not diffrent with others rought endoplasmatic reticulum(RER). It same pourpose as normal RER.


text:
Help identifying a weird creature
Okay, so there is this weird creature, which has been crawling around our house.
I can hear it moving around, and it's especially active in the dark. I've however been able to take a picture of it.
If it helps, it's a carnivore (I've thrown some hot dogs and such).
This weird thing is 25-30cm long, and the picture of it was taken from a balcony on the second floor. I've only been able to photograph it once, but never came close to it otherwise. We live in central Europe, in a small town that somehow resembles a village. As for the ecosystem, I don't quite know. Fields, rivers and forests are all in proximity of our house.
Thank you for your anwsers,

Can you please add more information? What is the approximate size? Where do you live (country, region, type of ecosystem, urban or rural, ...)? How close did you get? Did you take this picture from two meters away, from a window at the second floor, ...?

The black and white colours on the front and the grey back as well as the overall shape make me think it could be a badger. Given the location, it could be the European badger (Meles meles). The size matches, and badgers are omnivorous, so they can eat meat.

It looks most like a hedgehog to me.  If you want to encourage a hedgehog, a bowl of fresh water is always important, and some cat food.  If you see a hedgehog in the day time, it is possibly in distress.


text:
Slightly different sequences returned by BLASTP
Probably this is very trivial but I am self-learning bioinformatics and I don't know who to ask for this kind of stuff. Also, apparently it is really hard to find information on general topics like this.
I am learning how to use BLAST. I tried to use the sequence of the COVID-19 delta variant spike protein. I used BLASTP and I obtain as results a lot of proteins (all classified as surface glycoprotein [Severe acute respiratory syndrome coronavirus 2]) that vary just for a single aminoacid. The majority of these changes is I to V or viceversa.
What does it mean? Are these all variants of the protein? Are these all sequences with mistakes? And why does it entail only the interchange between I and V?

It would help to know the blastp database you use (e.g. just default with the "run blast" button?), what the output is, what the position is, etc. Briefly, we would expect those to all be real variants, it is comforting that they are replicated in different isolates.

Note: by default blastp web interface or the command-line program may only return some number of the most similar sequences ("Max target sequences" under "Algorithm Parameters" on the web interface). You may want to look into adjusting this parameter if you want more, less similar seqs.

For the moment I just tried to get the best 50 candidates. I don't really care, it's just to try it out. I just changed the expected value to be less than 0.05. The other parameters are left to default. So from what you are saying I assume those are all genuine variants of the protein, is it correct?

Unless you have some reason to expect systematic error, that is my expectation. Viral protein sequences vary significantly, that is normal. Unfortunately in this case!

However what really leaves me wondering is that (at least in the top 50 candidates) we can only see interchange of I and V. Any idea why it might be the case?

Probably because there are so many publicly available sequences now that you will highly sample closely related sequences!! What blast is doing is just saying "give me the 50 most similar sequences to the one that i put in", and it's doing its job, it just turns out that we have so many covid genomes now that the top 50 most similar are indeed very similar!

The answer is that I and V are similar in their biochemical properties. By the way I see some V-I substitutions as well as the I-V in query vs subject and also some others (e.g. B-D, L-M). These are all real and natural variations in the sequence.
If you look at the table here, you will see that Valine and Isoleucine are both hydrophobic and similar in structure. If you delve deeper into the numbers, you will see further that they have similar charges, similar sizes, and are aliphatic. This means that they are likely to conserve protein structure in the folded form. Valine is less energy expensive in synthesis for the cell, so perhaps this plays into it a bit, but as this is a virus that is hijacking the cell processes I have no real idea if the energetic cost comes into it.
BLAST, as mentioned in the comments, returns a certain number (usually 50) of the most similar sequences to the query. You can adjust the number and specificity limits during your setting of the search parameters.  If you do something like blast the spike reference sequence from Wuhan-Hu-1 (YP_009724390.1) against your sequence (put yours in query, and the Wuhan-Hu-1 one in the subject or vice-versa), you will see a number of substitutions, indels etc, none of which are I-V. From this you can deduce that your findings of I-V and V-I are simply a matter of sampling based on the most similar sequences.
I don't know the algorithm for BLAST (or anything else for that matter), but it may well take similarity of biochemical properties into account when searching for most similar sequences. Given that there are millions of submitted sequences for the spike of SARS-CoV-2, there are likely to be many thousands of highly similar sequences in the database.


text:
what is the source of data in biological database like Genbank
What is the source of data  in international biological data bases like Genbank and what is it meant for?

The data sources of GenBank, and the intention of GenBank are stated on their welcome page: https://www.ncbi.nlm.nih.gov/genbank/

The data comes from scientists who gather data in their labs, such as DNA sequences. It is meant for a number of purposes. First, if science is to repeatable, these data can be checked against other data to see if the conclusions of a paper are valid. They are also used to reduce redundancy in data collection (sequences already exist for a particular species at a particular location, then perhaps further sequencing efforts might be better spent on another species or location). Finally, they can be used as raw data in asking new research questions.


text:
How can a layperson get their hands on a specific strain that's not readily available commercially?
I'm mostly interested to get my hands on L.plantarum D-103, but there are a few other strains as well. D-103 is e.g. mentioned here https://meridian.allenpress.com/jfp/article/80/10/1682/199965/Degradation-of-Histamine-by-Lactobacillus . It's commonly found in miso. My understanding is that the usual way is to find out an active culture collection like the ATCC, and the number that strain hast at that culture collection. But how do I find out this number? (I think it's called the type number).
With D-103 specifically the problem seems to be that it's not available at any active culture collection. It's listed as IMAU70005 (I had to google for ages to figure this out, how would you guys figure this out?), but the IMAU is not an active culture collection. What do I do then?
I'm not a biologist, just a lay person.

Generally what happens in the scientific community is you go to a culture collection - there are lots of different ones around the world. If they don't have it available, then you write to the authors of a paper on it and ask if they can share some.
In the past this used to be simple; however, now that universities and similar institutes have become much more commercially focussed, they have started to put Material Transfer Agreements (MTA) on any product coming out of them. This means that if you write to an author, they may not be able to share things with you as they also received it under a MTA - though they might be able to direct you to their source. You would also likely have to sign a MTA with the supplying institute (even the ATCC and similar usually have MTA these days), which would restrict what you could do with the material and how long you can keep it and any derivatives for. You would need a lawyer to look over an MTA if you went down that route.
Another complicating factor is that they will be very reluctant to share anything with someone outside of a research institute, for biological safety reasons among many others.
Long story short: you probably can't get these sorts of things easily.


text:
Human Anatomy and Physiology - The Muscoskeletal System
In the human limb skeleton can you identify a bone which is rather feeble and does not have much role in supporting body weight or maintain posture, and doctors use pieces of it to transplant to other broken bones, where necessary?

For bone grafts, they usually use parts of the bones, so their removal should not result in problems with the "body weight maintenance" or "posture."
Parts of the fibula (calf bone) can be used, for example, as a graft to repair avascular necrosis of the femoral neck or congenital pseudoarthrosis of the tibia (shinbone) (International Orthopaedics).
For spinal fusion (joining the vertebra in the spine), they typically use the bone from the iliac crest (the top part of the pelvis) (OrthoInfo).
Other bones that can be used as grafts:

Parts of the ribs and certain skull bones for reconstruction of the facial bones
Parts of the mandible for tooth implants
Upper part of the tibia for various purposes
Distal part of the ulna for correction of the wrist in rheumatoid arthritis


text:
Why is iodine added to salt? As opposed to fluor or fats/oils like iron and vitamin A?
Is there a particular reason why certain foods are enriched or fortified with certain nutrients?  Such as salt with iodine?  Or did we just get used to doing things a certain way since we started enriching foods about a century ago?

Where I live, supermarkets offer cooking salt enriched with iodates and fluorides. "Food grade salt shall be used when salt is used as a carrier for food additives or nutrients for technological or public health reasons. Examples of such preparations are mixtures of salt with nitrate and/or nitrite (curing salt) and salt mixed with small
amounts of fluoride, iodide or iodate, iron, vitamins, etc., and additives used to carry or stabilize such additions." (FAO, 1985)

Please demonstrate the research you have put into this question (which is to do with health policy, rather than biology) yourself. Did you look at the Wikipedia article on this topic, for example?


text:
Based on morphology alone, what type of claw does the Tyrannosaur have?
I understand that the exact use of Tyrannosaur Rex's claw is a mystery, or at least debated. I also understand that claws can be used for a variety of different purposes, selective pressure adapts their morphological to be better optimized for certain tasks. Some are used for hunting and killing, like large cats' claws, some are used for digging, like bear's claws, while others are used for climbing, like squirrel's claws.
My question is, all other clues and bits of information about if and how T. Rex might have used its arms, what 'type' of claws did it possess? I'm not asking, in this question, about its arm, the arm's musculature, its mouth or jaw, or about any of the rest of the animal. Based on the morphology of the claw alone, and comparing it to known uses of similarly shaped claws, what types of tasks were the claws geared towards?

unfortunately they have fairly generic claws, they are not specialized enough to point to a use. They are curved enough to be used to grasp something but that is true for their ancestral line too so there is no sign of a specific directional selection.


text:
How does protein help to cure wound?
I understand that the protein helps to repair body tissues. If I increase the intake of protein, would it help to cure the wound more quickly? I would like to know how does the protein reaches the wound and how does it help to heal?

There are thousands of different proteins in our body, some will make a wound heal, some will not make a difference, some could make the situation even worse, you cannot generalise.

Do you mean it is impossible to know and intake those proteins that heal wound?

I am just saying that speaking about "the protein" is not meaningful, as there is not just one type of protein. Also, proteins taken through food do not enter the body as such, but are first destroyed to their components (called aminoacids) in the stomach and the intestine. See Armatus answer for example of proteins produced by the body to help wound healing.

This question seems to be based on some fundamental misunderstanding, there are hundreds of thousands of different proteins. If you're interested in specific aspects of wound healing I recommend you to start with a basic biology textbook first.

Saying protein in general helps to heal wounds is a very far step. Different proteins are essential for nearly every process that happens anywhere in your body.
There is a range of proteins which is required specifically for wound healing. The first step of wound healing is blood clotting in order to close wounds. This uses several so-called clotting factors, all of which are proteins. Some of these help the platelets (small cells in the blood) stick to the walls of the blood vessels which have been damaged, others are responsible for forming a tight clot around them to make sure no more blood leaks out. Most clotting factors also require vitamin K for their production.
The next step is wound healing. This involves several cell types gathering at the wound and laying down what is called connective tissue, a network made mostly of proteins. Cells of the skin will need to replicate themselves in order to close the wound, and they will require lots of proteins for this.
Protein reaches all cells of the body from the intestines via the blood flow.
Eating a diet high in protein would surely not be a bad thing to do - your body needs it everywhere. But it is important that you consume it mixed with healthy amounts of carbohydrate (needed for energy) and fats (needed for many structures and hormones).


text:
How do Mockingbirds find each other during mating season?
Since mockingbirds imitate songs of other birds, how do they find each other during mating season? How can they tell it's a mockingbird singing, instead of other birds? Is there something in their imitations that still identifies them as a Mockingbird?

Wildlife biologist Daniel Edelstein implies as much here: he says that there are in fact variations in tone and context that distinguish mockingbirds from other birds they imitate. (He was writing about the possibility of mockingbirds attracting the birds they are imitating, which doesn't happen. I can't find much about what specifically attracts female mockingbirds, except for the variety he alludes to.)


text:
Do ectotherms think slower when they are cold?
Animals near the ectotherm side of the endotherm-ectotherm spectrum rely on external heat sources to regulate their body temperature. When they are cold, overal enzyme activity and metabolic rate is lower.
My question is if these animal tend to 'think' slower when cold?
To be honest, my knowledge of brain physiology is very sketchy, I'm not sure biochemical activity plays a large role vs. electrical and diffusion processes and the latter would be less temperature dependant. So I'm not sure we would expect ectotherms to 'think' slower.
OTOH, wikipedia on endotherms states ...

Some ectotherms, including several species of fish and reptiles, have been shown to make use of regional endothermy, where muscle activity causes certain parts of the body to remain at higher temperatures than the rest of the body. This allows for better locomotion and use of the senses in cold environments.

The source for this claim is on google books, just not the relevant pages (Willmer, Pat; Stone, Graham; Johnston, Ian (2009). Environmental Physiology of Animals)
I'm also not sure how to define 'thinking' within this wide range of animals, I'll take any metric for  speed at cognitive tasks or reacting to external stimuli.

if the lower temperature would make the transmembrane proteins responsible for the maintenance and restore of resting potential, and creation of action potential, work slower or less, I believe it would make the thinking slower. On the other hand, the lower temperature may only alter the strength of the stimulus necessary for the action potential, in which case I don't know if the thinking would be slower or if the only change would be that there would simply be less thinking. I believe both happen, but to be sure one needs to analyze this to a deeper physiologic level and do some calculations

temperature definitely affects insect response time, not sure about other ectotherms. https://www.biorxiv.org/content/biorxiv/early/2016/06/09/056051.full.pdf

I would assume as the temperature decreases, even as an ectotherm organism that the neuro processes would decrease. From my experience in chemistry, the colder the temperature the slower the molecules vibrate. As a result, it would take a longer time for the sodium and calcium molecules to move from the end of the neurons to the synapses resulting in delayed thinking. If they are absorbing the energy necessary, then their neuro processes should be functioning normally.

Welcome to Biology SE and thank you for your contribution! However, we tend to prefer answers that are backed-up by references in this community. As it stands this is really a comment, not an answer. Additionally you seem to be contradicting yourself: will the "molecules" diffuse slower or will the "processes" be functioning properly?

It's usually not simply that it would take longer for the ions to move during depolarization. It's much more complicated than that, usually involving a myriad of interactions. A large part of it is that metabolic processes slow down (remember, activation energy often requires heat), and less energy in neurons means they will respond sluggishly.

I can't see why it would be different for ectothermal animals than endothermal animals. By lower temperatures, I'm not considering a few degrees one way or the other; there is probably a maximal temperature range for the nervous system to operate, followed by decreases in lower ranges.
You write

Some ectotherms, including several species of fish and reptiles, have been shown to make use of regional endothermy, where muscle activity causes certain parts of the body to remain at higher temperatures than the rest of the body. This allows for better locomotion and use of the senses in cold environments.

Protective mechanisms are also in place in humans, where shivering generates heat, and blood is shunted away from cold areas to core (warmer) areas to protect executive functioning (thinking) and heartbeat regularity. It doesn't mean that once thes compensatory mechanism (and others) are overcome by falling temperatures, that cognition remains unaffected.
Given extremes, there are iguanas falling frozen (not necessarily dead, though) from the trees in Florida. I doubt they even know they're falling. Maybe a muddled "Huh?" when they hit the ground, a car, etc. But I would wager that, could we read their thoughts, they are not racing with anxiety:

My ---, I'm stiff as a board! Someone help me, I can't move a muscle! What's happening? Is this a bad dream where I can't move? Am I dead? Is this HELL? Oh, ---, I wish I had spent more time with my wives and kids! Is a deathbed confession acceptable now? Can anyone hear me? Am I even talking? How could I be talking if I can't move my mouth?!

Hypothermia definitely slows down thinking in humans, e.g. in studies to try to understand the effect of cold on astronauts (not done on astronauts, though):

Chronic multifactorial stress impaired cognitive function and mood; the addition of moderate, acute cold stress further degraded vigilance and mood. When such circumstances occur, such as during disasters or military operations, measures to prevent adverse cognitive and physiological outcomes are recommended.

and

Cold stress is experienced in occupational (military, fishing trawlers, emergency disaster workers) and athletic (winter sports) settings (Muller et al., 2012). It appears that both moderate and extreme reductions in ambient temperature may have a negative effect on cognitive function (Banderet et al., 1986; Palinkas, 2001). Specifically, cold exposure (−20 to 10°C) has led to decrements in memory [complex task (Thomas et al., 1989; Patil et al., 1995)], vigilance [complex task (Flouris et al., 2007)], reaction time [simple task (Teichner, 1958; Ellis, 1982)], and decision making [complex task; see Table Table4;4; (Watkins et al., 2014)]. Such consistent findings across such diverse ambient temperatures may be explained by traditional theories of cold induced cognitive decrement (Teichner, 1958; Enander, 1987; Muller et al., 2012). ... Regression analysis from a recent study (Watkins et al., 2014) reported a significant relationship between alterations in thermal comfort and cognitive function in the cold.

So, yes, at sufficiently lower temperatures, cognition is decreased. One theory is that initially it is decreased because attention is directed at the discomfort of being cold (1958), but fMRI studies might clear up that issue nicely.
Cognitive function and mood during acute cold stress after extended military training and recovery.
The Impact of Different Environmental Conditions on Cognitive Function: A Focused Review


text:
Difference between flexion and contraction?
i asked this to my anatomy teacher and he said there is no difference but when it comes to specialy in body building when you say to flex their bicep they freeze their upper limb in order to do that but when you say contract your bicep they only isolate it an shortens it.
am I right with my reason?

Flexion: the movement that decreases the angle between two parts [1]. Examples: clenching the hand into fist, sitting down.
Contraction: the property of muscle to generate tension when actin and myosin filaments are crossing. There are a few types of contractions. The isometric contraction is when the muscle generates tension but its length doesn't change (for example when you try to lift something that you can't). The isotonic contraction is when the muscle changes its length [2]. This kind of contraction leads to movements and can lead to flexion too.

References:

Wikipedia contributors, "Anatomical terms of motion," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Anatomical_terms_of_motion&oldid=612679254 (accessed June 26, 2014).
Wikipedia contributors, "Muscle contraction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Muscle_contraction&oldid=609265714 (accessed June 26, 2014).


text:
How many birds in this population would be expected to have either red or white feathers?
Question: The red and white feather pattern of a  bird is determined by a gene that has two alleles, band R and W,which show codominance.  Some birds have completely red feathers (RR),some parrots have completely white feathers (WW), and others have red and white feathers (RW).In a population of 630 birds that is at Hardy-Weinberg equilibrium, 202 parrots have completely red feathers. How many birds in this population would be expected to have either red or white feathers?
Is this question asking for what is the carrier proportion-2pq? The answer is supposed to be 321 but I keep getting 309. I did 202/630= p^2=0.32= 0.566. Then q=1-0.566 =0.434. Then I did 2(0.434)(0.5662)= 0.49. Then I multiplied 0.49 x 630 to get 309. If any one can point out what I did wrong I would really appreciate it!!

If this is homework, please add the homework tag.

Its nice to see someone actually do something before to post it on SE. :)

The solution
$$p^2 = 202 / 630 ≈ 0.32$$
$$p = \sqrt{202/630}$$
$$(1-p) = 1 - \sqrt{202/630}$$
$$(1-p)^2 = \left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$$
There is a fraction of $202 / 630 ≈ 0.32$ of red birds. There is a fraction of $\left(1 - \sqrt{202/630}\right)^2 ≈ 0.188$ of white birds. There is therefore a fraction of $0.32 + 0.188 = 0.508$ of birds that are either all white or all red. In a population of 630 individuals, it therefore represents $630 * 0.508 ≈ 320.53$. A result that is apparently rounded up at $321$ in your answer key.
Your mistake
You computed the number of birds that have both white and red feathers (WR) while the question was asking for either red or white feathers. You calculated the expected number of heterozygotes instead of calculating the expected number of homozygotes.
Of course the number of heterozygotes and the number of homozygotes should add up to the number of individuals in the population ($321 + 309 = 630$).


text:
What kind of bug is it?
I really wonder what this is:

I find it near pound in Czech Republic (Central Europe). It's 2 inches long, AP. half wide. It was quite fast.

It is a Coleopteran insect (Beetle order) in the Ground beetle (Carabidae) family. Based on the elytra (protective wings) and the dark first antennal segment, it looks like Carabus granulatus. C. cancellatus is very similar, but has reddish first antennal segments. I don't think there are any other similar species in the Czech republic, but don't know the fauna there well. Overall, Carabus has many species and several are native to Eurasia and can be a size of 2 inches.
https://en.wikipedia.org/wiki/Beetle#Wings
https://en.wikipedia.org/wiki/Carabus
https://en.wikipedia.org/wiki/Carabus_granulatus
https://www.insecte.org/forum/viewtopic.php?t=160369

I agree, based on the european species I know of, it should be Carabus granulatus, C. clathratus or C. cancellatus. I suspect all of them are found in the Czech republic.

Scratch C. clathratus, which has pits between the elytra lines (instead of raised bumps). In my literature, the other two are separated by the color of the first antennal segment, which cannot be seen clearly in the picture.

I am so sorry. I wanted to do better picture, but it run away as soon as it noticed me. But I have a picture, where it can be seen (I think so). Anyway I didn't put it there in first place because don't have clue how to identify a bug in science way.

@user40760 The dark first antennal segment in your second picture says that it is Carabus granulatus. On C. cancellatus it is reddish in colour.

Sorry for the late answer. I only bumped into this photo today. And sorry, guys. It is neither granulatus or cancellatus. This is a Carabus ullrichi. Without a single doubt. granulatus is narrow and elongated. Primary and secondary keels with cancellatus are more narrow. This one is convex, plump with very distinct keels.
Carabus ullrichi. For sure.

Can you add sources to your answer, and an image showing that it is indeed this speccies?


text:
RNA product storage in isopropyl alcohol
I have an issue. I isolated RNA from cortex a few days ago. For isolation of RNA i used this procedure:
I homogenizised my sample (mouse cortex) with Trizol. Then to the sample add chloroform, shooke and centrifugate it. After this part i took away the aquatic phase with RNA from mixture and add it to the eppendorf tube with beforehead prepared isopropyl alcohol with glykogen. Again i shook and centrifugate it. In this part i removed isopropyl and let only RNA pelet. Afterwards i did same thing with 75% ethanole. Last but not least i dissolved the pellet with DEPC, checked its concentration on nanodrop.
From nanodrop i saw that one of the sample had been contaminate with guanidine isothiocyanete. So i just desided to repeat steps od my isolation from isopropyl alcohol. To increase precipitation of RNA and increase chance od decontamination i decided to let RNA in isopropyl alcohol precipitate in -80 °C freezer for a night. Unfortunately i fail to remember it untill now.
My question is: Will it affect any integrity of my RNA sample?

It would generally not be an issue to leave RNA in alcohol but you should clarify your question. What do you mean by "let it clean"? Why are you doing it after the extraction and quantification? What was the concentration of alcohol?

WYSIWYG i try at least write down the steps i did. Today i was at lab but i forgot check the concentration. But i usually use all chemicals in proportion  to volume of trizol. So the isopropyl alkohol is from bought storage bottle.


text:
What is the oxygen carrying capacity of reticulocytes?
What is the oxygen carrying capacity of immature red blood cells, or reticulocytes? Is there any difference between oxygen carrying capacity of mature and immature red blood cells?

This was studied by Steve Fishbone et al and concluded that the Hb content of a Reticulocyte is slightly higher than that of a mature RBC. The CHr, which is the Hb content of a reticulocyte in CRF patients receiving Erythropoetin is around 27.5 +/- 2.5 pg
Ref: Fishbone S, et al. Reticulocyte Hemoglobin Content in the Evaluation of Iron Status of Hemodialysis Patients. Kid. Int., 1997; 52: 217-222

Interesting.  Is this the Hb content per cell?  Is it considered a normal value?

Hi Roland! Thats the value in CRF patients! It could be slightly lesser by about 5-10% in normal individuals


text:
What evolved to produce sweetness, plants or consumers?
I couldn't find an existing answer on this site, although I may be wrong.
What evolved to produce "sweetness", a pleasant reaction to the presence of sugar?
(A) Plants, using it to lure in consumers and spread seed
(B) Animals / consumers, which used sugar as a vital nutrient, to identify nutritious food, or
(C) Neither of the above; something else?

sounds like A and B could easily be answers - what do you think?

@VanceLAlbaugh I think either is plausible. I'm just wondering if there is one that can be proven or one that is widely accepted

I don't understand the question. Is the question "do plants evolved sweetness first or did animals evolved attraction to sweetness first?". When reading a question of the type "What evolved for ...", it sounds like you are searching for a physiological explanation but the suggested answer don't go toward this direction.

@Remi.b I'm not exactly sure how to answer that, the idea of something evolving in response to something else seemed somewhat clear to me; answer however you think you can explain what occurred.

None of the above.
Seeking sugar evolved long before animals, before multicellular organisms even.
Plant evolved a strategy to exploit it much much later with the evolution of fruit and nectar.
Animals evolved to like the taste of sugar since it is the primary fuel almost all life metabolizes to live in an easy to digest form, literally a simple carbohydrate. plants use sugar substances as lures becasue that's what animals already wanted and plants were already making it. Also a lure is not going to evolve before the seeking behavior that would actually make it a lure. fruit and nectar are new sugar is one of the oldest metabolic compounds in existence.
Metabolizing glucose is one of the shared characteristics between Eukaryotes and Bacteria and is present in nearly all life,source. Meaning it is was likely present in their common ancestor. This means plants and animals have been eating sugars since before they diverged into plants and animals. . Chemotaxis  of motile bacteria towards glucose is well understood, and likely predates the existence of eukaryotes. source
The production of sugar by photosynthetic bacteria predates the merging of Eukaryotic cells and chloroplast ancestors. It was present in the Cyanobacteria that gave rise to chloroplasts, meaning sugars were produced long before plants existed. source the attractive aspect was only exploited later with evolution of nectar and fruit.

Plants have been making sugar since before they were plants and animals have been eating sugars since before they were animals... Perhaps you should clarify this statement (make it scientifically accurate so that it is not misleading).

Please add valid references (with links) to support your claims. Unsourced material may be disputed or deleted.


text:
Why do we have the tibia and fibula (a 2nd bone) in the lower leg?
Does fibula participate in rotational movement of ankle or not (just like the radius in forearm)? If not, what is the purpose of that bone?

the Tibia is just like the Ulna.

@GlebVoronchikhin - The tibia is not really like the ulna. If you take a closer look at the articulation of the tibia/fibula with the talus, you'll see that the fibula allows a nice fit with stability.

@anongoodnurse so the fibula's main function is not rotation of the foot?

Two bones in lower limb (forearm or leg) is the ancestral condition for mammals. But, depending on size, there can be some degree of fusion between the two bones. Mammoth and rhino skeletons can show this. The hypothesized biomechanical trade-off is stability on uneven terrain (so, joint flexibilty is useful) vs weight support (robust limb is useful). Need to hunt down appropriate refs and skeleton images, though.

It does function in the rotation and stabilization of the foot, but that is not why we have it, even species in which it serves no function still have it. A bone does not necessarily have to have a purpose in an organism, instead it can have on in its ancestors.
We have this arrangement becasue we inherited the basic limb bone arrangement from our fishy ancestors. Basically all tetrapods share the same pattern of bones in their limbs, one bone, two bones, many small bones, followed by several groups of long thing bones. this goes for front and hind limbs.

tetrapod evolution


text:
Annotation for non-model organism
I want to annotate data while analyzing transcritpome data using DESeq2 , usually Biomart R-package (https://www.bioconductor.org/packages/release/bioc/html/biomaRt.html) does the needful , but for non-model organism for which link to Biomart R package is not available seems troublesome, any way to use the custom annotation file( I have one annotation file obtained from Uniprot) or any other alternative to do so?

Can you elaborate? DESeq2 takes count data where the row names are labeled sequence features and allows you to test for differential expression. If you want to associate an annotation with a given sequence you don't need DESeq2, either the sequence features can be matched to the annotation or you need to go back to how the transcripts were assembled.

What kind of annotation file are you looking for? Can you clarify a bit on what exactly do you intend to do?

I'm voting to close this question as off-topic because this is a question about computation (how should I accomplish X in R), not about biological concepts.


text:
How is randomness of the branch migration process ensured?
Branch migration (part of genetic recombination) is a random process. It looks like Ruv-ABC proteins are mainly responsible for this process, but how is randomness ensured? After all, it can only be a quasi-random process - i.e. molecules don't behave randomly. Is it thermal motion perhaps?


text:
Why are archae and bacteria grouped into separate domains?
Archae and bacteria are both Prokaryotes. Why are they group into two separate domain?

have you tried google - there is plenty out there for you to discover about this...google "why are archaea in a different domain from bacteria"

Homework questions and questions that show little or no prior research effort are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Reducing your question to its fundamental misunderstanding
Similarly one could ask "Mammals and birds are vertebrates. Why are they grouped into two separate taxa?" (Bacteria and Archea include all procaryotes unlike my example). Or even better, one could ask "procaryotes and eukaryote are all alive. Why are they grouped into two separate taxa?" At the end of the day, your question boils down to why do we group lineages together?.
Why do we group lineages together?
Population tend to diverge through time. For this reason we end up with a multitude of different lineages. As humans we can enjoy grouping lineages as we like to. One might group all yellow flowers together for example. However, a grouping which is of particular interest is one which represent evolutionary relationship. Insecta for example represents a group that include all currently living insects and all of their ancestors until the most recent common ancestor of all insects (that is the individual toward which all currently existing lineages coalesce). Such groups are called monophyletic.
You should have a look at this post where I made an intro to phylogenetic.
In short, to answer your question,

[W]hy are [Bacteria and Archea] grouped into two separate domain?

Because they represent two separate lineages.
Phenotypic differences
Of course, different lineages often have distinct phenotypes which makes their grouping intuitive to a naturalist. For Bacteria and Archae, it takes some knowledge in molecular biology to tell how different they are phenotypically. This document from Colorado University does a good job in introducing the similarities and differences between Bacteria and Archae

I would add to this that an important element of this classification is that bacteria and archea are at least as different from each other as plants and animals; our bias as eukaryotes might be to split the eukaryotes into all sorts of classes and lump prokaryotes together as just being sufficiently different from us, but if we try to be slightly less biased it is clear there is just as much (and by most definitions more) variation within the prokaryotes.


text:
If targeting a certain daily water intake, do you have to compensate for beverages that promote diuresis?
Please forgive my ignorance on the topic and I hope this is a "on topic" question here. It was a toss up between this SE and Physical Fitness SE but I want a more scientific answer.

I came at a impasse in a conversation with another fitness enthusiast. They stated that if you are targeting your water intake during the day then drinks with a diuretic effect (tea/coffee) count negatively towards that water intake total.
So, is it true that one should over-compensate if drinking these diuretics? Or does the water content of drinks like coffee and tea balance out or even positively hydrate you?

The notion that tea and coffee are diuretic and don't count in your daily waterbalance, is an urban myth. At most, both are mildly diuretic (if any).
The assumption is based from an old study from 1928 with only three participants. While the small number of participants alone is a good reason to reject the study (it would never get published today) because the findings would lack any statistical power, the design is also questionable. You can find this story in reference 1 if you want to read it.
It is known that large amounts of caffeine indeed have a diuretic effect by increasing the blood flow to the kidneys and inhibiting the reabsorption of sodium. This leads to the outflow of water and an increased production of urine. See reference 2.
However, reference 3 found that this diuretic effect (which is only present at high concentrations of caffeine) diminishes due to tolerance when people regulary drink tea or coffee. They do not see any diuretic effect from normal tea, coffee or caffeinated beverages.
The explanation for this effect is most likely a misinterpretation of our observation. We seem to produce more urine when we drank tea or coffee, but we wrongly compare it to a time when we drunk nothing. If we would compare it with a time, when we drank the same amount of water, the effect (you have to pee more when you drank something) would be the same.
Drinking tea and coffee will therefore help to keep our waterbalance, as would water, juice or softdrinks.
References:

TOLERANCE AND CROSS-TOLERANCE IN THE HUMAN SUBJECT TO THE DIURETIC
EFFECT OF CAFFEINE, THEOBROMINE AND THEOPHYLLINE
Caffeine and the Kidney: What Evidence Right Now?
Caffeine ingestion and fluid balance: a review.


text:
Do plant viruses attack animals? examples?
Do plant viruses attack animals, if yes please give an example of the virus.
I feel both plant and animal viruses are different, and they cannot attack each other hosts.

Plant viruses attacking animals or vice versa would mean that an animal serves as a biological vector to a plant or that a plant serves as a biological vector to an animal (depending on whose prospective you take by considering it as the host). This is highly unlikely

due to very different properties of the plant and the animal cells, while the virus has to be adapted to replicating in both
due to the nature of the interactions between the plants and the animals which are unfavorable to transmission between viral habitats (unlike, e.g., direct blood exchange between an animal and a stinging insect).

On the other hand, plants and insects routinely serve as mechanical vectors for transmitting viruses: an insect feeding on one plant may carry virus particles to another plant, and similarly a plant may mediate viral particles exchange between insects.
See Viral Ecology by Hurst et al.

WRT different properties, note that many (most/all?) animal viruses are even more specific.  They attack only one or a few cell types in the animal.

@jamesqf indeed, but they can attack different species - e.g., a human and a mosquito.

But are mosquito-borne viruses actively infecting the mosquito, or are they just carried by it, in the same way that airborne viruses are carried in droplets?  That is, mosquito sucks some blood from an infected person, virus floating around in that blood gets transmitted to the next person bitten.

@jamesqf It depends on the virus and the insect. In your scenario the insect is still a mechanical vector - it only carried the virus. However some viruses do take active use of the alternate hosts. Flaviviruses (Zika, Dengue, Yellow fever, West Nile) are an example. Not only they reproduce in a mosquitor, but they can even be passed vertically to their progeny. On the other hand, there is no horisontal tarnsmission between mosquitoes for physiological reasons (mosquitoes do not exchange body fluids). It is still specific in the sense that it infects a particular species of mosquito.

Interesting.  I learned something new :-)


text:
Reference to hypothesis about breast sexual attractiveness?
Some time ago there was a hypothesis published,suggesting evolution made breasts mimic buttocks for either primitive men being attracted to women when they started to walk on two legs, or to discourage sexual intercourse from behind for other reasons I can’t remember. I can find many posts about this online, but I can’t find any reference to the original idea. Can anyone provide information about this?

Do breast ressemble buttocks so much?! You can use google scholar for example to search for papers. Among the first results I got there are Furnham and Viren 2007 and Anderson 1988. Note by the way that you are confounding the term theory with hypothesis.

What is the difference between theory and hypothesis? arent they both unconfirmed?

@Remi.b those researchs you linked are interesting, but they arent the one I'm looking for. The one I'm looking for states the opposite to the second one.

In science, a theory is a set of hypotheses that are highly supported by many evidences (e.g. theory of gravity, theory of evolution, ...). The definitions of these terms are up the the field of philosophy of science but we have one post on Biology.SE that explain them brielfy (here).

I know it is not exactly what you were looking for that's why I posted it as a comment rather than an answer.

We use a different meaning for theory in my country. In the universities I attend, in subjects like research methodology or philosophy of science, theories are unconfirmed or unvalidated statements, which might have support, but not conclusive evidence. I dont think we are the only ones who uses the term this way, because I've seen the term being used in this way amongst american  Psychologists for example. What is different to a hypothesis or a theory is a scientific law. I didnt mean theory as a synonymous of scientific law, if that's what you understood from what I wrote

I have modified your question, improving the English and scientific statement. If I have changed your meaning please say. I am still not sure this is on-topic. It is not really a question about science — you just want a reference. However I will leave others to decide on that.

A scientific law differs from a scientific theory. A law does not attempt to explain a natural phenomena, they just posits a causality relationship (e.g. law of thermodynamic) while a theory attempts to explain a natural phenomena (e.g. theory of gravity). A hypothesis is a guess about nature (e.g. the hygiene hypothesis). Anyway, it is not the place to discuss this. Just have a look at any intro course to philosophy of science or philosophy of knowledge (or even just wikipedia) or ask questions on Philosophy.SE. Note that the term theory is often misused in the popular culture.

and what do big and red lips look like? why do men and women have equally large big lips? your theories are only components of a larger image, and in a concensus of all theories on breast shape, that theory is only one dimension of it.

Eventually, I found it, here it is:

In considering the human animal, zoologists proposed that the human
  female is the only primate that possesses permanent, full-form breasts
  when not pregnant. Other mammal females develop full breasts only when
  pregnant. The zoologist Desmond Morris proposed that the rounded shape
  of a woman's breasts evolved as frontal, secondary sex characteristic
  that is a sexual-attraction counterpart to the buttocks, and so
  encouraged frontal copulation, the reason being that while other
  primates mate by means of the rear-entry position, the upright,
  bipedal human being was likelier to successfully copulate face to face
  in the missionary position.

https://www.reddit.com/r/askscience/comments/uflgy/why_are_breasts_so_attractive_after_all_theyre/

I said I was looking for a hypothesis which refered to that. That's the hypothesis I was looking for, I didnt say the hypothesis was confirmed or denied as being "right" or "wrong".


text:
Why can't two different genetically species reproduce to give a viable offspring?
What is the reason that only organisms belong to same species can produce a viable and reproductively healthy offspring but organisms of two different species cannot?

Viable - it should be living atleast and I meant reproductively healthy as healthy.

This question is based on a false premise and shows lack of research — there are many examples of interspecies hybrids that are able to reproduce with other hybrids and/or one or both progenitor species. These hybrids include many modern Homo sapiens, wolves and coyotes, several species of "new world" warblers, and many plants.

The short answer is that "different species" are defined as "not being able to produce viable offspring".  So the answer to your question is that it's a tautology; it's that way because that's how it's defined.  You're asking a question about words, not about biology.  If you were able to persuade people that a "species" was "anything living in the same area", then "different species" would be perfectly able to reproduce.
More specifically, there are many different definitions of "species", and you're asking a question about one particular definition, the "biological species" concept that was first presented by Ernst Mayr in 1942 in his book Systematics and the Origin of Species.  Mayr's definition is a useful one, but it's far from the only one; there are literally dozens of other definitions of "species".  See Wikipedia's The Species Problem for more information.
Still, it's worth asking why there biology does (to some extent) have "species" that don't interbreed; Mayr's definition has stuck because it is useful.  The first thing to consider is how remarkable it is that any two individuals (of the same species) can interbreed at all.  It's not the default option! There are thousands of highly specialized quirks that allow fertilization to happen at all. Males and females have to be incredibly fine-tuned to recognize each other, to have sperm and egg meet each other, to have the sperm identify the egg, to enter and mix genetic material ... the cascade is tremendously unlikely and has to be rigorously maintained.
So when it's not maintained -- when there's no selection pressure on two populations -- inevitably there will be genetic drift that will randomly disrupt this fine-tuned system. If a population of, say, voles is isolated on an island, they will continue to have pressure to be able to interbreed with other voles on the island, but if they can't interbreed with those on the mainland there won't be any consequences, and so over long enough time they'll drift and lose that ability -- just as many apes, not suffering any consequences from not synthesizing vitamin C, gradually lost that ability from random drift.
There's another side to it. Two populations in the same location may be positively selected to not be able to interbreed. Think about two groups of finches, one with small fine beaks that eat tiny seeds deep inside pine cones, and one with heavy beaks that crush and eat thick-shelled nuts. They each do fine, but they can interbreed and produce offspring that have intermediate beaks -- too thick to reach the fine seeds that one parent eats, but too delicate to crush the nuts that the other parent eats. Those intermediate offspring will die off, and both parents will have wasted their resources raising them.  Both parents would be better off not breeding with each other,  but only breeding with their own kind to produce specialized and efficient offspring. There is now selection pressure on the birds to recognize their own kind (perhaps through songs or mating displays) and ultimately to be inter-sterile, so they never waste resources on the un-fit offspring. There's a gradation of separation over time, in which the different populations become more and more distinct. Eventually, at some arbitrary point, humans start calling them "species", but that's just us, not biology.
"Species" is an important concept, but it's not special in evolution; speciation is just one aspect of natural selection, there's nothing magical about it.

Nice! Taxonomy isn't carved in stone. The nomenclature changes over time. The scientist decide that some subspecies should actually be different species, species are moved to another genus, etc. Are dog Canis familiaris and wolf Canis lupus different species? They can interbreed and produce fertile offspring.

In sexually reproducing organisms, fusion of gametes starts of the process of embryonic development.
If union of gametes between two genetically distinct species takes place, there may be two situations -

Same number of chromosomes - Though the number of chromosomes are same, during the first mitosis, their centromeres may not be arranged in the same plane. As a result, cell division cycle arrest occurs, halting further development.
Different number of chromosomes - The extra chromosomes which are not paired lead to differential tension on the microtubules which again disrupts the cell division cycle.

Description of cell division checkpoints.

But still there are mules, and they themselves are infertile.

There are numerous examples of viable interspecific hybrids, many of which are reproductively competent. Your answer seems to assume that these don't exist. Your answer also seems to be about post-zygotic inviability (rather than sterility) and provides no references or other support for either mechanism. One example — mules (and hinnies) have an odd number of chromosomes and while usually sterile they are very robust. This shows that your point 2 is incorrect (it may help explain meiotic failure in the hybrid, but it definitely doesn't prevent development of that hybrid).

@tyersome I agree that there are viable interspecific hybrids but the way the question is asked, it seemed to me that they want to know the reason why such hybrids are rare which is why i listed (simple) causes to explain it. I also agree that the factors I have listed are post zygotic ones. Truth be told at that point in 2017 I did not know enough about evolution (and I still don't).


text:
Less oxygen in winter?
Since Oxygen is produced by photosynthesis, would there be less oxygen in the air in winter, where the trees shed their leaves and the sun generally shines a lot less? If yes, would that be a noticable difference?

Pretty interesting question: The short answer to it is: Yes, the seasonal O2 levels vary with the season and this can be measured.
The paper in reference 1 says that this is connected to two phenomena: Production of O2 by photosynthesis and also the uptake and release of O2 in the oceans due to higher temperatures (warmer water dissolves less gases).
The paper in reference 2 says that the northern and the southern hemisphere are basically decoupled from each other. The northern hemisphere reaches its peak of maximum O2 concentration in June/July while the southern reaches its peak around January due to the slow mixing in the athmosphere. They also say that due to more ocean area on the southern hemisphere the uptake/release processes in the ocean play a much more important role there.
The graph from paper 3 also shows that the CO2 concentration is inverse compared to O2, since during the photosynthetic period of the year CO2 is consumed.

The following figure is taken from the website of "2° Institute" and is interactive, so can actually check, when the concentration is at which level. The general O2 concentration is getting lower, it is assumed that this happens due to the human CO2 production, the source can be found here.

References (please let me know in the comments, if you can't access the articles):

Seasonal and interannual variations in atmospheric oxygen and
implications for the global carbon cycle
Seasonal variations in the atmospheric O2/N2 ratio in relation to the  kinetics of air-sea gas exchange
Seasonal and short-term variations in atmospheric potential oxygen
at Ny- Ålesund, Svalbard


text:
Why slow worm lost ability to walk in evolution/ecology perpective?
Can  lost of legs for slow worm be considered as Batesian mimicry?

I just want to be sure why does it lost its  legs.

Your first link is broken

For what reason does losing its legs could be an anti-predator adaptation? Can you please explain your thoughts?

i am sorry but i dont know how to fix this. But anyway i hope this is clear what i am askingfor.

He is looks like a viper commune, most common poisonous snake in middle europe so i thought that can be possible connection.

You can use the edit button to fix it. If you are uneasy with the formatting you can see how I fixed it. Can you please explain your thoughts for why being legless in slowworm could be an anti-predator adaptation?

I thought it is because slow worm looks like a snake and snakes are usually danger with their venom, so part of the slow worm population whose looked more like snake had advantage. In the end the the subtype of slow worm spread in whole species. But  I am quite confused with the part of the lost legs, because it is logicaly much more disadvantage in live (possible trade-off to look like snake?).

Oh you mean Batesian mimicry then, isn't it? You should edit that!

@L.Diago Your last comment suggests that a loss of legs is generally a disadvantage. That is hardly the case, since a loss of legs has evolved independently with Squamata multiple times (>20 it seems). With your assuption, you could just as well argue that all snakes should have legs. So the premise of the question is probably incorrect, and mimicry is not likely to be the explanation (at least from what I've seen).

I actually quite dont see a any diffrence between Batesian mimicry and muller actually (even dont know about batesian). I didnt know that lost of legs was multiple times, but i thought thet slow worm is diffrent case because it is actually lizard. That why i thought this  case is adaptation after the snakes lost legs (secondary). Anyway i got your point with my premise.

@L.Diago Batesian~= harmless species mimicing dangerous species (eg hoverflies vs wasp) ; müllerian~= several distasteful/poisonous species having warning patterns that resemble eachother.


text:
GABA in plants (article about its mechanism)
I am studing to plant physiology exam and i cross over the statment about GABA in plants.
It said that level of GABA increasing my thermal shock. But mechanism of effect on plants is unknown.
Can anybody give me a tipe about proper article about it?

I am sorry for not doing my research part but i am quite busy.

Your comment perfectly nails down the main issue with your post. Respectfully, we are not here to do your work. Wether you are busy or not is irrelevant. We are all busy people and we would all be very pleased to have someone to work for us for free. I am VTC as homework question lacking effort. Good luck!

Unlike in Europe, in the US and Canada, there is actually loads of homework at the University. I dunno about other continents.


text:
FIbroblast vs fibrocyte
After i had been studing for histology examp i tried to solved one nominclature dilema.Its about fibrocytes and fibroblast.
In my histology book is statment, that fibrocytes is special type of cell which can be differentiated to different cell types by specific occasion ( for example exposure to transcript factors).
Then fibroblast is cell of connective tissue. Its differentiated.
Why is differentiated cell named with blast (usually active type) istead fibrocyte (usually the differentiated one)?

If i  misunderstand something i ll be grafull for correction.

See the second part of the answer marked as duplicate: Blast cells may also be cells that produce materials applies to fibroblasts. There isn't anything particularly unique about this example, you've just focused on one but not both of the meanings of the -blast suffix.


text:
Hepatocytes polyploidy
Why are some hepatocytes polyploid?


text:
Hemispherectomy and brain changes
As far as i know hemispherectomy is a rare procedure when individual will going to have half brain removed in very young age. Because brain has quite remarkeble neuroplasticity patient usually will survived only with half of brain.

My questions is?
How much brain can be removed to not to negatively influence brain activity?
Does anatomy hemispherectomy alter secretion of glands for example pineal gland?

The glands are not a part of cerebral hemispheres; so they would not be removed. The wiki link also says that surgeons prefer to leave the sensorimotor cortex intact.

I didn't think functional hemispherectomy but anatomical one. I am sorry that I forget to mention that


text:
Do all retroviruses evolve into dna viruses?
Since even nonprocreative sex transfers genetic material it seems redundant for viruses to destroy the host. Retroviruses are sufficiently simple to fit into DNA. So why not just become DNA viruses?

Why is this question tagged proteins? Unrelated, I've been contemplating that life change myself...

First of all we need to be clear with the differences between DNA and RNA.

This is the typical picture that comes to our mind after high school biology classes when anybody mentions RNA and DNA. But this is actually not 100% accurate. Fact that in DNA is only 5-methyluracil (thymine), not uracil and in RNA is only uracil, not 5-methyluracil is not true.
Uracile
One of the example of Uracil occurring in DNA is deamination of cytosine. Basically it's a type of mutation. But the occurrence doesn't have to be just by mutation. According to this article:

The other main source of uracil in DNA is by incorporation of dUMP instead of dTMP during DNA replication. dUTP is a normally occurring intermediate in nucleotide metabolism, but the level is kept very low due to an efficient dUTPase which prevents incorporation of dUMP. Although incorporation of dUMP into DNA was demonstrated both in bacteria (Tye et al., 1977; Wist et al., 1978) and isolated mammalian nuclei 25 years ago (Wist et al., 1978), the extent and significance remains unclear.

Double helix structure
Even the claim that only DNA has double helix structure is not true. You can easily disprove it by seeing tRNA´s 3D structure.
2C ribose ring
So the only difference is on the 2C of ribose ring. In RNA there is one extra -OH group which makes it more unstable than DNA (which doesn't have an extra -OH group). Although, C-OH has more bond energy than C-H, the true reason that it is so reactive is in the electronegativity of Oxygen (2nd most electronegative element after fluorine).
Why RNA viruses use RNA?
So, why is it better to be RNA virus for the HIV?  According to this study:

Multiple factors influence evolutionary rates, including
  generation times, fidelity of copying genes, and selective
  pressures. Microbes often have very short generation times.
  Ribonucleic acid (RNA) viruses, typically lacking proofreading,
  have high error rates when they make copies. As a result,
  evolution rates in microbes tend to be rapid, and RNA viruses
  are the most rapidly evolving organisms. This is useful
  for rapid adaptation to novel selective pressures such as immune
  selection and antimicrobial drug use. To compensate,
  the most rapidly evolving genes in vertebrates are immune
  related.

Basically, it says the  RNA form can increase your evolution rate and your chance to avoid the host immune system. In the end take it logical. Viruses have special life strategy (technically viruses are not living form of matter so apologies for that). They wanted to replicate itself as much as it can. So if the virus is made from DNA the proces takes much more time (it has to be transcribed into mRNA and after that translation). So RNA virus have to only translate the RNA to make as much as it can (my claim is confirm by viruses classification on wikipedia).

You have to remember that evolution has no logic, in the sense that "if it works, it ain't stupid"! There are many creatures that, by our perspectives, we would ask the question, "why?".
What makes retroviruses so well evolutionary adapted is their high mutation rates with each replication cycle and destroying the host cells are like leaving no witnesses. High mutation rates are associated with RNA molecules, because they are   not as stable as DNA. This can make the virus difficult to identify by a host cell and initiate defense mechanisms because they are changing all the time. We see this with the HIV virus, which is why we can't seen to find a cure, we cant lock on a single version on the virus.
The take home message is that if an organism, even viruses, have evolved in a strange way, it is probably because they function uniquely and efficiently within their niche. Natural selection knows best!


text:
Is this a Tsetse fly?
I found this on my back while looking in the mirror.It took me 10 minutes to kill it.I hit it well at least 5 times before it died.It kept flying to me every time i tried to hit it,trying to go under my shorts
Is this a TseTse fly?

what fly is this?

Why the downvote?

This is a species of Hippobosca, looks like H. equina. There aren't too many species of this genus, so the species may be this one, which is rather common in Europe, Africa and parts of Asia - see https://www.biodiversidadvirtual.org/insectarium/Hippobosca-equina-Linnaeus-1758-img485046.html. Since you suggested it could be a tsetse fly, I assume you are in Africa. Hippobosca equina occurs in Africa as well. Other hippoboscids are not as strong fliers as Hippobosca species, which would explain its flying back to you over and over.

Thanks a lot Steve.I am actually from Greece.The title was for click-bait and the suspense :P ! The smartest fly i have ever seen.


text:
How much blood flows to female breasts?
How much of the entire blood in the body blood flows to the breast (while resting). If you know the percentage or absolute values , as well as the total cardiac output, I would appreciate it answers or referrals to publications or tables. Thanks.

Maybe this paper is relevant, but I don't have access to it.

This paper has an answer for a normal tissue in a patient with cancer. It is known that also blood flow of normal tissue increases near the presence of a cancerous tumor.

By resting do you mean supine or upright?

Resting = sitting on a chair.


text:
I haven't seen any gel lanes
I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them. This is not my first time performing 1.2% agarose gel electrophoresis.
I see gel lanes when I take the gel out the apparatus, but when I go to photograph them: nothing shows up. I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).
Tried using different markers: no luck.
Re-added some more EtBr to better stain the gel: no luck.
I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).
What could I be doing wrong? Am I taking the film out too early?

Do you see something on the gel when you put it on UV light?

Are you using a digital gel box or the old school one that uses UV light and requires orange-tinted glasses?
We had a similar problem like that in our lab. The best solution was to properly add the correct concentration of SYBR to our gels. However, we never worked with ethidium. But it might be a concentration problem.
Running your dye off the gel is never a good idea. I usually take a photo at about 2/3 of the way running it. Remember that the loading dye lets our naked eyes see the travel of our PCR product, whereas the Nucleic staining dye is what will be picked up by the UV transmission photography.
Have you tried adding it directly with your PCR product so that it’ll bind? How much are you adding to your gel when you make it? The Nucleic dye is essentially binding to the major/minor grooves of your DNA and thus lighting with UV exposure.
Have you checked to see if you’re also using the correct restriction enzyme or primers?


text:
Does a software exist to automatically design antibodies that target a given protein or antigen?
I'm looking for software to automatically design antibodies that target a given protein or antigen.

No, there does not. It is possible to do in silico tweaking of sequences to do some affinity maturation, for example, but I've never heard of a method for de novo CDR design. Nature is much better at doing that for us. Also, even if such software existed, the computing power required would be enormous - much much more than an individual computer.

Much easier said than done!
If I had sufficient funds and time to pursue your goal what I would do is comb the Protein Data Bank for all the PDB files of interest. Surely you have some protein that interest you. Might consider doing the following:

Figure out what family your protein belongs in, considering it's number and presence of motifs: coils, helices, beta sheets, etc...
Do a literature review of any protein that has already been studied belonging to this family. So when a protein in this family catalyzes a reaction what are its flexible and restrained regions?
Use a program like Autodock to dock your protein to a protein that its protein family might interact with.
Calculate the interaction energies using Gromacs, NAMD, or Gaussian. You can do a zero time calculation of initial states or pursue a molecular dynamics approach as the proteins move randomly to their most stable configurations, or even a molecular mechanics approach. Which systems are most favorable?
You got this far. Now what? But then none of these steps creates your candidates. It just gives you an idea of the physics involved in already structurally identified compounds. Yes, you can make point mutations in VMD and Pymol. But, if you want to add a new motif to an existing protein structure it will not work because more than 20 amino acids in a peptide do not fold properly.

To do some of the biological statistics, the research collaboratory of structural bioinformatics is right here: http://www.rcsb.org/pdb/home/home.do
You can parse through their folders with wget or curl in bash scripting
at http://files.rcsb.org/
But then assuming you do figure out a candidate protein that doesn't exist yet. How are you going to make it in the lab? It appears that it would be better to do microbial studies. Maybe you can screen for a match with micro-array plates.