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The term "domain" in biochemistry and molecular biology is usually used to refer to a part of a protein that has a conserved structure and function, is similar between related proteins, and can generally exist or function on its own if it was separated from the rest of the protein. A DNA-binding domain is a protein structure that has a high affinity for DNA, and so binds to it when the two molecules are in the same vicinity. An example is a type of protein called a transcription factor, which binds to DNA in the nucleus of the cell (in Eukaryotes, bacteria and Archaea don't have nuclei - the DNA just floats free) and causes changes in the transcription of genes. The following image from WikiMedia shows how transcription factors work in general.

"DNA coiling" is a very generic term that describes many different things. The basic structure of DNA itself is a coil, with two sugar chains (the deoxyribose in DeoxyriboNucleic Acid or DNA) coiling around each other, and attached by nucleic acid bases. In the eukaryotic cell, individual strands of DNA are associated with structural proteins to create chromatin, which is what makes up chromosomes in the nucleus of each cell. In the first stage, naked DNA is wrapped or coiled around structural proteins called histones into a structure called a nucleosome. These then stack into a "solenoid" or fiber structure, which makes up so-called "relaxed" chromatin - regions of the genome where active transcription is taking place. If a part of a chromosome has been marked as inactive, or during certain steps in the cell cycle when one cell splits into two (mitosis), the fibers further coil into condensed chromatin, forming the typical structure many people associate with chromosomes. This image, from Wikipedia, visualizes each step in the process.

The word "motif" can sometimes mean the same thing as domain - for example, someone might refer to a "DNA-binding motif" in a protein. However, a motif is typically smaller than a domain, can occur in DNA, RNA, and proteins, and has to do with the specific sequence. A "structural motif" in a protein is something like a helix-loop-helix or a beta-hairpin turn that can appear in multiple different kinds of protein domains, and doesn't necessarily have the same exact function in those different domains, but typically has a fairly conserved sequence that is very similar. As an example, the zinc finger motif is found in protein domains that bind DNA, RNA, and other proteins.

All of this terminology can be very confusing at first, but if you stick with it it'll get easier over time. Biochemistry and molecular biology are fascinating fields, so keep up your studies!


Did the Swedish cod fishery expand in the past years?

If by 'fishery' you mean "amount of fish caught", the answer is a qualified no. Sweden's catch has been stable or perhaps slightly increasing since a low in 2005, but the catch is still much lower than a decade ago (Statistics Sweden). This is presumably due in large part to the quotas set on Total Allowable Catch for various sea regions.

If by 'fishery' you mean "amount of fish in the sea", the answer is a qualified yes. Most Swedish cod catch (>90%) comes from the Baltic, where stocks have been recovering since 2006 after steep declines in the eighties (ICES full report and executive summary for Eastern Baltic). Presumably, this recovery is also due in large part to the quotas set on Total Allowable Catch, i.e. to the reduction in cod mortality due to fishing.

Sweden's cod catch for all regions, and the ICES estimated Spawning Stock Biomass of cod in the Eastern Baltic. Both are in thousands of metric tons, but note that the scales differ by a factor of ten)

No idea how this is affecting import/export, although Statistics Sweden might have that data. One biology related possibility is that Eastern Baltic stocks (presumably accessed more by Sweden) are doing better than North Sea stocks (presumably accessed more by Norway), but that's just a guess, you'd have to check the data.


To date, there isn't a single species that may be considered pathogenic to animals or plants. There are archeon who live in association with animals (in the case of human, they have been found in the gut microbiota aswell as certain skin surfaces) that are mainly methanogens. This could lead to think that archaons could produce "pathologic farting", but that condition has never been described.

In the case of ascidians and other marine invertebrates, some archeon have been found living in symbiosis, with the microbe aiding the animal by means of nitrogen fixation. One could think that, since they're able to live inside the organisms, they could behave as opportunistic pathogens, but none has been described.

Furthermore, it actually exists at least one known species who could be classified as parasitic, the nanoarchaeota Nanoarchaeum equitans, which has been described as a symbiont of some hyperthermophilic archaeon. Despite that description as symbiont, Nanoarchaeum cannot live by its own, while its companion does. Moreover, its genome contains the typical traits associated to parasitism, with great reduction in genome size and loss of many key pathways and cell functions, including methabolic pathways an even some key components of its transcriptional and translational machinery. Since there is no known function of the Nanoarchaeum itself, it should be considered as a parasite.

However, the lack of evidence may be biased, since few people has used metagenomic approach to look for archeon in clinical samples, and some rare cases may be found in the future.


Why are female not competitive for reproduction like males?

As @Dexter said, there are examples of species where female compete for the access to the males but most often it is the other way around; males compete for the access to the females.

The reason for this discrepancy is mainly explained by Bateman's principle. Citing wikipedia:

  Bateman's principle suggests that in most species, variability in reproductive success, or "reproductive variance," is greater in males than in females. This is ultimately a consequent of anisogamy. Females, especially mammalian females, almost always invest more energy into producing offspring than males invest. Bateman's principle anticipated and is consistent with Robert Trivers's theory of Parental investment—in most species females are a limiting factor over which males will compete. This competition results in some males being more successful than others, leading to greater reproductive variance among males than females


How is RNAse contamination in RNA based experiments prevented?

You need to be careful about everything that comes in contact with your samples. Every spatula, beaker and every magnetic stir bar need to be RNAse-free.

For metal- and glassware we usually put everything into a drying closet at 200-250 °C for a few hours. That should get rid of RNAses pretty efficiently.

The RNA chemicals should be seperated from other chemicals if not everyone in the lab is working with RNA. They shouldn't be weighed using spatulas, but just poured into an RNAse-free container to avoid contaminating the storage container.

Use disposable plastic wherever possible, you should be able to perform most stuff in falcons and Eppendorf tubes.

Be careful with performing e.g. a DNA-prep at the same bench as the RNA work. The first buffer for the DNA-prep contains RNAse.

Avoid keeping your Eppendorf tubes or falcons open for long, that should reduce the potential for contamination.

We've had pretty good experience with just using water from a Millipore system and autoclave it once, that seems to get rid of the RNAses. I know that this is not a sure thing as the RNAses can survive autoclaving, but it seems to work well enough.


Why do large, aromatic residues prefer beta-pleated sheets?

This table is from the Wikipedia page for α-helix:

As you can see aromatics are not the worst offenders. In fact, barring proline (whose backbone torsion angles are unsuited to helices), Gly is the worst offender. A likely reason for this is Gly being too flexible i.e. its small side chain H allows it to adopt backbone torsion angles unsuited for α-helix.
As another example let's look at silk, an extended anti parallel β-sheet structure, from libretexts.

As you can see, the small side chains of Ala and Gly in fact allows the β-strands to come close enough to form backbone hydrogen bonds. In fact, from the same reference I quote - "Unlike the α helix, though, the side chains are squeezed rather close together in a pleated-sheet arrangement. In consequence very bulky side chains make the structure unstable."
So it is not entirely true that aromatic amino acids prefer pleated β-sheets.
So what are we missing? We are missing the chemical environment in which the the amino acid residues are placed. Remember, most of the propensity charts we look at are average propensities across known protein structures. In a specific protein, its specific chemical context can radically change the secondary structure propensities.


Relative rates of migration of circular, linear and supercoiled DNA in agarous gel electrophoresis

First let me supply an illustration of the situation described in the question, together with a reference.

Although you can see this sort of thing, just by searching for “plasmid migration on agarose gel”, this is one of my own from the last millennium (plasmid pBR322), appearing in a text from the last millennium, Adams et al. The Biochemistry of the Nucleic Acids (11th ed).

The poster’s attempt to rationalize the results, though expressing the quandary, is marred by the loose use of the word small, and the absence of any statement as to why ‘small’ pieces of DNA should migrate more rapidly.

The different forms of the plasmid have exactly the same molecular mass, so what is meant by small? My own initial way of looking at this is to consider the agarose gel as a mesh or sieve through which the molecules must pass, so that the larger the volume they occupy in space, the less likely they are to pass through the ‘holes’ in the mesh. The volume that they occupy in space might be regarded as that generated by rotating them from their midpoint in three dimensions. On this basis the supercoils, in which the DNA is collapsed into a short fat pseudo-linear shape should occupy the least volume in space, and the long thin linear the greatest. The diameter of the circle should place it somewhere between the other two.

So, we reach the same conclusion as the poster: the faster migration of the ‘linears’ than the nicked circles does not fit this simple model. In the text accompanying the figure I wrote “…a result that is a little unexpected” without attempting to explain it.

Am I able to explain this somewhat unexpected result now? An internet search produces either hand-waving or evasion (I stand to be corrected on this), so that I can only imagine that the result has something to do with the linear molecules having a greater chance of their ends being directed to the holes in the ‘mesh’ than the nicked circles, because of the open nature of the latter. One can perhaps imagine an hour-glass shaped portion of the sphere for the rotation of the linears that allows the ends to be directed at the holes.

More waving of hands? Perhaps. But the main point is that the physical explanation for the migration of molecules of different shapes during electrophoresis is more complex than a mere biologist might have hoped.


Mean and standard deviation of human bone density?

Interesting question that I'd not considered before.

Bone density is commonly measured by assessing the bone mineral density (BMD) using dual-energy x-ray absorptiometry (DMA), literally the g/cm2 of minerals in the bone.

Having had a search I can only find values for a small number of bones commonly measured when testing for osteoporosis (characterised by reduced BMD). Unsurprisingly the age and sex of the individual has a large effect on BMD; after puberty males have higher BMD (1) and during ageing this then declines, sometimes dramatically (2).

These values are from a Vietnamese study (3) show that the hip and the spine are different.

Men [ mean (SD) ]

Femoral neck: 0.85 (0.13)
Total hip: 1.00 (0.13)
Lumbar spine: 1.05 (0.12)

Women  [ mean (SD) ]

Femoral neck: 0.80 (0.11)
Total hip: 0.95 (0.12)
Lumbar spine: 0.96 (0.11)

There must be other reference values for other bones in different populations but I don't have time to look them up now! Good luck in your own research.

I found this website by the US National Institute of Health and this PDF by the World Health Organisation immeasurably enlightening.

Bonjour JP, Rizzoli R. Bone acquisition in adolescence. In: Marcus R, Feldman D, Kelsey J, eds. Osteoporosis. San Diego, CA, Academic Press, 1996:465–476
Cummings SR, Kelsey JL, Nevitt MC, O’Dowd KJ (1985) Epidemiology of osteoporosis and osteoporotic fractures. Epidemiol Rev 7:178–208
Ho-Pham, et al. (2011) Reference Ranges for Bone Mineral Density and Prevalence of Osteoporosis in Vietnamese Men and Women. BMC Musculoskeletal Disorders, 12:182  doi:10.1186/1471-2474-12-182


Does bright environment strain eyes more than dim?

I think the principle is "everything in moderation". Environment should be not very bright and not very dimmed. Also, the contrast should be moderate too, i.e. having bright screen in dark room is not good. Also, he type of work should not be very constant, i.e. you should sometimes change looking at the screen to looking in the window and similar.

Remember, that the light is required for stimulating the brain activity.


Prediction of transmembrane beta barrels?

I could tell only from my pretty poor experience.
I had all PDB entries processed with DSSP and then I've tried to find any trends in amino acid preferences. I did not find any except the pretty obvious absence of proline in double (i.e. with two neighbours) strands. Also, negative charged amino acids (I, L, V) were slightly more frequent in parallel strands. After that, I tried a sort of naive Bayes classifier for the amino acid and it's neighbours in two neighbour strands and +/-2 amino acids up/downstream. For single\double parallel\antiparallel strands, the prediction precision was about 60%.


Does methanol fixation deform cultured cells?

Yes, fixation of almost any kind can have effects on morphology.  When you take a free flowing, protein spiked fat-blob (ie cell membrane), and make it rigid, you are going to get some differences.

A fun visualization of this can be done by wrapping cellophane/shrink wrap around a serological pipette and dipping it in a dry ice and methanol bath.  It's something I show students all the time before getting into histology work.

Back to what you need.  What cells are you using and what are you growing them on?  Have you tried acetone fixation and you know it destroyed your plastic?  The amount of time and concentration needed for acetone fixation is low enough that most modern chamber slides can handle it.  Do you need the membrane to be permeabilized in fixation?

I don't know the main effect you are measuring, but assuming you have good controls, you should be able to see it past the fixation.  The effect in your controls should be similar to your treated groups, unless the treatment is specifically effected by your fixative.

Moving to some more general recommendations.  I think you should reconsider the fixative’s you’ve ruled out, because I am unconfident about their application.  The base source I always recommend students to turn to is the Wiley "Current Protocols in X" book that is relevant to the task at hand.  In this case, I think the most relevant text is Current Protocols in Immunology, and the appropriate unit is 21.4 "Immunohistochemistry."

I think a particularly useful, and relevant to this question if you are concerned with formalin masking, is Table 21.4.3.

That is for human antigens, but the “antigen retrieval” process works for murine cells in most cases.  You are right that you antigen could be blocked by formalin, but the solution is often unmasking as MtOH are often more harsh to morphology.  To support protocol 1:

  Formalin or paraformaldehyde fixation cross-links protein, often
  making antigens inaccessible to specific antibodies. The antigen
  retrieval protocol, which combines high temperature with buffers at
  different pH, has been very effective in unmasking antigenic
  determinants which may be masked in fixed tissue or fixed cell
  preparations, particularly determinants within the nucleus or
  cytoplasm (Taylor and Shi, 2013).

My modification of the protocol is:

Sodium citrate buffer: 0.1 M citric acid/0.1 M sodium citrate, pH 6.0

Wash sample on a liner rocker for 5 min w/2x culture volume of d.i. H2O
Place your slides in 1mM citrate buffer in Coplin jars with the lid slightly off
Weigh the jar in final state so you know how much water to add back
Microwave 4-7 min.  You don’t want it to go to a boil, and you need to remember to allow for venting
Weigh the jar again and add back water
Microwave another 4-7 min, again you don’t want a boil
Take out of the oven and allow it to come to room temp by sitting it on the bench.  If you do it too fast you’re going to disrupt the membrane.
After it’s back to room temp, wash 2x PBS+0.05% Tween20 for 10 min each
Try your IHC again, it will probably work now.


Insect identification - Possible grasshopper or grass beetle

Neither beetle nor grasshopper, it is a hemipteran, Coreidae. Leptoglossus occidentalis or
Western Conifer Seed Bug.  https://www.britishbugs.org.uk/heteroptera/Coreidae/leptoglossus_occidentalis.html


You can use Gelatin - actually this was used by microbiologists before agar came in use. That gelatin is more or less completely abandoned in this field tells quite a story, right?

Gelatin has the main disadvantage that it cannot be autoclaved together with the medium to sterilize it. Using it would need some experience and probably advanced techniques to which you have no access.
But there are some good news as well: Agar is also used as a geling agent when making food, and when you cannot find it in your local supermarket, Amazon can deliver it. You don't need much, around 15 gram/litre.


How do I read a species description that uses both ≡ (triple bar) and "incl." to denote synonymy?

According to the Taxon guidelines for authors (pdf, pg 205), a triple-bar (≡) indicates a homotypic synonym:

  Homotypic names are cited in chronological order in a single paragraph with
  the identity sign (≡), followed by the type.

So, in your example, Dorstenia foetida was described on the basis of the same type specimen used by Forsskål in 1775 to describe Kosaria foetida -- or possibly a neotype was designated linking these two names, possibly by Schweinfurth in Bull. Herb. Boissier 4(App. 2): 120 in 1896. More information about the relevant type specimens would help sort this out.


What are the differences between HPRD and BIOGRID databases?

Short Answer

In a nutshell, there are two major differences:

Species range: BioGRID integrates multiple species' protein-protein interaction (PPI) data, whereas HPRD focuses mainly on Human data.
Functionality: HPRD has some GUI tools that can interact directly with it's database (e.g. BLAST - for searching proteins and their binding partners via sequence alignment) whereas BioGRID is mostly just a database.

Long Answer

In bold are the unique features of each database.

About HPRD:

  The Human Protein Reference Database represents a
  centralized platform to visually depict and integrate information
  pertaining to domain architecture, post-translational modifications,
  interaction networks and disease association for each protein in the
  human proteome. All the information in HPRD has been manually
  extracted from the literature by expert biologists who read, interpret
  and analyze the published data. HPRD has been created using an object
  oriented database in Zope, an open source web application server, that
  provides versatility in query functions and allows data to be
  displayed dynamically.

  FAQ HPRD: Why did you decide to develop yet another database instead of integrating other existing databases?"
  We believe that biological databases are still in their early stages
  and no protein database can be considered as an established standard.
  We feel that a variety of databases trying to solve problems in
  diverse ways provide the biologists the possibility of choosing their
  favorite. Our approach is radically different from existing databases
  and we want to offer biologists the possibility of choosing instead of
  imposing one database by default. Besides, most of the databases are
  automated and ours is manually curated to avoid errors. We are also
  trying to provide information that few other databases provide.

About Biogrid:

  The Biological General Repository for Interaction Datasets (BioGRID)
  is a public database that archives and disseminates genetic and
  protein interaction data from model organisms and humans
  (thebiogrid.org). BioGRID currently holds over 720,000 interactions
  curated from both high-throughput datasets and individual focused
  studies, as derived from over 41,000 publications in the primary
  literature. Complete coverage of the entire literature is maintained
  for budding yeast (S. cerevisiae), fission yeast (S. pombe) and thale
  cress (A. thaliana), and efforts to expand curation across multiple
  metazoan species are underway. Current curation drives are focused on
  particular areas of biology to enable insights into conserved networks
  and pathways that are relevant to human health. The BioGRID 3.2 web
  interface contains new search and display features that enable rapid
  queries across multiple data types and sources. BioGRID provides
  interaction data to several model organism databases, resources such
  as Entrez-Gene, SGD, TAIR, FlyBase and other interaction
  meta-databases. The entire BioGRID 3.2 data collection may be
  downloaded in multiple file formats, including IMEx compatible PSI MI
  XML. For developers, BioGRID interactions are also available via a
  REST based Web Service and Cytoscape plugin. All BioGRID documentation
  is available online in the BioGRID Wiki.


Why do some mammals not have testes in a scrotum?

Having descended testes is a derived characteristic within mammals; monotremes and the Afrotheria (including elephants) all retain the ancestral character state (Kleisner, et al., 2010)2. Among those mammals with descended testes, these can be ascrotal or scrotal. Testicular descent is hypothesized to have only occurred once within Mammalia, with the ascrotal Laurasiatheria. Descended ascrotal testes are found in cetaceans, phocid seals, hippos, tapirs, rhinos, and some bats. Descended scrotal testes are found in horses, pigs, camels, and Carnivora.

Since basal mammals would presumably have to regulate testicular temperature just as much as derived mammals, the temperature regulation hypothesis seems to not hold up. So the real question is: why have a scrotum? One hypothesis has to do with evolution of fast locomotion (e.g., galloping).

According to Frey (1991, 40)4:

  The strong flexions and extensions of the vertebral column during
  gallop should cause intense fluctuations of intra-abdominal pressure.
  Fluctuations of intra-abdominal pressure severely impede continuous
  flow of blood in the abdominal veins. Periodically reduced venous
  drainage resulting in fluctuations of intra-testicular pressure would
  impair the process of spermiohistogenesis, which is dependent on an
  absolutely constant pressure within the testis.

Chance (1996)5 suggests that the temperature hypothesis might represent a secondary adaptation:

  Because in the human male, scrotal testes function optimally at
  temperatures below that of the body, much speculation, and a
  considerable amount of research, has gone into attempting to see what
  (metabolic) advantage might accrue from this lower temperature,
  without considering the possibility that this is a secondary
  adaptation to an enforced external position.

Kleisner, K., Ivell, R., and Flegr, J. 2010. The evolutionary history of testicular externalization and the origin of the scrotum. J Biosci 35:27-37

Frey, R. 1991. Zur Ursache des Hodenabstiegs (Descensus testiculorum) bei Säugetieren. Z Zool Sys Evolut-Forsch 29:40–65

Chance, M.R.A. 1996. Reason for externalization of the testis of mammals. J Zool 239:691–695


How do we know that ammonites are a kind of cephalopod rather than another type of mollusc?

It really is mostly the siphuncle as @augurar mentioned. The siphuncle is present in modern ammonites, cuttlefish, and Spirula(a deep-sea squid with an internal chambered shell). It links shelled cephalopods neatly with other cephalopods(both extant and extinct) and distinguishes them from other shelled things like snails.


When life evolved, first came heterotrophs that obtained their organic molecules from their environment. Then came autrotrophs who made their own organic lecyles. The most important autotrophs are photosynthetic organisms. These photosynthetic organisms lived in the water and made glucose from CO2 and H2O. A byproduct of this reaction was O2.

Now, O2 killed off many of the species since it is very reactive. But the remaining species used the O2 for cellular respiration. Before, the cellular respiration was done anaerobically, without oxygen. The way this wroked was that the glucose was oxidated and the electrons from the glucose was used to make ATP, the main source of cellular energy. Once those electrons were used, they were deposited in a highly electronegative element compound, such as Nitrogen containing compounds. When plants produced O2, instead organisms doing anaerobic respiration, since oxygen is an extremely electronegative element, organisms deposited the electrons in the oxygen molecule. This is aerobic respiration. This from of respiration was more efficient and advantageous for land organisms. That is why we use oxygen.

Lungs and breathing is one of the many ways organisms obtain oxygen for delivering to cells to do cellular respiration. Fishes use gills. Most mammals use lungs. Many single celled organisms just obtain their oxygen through diffusion.


Pyruvate as a final electron acceptor in the electron transport chain

Someone else may come along later with a definitive answer but I found this question intriguing so here are my thoughts:

The standard redox potentials of the mitochondrial ETC carriers are:

NAD⁺/NADH              -0.32 V
complex I (Fe-S)       -0.27 V
complex II (cyt b₅₆₀)  -0.08 V
complex III ((cyt c₁)  +0.23 V
complex IV (cyt a₃)    +0.38 V
O₂/H₂O                 +0.82 V

Note that electron transport is carried out from negative to positive.

Now, for pyruvate/lactate the standard redox potential is -0.19 V so on the basis of this pyruvate could in theory accept electrons from complex I, but not any further down the chain. However, complex I normally transfers electrons to coenzyme Q within the membrane. The standard redox potential of CoQ is +0.04 V which is already too positive to be able to then reduce pyruvate at the membrane surface. Thus there would have to be a novel way of transferring electrons from the final FeS centre of complex I, which is within the membrane, to pyruvate. Pyruvate is, of course, soluble and is generated by cytoplasmic glycolysis, so this transfer would have be at the membrane surface that faces the intermembrane space of the mitochondria.

If such a scheme had evolved then it might be possible to achieve some proton pumping through the novel version of complex I, which would be  energetically advantageous.

Another complication is – assuming that a complex I with pyruvate as electron acceptor had evolved – how would the cell/ mitochondrion regulate electron flow during aerobic respiration? Presumably the pyruvate-accepting version of complex I would have to be kept inactive somehow until needed.

Clearly it is much simpler to have a soluble lactate dehydrogenase to deal with the pyruvate and regenerate NAD⁺.


Can an electrocardiogram be recorded with a single electrode?

Short answer
Any electrophysiological recording of potentials, including the electrocardiogram (ECG or EKG), measures a potential difference. Hence, two or more electrodes are necessary.

Background
The ECG measures the rhythmic voltages changes generated by the heart muscle. Voltage is defined as a potential difference between two points. Therefore, a voltage is always measured across two or more points. For example, when
you measure voltage when holding one out of two recording electrodes to one of the two poles of a battery, nothing will be recorded. This, because no current will flow through the potentiometer by connecting just one pole of the battery. Likewise, electrophysiology needs at least two recording channels to determine the voltage differential between the two. One channel is typically called the active electrode, the other the reference. The configuration of active and reference determines the polarity of the recorded voltage. Often a ground electrode is added to remove background noise.


how to change format of ent file into PDB format?

Just rename the file to .pdb - in other words, .ent files are PDB format:

  The archival PDB files will be distributed with the reserved conventional names, in the form pdbentry_id.ent, where entry_id is a PDB 4-letter code, e.g. pdb1abc.ent, for PDB format entries; rentry_idsf.ent, e.g. r1abcsf.ent, for X-ray experimental data; entry_id.mr, e.g. 1abc.mr, for NMR experimental/constraints; entry_id.cif, e.g. 1abc.cif, for mmCIF format entries; and entry_id.xml, e.g. 1abc.xml, for canonical XML format entries.

From http://www.wwpdb.org/about/faq


How can I fit the A595 of my unknown samples to the data?

You could, depending on what you are doing, extrapolate your standard curve to include the absorbance of your samples. This, however, is not recommended since absorbance is linear only within a certain range. It's best to dilute your samples so that they fall within the range of the standard curve while also ensuring that your standard curve is, in fact, linear.


Microbes can produce several gasses other than methane.

All microbes produce $CO_2$ through the oxidation of reduced carbon

Additionally some metabolic pathways produce other gases.

Photosynthetic microbes produce $O_2$
Sulfur reducing bacteria can produce $H_2S$ (as @ohcanada points out)
Denitrifying bacteria produce $NO$, $N_2O$, and $N_2$
Fermenters produce $H_2$ (as @mart indicates)

There may be others that I am not thinking of but these are some of the major players...


How to pipette accurate volumes from BSA solution without air bubbles?

Never vortex the BSA solution. The best way to prepare a BSA solution is to put the BSA powder on the buffer solution (or water) instead of the other way round. Tap or rock the tube to dissolve the BSA. If there are some tiny clumps then pipette very gently (use 1ml tips; cut the tips if needed) but tapping/rocking should usually do the job.

From CSHL protocols:

  For a 10% (100 mg/mL) stock solution of BSA, dissolve 1 g powdered
  Fraction V or molecular biology grade BSA in 10 mL of distilled H2O;
  to avoid clumping, dissolve by layering the powder on the surface of
  the liquid. Gently rock the capped tube until the BSA has dissolved
  completely. Do not stir. Store in aliquots at −20°C.


regarding genetic disorders related to protein production

There are many protein deficiency issues caused by genetic mutation for eg: Protein C whose deficiency causes abnormal blood clots. This protein is controlled by the PROC gene whose mutation causes Type I Protein C deficiency (reference).

There are treatments of replacing proteins like in the case of Protein C deficiency, protein C concentrates are used (reference). In the case of Alpha-1-antitrypsin (AAT) deficiency, augmentation is done with weekly intravenous infusion of the AAT protein (reference).

So in many cases protein is actually supplied from outside the body and also many protein deficiency conditions can actually be controlled with balanced diets (reference) which unfortunately is not a solution for insulin deficiency.


Some moth actually do use clicks for their own echolocation: "Noctuid moths (Noctuidae) are the only group of invertebrates for whom echolocation was
demonstrated":

Lapshin & Vorontsov 1998
Lapshin et al 1994.


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

She is referring to a mixture of chromogenic substrates: molecules which are more or less colourless until cleaved by a specific enzyme, releasing a coloured product.

For example X-gal is colourless until the enzyme beta-galactosidase hydrolyzes it, releasing a blue coloured product. If you spread a mixture of bacteria onto a plate, with some expressing beta-galactosidase and some not, you will see both blue and colourless colonies, as seen here:

[source]

Chromogenic substrates are often used to create differential media that allow the differentiation of different species of bacteria. This plate, for example, contains several different chromogenic substrates (a mixture, if you will) for identifying the bacteria commonly found in urinary tract infections:

[source]

If you wanted to make a picture with this plate, you could “paint” with Enterobacter spp. for blue, Staphylococcus aureus for yellow and S. saprophyticus for pink. Each species produces a specific enzyme that acts on a specific chromogenic substrate in the plate, changing its colour.

Alternatively, you could express the desired enzymes recombinantly in one species.


16S sequencing: pooled or individual samples?

Ultimately, it depends on what insights you are trying to glean from your sequencing data, but from a purely scientific perspective, there's almost never a reason to pool samples in the the way you described. You pro-con list is not far off, in terms of information lost or gained, but I think it overlooks some of the down-stream consequences of losing that information on your analysis. For one thing, pooling limits your ability to make biologically or statistically meaningful comparisons. For example, if your individual samples are pooled by country of origin prior to sequencing, you have no way to estimate varation within those pooled samples. Because of that, not much can be said about any observed difference between countries beyond simple descriptions of richness and taxonomy. Treated as individual communities, you can look for differing trends, make meaningful beta-diversity comparisons, and actually analyze them with statistics. If you have environmental data, you might even be able to do some meaningful ecological analyses.

Second, as you mentioned, a pooled sample should theoretically have more diversity than the individual samples it was pooled from (at least it should have no fewer unique sequence variants than the richest of the pooled communities), but pooling could also mask community diversity. If one of the pooled samples has a particularly high abundance community that is dominated by just one or two organisms, it could create the appearance that some organisms at moderate abundance in other more diverse communities are actually vary rare, or non-existant. Even at a much greater depth of sequencing, diversity metrics accounting for abundance lose value, since any outlier sample could skew pooled results, creating a false impression of overall community profile.

Lastly, all of the cost-savings assumptions in your post are going to depend on the sequencing center you use and how they bill samples, so there isn't really a straight answer to give. But I will say that the per-sample cost of Illumina 16s amplicon sequencing is pretty cheap (especially compared to the cost of collecting insects from 5 different countries). And because of how sequencing is performed, pooling samples might not even save you much money. Sequencing is often billed per sequencing kit or per lane of sequencing used, not per individual sample you send. So, unless you have someone to share your sequencing run, it's possible that you'd pay roughly the same amount for 5 samples as you would for 95, with only minimal cost savings on library prep and extraction kits.

To summarize, pooling samples reduces your effective sampling effort and limits your potential scope of inferrence. The only valid reason I can think of for pooling samples in such a way would be if you cannont isolate enough bacterial DNA for sequencing from any one individual (which could be the case, depending on what type of insects you're working with). Like I said at the start, though, it really depends on what you want to learn from your 16s data. If the microbiome comparison is crucial to the outcome of your study, I'd suggest sequencing as many individual communities as possible, or at least a subset of individuals from each country (depending on how many you collected). If you don't plan on doing much analysis beyond describing microbial richness and maybe some taxonomic classifications, maybe pooled samples are sufficient for you needs.


Can neutrophils kill bacteria inside other cells?

Are neutrophils able to get inside epithelial cells in order to kill bacteria.
  Therefore, even if a bacteria gets inside the epithelial cells can the neutrophils get inside the epithelium to kill the bacteria?

No. Firstly because bacteria (except for very special cases) do not enter epithelial(or other) cells - that's what viruses do. Second, neutrophils recognise bacteria based on markers on their cell wall. These markers can come from the bacteria themselves, or from the innate immune system (see complement system) that 'marks' the bacteria, in any case being inside another cell would protect bacteria from neutrophils. Cases are like these are handled by the CD8+ T-cells of the adaptive immune system.

  Also when the bacteria get into blood stream can neutrophils kill the bacteria?

Yes, that's their job and neutrophils are usually inside of the blood(stream), so they could find and kill bacteria there.


How to inactivate trypsin permanently by boiling?

In my experience 10min at 100°C are sufficient, this is also supported by the paper linked below. Heat inactivation works by denaturing the protein and is therefore final.
Depending on what you want to do with you sample, it might be problematic, as this is probably also denaturated at least to some degree.

You can also chemically inactivate trypsin, either by adding fetal bovine serum (which is done in cell culture), which contains protease inhibitors as α1-antitrypsin and α2-macroglobulin or by using commercially available inhibitors. Trypsin is also inhibited by calcium and magnesium ions, so your reaction buffers shouldn't contain any of them.

A Simple Procedure for Effective Quenching of Trypsin Activity and
Prevention of 18O-Labeling Back-Exchange


What was the reason for some plant and animals to become giant in course of evolution?

Thanks for asking an interesting question which made me think.

The short answer is that something evolves if there is an advantage to the genes involved, and, by 'advantage' I mean it produces more copies of the genes in the next generation so more individuals with that characteristic will be present in the population.

As to what particular advantage increased body mass had to any particular species that would depend on the particular species and its environment at the time.  There is almost certainly not a 'one-fits-all' answer.

Most very big land mammals are herbivores and there is an advantage in having a large digestive tract when you eat a lot of plant material with a fairly low nutrient level.  However, when there are also predators around, getting big and slow might be more of a disadvantage than staying small and fast. With evolution there is often a balance of competing forces which are traded of against one another.

Where large mammals have become isolated on islands with no predators, such as a species of now-extinct elephant on the Flores Island, they tend to become smaller so this suggests avoiding predators by simply being too big for them to kill might be an important factor.

And of course with many species we have the effect of sex-selection. If females select for the biggest males, there will be a selection pressure towards greater size.

With plants it could be something else entirely. Trees, for example, have long trunks basically for one of two reasons.

Firstly to put their leaves and seeds out of the reach of herbivores, so we have a kind of arms race like that between giraffes and acacia trees in Africa.

Secondly, when they grow in close clumps like woods and forests, there will be competition for sunlight and soil resources like water. A species which can reach higher and put it's leaves above those of it's neighbours will win the competition and there will also then be pressure on it's neighbours to evolve longer trunks.  Long trunks mean that water must be pumped a long way to the leaves so the tree with the longest trunks will also need bigger root systems.  Again a trade off between making a long trunk and dominating the water supply underground.

Many trees are also believed to have formed symbiotic associations with fungi in their root systems which help them take in the nutrients and water required to 'service' a long trunk and high-up leaf crown so they may be the only types of plants capable of doing this anyway.

One thing you might like to think about is why some whales are very big and some are relatively small (dolphins, porpoises, killer whales). What is the difference in their life-style, food, habitat, and so on, which could drive these evolutionary differences.


Why do humans alone have the capability to have religious/spiritual experiences?

Its not clear that this is true.

Working with animals has been a little disconcerting over the past 50-60 years.  In the distant past, I think most evolutionary anthropologists and their like bought into the idea that humans were completely uniquely intelligent and spiritual.  But the more we try to define human sensibilities apart from other animals, the more we find its difficult to see animals as being completely incapable of human feelings and even thoughts.

I refer you to this question which describes the shift in intelligence theories over the years: Why have humans evolved conciousness?

The above reference is just to say that every definition of intelligence that is fairly broad has been overturned by animals (thumbs, socialization, tool use, self awareness, communication and language).

If you want to say 'I know we're special, but I just can't say how' you are in lots of good company... it's become pretty hard to lay down a definition that includes all human beings and excludes animals.

Lately it seems as if the definition of spiritual experience is similarly hard to define. What is your definition?  The capacity to receive and reciprocate affection or love is almost never brought up - that seems to be half of the internet.  Yet, that's a common component to many ideas of spirituality.   It was found a while ago that primates have some form of self-awareness to identify themselves as distinct from other individuals.  True this was only demonstrating that they know themselves in a mirror, but other experiments show it probably is deeper than just that.

I think the most confounding evidence is the work with animals who have been trained from infanthood to communicate to humans through sign language or symbols.  The most astounding example I know if is Koko the gorilla. She had the vocabulary of a 5 year old and the capacity to joke around, reason, and adopted pets as children including a cat called All Ball.  When All Ball who was killed by a car she mourned and remembered her adopted cat for years.  This page outlines all that, though there is a book that describes Koko's life.

  The human staff sought to discover what Koko thought about death.  So they asked, “Where do gorillas go when they die?”  Koko answered, “Comfortable / hole / goodbye.”
  They asked, “When do gorillas die?”  Koko answered, “Trouble / old.”
  They asked, “How do gorillas feel when they die:  happy, sad, afraid?”  Koko answered, “Sleep.”

So this has been taken as evidence that gorillas have a concept of their own mortality or possibly even life after death.

So what is left?  Not clear to me.  Any thoughts?

Some regions of the brain and control of electrical activity in the brain have been associated with spiritual experiences or acts like prayer and meditation.  The temporal lobe is exciting because magnetic stimulation of that region can create the sensation that there is a presence in the room with you. there appear to be many regions which are active in different instances though, which is something you might expect.

There is no evidence yet that animals do not experience similar effects in their brains, though primates have very much the same structures as we do.   Its too bad Koko has died - she might have told us.


Why is beta thalassemia major not lethal while alpha thalassemia with loss of all 4 genes lethal?

This has to do with the fact that fetal hemoglobin (HbF) isn't made of the same chains as adult hemoglobin. The latter comes with 2 alpha chains and 2 beta chains while the main fetal hemoglobin is made of 2 alpha chains and 2 gamma chains. Hence any disease affecting the quality or quantity of beta chains won't have nearly as much impact on a fetus as it does on an adult.

Reference: https://www.uptodate.com/contents/fetal-hemoglobin-hemoglobin-f-in-health-and-disease


How can I fetch nucleotide sequences based on ENA accession numbers and positions?

From ENA

  To retrieve results by a single identifier for all records other than
  Taxon and Project please, use the following URL syntax:

  http://www.ebi.ac.uk/ena/data/view/

  For example, the following URL returns the EMBL-Bank entry with
  accession number A00145 in HTML format:
  http://www.ebi.ac.uk/ena/data/view/A00145

Check this.

If you use a *nix system (such as Linux, Unix, or OSX) then you can do this:

[ if list.txt contains all your ids ]

for i in `cat list.txt`; do wget -q -O $i".fa" "http://www.ebi.ac.uk/ena/data/view/"$i"&display=fasta"; done

OR ELSE

Download the entire database and pick up sequences based on your identifiers, offline. You can use your favourite programming language to retrieve sequences. [I prefer awk but python is also good]


Can I do an MS in biotechnology after a bachelors degree in chemical engineering?

This will probably to a high degree depend on the (exact) curriculum and prerequisites of your chosen bachelor and master.
Also note that I'm not from the US and judging from the terms you are using, it seems that you are, so everything I say is also a bit speculative.

In general biochemistry and to some degrees also biotechnology will have a lot of overlap with many aspects of chemistry (or at least organic chemistry). Depending of the focus of each program this might, make it possible to switch over from one to the other. One thing you will definitely not learn in any chemical mayor is molecular biology, which may well be a requirement for studying in any biotech related field later on.

If both your majors focus more on the technological aspect and less on the biological or chemical you should probably be fine. The equipments used in (modern) biology and chemistry is in many cases similar, though biotech involves more equipment specialised for the handling and analysis of cells. The underlying principles are still the same though.

In your case I would recommend you to check the requirements of different MS or grad schools, that you'd be interested in first, and the see if you can meet these with a chemical engineering mayor (and maybe/probably some added courses like molecular biology).


Does a full tear of the gluteus minimus tendon has any functional implications?

You’re correct that the gluteus minimus is redundant in function with the gluteus medius, but an isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response and subsequent pain deemed “greater trochanteric pain syndrome,” as the greater trochanter is the insertion site for hip abductor muscles like the gluteus minimus and medius:

  MRI Web Clinic — May 2004,
  Gluteus Minimus Tear & Trochanteric Bursitis,
  Michael E. Stadnick, M.D. (mirror)

    Clinical History: 70 year-old female with chronic left hip pain...What is your diagnosis?

    Diagnosis: Gluteus minimus tear of the left hip with associated trochanteric bursitis.

    Discussion: Lateral hip pain is frequently a challenging diagnostic and therapeutic problem. In the past, the presentation of chronic lateral hip pain with tenderness over the greater trochanter was attributed to trochanteric bursitis. This symptom complex, called greater trochanteric pain syndrome (GTPS), can mimic other serious causes of hip pain...Abductor tendon (gluteus minimus and gluteus medius) tears are becoming increasingly recognized as a frequent cause of pain at the hip. In fact, tears of the abductor tendons, instead of trochanteric bursitis, are likely the most common cause of GTPS.

    In a large majority of patients, trochanteric bursitis or distension will accompany an abductor tendon tear. The frequent coexistence of trochanteric bursitis and abductor tendinopathy has led some authors to suggest that bursitis may in fact be a result of the underlying tendinopathy.

    Early descriptions of abductor tendon tears at the hip emphasized involvement of the gluteus medius tendon as being most common. However, subsequent papers have revealed a roughly equal frequency of involvement of the gluteus minimus and medius tendons.


How to find the concentration of an enzyme?

The enzyme unit U is not a measure of enzyme concentration but its activity, defined as the conversion of 1 micro mole ($\mu$mol) of substrate per minute (under a specified condition such as pH and T)

Absorbance (O.D. at a specific wavelength) of the enzyme is a measure of enzyme concentration, regardless of its activity. Depending on the unit of the extinction coefficient, Absorbance can be converted directly by Beer's Law to enzyme concentration, typically in mg/mL or in the standard mM.

5U/mg is the specific activity of pectinase, and the bottle contains a total of 5 kilo U (KU), meaning that there is a equivalent of 1g of active enzyme inside (often in powder). If you assume all pectinase molecules inside the bottle are active, when dissolved in 10mL water, you have a pectinase concentration of 100mg/mL. If the molecular weight of pectinase is 31kDa (31000 g/mol), then 100mg/mL is the same as 3.2mM in concentration.

By the way, Lowry protein assay measures enzyme concentration, not activity in U while DNS assay measures activity (of enzyme that produces reducing sugars), not enzyme concentration.


Is the Andraka pancreatic cancer test real?

Basically, Andraka's method measures mesothelin. There's two key questions being asked about it (as it stands right now), falling into two categories:

1) There is some doubt as to the significance of serum mesothelin levels as a biomarker in pancreatic and biliary cancers. Some studies (e.g. Sharon et al (1)) suggest that there is no significant difference in levels - others (e.g. Hassan et al (2)) suggest that mesothelin may be a valid biomarker in some conditions but not others.

2) There are questions around the test itself. Andraka's work is promising and quite impressive. There are, however, some claims about it are being made that there's just not the evidence to support. I suspect that any fault for this lies with the journalists reporting on the story or PR people for various companies or institutions. The device may stand up to clinical trials and testing and be as revolutionary as it's claimed to be, but it does need to be fully tested.


How do animals decide what to eat and what not?

To answer with a question: How do you decide what to eat (if you don't know whether something is edible)?

All animals have evolved taste and smell (and I'm sure even prior to eyesight). The purpose of taste and smell in terms of nutrition is to determine if something is edible. If something tastes bitter or extremely sour, this is mostly a warning sign for toxins or advanced microbial degradation. The same accounts for smell: If you let raw meat foul, the smell is unbearable. Why? Because our brain is telling us not to eat this.


How is there no limit to a human lifespan again?

You're probably reading about the recently-published responses to a publication that argued there is a limit to human lifespan.

The original article is Evidence for a limit to human lifespan, and in the June 29 issue of Nature there are five responses to it:

Contesting the evidence for limited human lifespan
Many possible maximum lifespan trajectories
Is there evidence for a limit to human lifespan?
Questionable evidence for a limit to human lifespan
Maximum human lifespan may increase to 125 years

Each of these responses has, in turn, a reply from the original authors.

The arguments turn on fairly intricate details of statistical analysis and database interpretation, and I think it's fair to say that outside experts remain unconvinced either way -- neither the original article, nor any of the five responses, nor any of the five responses to the responses, presents a slam-dunk case for or against a limit to human lifespan.


Is there biological evidence for self-awareness in animals?

Yes, there is a lot of evidence for self-awareness in animals. The gold standard test for self-awareness is the mirror self-recognition test (MSR)--we can tell from the behavior of an animal exposed to a mirror whether or not it can tell itself apart from other animals of the same species:

  Animals that possess MSR typically progress through four stages of behavior when facing a mirror: (i) social responses, (ii) physical inspection (e.g., looking behind the mirror), (iii) repetitive mirror-testing behavior, and (iv) realization of seeing themselves. (Plotnik et al. 2006)

That quote was taken from the abstract of a paper showing self-recognition in a single African elephant, but there is evidence for self-awareness in magpies (Prior et al. 2008), dolphins (Harley 2013), chimpanzees (Povinelli et al. 2006) and orangutans (Suarez and Gallup 1981). Many of these studies use the Gallup mark test (Wikipedia):

  Gallup anaesthetised the chimpanzees and then painted a red alcohol-soluble dye on the eyebrow ridge and on the top half of the opposite ear. When the dye dried, it had virtually no olfactory or tactile cues. Gallup then returned the chimpanzees to the cage (with the mirror removed) and allowed them to regain full consciousness. He then recorded the frequency which the chimpanzees spontaneously touched the marked areas of skin. After 30 minutes, the mirror was re-introduced into the room and the frequency of touching the marked areas again determined. The frequency of touching increased to 4-10 with the mirror present compared to only 1 when the mirror had been removed. The chimpanzees sometimes inspected their fingers visually or olfactorily after touching the marks.

Basically, an animal which has seen and recognized itself in a mirror recognizes the mark as being new, so it touches its own body on the marked area, which shows that the animal recognizes the image in the mirror as itself.


This is a fairly broad question and a book or two will give a more complete answer.  I'm assuming you are interested in expression microarrays.  Genotyping microarrays are also very popular these days and are quite different though.

Where can I understand the matrix of the dataset ?
This is a little unclear as a question, but I'll start with a numerical description.  Microarray data is reducible to a one dimensional array of intensities.  As a vector of numbers, each representing the amount of a given species of RNA in a sample, it has many interpretations.  Most of what is said here applies to RNASeq data too.

These numbers are sequence dependent - that is, they should not be interpreted as an absolute count of a specific mRNA in the sample, so comparing two entries in the vector (e.g. "gene A has 10% more RNA than gene B") will probably not be useful.

For this reason, microarray experiments are typically done as difference experiments, where two or more conditions are compared, producing a matrix of numbers, where N rows represent N experiments, and the M columns each represent a probe set / gene.  The transpose of this matrix is also common.

**Methods to classify microarray results. **
Taking the matrix of data, there are many ways of interpreting data in matrix form and most of them have been tried credibly with microarray data.

The most common are to take a set of probe sets whose biological action are related (e.g. all in a metabolic pathway and display them as a heat map where the columns have been clustered by a distance based algorithm to produce a tree, where neighbors have the greatest numerical similarity.

For purely numerical methods, Principal Component Analysis is often used (despite the fact that this is not a great method), but Self Organizing Maps, neural nets and just about any machine learning algorithm have been used.

Most common method by far though, is Analysis of Variants (ANOVA), where the probe sets/ genes have been scored by their greatest to smallest variance.  The most common case of this is a two condition difference experiment where the largest differences are taken as results.  This is not a great experiment, but the data is not super cheap to produce.

**Microarray data repositories **
Gene Expression Omnibus (GEO) is a highly regarded repository for microarray data, with over a million sets of data. They also have some tools, see below.

EMBL ArrayExpress claims to have slightly more data than GEO (1.2 M assays).

There are many many specialized microarray websites, mostly focusing on a particular organism (E coli for instance) or problem (like cancer).  Google is pretty helpful for this sort of thing once you have the right keywords.

**Web based tools for microarray analysis **
There are several tools you will use for microarray analysis and there are lots of websites for different aspects of this data.  I'm going to cite a couple, but the most commonly used tools are command line tools like R/bioconductor or the software that comes from the array manufacturer.

GEO2R is a great tool to browse expression data experiments.  It does a simple version of ANOVA and will really help you find some cool biology quickly.

VAMPIRE is a web analysis suite for microarray analysis.  Scaling the data into numbers from images to intensities to data analysis to compare several arrays.  Its probably one of the most comprehensive analysis sites out there.


Difference between 'fitness' and 'fitness effects'

Fitness

Fitness is some function of the probability of survival and fecundity for a given genotype. Fitness is therefore a single value per genotype.

Fitness effect

A fitness effect is a component of fitness. For example, for a given bi-allelic locus, the fitness effect of allele A is -0.05 in comparison to the allele B, meaning that the allele A is deleterious and the allele B is beneficial. There is a fitness effect for each allele, for each trait and, if you interested in  genetic interaction (epistasis) and genetic-environment interaction, then there can be a fitness effect for each gene and each trait in each genotype in each environment.

Example

It is typically common to assume a model of $n$ loci, where the fitness effects at each loci are $1$, $1-hs$ and $1-s$ for the three genotypes AA, AB and BB respectively (diploid population). $s$ is the selection coefficients and $h$ is the dominance coefficient. The fitness of the individual is often obtained by multiplying out the fitness effects at each loci. The worst possible fitness is therefore $\left(1-s\right)^n$.


Recessiveness of allele for protection of organism

Instead of dividing mutations into two classes, dominant vs. recessive, consider categorizing them into classes based on how the mutation affects the gene--or the gene product.  This yields loss-of-function (lf) alleles, that reduce the activity of the gene, or its product, and gain-of-function (gf) alleles that act as if they somehow increase the activity of the gene, or its product.

The logic underlying this classification was described in this classic reference: Muller, H. J. 1932. Further studies on the nature and causes of gene mutations. Proceedings of the 6th International Congress of Genetics, pp. 213–255.  Since this was before DNA had been shown to be the genetic material his arguments are based solely on the phenotype of animals carrying various combinations of chromosomes.  In particular he relies on genetic duplications and deficiencies (or deletions).  In this nomenclature + indicates a chromosome carrying a wild-type (wt) allele of the gene, and m indicates a chromosome carrying a mutant allele of the gene.  So if an +/m animal appears Wild-Type then that allele is recessive.  Similarly, if an +/m animal has a Mutant phenotype then the allele is dominant.

There are two types of lf alleles:

a hypomorph is a partial reduction in function and retains some residual gene function (e.g., a weak missense mutation, or a temperature-sensitive (ts) mutation. A hypomorph is recessive to a wt allele.
an amorph is what we would call a true genetic and molecular null allele, a complete knockout of the gene, where there is no measurable function left (e.g., a nonsense mutation early in the protein coding region, or a small deletion that only removes a single gene).  Amorphs are normally recessive to a wt allele (but see below for an exception)

There are three types of gf alleles:

a hypermorph that elevates the level of the wt gene function (e.g., a promoter mutation that removes a negative regulatory site, leading to increased expression). Hypermorphs are dominant.
an antimorph, or so-called dominant-negative (dn) allele that produces a mutant gene product that somehow interferes with the wt gene product (think poison product as one model). Antimorphs are always dominant over wt.
a neomorph, an allele the results in a completely new gene function (e.g., if a glycolytic enzyme acquired sequence-specific DNA-binding activity, perhaps from a gene fusion event(?)). Neomorphic alleles are extremely rare and almost always dominant over wt.

So we have a straightforward mapping of lf alleles to recessive phenotypes, and gf alleles to dominant phenotypes.  However there is an important exception to this simple scheme for genes that are dose-sensitive, or haploinsufficient. These are dominant lf alleles. For example, when halving the level of the gene product causes a mutant phenotype: +/null. Some well-known examples from the developmental genetics of model organisms are the Ubx gene, and the Notch gene from D. melanogaster.

Further discussion of these terms can also be found in Wikipedia


Technically men do have a mons pubis but it is less pronounced. With increased estrogen in females it becomes more pronounced.

Wikipedia


Are there any organisms that lack ATP synthase?

As Superbest mentioned, substrate level phosphorylation (SLP) is alternative pathway by which ADP is phosphorylated to ATP. In SLP, phosphorylation is coupled with a highly exergonic chemical reaction. Fermentative organisms (both fully and temporally fermentative) organisms depend on SLP for ATP.

Note: fermentative $\neq$  anaerobic

Fermentation can either be a temporary situation, depending on the growth substrate (for e.g. yeast) or the only option as in the case of amitochondriate organisms like Entamoeba. You can refer this book if it is available to you. See this article too.

You can also see the wikipedia page on fermentation; it mentions the SLP steps.


It seem's you are assuming that your / the adult human brain produces new neurons over time- this is (largely) incorrect: neurons are non-dividing cells and are all formed throughout embryogenesis and very early childhood / infancy (see also this question).

Only very exceptions to this are known as adult neurogenesis (generation of new neurons), the most likely or active region in humans would be the hippocampus, however the extent or importance of the process in humans is still not really known. Additionally the hippocampus is an area of the brain that mostly holds memories and is not really related to reasoning skills or body / motor control.


The first 30 days involve rapid growth, but generally, fall within a standard proximal range of 5 - 7mL on day one. By day 3 the stomach has expanded vastly to nearly 23 - 27 mL. From this point on, growth and size to age ratio will vary a bit.

https://themomivist.com/2016/10/10/the-newborn-stomach-size-myth-it-is-not-5-7ml/

Here's a link to an article that has some efficacy. Many hospitals and physicians use different techniques and believe differently on this particular subject. Considering the laws surrounding experimentation on fetus and children, the "Size" of the stomach debate only has efficacy if we were able to case study THOUSANDS of infant stomachs which isn't likely to happen anytime soon. I hope the link helps and maybe points you in the right direction. There really is no 100% correct way to answer this as the studies surrounding it just don't have any weight to them.


Why do doctors still advise HIV+ couples to wear a condom during sex?

Doctors would recommend the use of barrier protection for couples where both partners are HIV+ because the virus can mutate. Mutated forms of the virus can become resistant to Highly Active Antiretroviral Therapy (HAART) treatments, rendering them ineffective.

The use of barrier protection reduces the risk that a resistant mutant strain of HIV is transferred into the population.

Also a child conceived by a couple that is HIV+ is at high risk of being born with the infection.

This link explains some of the risks and ways to attempt to prevent mother to child transmission of HIV.

Edit

In retrospect, I have been thinking about the answer I gave, and while I still think that what I said above is relevant, I feel that I left out an import aspect of why a medical doctor would recommend the use of barrier protection during sexual activity, even if both partners are HIV+.

One thing that we should remember is that a person with HIV, even when the virus is suppressed by HAART is immunocompromised to some extent and they will likely be more susceptible to secondary pathogens and cancers initiated by oncogenic viruses.

An HIV+ person will be more vulnerable to sexually transmitted diseases such as human papilloma virus, herpes, hepatitis, chlamydia, gonorrhea , or simply opportunistic pathogens such as C. albicans than they would have been had they not been HIV+. Cells that mediate innate immune response are affected by HIV as well as cells of the adaptive immune system, so any dysregulation of the immune system creates an opportunity that a pathogen would not normally have.

Not only will these diseases have an easier time infecting an immunocompromised patient, but these infections will also be more difficult to cure once they have taken hold, as the person's immune system will likely not be able to mount as robust a response as it would have if the person was not HIV+. So barrier protection provides a means to help protect a person from secondary infections as well as for the reasons given previously.

Use of barrier protection during sexual activity to prevent the transmission of sexually transmitted diseases is just as relevant for people who have HIV as for those whose HIV status is negative.


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

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

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

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

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

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

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


How can I tell if regulation is at the transcriptional or translational level?

From the Methods section:

  Human TfR in plasmid cDNA was a gift from Tim McGraw (Weill-Cornell
  Medical College, New York, NY). Human TfR cDNA was subcloned in frame
  with EGFP in the Clontech pEGFP-N1 vector at the XhoI and BamHI
  restriction sites.

This TfR-GFP fusion protein does not have the endogenous TfR promoter. So it is not likely to be regulated by any TF that would directly regulate TfR transcription.

So they conclude that Rabenosyn-5 does not specifically regulate TfR expression.


I will respond with a "story-like" approach. You may already know some info but I want to be sure I can help you fully understand!

Unlike RBC, you are born with all the CD4+ (or Th, as I refer to them) you will ever need in your lifetime in the primary organs of the immune system -- they are already specialized and ready to be used, and this has taken place in the thymus. On the other hand, RBC get renewed through erythropoiesis every ~120 days.

In utero, the thymus and bone marrow (primary organs) now supply secondary organs (lymph nodes, the spleen, the MALT) with the various cells they’ve made (B&T). However, only 5% leave the thymus, as 95% are recognized as "anti-self" and are killed. So this would be the first "killing" of Th cells. B cells live in the peripheral layer, while T cells live in the deep lymphoid tissue and the lymphoid dullet.

The dendritic cell will "wander" into the lymph node, carrying the fragment of antigen presentation on the MHC class 2 molecule-Dendritic cell resides between the B cell area and the T cell area. Now, the first specific thing occurs in the immune response, when the T cell receptor attaches to the antigen and tells cell says to make antibodies.

Now -- as of here, we have a lot of Th (and B) cells doing nothing while the antibody is being produced. Some of the Th will be killed, while some will serve as "memory Th cells" so that the next time such an antigen is present in your body, the response will be quicker. At this point, it's hard to distinguish which Th cells are dividing, and which are dying. The average lifespan has been reported to be >17 years.
 Source: https://www.ncbi.nlm.nih.gov/pubmed/24492253

I hope I have been able to help.


Macromolecule levels in daughter cells after fission

Many years ago I worked in the field of bacterial chemotaxis, and your question brought this paper to mind:

  JL Spudich & DE Koshland Jr. (1976) Non-genetic individuality: chance in the single cell. Nature 262:467-471.

The authors report an analysis of the chemotactic behaviour of individual bacterial cells from a single homogeneous culture. They find marked differences between individuals, and their favoured model is what they refer to as a Poissonian variation in the inheritance of key proteins that are present in small numbers.

According to ISI Web of Science this paper has been cited 241 times - presumably at least some of those papers might be about other more recent examples of this type of phenomenon.


Gene expression is the production of a functional gene product from a gene. So protein expression is a functional read-out of gene expression for gene loci that encode proteins.

However, gene expression is frequently, and erroneously, used to refer to measures of mRNA levels. The production of mRNA is a prerequisite step for the production of protein from a gene and it provides information about the transcriptional activity of a gene loci.

Translation of mRNA is a highly regulated process and
global assays highlight that mRNA transcript levels explain less than half of the variation in protein concentrations.

  For example, if I replace the DNA sequence of a gene of interest with the GFP DNA; and then subsequently quantify the fluorescence levels, am I measuring the gene expression of the gene of interest OR the protein expression?

You are measuring both gene expression and protein expression from the promoter + GFP gene loci. If you are interested in transcription from the promoter then measuring transcript would provide a more direct measure.


Are tuna fish present in the Baltic sea?

Indeed tuna are present in the Baltic sea, and they can also grow in the Pacific and Indian oceans. A lot of the tuna we see in tuna cans in supermarkets comes from the stocks in the Indian ocean, but it is possible to have fresh tuna from the Baltic.

Sorry, I only found a French answer from a famous French news paper: http://sante.lefigaro.fr/mieux-etre/nutrition-aliments/thon/dou-vient-thon


Is telomere shortening consistant over consecutive cell divisions from zygote to a differentiated cell?

It is not consistent, and so cannot function as a temporal or generational signal. Not because the telomere shortening is unpredictable, but because of telomerase activity in the embryo.

If it did, gamete production in specialized tissues like the ovaries or testes would have shorter telomeres than the zygote they originated from. Each generation would have shorter telomeres than their parents. They would be genetically 'older', which can't go on forever.

Development is incredibly complicated and mediated by a large number of genes. Try homeobox genes for developmental layout.


You can see this review.

  There are several different types of alternative splicing (AS) events,
  which can be classified into four main subgroups. The first type is
  exon skipping, in which a type of exon known as a cassette exon is
  spliced out of the transcript together with its flanking introns (see
  the figure, part a). Exon skipping accounts for nearly 40% of AS
  events in higher eukaryotes [17, 111] but is extremely rare in lower
  eukaryotes.


Is human "sperm warfare" a concept supported by biology?

I wanted to respond to your question because while I don't know very much about this particular subject myself, I did have the pleasure of attending a talk by Robert Martin, author of How We Do It (https://www.amazon.com/How-We-Do-Evolution-Reproduction/dp/0465030157/ref=sr_1_2?ie=UTF8&qid=1492260860&sr=8-2&keywords=how+we+do+it).  In the talk and in his book he does address this topic (and the book Sperm Wars) and basically says that while it was a highly influential idea, the underlying science isn't reliable.  He argues that evidence suggests that humans have not evolved under multi-male types of mating systems. There is a lot of evidence to back this up, and revoke the idea of "killer sperms."  Check it out and see what you think!  If anything it is an interesting read.


Can microorganisms (e.g. bacteria) be damaged or killed by 253,7 nm light?

This is UV-C radiation and light of this wavelength (which is emitted by low pressure mecury lamps) can indeed be used for disinfection purposes. The nucleic acids (DNA and RNA) has an absorption maximum for UVC radiation at 265nm, causing DNA/RNA damage. The radiation of the mercury lamps is only a little below, making them still quite effective (see the image from here):

This is used in "Ultraviolett germicidal irradiation" for example in water disinfection systems or also for workplaces. The problem with this irradiation is that it causes severe sunburns (and very fast) and also causes plastic materials to decompose (like leaving them in sunlight but much faster). Since I know the precautions for using such devices at workplaces, I wouldn't consider them safe for home use.

The other problem is that you need a pretty clean area for the radiation to be effective. We have to clean our work benches for doing cell culture work entirely so that no shadows are cast in which the UV radiation wouldn't be working since the area is shielded. Imagine this for your home. Additionally I think the fear for germs at home is massively overrated and that there is not need for theses devices at home.


Is the chitin in an insect's exoskeleton cross-linked?

much like cellulose, chitin strands are bonded to other strands by hydrogen bonds. here is a slide share with a breakdown of the structure.

It is crosslinked in the sense strands are linked to other strands in such a way that most enzymes cannot access it to break it down. this is the same thing that makes wood last untreated. In a strictly chemistry sense it is not a crosslinked polymer (which requires covalent or ionic bonding) but it still has crosslinking. Your hitting a difficulty in jargon.

source.


Gene expression: which allele is considered?

Genome assemblies usually feature a haploid set of genes, unless particular effort is applied to assemble separately the homeologs. With that said, the gene copy you have in the assembly is usually one of the two, and usually the one you had more genomic reads for.

In terms of gene expression, if you measure it by RNASeq you will get reads from both and both of the read pools will map on the same gene. The ones that come directly from it will map with no mismatches (ideally) and the ones that come from the homeolog chromosome will map with a few mismatches (probably).

The expression of the "gene" will therefore be the expression of both genes, summed together. If we consider it as the same gene, though, it doesn't really make a difference if you sum them up or count them twice separately; unless we are talking about specific homeolog silencing like the Xist mechanism, in which it is important to remember that one copy of the two is off.


How can cats' claw grow sharper without replacing the claw?

The horn has a specific structure which is different from the round edge that we see on our fingers. It splinters and cracks into flakes, so it is more similar to a flint than a chalk.
The outside of the cone dries out and flakes and is scratched off by the cat, while the inside of the cone is the newer horn that grows towards the apex as a new blade edge.

The image is from this research. If you search "sharp" you will find astonishing vetinary descriptions quoted. Also see page 641 for the conclusion of the research. He sais that it seems to have evolved in the aim of keeping the feline claws sharp.

If someone has the technical ability to rewrite the researcher's descriptions into everyday words, you would be a first.

Vetinary research quote:

The horn-generating living blade epidermis that is
located most centrally on the slanted face of the curved
ledge is continuous with the parietal epidermis (Fig. 9b),
so that the blade epidermal cells generated here lie next
to the parietal epidermal cells. Therefore, the cornifying
parietal epidermal cells are deflected and entrained apically
as the blade horn is pushed apically by the proliferating living
blade epidermis. The direction in which the blade horn is
pushed forward can also be inferred from the arrangement
of the ridges visible on the dermo–epidermal interface of
the parietal horn (Fig. 7). The living blade epidermis that
is located at the outer edge of the face of the curved ledge
is continuous with the living epidermis of the proximal
cone horn (Fig. 9b). These lateralmost blade epidermal
cells, therefore, form a layer that lies directly underneath
the deepest layer of proximal cone horn, so that the
boundary between the blade horn and proximal cone horn
is indistinct. Hence, the layers of horn that are generated
in the dorso-proximal bend of the curved ledge underneath the combined horn layer of the external coronary
and proximal cone horn cover the sides of the apical cone
horn and are designated as part of the blade horn. As
the superficial coronary horn on the dorsal side of the
cornified claw sheath is worn off through normal use, the
superficial layers of the blade horn are exposed and are
shown to hug the sides of the apical cone horn (Fig. 13a).
Remnants of these blade horn layers are discernible near
the very tip of the cornified claw sheath, which consists
mostly of apical cone horn, because the rest of the coronary
horn, including most of the blade horn, has been worn off
(Fig. 13b,c).
The remaining soft-cornified horn segments of the
cornified claw sheath are found in places where the
hard-cornified horn divisions need to be supported and
cushioned.
The soft-cornified terminal horn is a segment of the
third major horn division (i.e. the Hyponychium; see Table 2).
It is generated by the living terminal epidermis, which is
continuous caudally with the parietal living epidermis and
is supported by the dermis that covers the medial, lateral
and palmar sides of the tip of the bony unguicular process
(Figs 3a, 4a,c, 7, 9b, 11a, 12a–j). It supports the apical cone
and crest horn on its dorso-distal side (Figs 3a, 4a,c, 7, 9b,
13b) and the blade horn on its lateral and medial sides
(Figs 4b, 8, 9b–d, 13a,b). By filling the space created by
these converging segments of hard-cornified internal
coronary horn, it is shaped into an elongated, pointed
cone and extends proximally between the blade and
sole horn (Figs 12c,d,f,h,j, 13a,b). Because the terminal
horn is soft-cornified, it can adjust its shape to the
changing conformation of the space it fills in the course of
the deformations of the cornified claw sheath during its
normal use.
The friable soft-cornified sole horn is generated by the
living sole epidermis, which is supported by the dermis
that covers the proximo-palmar side of the bony unguicular
process (Figs 3a, 4, 7, 8, 9b–e, 12c,d, 13a,b). Along its medial
and lateral sides, it is embraced by the terminal and parietal
horn (Figs 1b, 4b, 8, 9c,d, 13a,b). The sole horn, therefore, fills
the space between the paired cutting edges of the cornified
claw sheath. It is worn off through natural wear and tear,
as well as through repeated compression and release, as
the cornified claw sheaths are deformed when they are
subjected to tensile forces during climbing and prey capture.


Subset of Protein Crystal Structures (from PDB)

Richardsons' Lab has a top8000 list.
See their paper from 2016.

They also have top500 list, but it hasn't been updated for many years.


What is the purpose of the adrenal medulla?

I have found the answer to the purpose of the adrenal medulla to be flexibility. Just like regulation for example of gene expression or metabolism occurs on many levels with different speeds and permanences of their effects, signalling needs to be available both quick and short-lived, and slower but with more long-lasting effects. The adrenal medulla provides exactly that.

Sympathetic adrenergic neurons are quick, but as quickly as they release their neurotransmitter, the effect is only of short duration and adrenalin is quickly cleared from the target area. Rather than giving off short bursts of adrenalin, the medulla maintains a constant systemic level of it and in response to stimulation raises or lowers that level. This response takes more time as blood circulates much slower than neurons respond, but its effects last longer.


Rhinitis is irritation and inflammation of the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic rhinitis, which is usually triggered by airborne allergens such as pollen and dander [1].

Many questions regarding sublingual immunization still remain to be addressed, including the use of proper adjuvant and the optimization of vaccine formulation to further enhance the vaccine efficacy [2].

Sublingual immunization can induce both systemic and mucosal immune responses against a variety of antigens, including soluble proteins, inter particulate antigens, and live-attenuated viruses [2].

Sublingual immunization has been shown to be safe and highly effective in generating robust immune responses against the administered antigen. Moreover, it has been shown to confer protective immunity by simultaneously eliciting systemic IgG and mucosal IgA antibodies as well as cytotoxic T lymphocyte responses in the peripheral lymphoid organs and mucosal tissues. Studies also suggest that sublingual immunization could be a better alternative to the traditional parental route of vaccine delivery against both genital and respiratory pathogens [2].

Although the s.l. mucosa does not allow passage of macromolecules into blood, s.l. immunization with ovalbumin, a model soluble protein antigen, administered
alone or together with cholera toxin adjuvant, induces mucosal antibody responses as well as systemic immune responses in mice. The magnitude of serum antibody responses induced by s.l. immunization was in fact comparable to that seen after intranasal (i.n.) immunization and far superior to that after o.g. (oro-gastric) immunization [3].

Upon stimulation of mucosal surfaces by foreign antigens, dendritic cells among the antigen presenting cells are immediately processed and transport antigen via afferent lymph to draining lymph node for presentation to T cells. Subsequently they induce secretory IgA antibodies. This suggestive link between trafic pattern of dendritic cells and their functions led to the investigation of the chemokine responsiveness of dendritic cells during their development and maturation. It has been observed that type II mucosa tissues (e.g., skin, vaginal, and buccal), which are covered with stratiﬁed epithelia and devoid of
mucosa-associated lymphoid tissues, mainly express CCL20, CCL19/CCL21, or CCL27/CCL28 individually [4].

CCR7 (chemokine receptor) expressed CD8α-CD11c+ cells ferry antigens in the sublingual mucosa, migrate into the cervical lymph nodes, and share the antigen with resident CD8α+CD11c+ cells for the initiation of antigen-specific T and B cell responses following sublingual challenge. The sublingual mucosa is one of the effective mucosal inductive sites regulated by the CCR7-CCL19/CCL21 pathway [4].

References:

Wikipedia, Rhinitis
Byoung-Shik Shim, Youngjoo Choi, In Su Cheon, and Man Ki Song. Sublingual Delivery of Vaccines for the Induction of Mucosal Immunity.
Cecil Czerkinsky, Nicolas Çuburu, Mi-Na Kweon, Fabienne Anjuere and Jan Holmgren. Sublingual vaccination.
Joo-Hye Song, Jung-Im Kim, Hyung-Joon Kwon, Doo-Hee Shim, Nirmala Parajuli, Nicolas Cuburu, Cecil Czerkinsky and Mi-Na Kweon. CCR7-CCL19/CCL21-Regulated Dendritic Cells Are Responsible for Effectiveness of Sublingual Vaccination.


Is "Cisternal Twins" an actual classification of twin types and if so, describe it

Cisternal doesn't make sense in this context, so either your mother is using an obscure term (quite possible, these things change a lot) or just has the wrong word.

However, mirror twins are a known thing (and quite cool): http://www.twinsuk.co.uk/twinstips/4/140/twin-pregnancy--multiple-births/types-of-twins--identical-fraternal--unusual-twinning/.

She may have meant something like "chiral twins" or "cis-trans twins", which would be borrowing from a similar concept in chemistry to describe your mirror-image nature (but is, again, not a phrase I've heard in the twin literature.)


Why does cyanide inhibit CuZnSOD, but not MnSOD or FeSOD?

I'm just taking a stab, because my inorganic chemistry is rusty.

cyanate (CN-) is well known to bind to iron (it inhibits hemoglobin and causes anoxia), and it also forms a pretty strong complex with Zinc:

http://en.wikipedia.org/wiki/Zinc_cyanide

I would guess that in the case of the SOD that the other liganding amino acids and the pocket of the enzyme are such that the affinity for cyanide is lowered to the point that oxygen can displace it.

In the case of hemoglobin, CN will coordinate to the heme iron in much the same fashion that O2 does, but it doesn't come off.   In the case of SOD, the enzyme will be looking to coordinate to superoxide O2(2-) which would be at a roughly tetrahedral angle to the metal.   This is not a favored geometry for CN coordination, which prefers to linearly coordinate to things.

In the case CuZnSOD it seems likely that this enzyme has enough room and its Zn and Cu binding envirionments don't forbid CN binding. it would be an evolutionary accident really as to why one is sensitive and another is not.

some structures at rcsb:

SODs:
http://www.rcsb.org/pdb/results/results.do?qrid=C0740111&tabtoshow=Current

thiocyanate bound. the pocket is pretty open between the two ions.  no CN bound structure.
http://www.rcsb.org/pdb/explore/jmol.do?structureId=1SXS&bionumber=1


What is the silencing mechanism of AGO1,AGO3 and AGO4?

Paper by Zinovyev and colleagues in the paper "Mathematical modeling of microRNA‐mediated mechanisms of translation repression" find that there are reports to 9 different mechanisms of miRNA-regulation.

Here we are reviewing available experimental data on all reported mechanisms of microRNA action, grouping them in a way which elucidates the main details supporting each of these proposed mechanisms.

Here is a list of the mentioned mechanisms:

M1: Cap-40S Initiation Inhibition
M2: 60S Ribosomal Unit Joining Inhibition
M3: Elongation Inhibition
M4: Ribosome Drop-Off
M5: Co-translational Nascent Protein Degradation
M6: Sequestration in P-Bodies
M7: mRNA Decay
M8:  mRNA Cleavage
M9: Transcriptional Inhibition Through microRNA-Mediated Chromatin Reorganization Following by Gene Silencing

Also here is a link to the Pubmed entry of the article:


Do adult humans exchange beneficial bacteria? If so, how?

Nonpathological bacteria Staphylococcus epidermidis on the human skin are part of normal bacterial flora that help to protect against pathogenic bacteria, such as Staphylococcus aureus. You can get "infected" by Staphylococcus epidermidis the same way as by other skin bacteria and you get a potential benefit from them.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807625/
You can get beneficial effects from pathological bacteria passed from someone, if you you develop antibodies to them, so you can become more or less resistant to them. For example, if you are from US or Europe and travel to South Asia, you at high risk to get food poisoning from either bacteria or viruses, bot local people are at much lower risk, because they have "shared" microbes one from another.
You can get beneficial effects from probiotic supplements (live nonpathological bacteria), which prevent overgrowth of pathological bacteria in your large intestine. The bacteria in probiotics are similar than those in the human gut.


To what extent can bacteria actually see?

Simple answer is that many simple organisms, including bacteria, carry light-sensitive molecules. One example is halorhodopsin (not bacterial but archaeic). This is a molecule, light-gated ion pump, that reacts to light, thus allowing organism to react to photons by changing concentration of certain ions inside the cell.

Study from Stanford described similar molecule found in bacteria.

In conclusion, if by "vision" you understand ability to react to light in the visible part of the spectrum, then a lot of organisms possess such ability. However, they lack other crutial parts of human vision.


It's a larva of a green lacewing (Family Chrysopidae). Yes, they can bite hard but you're not its intended victim and they're not only harmless but beneficial as they're aggressive predators of aphids and other soft bodied plant pests. I can't be specific to what species of lacewing as they look fairly similar.

Another larva that looks very similar to yours.

Source from BugGuide.net

What the adult looks like (remember,they're an entire insect family so there are differences but not to most people).

Source also from BugGuide.net


Trial pre-registration service that accepts non-clinical trials, or specifically ecology?

Did you try OSF.io?

They offer a free service where you can preregister trials and give them a timestamp with a DOI number etc.

I do not know if this is exactly what you are looking for, but it's the easiest solution for preregistering and I am quite sure that it would be enough to get the "preregistration" badge when you are finally ready to publish.

Here is more info on how to do it and what is essential for preregistration.


Why summation takes place at Initial segment?

Why don't EPSPs travel passively through axons?

EPSPs decay over distance. The decay is described by the length constant, which can be calculated based on the electrical properties of some compartment (i.e., a length of dendrite or axon). By definition, the length constant is the distance at which the amplitude of the signal will decay by about 37%. If you are familiar with the concept of a "time constant," the math is exactly the same.

There are two main factors that influence the length constant: the number of open channels (i.e., how "leaky" the membrane is) and the diameter of the neurite. The "leakiness" of different parts of the cell is often modulated by inhibition. Preventing EPSPs from reaching the soma or decreasing their amplitude by increasing leak is called shunting inhibition. However, for your question, it is the diameter and overall length that is important.

Dendrites tend to be a bit bigger than axons, so they have a longer length constant: that is, EPSPs travel further. Dendrites are also not entirely passive: dendrites can actively propagate signals (see review by Yuste and Tank) using voltage-gated channels to boost EPSPs, especially in cells that have a long distal dendrite, such as the deep-layer pyramidal cells in neocortex. These voltage-gated channels give the dendrite a longer effective length constant

The most important thing is that even relatively short axons are just way too long for passive conduction: that's the reason for action potentials. Length constants depend greatly on the size of the neurite, but you can expect the distances to be on the order of millimeters to 10s of microns.

That said, it isn't ever true that a subthreshold EPSP won't flow into an axon: it just will get weaker and weaker with distance. Neurotransmitter release depends on a substantial depolarization which opens voltage-gated calcium channels; a small little EPSP that has decayed several-fold from the soma has no chance to cause calcium influx and subsequent vesicle release.

Spatial and temporal summation

EPSPs don't 'wait' anywhere, the EPSP is constantly decaying because all membranes are somewhat leaky, and current isn't restricted to any compartment. Current is constantly flowing out of the membrane and out into all the other processes of the neuron (and then out through those parts of membrane too!). In fact, if you are talking about passive conduction of EPSPs, you are really talking about a form of "leak", not through the membrane but through the cytosol! The EPSP isn't traveling to the soma in any directed way, there is current "leaking" in all directions, and some of it happens to go towards the soma. To get summation at the soma or anywhere else, EPSPs have to arrive both close enough in time and close enough in space.

EPSPs can sum with each other in the dendrites if they occur close enough in space, but of course that also only works if they occur around the same time. Similarly, at the soma, an EPSP slightly depolarizes the soma but only for a brief time. If one EPSP has an amplitude of, for example, 5 mV, and another EPSP has an amplitude of 3 mV, they will only sum to close to 8 mV if they occur simultaneously. If the 3 mV EPSP comes a few milliseconds later, the peak voltage might only be 6 mV, or if they are separated even more in time, there may be no summation at all.

Why do spikes start at the axon hillock?

The axon hillock is a special part of axon, right at the beginning of the axon. This area is more than just the first section of axon, it also typically has the lowest threshold for initiating an action potential due to a greater density of voltage-gated sodium channels. Sort of by definition, a cell's threshold is going to be the threshold for whatever part of that cell has the lowest threshold (at least near the soma, which is so big compared to axons/dendrites that it is nearly isopotential).

For example, take an example cell whose overall threshold is at -45 mV. If you were to somehow remove the axon hillock, leaving just the rest of the soma and the dendrites, the threshold wouldn't be -45 mV anymore, it would be much higher, maybe -10 mV. Even if you had some really huge EPSP (or manually injected some current) to bring the cell towards -10 mV, the axon hillock would still hit its threshold first and start the action potential well before the EPSP reaches a peak sufficient to start a spike in the soma proper.

If it helps you could think of a balloon analogy. The EPSP is air flowing into the balloon, and the action potential is the balloon popping. If one part of the balloon is thinned/weakened, that part will always be the site where the popping starts. It doesn't matter if you put in enough pressure to cause the thick part of the balloon to pop, because before you can possibly get it to that pressure the weak part has already burst.

Also note that for this analogy to fit with all the rest of this answer, it has to be a leaky balloon, so it only pops if you put enough air in fast enough before it has a chance to leak out.

References

Yuste, R., & Tank, D. W. (1996). Dendritic integration in mammalian neurons, a century after Cajal. Neuron, 16(4), 701-716.


What is the literal meaning of the scientific name for the cactus wren?

According to the Helm Dictionary of Scientific Bird Names:

Kampylos, καμπúλος (Greek): curved, bent;
Rhynchos, ῥύγχος (Greek): bill.

Also, for the specific epithet:

Brunneus (late Latin): brown;
Capillus (Latin): hair.

Page with the Genus name: https://books.google.com.au/books?id=-RfSBAAAQBAJ&lpg=PP1&pg=PA87#v=onepage&q&f=false

Page with the specific epithet: https://books.google.com.au/books?id=-RfSBAAAQBAJ&lpg=PP1&pg=PA78#v=onepage&q&f=false