What is protein folding and how is it relevant to disease?

Protein folding is a complex thing. There are huge computer algorithms and huge mainframes which are trying to predict the final 3D structure of a protein.

Knowing the tertiary and the quaternary structure of a protein, allows us to understand why diseases happen. In many cases a mutation of the gene provokes an aberrant protein folding. When the protein is misfolded, it is not able to do its function. This particular condition is called "Proteopathy".

http://link.springer.com/article/10.1385%2FMN%3A21%3A1-2%3A083

If you know the structure of a protein, you are able to design or improve drugs which can directly influence the protein structure and/or function, for example antibody therapies against cancer (Cetuximab-->against EGFR, in colorectal cancer; it is a drug which was very much improved when computers prediction/simulations are used).

https://en.wikipedia.org/wiki/Cetuximab

It is hard to find out a protein's structure - for some proteins it can require years!

So you first go from the sequence of the healthy people, then you sequence their genomes, and you use this as reference for the people with certain diseases. You might find eventually some mutation is in certain loci in the genomes of people with a certain disease. Then you can study the protein structures, so you can design some new drugs which might tackle this protein. If the protein is misfolded, like the tau protein in the neurodegenerative diseases, then is good to study the structure of this misfolded protein so you can design some drugs for these protein too.

So in the end the structure is extremely important, but often times you have to study many stages of the protein folding process to understand the possible final structure that one protein might have in the body and/or in a certain disease.

I hope this can help!


It's not entirely true.
For example, a 2014 study demonstrates bed bugs can transmit Chagas disease. From Penn Medicine News:

  The bed bug may be just as dangerous as its sinister cousin, the triatomine, or “kissing” bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

(I'll update with more details when I get off the road)


How, on a physical level, does ATP confer energy?

Usually in biology (and being ATP, it most probably is biology), it's one of two things.

The gamma-phosphate (the third one, the one farthest from the adenosine) is very unstable, meaning the phosphoanhydride bond is easy to break.  The cell "allows" it to break, but only at the cost of moving the phosphate to some other molecule, such as a serine or glycerol or fructose or whatever.  This phosphorylation creates a bond with lower energy than the phosphoanhydride, and so is overall favored.  Imagine the personification: the gamma phosphate hates being attached to anything, but hates being attached to an ADP the most.

Alternatively, if ATP hydrolysis is coupled via an enzyme, it is usually done through transient storage of the energy is protein conformation.  An enzyme binds ATP, which makes the protein structure "bend" or conform around the ATP.  This puts loads of strain (energy = A) on the protein which is offset by the stabilization of binding the ATP (energy = B).  This strain can make an enzymatic surface open up on the protein which itself takes a lot of energy to make (energy = C).  The surface can catalyze some reaction (X+Y->Z in your example) that costs some energy (energy = D).  The completion of that reaction alters the enzyme's catalytic site to something new and higher energy (energy = E), which can be alleviated by cleavage of the ATP (-7.3 kcal/mol).  Alas, ADP and P do not fit well into that site of the enzyme, so they float out, restoring that original ATP-binding surface to it's original state.  Provided A>B>C>D>E>-7.3, the cycle will continue until the ATP is exhausted or you have no more Z to make.

Typing "enzyme catalysis cycle ATP" gives a few examples. Here's a few:
DNA gyrase
Actin-myosin cycle


Using high concentration of primers ensures that after denaturation template DNA binds to primers instead of binding to each other. Also higher primer concentration enhanced product yield, as primers act as limiting factor for annealing.

(Reference: https://academic.oup.com/nar/article/24/5/985/1047654)


According to this:

Yet another significant finding was the discovery of HCO3− absorbing mechanisms like NHE3 and NBC3 (NBCn1-A) at the luminal membrane of the ducts, which suggested the ducts absorb and scavenge HCO3− in the resting state.

So, initially saliva is isotonic to plasma, it is both reabsorbed and secreted, if its flow is slow, more of bicarbonate is reabsorbed, if the flow is high less bicarbonate is reabsorbed. Therefore when flow rate increases bicarbonate concentration increases.

Source of image:

At low salivary flow rates, HCO3- is reabsorbed by the striated duct cells and so very little reaches the mouth. At high flow rates, the striated ducts can't keep up and so HCO3- reaches the mouth at high concentration (<25mM)).
This makes perfect sense, from a physiological point of view. HCO3- is valuable to the body and not something to throw into the gut for no reason. The main purpose of unstimulated saliva is to keep the mouth lubricated, help you to talk and so on. Unless you are feeding the plaque bacteria, there is no great amount of acid to neutralise and therefore no need for a high HCO3- saliva. When you feed yourelf, and also your plaque bacteria, you stimulate salivary flow and produce a high HCO3- saliva, with a high buffering capacity, just when you need it.(Source)


Are all dead plant cells (that die to do a job), have secondary wall?

Not all plant cells perform a function when they die.
But a lot do.
Sclerenchyma is refereed to as:

Sclerenchyma is the tissue which makes the plant hard and stiff...

Mature sclerenchyma is composed of dead cells with extremely thick cell walls (secondary walls).

Plant cell death includes necrosis, apoptosis and autophagy and studying how and why they occur is an active area of plant research.
Some plant cells die because they are not provided enough energy. Plants garner energy via the sun and biochemical process known as photosynthesis.
When the days start to become shorter there is less sunlight and parts of some plants die.
E.g. Leaves die.


Why is this spider wound in such a dense web?

From the look of the spider outline, it looks to have short legs and is dark. A yellow sac spider is quite light-coloured and has long legs. Yellow sacs and clubionids will sometimes make themselves a sac for resting or eating or molting or laying eggs. Yours is probably a jumping spider, and here is a youtube timelapse video of a jumping spider laying eggs while inside its own protective sac:
https://www.youtube.com/watch?v=yoqMNX0RWuc


Function of NaCl in yeast shuttle prep of plasmids

High salt concentrations will cause the proteins and lipids to precipitate out, as in salting out. Free Na+ ions may also bind the negatively charged DNA backbone and give the molecules a neutral net charge, allowing them to concentrate as well.


Which human cells have the longest and shortest lifespan?

If we define lifespan of a human cell to mean the period during which the cell survives with the same function in a human then..

LONGEST (LIFETIME)

Stem cells. Many types of stem cell form during embryogenesis and persist with the same functionality through to death. would be the longest lived (e.g stem cells that form blood cells such as lymphocytes, red blood cells and platelets).  Stem cells are found in many tissues including self-renewing ones such as the blood/bone marrow, gut epithelium and skin.

VERY LONG (YEARS-DECADES)

Neurons are long lived and are generally non-mitotic.  However, recent studies are raising questions about the degree of cell division in the 'mature neurons' of the brain.

Memory T-cells and memory B-cell (which can be activated and secrete antibodies as 'plasma cells') can provide long-lasting immunity from exposure to antigens in the environment and vaccines.

LONG (FEWER YEARS-DECADES)

Oocytes (eggs)..which are present at birth but which become functionally mature in waves  during puberty.

RACE FOR THE SHORTEST

Labeling studies show that mature gastric epithelial cells live for a few days.

The top layer of skin epithelium is sloughed off every few days.

Sperm cells live for days and are expended or re-cycled.

Mature neutrophils have a circulating half-life of around 8 hours but they can persist as mature forms within the bone marrow for a few days before entering the circulation and they may exit the circulation into depots such as the lung.  So the 8 hours is too short for their actual lifespan.


Why do living things go belly up as they die?

limbs are light weight compared to bodies, if you knock an animal around (and it has no active correction AKA is not alive) it will tend to end up on its back just due to where its center of gravity is.


It's well known that obese patients have slower wound healing, but the specific cause isn't known; most likely there are multiple causes acting together.

  The correlation between obesity and deficient wound healing has long been established. ... Substantial evidence exists demonstrating that obesity is associated with a number of postoperative complications. Specifically in relation to wound healing, explanations include inherent anatomic features of adipose tissue, vascular insufficiencies, cellular and composition modifications, oxidative stress, alterations in immune mediators, and nutritional deficiencies.

--Obesity and Surgical Wound Healing: A Current Review  (This is an open-access article that nicely summarizes the open questions)

  Obesity has been shown in a number of studies to impair wound healing, and chronic nonhealing wounds in obesity and diabetes are a major cause of limb amputations in the United States. ... Recent evidence indicates that aberrant wound site inflammation may be an underlying cause for delayed healing. Obesity, diabetes, and other conditions such as stress and aging can result in a chronic low-level inflammatory state, thereby potentially affecting wound healing negatively.

--Exercise, Obesity, and Cutaneous Wound Healing: Evidence from Rodent and Human Studies (Also open-access, a little more recent but less wide-ranging)


Growth rate oscillation in the a population of non-interacting bacteria

The theoretical article concerns growth rates of single cells. There are many studies that model cell cycle as a non-linear oscillator (see Tyson and Novák, 2015).

However, growth rate measurements in microbiology are usually done on cell populations consisting several cells. You generally do not observe any oscillation because:

Cells are not synchronized
There can be variations in growth rate of different cells because of noise
The measurement time points are much larger than the period of oscillation

Some of these reasons are already mentioned in the paper you linked (Jafarpour, 2019).

I do see some ups and downs in the growth rate in my own data; E. coli growing in LB in a 96 well plate.

X-axis is the time in seconds; measurement was made every 15minutes. Y-axis denotes difference in OD between two consecutive measurements. The different colors are biological replicates. However, I cannot say that this is the kind of oscillation that Jafarpour talks about. It appears more like stochastic fluctuations in growth rate or measurement errors (they are also not damping by the end of growth).


How far can a mosquito fly over the sea?

If we ignore the weather effects mentioned by Count Iblis we can do a fairly simple calculation.

The lifespan of a male mosquito is about 10 days whereas females live to about 50 days.

Their flying speed is generally about 1.2mph.

So if we assume that they can fly whilst asleep and maintain a constant velocity for their entire lifespan (obviously ridiculous because of the need to eat etc), their maximum ranges would be:

Male: 1.2 * 24 * 10 = 288 miles.

Female: 1.2 * 24 * 50 = 1440 miles.

It should be noted that these are absolute theoretical maximums. I would suspect real life values to be somewhere in the region of 10%-20% of these. However, once wind is taken into account they can easily spread globally.


How to name a case of convergent evolution where the same mutation is involved in both lineages?

I'm not aware of a specific term for this. In the places I can find the concept discussed in the literature (here and here), the authors simply describe the pattern as "the same [...] mutation in two lineages" and "parallel mutation in two lineages".


A: wild-type allele / a: color blind allele

Because color blindness is recessive and X-linked your assumption $p=F(a)=4\%$ is correct as men do only have one copy of the allele. Subsequently $F(A)=q=1-p=0.96$ is also correct. Therefore:

a) $F(Aa)=2pq=7.68\%$ is correct and b) is wrong, a is the color blind allele and $F(a)=0.04$ therefore it's $p^2=0.04^2=0.0016=0.16\%$.

92% color blind among females seems a bit high :).


I don't believe either is the reason. Back in the day of early man, the different intensity levels of light was used as a signal to our body's "master clock" to tell us when it was time to go to sleep. So to simply put it, when exposed to less intense light, such as artificial light, its picked up as the dimmer, less intense, light akin to when historically we would be getting ready to go to sleep.


What values to be taken for x-axis and y-axis?

It doesn't matter really, but for aesthetics sake, you'd plot the wavelength on x and the absorbance on y. We tend to visualize such data as spectral or absorbance as "peaks" on the range of interest. There's a fairly good example here. It has something to do with convention: traditionally
 the independent variable on x and the dependent variable on y. There's a good answer on cross-validated on the matter, too.


The "chain identifier" does exactly what it says: it identifies the polypeptide or other molecular chain. For some structures, there is only one, so you'll only see an identifier A. However, many structures show two or more proteins bound together, or an enzyme complexed to a substrate, or a small molecule inhibitor in a binding pocket - there are many different possibilities. Each individual chain of atoms has its own identifier.

For example, 1VKX shows my favorite transcription factor NF-κB bound to the κB DNA enhancer sequence. There are four chains in the structure: two polypeptide chains, the p65 subunit A and the p50 subunit B, and two DNA chains C and D, one for each strand (forward and reverse).


The term you are looking for is psychrophile or cryophile. There are examples of microbes adapted to very cold conditions in Bacteria, Archaea, and Eukarya. There are also fairly complex animals capable of surviving very low temperatures -  Tardigrades, for example. There are multiple issues that organisms face in withstanding extremely low temperatures - protein denaturation, membrane fluidity, intracellular ice-formation, just to name a few.

There is this review that might be useful to you.

D'Amico, S., Collins, T., Marx, J.-C., Feller, G., Gerday, C. Psychrophilic microorganisms: Challenges for life (2006) EMBO Reports, 7 (4), pp. 385-389. link


The propensity for heterozygotic twins seems to be driven primarily by genetics, with additional factors playing a role (http://152.98.160.29/contents/p/staff/CV162Lewis_UQ_Copy.pdf', info site):

hormones ("Mothers of fraternal twins tend to be taller, and have earlier and shorter menstrual cycles")
ethnic background (which is really genetic) - African women are more likely than Caucasian women to have them, and Caucasian women are more likely than Asian women to have fraternal twins
mother's age
nutrition
previous births
fertility drugs

I also found a link to a genetic study published in Nature that claims to have linked a DNA region to dyzotic twins, but the Nature website seems to be down - maybe it will work later: A region on chromosome 3 is linked to dizygotic twinning - Nature.

Note that the father does not contribute to the chance of having heterozygotic twins, but a male offspring could pass the gene to daughter.


Bending your little finger without bending ring finger

This does not have to be the case always, For example if you are a pianist you need all your finger to work independently.

OK, So coming to the main question.

In simple words, They are all interconnected. See the image [Source: Google Images]

They share flexor tendons (The flexor tendons allow you to bend your fingers) , If you try to move one, other is objected to come along.

Yes it is possible, As I mentioned before if you are a pianist, you don't have much choice. It is possible by little bit training.


Well, $Cl = R/Cp$ is correct, but $R$ is not $Cp \cdot k$.

Given $X(t)$, the actual quantity (ie weight or moles) of drug in the system, $R$ should have the dimension of $\frac{dX(t)}{dt}$, that is $weight \cdot time^{-1}$ or $mole \cdot time^{-1}$ because the base definition of clearance is given by $$- \frac{dX(t)}{dt} = Cl \cdot C(t)$$.

The volume of distribution $Vd$ comes into play when converting from $X(t)$ to $C(t)$. Following the same steps as you did :

$$ R = \frac{dX(t)}{dt} = \frac{dC(t)}{dt} * Vd = C_p  \cdot k \cdot V_d$$
because (due to 1st order kinetics)
$$\frac{dC(t)}{dt} = Cp \cdot k$$

  Substituting,
  $$ t_{\frac{1}{2}} = \frac{\ln(2)}{k}$$
  $$ t_{\frac{1}{2}} = \frac{\ln(2) \cdot C_p \cdot V_d}{R}$$
  Since $ Cl = \frac{R}{Cp}$, substituting would give,
  $$ t_{\frac{1}{2}} = \ln(2) \cdot \frac{1}{Cl}  \cdot V_d$$
  $$ Cl = \ln(2) \cdot \frac{1}{t_{\frac{1}{2}}}  \cdot V_d$$
  $$ Cl = k  \cdot V_d$$
  $$ k = \frac{Cl}{V_d}$$


Melanine is produced and stored in melanocytes. They contain melanosomes that are organelles that store melanine.


Lets define the nomenclature first: An antigen is a large structure (protein, virus, bacteria and so an) which is recognized by the immune system as foreign. The word antigen derives from the abbreviation ANTIbody GENerator. Exposure of our immune system to an antigen results in an immune response and the generation of many antibodies.

An epitope is a small part of an antigen - typically these are small structural elements or small peptides (8-11 amino acids in length) which are recognized by the binding site of an antibody. See the picture below (from here):

Here the antigen is the albumin protein. On the surface you can see 8 different epitopes which lead to the generation of 8 highly specific antibodies against the epitopes (antikörper is the german word for antibody). Every antibodies is highly specific for its epitope and will recognize no other epitope and helps raising an immune response against it. What happens after an antibody bound to its epitope can be read here.

Antibodies directed against a protective epitope are directed against (highly) conserved structures of the antigen. For example the recognize a highly conserved structure of a virus which means that even when this virus mutates (like influenza does) it will still recognize the conserved epitope and give protection against this virus (or better: antigen).


an umbrella term for homeolog and ohnolog?

Unfortunately, there is no such term. Look at Glover et al. 2016 for a proposal how to unify the ploidy related homology terms, none of the words describes exactly what I searched for, so I at least compiled the relevant vocabulary

homoeolog/homeolog - homologous chromosomal sets in an organism diverged in isolated populations/subspecies and broght back by a hybridization event; note that the two spellings with exactly the same meaning are possible
ohnolog - homologous chromosomal sets originated from a whole-genome duplication (WGD) event; however usually this is used for ancient WGD events (like the R1 and R2 at the base of vertebrates, or the WGD at the base of bony fishes). It is not really possible to distinguish between WGD and hybridization in these ancient cases and therefome ohnologs perhaps suit "unknown" category better.
homologous chromosomes - chromosomes that pair during meiosis (does not strictly correspond to the homology in the context of molecular evolution)
homologous sequences/homologs - any sequences that have a common ancestor (as used in molecular evolution; but does not have to be on a genome-scale or within a genome; tandem duplicates or orthologs in two species are also homologous sequences)

2020 update:
I asked when I was writing this paper. I needed the term to describe the heterozygosity structure of some polyploids and I ended up calling them homolog (A <-> A' divergence) and homoeolog heterozygosity (AA' <-> BB' divergence) or composite when I was unable to set them apart (the majority of cases in fact).


Why "Having chlorophyll without photosynthesis is actually very dangerous" and "like living with a bomb"?

Chlorophyll absorbs photons (light). The energy in the photon extracts an electron from a molecule of water. Electron transfer creates intermediate superoxide and hydroxyl radicals from the oxygen and hydrogen from the donor water molecule.

In normal photosynthesis, these radicals are quickly used to power the reduction of NADP to NADPH and the synthesis of ATP from ADP. NADPH and ATP in turn power the synthesis of sugars from carbon dioxide and water, via the Calvin cycle.

These radicals are highly reactive. If they hang around and don't get used properly in redox reactions, they will just as happily attack DNA, proteins, and structural lipids within the cell, and are therefore dangerous. In normal plant cells that get too much sun, for instance, free radicals can build up and cause cell damage.

My guess is that the author's "bomb" is made up of higher concentrations of these radicals within a cell with no apparent machinery to perform the downstream (photosynthetic) chemical reactions needed to consume them safely.

Edit

I skimmed the (sadly, paywalled) paper, and it sounds like my guess was right, that it is indeed these radicals that are the danger from having chlorophyll, with no light-independent (Calvin cycle) mediated reactions to safely consume the energy in them:

  Chlorophyll itself has no natural biological function outside of
  photosynthesis, so if photosystems are indeed absent, corallicolids
  must have evolved a novel use for either chlorophyll or its closely
  related precursors or derivatives. However, these molecules generally
  function in light harvesting, which would be destructive to cellular
  integrity without the coupling of the resulting high-energy compounds
  to photosynthesis. Other possibilities are functions in light sensing,
  photo-quenching or the regulation of haem synthesis, but these too
  leave open the question of what the cell would do with the highenergy end products.

What's not clear to me is that the genes that help generate chlorophyll are expressed, but the cells are unpigmented. I don't see any explanation where the chlorophyll and associated proteins are localized in the cell — seems like a missing part of the paper, or I missed that part when skimming. Or perhaps the organism has evolved interesting and novel ways to manage the damage caused by these oxygen radicals, or has other mechanisms for consuming them, yet to be identified.

Should motivate further research, especially if these organisms share ancestry with malaria and toxoplasmosis — there might be something interesting to learn that would help with eliminating these diseases. I imagine a biochemical "radical bomb" could be very handy for destroying parasites, if there was a way to expose them to light or some other source of photons; perhaps some drug therapies could target the relevant genes and induce the parasite to destroy itself. Interesting paper.


What is difference between breed, variant, subspecies and species?

A species is commonly defined as the largest group within which interbreeding produces viable offspring.

A sub-species is a subgroup below the level of a species.  One definition is a group which can interbreed successfully with other subspecies, but does not do so in practice (e.g. due to geographical isolation).  Other terms like variety, form, etc., may be used in some domains to indicate various groupings below the species level.

A breed usually refers to a population of a domestic animal that has been selectively bred for specific characteristics.

A population is a set of individuals within a species that live in the same geographical region.  Depending on rates of gene flow, different populations within a species may eventually differentiate into subspecies or distinct species — this is known as allopatric speciation.


I am not a MassSpec expert but this is what I understand from my spectroscopy basics:

In tandem MS (MS-MS), the ionized analyte generally undergoes or made to undergo fragmentation (breaking up into smaller ions). Fragmentation allows you to study finer details. It is also essential for de-novo peptide sequencing. Different fragmentation techniques, such as Collision Induced Dissociation (CID) or Photofragmentation, yield different kinds of secondary ions.

You can intuitively understand that Fragmentation of structural isomers will yield different kinds of secondary ions (using the same fragmentation technique). The choice of fragmentation technique depends on the molecular nature of the analyte. In the article that I mentioned previously, they use laser induced photofragmentation to dissociate glycan-ions.

Even small molecules, which had been classically studied by MassSpec, undergo isomerization after ionization in order to stabilize the ion. Reactions such as reverse-Diels-Adler can also happen. The pattern of reactions would differ between structural isomers. For basics you can refer to a book on Spectroscopic techniques by Silverstein


There is both an upper and lower limit which are species specific. The upper limit is caused by incomplete segregation of sister chromatids and subsequent trimming of the long arm(s). The reason for the lower limit is, as far as I can tell, unknown.

Upper Limit
Schubert I, Oud JL. 1997. There is an Upper Limit of Chromosome Size for Normal Development of an Organism. Cell 88:515-520.
Hudakova S, Künzel G, Endo TR, Schubert I. 2002. Barley chromosome arms longer than half of the spindle axis interfere with nuclear divisions. Cytogenet Genome Res 98:101-107.
Rens W, Torosantucci L, Degrassi F, Ferguson-Smith MA. 2006. Incomplete sister chromatid separation of long chromosome arms. Chromosoma 115(6):481-490.
In these papers they found that in mono- and dicotic plants and one animal, the chromosome arm length is limited to half of the average length of the spindle arm axis (the length between the centromeres). Due to the mechanism and its presence in both plants and animals, it might be reasonable to expect that other domains of life are subject to similar constraints. Schubert and Oud (1997) speculate that the spindle axis length is fixed species specifically.

These are confocal microscope images of dividing Vicia faba (bean) cells (Schubert and Oud, 1997). (a) Wild-type cell at anaphase. (b-d) When the chromosome arms are longer, the chromatids cannot be completely separated at anaphase. (e) Wild-type cell at telophase. (f, g) Longer chromatids cannot be separated sufficiently and a bridge forms between the two daughter nuclei. (h-j) The bridge is broken when the cell plate forms. (k) Wild-type cell at interphase. (l) Breaking of the bridge between cells with lengthened chromosomes creates irregularly shaped nuclei and micronuclei - these micronuclei represent loss of DNA from the genome and are eventually lost outright through further cell divisions.

Lower Limit
There is a lower limit, but it doesn't seem that anyone knows why, which makes it impossible to accurately define.

Schubert and Oud (1997): Data from various eukaryotic kingdoms indicate the existence of a lower limit of chromosome size for stable mitotic and meiotic segregation. Yeast artificial chromosomes do not exhibit normal meiotic stability until they are of a size between 120 to 500 kb which comes close to the order of size of native yeast chromosomes, in addition to functional telomere and centromere sequences (Niwa et al., 1989). For a Drosophila minichromosome, an island of complex DNA of 220 kb was shown to be necessary for proper centromere function (Murphy and Karpen, 1995). However, for stable mitotic and meiotic segregation an additional 200 kb of a flanking satellite sequence was required. For stable achiasmate disjunction of minichromosomes during meiosis in female Drosophila, 1000 kb of overlapping centric heterochromatin sequences are necessary (Karpen et al., 1996). Schriever-Schwemmer and Adler (1993) have shown that a minichromosome representing the small centric product of a translocation between chromosomes 7 and 15 of the mouse and comprising about 1% of the haploid genome got lost during meiosis in the female carrier organism while the corresponding product of a translocation involving chromosomes 4 and 8 did not. The latter was somewhat larger. Either this different behavior was due to the presence of essential genetic information on the small translocation product 4⁸, or the minichromosome 7¹⁵ was just too small for stable segregation, although it contained a complete centromere as well as telomeres. Finally, we have observed that the frequency of meiotic missegregation, but not of transmission to the next generations, is inversely correlated with the size of translocation chromosomes in Vicia faba (Schubert et al., 1986). Thus, the existence of a proper length range for eukaryotic chromosomes is obvious.
The physical reasons for the lower limit that still enables stable mitotic and meitotic segregation are less clear at present than the constraints for an upper limit of chromosome length

Of course, "present" in that paper refers to the late 90's but, in my admittedly brief search, I have been unable to find too much in the way of more recent results. The following paper seems somewhat promising, but I don't have access to it and can only quote from the abstract. It's not much more recent, either.
Schubert I. 2001. Alteration of chromosome numbers by generation of minichromosomes -- is there a lower limit of chromosome size for stable segregation? Cytogenet Cell Genet 93:175-181.

[A] lower size limit for a stable chromosome transmission … might be based, for instance, on insufficient lateral support of centromeres or on insufficient bivalent stability due to the incapability of chiasma formation.


How much mechanical stress can a skeletal muscle bear?

The skeletal muscle is not isotropic and therefore the effect of stress would be different from different axes. The strength also depends on the density of fibers and the composition of tendons (aponeurosis) that connect the muscle tissues; these can change (positively) with long term exercise [ref].

In this article the authors show the effect of different mechanical stresses on the skeletal muscle tissue — digitorum longus, from rabbit hindlimbs.

  Tests were performed on extensor digitorum longus (EDL) muscles,
  chosen for its regular cross-section and low pennation angle (Lieber
  and Blevins, 1989). To ensure that only muscle tissue was tested,
  aponeuroses were carefully dissected away

Figure from the same article by Morrow et al. (2010)

You can notice that the yielding point to longitudinal extension is somewhere near 180kPa. It can be assumed that a hook into the tissue on pulling would generate longitudinal extension stress (unless the hook pierces through the muscle tissue or has sharp edges that can rip the muscle transversely). The stress in the Bobby situation would be: $$\frac{\text{weight (mass)}\times \text{gravitational acceleration}\ (9.8\ ms^{-2})}{\text{area of the muscle covered by the hook} \times \text{number of hooks}}$$

This is the best I can answer your question based on data; this cannot be directly extrapolated to the Bobby situation because:

The muscle tissue is different
The strength of the tissue depends on how much has Bobby exercised his muscles.
There would be additional mechanical stresses in other directions because of his movement while being suspended from the hook.

Ribs are not very strong bones and attempt to hook something on it may cause punctured lungs, not pneumothorax. Death will depend on the severity of the wound.


Why are male gametes and female gametes not equally sized

Gerardo is correct that female designates the bigger gamete, so there's nothing important about the terms "male" and "female" here.  But I'd like to also respond to your initial question of how the difference in size would've evolved because I don't think it's trivial.

I can provide a rough summary of one explanation that was summarized in Dawkin's The Selfish Gene which was summarized from G. A. Parker's 1972 paper "The origin and evolution of gametic dimorphism and the male-female phenomenon."

It goes something like this:

The asymmetry could have evolved from originally equal sized gametes through the evolution of two divergent sexual strategies - a large investment strategy which opened the way for a small-investment exploitative strategy. The idea is that when gametes were all roughly the same size, some would have happened to be bigger than others. There may have been some advantage to this because the larger gamete could provide a larger initial food supply. However, this also could have created a condition for exploitation by individuals producing smaller than average gametes, especially if they could ensure their smaller gametes fused with the larger than average ones. This could be achieved by making the small ones more mobile and able to actively seek out the larger ones. Making smaller gametes would have allowed that individual to make more of them and potentially have more descendants, as they're not investing as much energy into any one gamete. The interplay of these two strategies would've continued in a runaway fashion, with the larger gametes evolving larger and larger to compensate for the ever-smaller contributions by the exploiters.  Eventually the larger gamete could become immobile since it's being sought out by the smaller gametes anyway. You can see where this is going, with the larger gamete becoming what we know of as eggs and the smaller as sperms.


Do pigeons have the smallest legs-to-body ratio of any bird?

That achievement probably belongs to the Swifts, specifically known for their short legs. Their name Apodidae derives from the word for "footless" in Greek.


Can sexual selection operate in temperature dependent sex determining organisms?

Yes! Crocodiles are indeed a good example as the sex in determined by the temperature (ref) and they have some traits evolving through sexual selection (ref).

I think you went almost all the way to the answer in your thoughts. Let's categorize things a little bit and talk about Genetic Sex Determination (GSD) and Environment Sex Determination (ESD) separately; that might help.

Note that ESD and GSD are two extremes of a continuum present in nature. Note also that I will talk about sexual dimorphism only and not specifically about sexual selection. Of course sexual selection is one process that can yield to sexual dimorphism. You can replace "locus involved in sexual dimorphism" by "locus involved in selection selection" in what follows and that will work as well expect that we will lose some generality.

Genetic Sex Determination (GSD)

Physical linkage

Indeed if you have sexual chromosomes, then you can have loci sitting on those sexual chromosomes that are affecting only one sex and therefore have genders with different appearances.

Gene expression

As you noted as well, those genes causing sexual dimorphism can also be sitting at different position in the genome and be regulated (directly or not) by the sex determining locus.

Environment Sex Determination (ESD)

If there is no genetic variance for sex but the whole variance is exclusively environmental (ESD), then phenotypic differences between males and females are just determine by whatever environmental variable (temperature for example) is used. In other words, you can have loci being under antagonist selection pressure between the two sexes that is regulated (more or less directly) by the temperature.

In short, you can have sexual dimorphism in ESD just like in GSD that...

the causal agent of the sexual dimorphism is not the sex determining locus but some environmental variable.
sexual dimorphism cannot occur through physical linkage (as there is no genetic variance to determine the sex) but only through regulation of expression.

I recommend this book (although a little expensive).

Do males of all sexual species have Y chromosomes is a somewhat related post but might be too introductory for you.

Here is a nice figure from Bachtrog et al. 2014 that offers an idea of the diversity of sex determination system (thanks @rg22)


How can the pressure during contraction vary between the left and right ventricles?

The key is vascular resistance.
Pumps like the heart don't move fluid, they exert force ("push") on it, increasing the pressure. The movement happens subsequently because there is somewhere for the fluid to go, so it moves down the pressure gradient from a place of high pressure to a place of lower pressure. If you clamped their outputs (increased resistance to infinity), neither ventricle would push any blood out.
We can say that the flow rate is proportional to the pressure difference and resistance:
Flow ~ ${\Delta}$P/R
If we assume that the two ventricles push out over the same time frame, you could easily get equal "Flow" with different "${\Delta}$P" if RLungs is different from RBody, and this is exactly the case: pulmonary vascular resistance is much lower than systemic vascular resistance. It's easier to pump the same volume through the lungs than through the rest of the body, so less pressure is needed.


What would be the effect of excess taq polymerase on the PCR?

Costly error.
And yes, it will affect your reaction, since the concentration of Magnesium ions, which are needed as a co-factor by the enzyme, is too low. If you need so much PCR product, you can now adjust the rest of the reagents or you could start over and put this on your personal list of errors. Always check the amount of volume, if it is suspiciously high, check again.

If you decide to proceed and work with a 10x larger volume, make sure that the single PCR reaction is not bigger than 50µl, because the bigger volume also affects how fast the reaction heats up and cools down. If your reaction is too slow to reach 72°C for example, the elongation time might not be long enough to get the full product. If denaturating is too short, your efficiency will drop.


The gold standard would be the isolation of infectious virus from mosquito saliva. Extraction of saliva from mosquitoes is fiddly if you have to do it in containment and the survival of mosquitoes collected from the field may be low. Alternatives, in roughly declining order of strength-of-evidence, would be

identification of virus from dissected salivary glands,
identification of RNA from saliva/salivary glands,
identification of virus or RNA from heads,
virus or RNA from whole bodies of insects that are not visibly
engorged with blood (and we're getting
into not-very-reliable-at-all territory at this point).
detection of viral RNA from pooled field-collected (unsorted) insects, possibly including those which have recently blood-fed.

There are also other technologies that are beginning to be used for field surveillance of arboviruses in vector populations, such as sugar-coated or honey-coated Whatman FTA cards (mosquitoes sugar-feed on the cards which preserve RNA).

Two other things are worth emphasising here. One is that not all mosquitoes which ingest infectious virus will develop a transmissible infection even if they survive to complete the necessary incubation period. Some will clear infection completely, others may develop a disseminated but non-transmissible infection due to the existence of barriers to replication within the vector's tissues (see this paper for a nice review).
The second is that the importance of a vector is not determined solely by its competence (the probability that a mosquito ingesting an infectious dose and surviving the extrinsic incubation period develops a transmissible infection) but also things like vector:host ratio, biting preferences, and typical lifespan. Vectorial capacity is more important (this is a recent paper pointing out the differences).


Why would we overexpress Sir2 by overexpressing its hypomorph (dSir2-EP2300) in C. elegans?

I have had a little time to look over this paper.

They do overexpress a native sir2 clone in high doses, called sir2.1 OE.  Which seems to be native and also appears in high copy numbers. This strain was found in previous publication to have a high lifespan... that is old news.

This paper sees sir2.1 expression levels as an oversimplification of the causes of longevity.  When they create crosses of the sir2.1 OE strain with wildtype, you can see the Outcross, which is verified to have a high level of sir2 expressed no longer has an extraordinary lifespan.

This can be seen in Figure 1.  http://www.nature.com/nature/journal/v477/n7365/fig_tab/nature10296_F1.html

So this paper is now asking, if sir2 levels do not convey the information that creates an extended lifespan, then what does?  It must be some modulation of some protein that sir2 affects.  They implies that the actual cause of the lifespan increase may have been a mutation somewhere else in the organism.

"However, longevity was not suppressed by sir-2.1 RNA interference (RNAi) ... indicating causation by factors other than sir-2.1, either on mDp4 or elsewhere in the genome."

"This implies that lifespan extension is due to transgene-linked genetic effects other than the overexpression of dSir2."

In the second half of the paper (figure2) the investigators have moved on to drosophila work, where they look at how expressing constructs or inhibiting sir2 protein levels might affect lifespan.  Although the dSir(EP2300) / + construct (drosophila sir2) with a wild type gene promoter did not live quite as long as dSir2(EP2300) with a fancy promoter (dSir2(EP2300) / tub-GAL4), the promoter construct (tub-GAL4/+) alone also had just as long a lifespan.  How can this be?  Not sure, but the expression of sir2 is clearly not the panacea we had hoped.  Note however that the reduced power gene still gave the same boost to lifetime.   This shows dramatically that sir2 activity alone does not drive the longer lifetime.

Lastly, deletion constructs (dSir4.5/1.7) , which should have lower than wild type protein levels for sir2 had completely normal lifetimes.

So the answer to your question; you need to test a hypothesis going in both directions - does increase of the protein really create a strong effect?  Does decreasing it have a negative effect then?  There are lots of other reasons to use knockouts and non functional genes in such an experiment, but those are the broad strokes.


The Body Story.

--Have to add some characters for the system to be happy--


Which of the response is faster? voice or hand action?

Assuming that we are talking about a situation at the physical limit of the brain:

Speaking a word will always be slower than pushing a button.
A whole word requires a contraction of the diaphragm to push out air so this air can be modulated by another sequence of contractions and relaxations of the vocal chords.

So contracting finger muscles is very similar to speech initiation however for a computer to respond (in the example you were playing a video game) the computer needs to recognize the full word and then map it to an output before actually implementing the left turn.

So adding the extra processing time of the computer and the actual extra production time of the vocalization you're better off pushing buttons.

As a matter of curiosity if the physical limit situation is relaxed; whenever there is a mismatch in both sensory receptors as well as outputs, the brain does its best to compensate. Think of something dropping on your foot, the visual information is actually delayed so that the sensory stream (that has to go up all of your leg and spine) catches up.


Why are pili more common in Gram negative bacteria than in Gram positive?

Pili were at least discovered more recently in gram-positive bacteria.

Pili are formed differently in gram-positive and gram-negative bacteria.  Here's a pretty good review on the differences: http://www.ncbi.nlm.nih.gov/pubmed/18953686

Researchers seem to think that pili might be involved in adhesion/formation of biofilms (adhesion is important for pathogenicity).  Certain types of pili are specifically involved in gene transfer. This is a good review on pili and pathogencity in gram-positive bacteria: http://www.nature.com/nrmicro/journal/v4/n7/pdf/nrmicro1443.pdf. If you can't access it, let me know, and I'll do my best to summarize.

EDIT:

The Wikipedia entry for pilin interprets the second paper I linked as saying that pili are more common in gram-negative bacteria and that pili are implicated in pathogenicity.

Straight from the paper:

Prevalence:

  Over the past five decades, several distinct pilus types
  have been identified, most of which were described
  and characterized in Gram-negative bacteria.

Function:

  A common feature of Gram-negative pili, however, is their role in adhesion to eukaryotic cells. It has been
  proposed that bacteria use these structures to form an
  initial association with host cells, which can then be
  followed by a more ‘intimate’ attachment that brings
  the bacterium into proximity to the host-cell surface.

and

  Pilus-like structures on the surface of Gram-positive
  bacteria were first detected in Corynebacterium renale,
  by electron microscopy. More recently, surface
  appendages were reported to be present in Actinomyces naeslundii
   and were subsequently found in other
  species, including Corynebacterium diphtheriae, Streptococcus parasanguis (Streptococcus parasanguinis), Streptococcus salivarius
   and Streptococcus sanguis (Streptococcus sanguinis). Finally, in the past
  year, pili were also characterized in all three of the
  principal streptococcal pathogens that cause invasive
  disease in humans — group A Streptococcus (GAS; that
  is, Streptococcus pyogenes), group B Streptococcus (GBS;
  that is, Streptococcus agalactiae) and Streptococcus
  pneumoniae — in which they have been shown to
  have key roles in the adhesion and invasion process and
  in pathogenesis. [emphasis added by me]


What causes the cardiac ventricular pressure change during the isovolumetric part of the cardiac cycle ?

Boyle's law doesn't apply to all fluids: only gasses, not liquids. Liquids like blood are (mostly) incompressible, so their volume does not change substantially when you add pressure.

During isovolumetric contraction, the ventricular walls are pushing in on the blood contained in the ventricle, causing the increase in pressure, but there is not yet sufficient pressure to force the blood out the pulmonary/aortic valve.

Source:

Hillegass, E. (2016). Essentials of cardiopulmonary physical therapy. Elsevier Health Sciences.


Why basement membrane thickens in diabetes mellitus?

The endothelial cells in small blood vessels take in more glucose (as glucose levels in blood are high due to diabetes.) Thus they form surface glycoproteins which causes the basement membrane to become thicker yet less strong. This leads to blood and protein leakage from the blood stream in other tissues in the space between cells. Blood leakage alters cellular blood supply for all cells.

Less blood means less oxygen and less nutrients. As you probably know nervous tissue gets damaged fastest without oxygen thus explaining diabetic neuropathy. Also retina and kidney contain cells that get easily damaged when there is not enough blood.

Probably the worst complication is neuropathy, because the person suffering from it may suffer a heart attack (caused by the accelerated process of atherosclerosis in diabetes) and feel less pain (http://medlineplus.gov).

Collagen and laminin poduction increases as a result of the fibrosis process that takes place when a tissue gets less nutrients than it needs.

Diabetes affects all blood vessels, even the larger ones. See macroangiopaty.

From http://en.wikipedia.org/wiki/Microangiopathy


Cold adaptation in proteins, at sequence & structural level

There are research groups working on this exact question; understanding cold adaptation in enzymes. You can read about this in several articles such as 'Computation of enzyme cold adaptation', or 'Molecular Structural Basis for the Cold Adaptedness of the Psychrophilic β-Glucosidase BglU in Micrococcus antarcticus', or 'Specific amino acids responsible for the cold adaptedness of Micrococcus antarcticus β-glucosidase BglU'
On a general level there are several sructural characteristics that are typically found. They are usually far more flexible (i.e. less salt-bridges and other such stabilising bonds). The flexibility come from having fewer strong bond between and within the polypeptide chain, and even containing disordered regions. The flexibility also means that they are usually far less stable, and more difficult to work with. They are industrially interesting, as developing enzymes that can work at low temperatures can reduce the cost of running reactions. This is essentially a step towards a greener-industry. There are also speculations about various ratios and abundance of the amino acid types, and where they are located.  You would have to read articles on specific proteins to investigate this.
From a practical view-point, cold adapted enzymes are usually isolated from arctic microorganisms and characterised in the lab - in order to determine their temperature tolerance. The structure of such enzymes are then solved (after lots of work) and form the basis for understanding cold-adaptation.
To answer the question more specifically, no its not realistic to know if something is coldadapted directly by looking at the protein sequence (on its own), this has to be determined experimentally in the lab. However, if the protein is from a cold adapted organism (typically arctic bacteria) there is reasons to assume it is cold adapted before you test it in the lab. You can also apply som bioinformatics (e.g. blast search) to determine if its related to cold adapted proteins.  Also, If that specific type of protein that you are looking at, is well studies, you could also try to make homology models and see if its structurally similar to cold-adapted relatives or if it is more structurally similar to its mesophilic or even thermophilic counterparts. This is however very speculative, and i would not put too much weight on theoretically assumed adaptations - you should at minimum know that the protein of interest is from a cold adapted organisms, to even begin to look (computationally) on why and how it could be cold adapted.


Need to make a library of mammalian coding sequences

Verify where these transcripts are generally present (this should not be difficult for common organisms)
If they are all expressed in a certain tissue use cDNA from that tissue
If not then pool the cDNAs from different tissues such that all genes can be amplified
cDNA libraries (including whole organism) are also available and you may obtain them from the nearest repository (I guess NCBI also provides).

Some other things you can do:

Ask the primer synthesis company to provide primer sets it in a
96well format.
DNA synthesis is also a decent option (it takes something like $0.5
per base pair), but that can be expensive if your cDNAs are huge.


How to isolate host cell RNA (tRNA,mRNA,rRNA) from viral RNA?

Thermo Fisher has a protocol for the separation of host mammalian RNA from prokaryotic RNA, optimized for E. coli vs human, mouse or rat sequences. Capture oligonucleotides bind portions of the mammalian RNA and hybridize. These hybridized oligo/RNA are then removed from solution via "oligonucleotide-derivatized magnetic beads," after which the remaining RNA assumed to be from whatever prokaryote can be precipitated out w/ ethanol. If you know enough about your virus and your host, I don't see why a similar assay can't be created. Otherwise, Thermo Fisher has additional links to RNA isolation protocol.. most of the viral assays, however, utilize serum, plasma, etc. because host DNA/RNA will elute along with the viral RNA if they're present, as in samples containing cells.


Relative concentration of enzyme vs reaction product

Remember that the concentrations you report are in mass units rather than mole units. If the protein has a mass of 40,000 Da, reasonable for many proteins, then 20 mg/liter means $0.5$ x $10^{-6}$ mol/liter. A typical small-mass product of an enzyme reaction might have a mass about 200, so its apparently lower mass concentration of 2 mg/liter is $10$ x $10^{-6}$ mol/liter, 20 times higher than the enzyme concentration in terms of numbers of molecules per liter. The mole or molecule ratios are what you should think about in terms of catalytic function.

Furthermore, from what you provide we don't know whether the enzyme was produced under circumstances that allowed it to express its activity; there may have been limitations on substrate availability, presence of inhibitors that would be removed in later purification, and so forth. In this scenario, evidently to obtain enzyme for downstream use, the emphasis is typically on getting large amounts of the specific enzyme regardless of whether some reaction product is formed. I don't find the enzyme concentration particularly high for something that the investigators are trying to over-express as in this case.

The Bradford reaction is a mainstay of standard biochemistry, as it's simple and straightforward. Different proteins can bind the reagent to somewhat different extents, so there is a second-order issue of whether the protein used for the standard curve and that being measured are similar enough in that respect. In practice, what's important is to provide enough information in the methods that are described so that someone could repeat the work to determine the relation between the Bradford measurement and some other more accurate method for this particular protein.


How do you determine if donated, stored blood is viable?

Blood can be stored as whole blood or packed red blood cells. The constituents of each are different. Which one will be used varies based on the patient, the availability and the situation. Whole blood (not necessarily warm) is used more often when there is massive blood loss, as it contains all the components of blood: clotting factors, platelets, plasma, etc. Packed red blood cells have had the white blood cells removed, most of the plasma, the platelets, etc. It is indicated for routine blood loss and to increase the oxygen carrying capacity of blood. The constituents of each are different.

The primary problems of stored blood viability are red blood cell deformability (red cells are normally very flexible in order to pass through capillaries) and red blood cell fragility (this results in fewer RBCs actually active in the recipient, as RBCs will break apart.) The viability of RBCs in storage depend on factors such as adequate ADP (the energy substrate). When RBSs are less viable for any reason (less deformable, more fragile, or hemolysis has started in the stored blood), this is termed red cell (or red blood cell/rbc) storage lesion.

Though there are probably many questions you may have about storage methods and viability, this will give you an idea of search terms for your reading. Good luck in your research efforts.

Fresh Warm Whole Blood (FWB
2012 Clinical Practice Guide on Red Blood Cell Transfusion
Blood Products
Deformability of stored red blood cells. Relationship to degree of packing
Microvascular perfusion upon exchange transfusion with stored red blood cells in normovolemic anemic conditions
Studies on the preservation of human blood. II. The relationship of erythrocyte adenosine triphosphate levels and other in vitro measures to red cell storageability
Nitric Oxide Scavenging by Red Blood Cell Microparticles and Cell-Free Hemoglobin as a Mechanism for the Red Cell Storage Lesion
Hemoglobin-driven pathophysiology is an in vivo consequence of the red blood cell storage lesion that can be attenuated in guinea pigs by haptoglobin therapy


Distribution of nutrients throuought a drink made of plants?

If we assume the drink was very well blended most of the water-soluble vitamis (B and C) as well sugars could dissolve in the juice. Fiber would mostly remain in the plant debris. Oils and fat-soluble vitamins (A, D, E, K) would form their own oily layer or be found in an emulsion with the fruit juice.


From Wikipedia:

Some biologists refer to wholly syncytial organisms as "acellular" because their bodies contain multiple nuclei which are not separated by cell walls.

As Albano pointed out, "cell walls" should probably be "cell membranes".

Paramecium and some types of amoeba like the Chaos genus have multiple nuclei so they fall under this definition.


Why do some trees hold their leaves through fall and winter?

The trait might not necessarily allow for an advantage, but a few possibilities have been proposed:

Nutrient return to the soil when needed in the spring
Less palatability to grazing animals

Source:

 http://northernwoodlands.org/articles/article/why-do-some-leaves-persist-on-beech-and-oak-trees-well-into-winter


Are people genetically predisposed to being interested in specific fields/ideas? How does specialization occur?

I think the concept you are looking for is the one of heritability.

In short, heritability represents the part of the variance for a trait that is caused by the genetic variance only. For more information, you can refer to this, this, this or this post or to wiki.

This wikipedia article talks about the heritability of IQ in human. It has been measured to be around 0.7.

Of course, heritability in IQ is not the same as heritability of "interests". But I don't know about any measure concerning the heritability of "interests". Such measure will be highly dependent on how you classify interests together. Does a mathematician specialist of probability theory have the same interests than a mathematician specialist of non-linear algebra? Does a Mathematician have the same interests than a chemist? and of a engineer? and of an electrician? Does a butcher have the same interests than a backer? and of a waiter? and of a bricklayer? .. Does anyone who work in business have the same interests? The fewer groups you make, the higher will the correlation between parents and offsprings and the higher is the part of the genetic variance that explain the variance in interests choice.


Hypotonic or Hypertonic solution and why?

Albumin wont form a true solution and wont affect the osmolarity greatly (colloid forming molecules like proteins can affect osmotic pressure to an extent. See oncotic pressure).. and since there is no solute the solution would be hypotonic..

But what effect it will have on the blood cells depends on how much solution was injected.


Lactobacillales vs LAB (Lactic acid bacteria)

Lactic acid fermentation is the most common type of fermentation among Eubacteria, and it's found on several genera.

Actually, regarding the fermentation types, we can say as a general rule:

Ethanol fermentation: found in Plants and Fungi.
Lactic acid fermentation: found in Bacteria and Animals.

That being said, according to the Todar's Online Textbook of Bacteriology,

  Although many genera of bacteria produce lactic acid as a primary or secondary end-product of fermentation, the term Lactic Acid Bacteria is conventionally reserved for genera in the Order Lactobacillales.

And according to Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition:

  They [LAB] belong to the Phylum Firmicutes, Class Bacilli and Order Lactobacillales.

These genera are: Lactobacillus, Leuconostoc, Pediococcus, Lactococcus, Streptococcus, Carnobacterium, Enterococcus, Oenococcus, Tetragenococcus, Vagococcus and Weisella.

The problem here is that not all lactic acid producing bacteria are called a LAB. Therefore, Lactobacillales and LAB can be used interchangeably. However, you cannot say that all bacteria that perform lactic acid fermentation are LAB.

Sources:

Textbookofbacteriology.net. (2017). Online Textbook of Bacteriology. [online] Available at: http://textbookofbacteriology.net/index.html [Accessed 3 May 2017].
Lactic Acid Bacteria: Microbiological and Functional Aspects, Fourth Edition
En.wikipedia.org. (2017). Lactobacillales. [online] Available at: https://en.wikipedia.org/wiki/Lactobacillales [Accessed 3 May 2017].


Can we remove impacted teeth by key hole surgery?

The impacted tooth is partially or fully enclosed in the bone. Even if accessed by a drill hole to reach the tooth. The tooth is too hard to be cut up into smaller sections with any of the conventional equipments available through an endoscope.

Tooth is a composite of three highly organized, mineralised tissues. The bulk of the tooth is formed by dentin and has around 30% organic content almost similar to that of bone. A large part of the organic content is collagen a tough fibre. Where as kidney stones etc are aggregates of minerals etc and are much more susceptible for pulverisation by shock waves from a lithotripter.

Besides an impacted tooth is either partially of fully inclosed in bone. So that too rules out the use of a lithotripter.


It looks like the parasitic wasp, Ichneumon stramentor, as found by my amazing girlfriend, and discussed on Nature Spot (UK). And it's a female to be even more precise:

  Description: Length 13 to18 mm. Female - Long tapered abdomen, first half yellow and rear half black, with yellow spot at the tip (both on the top and beneath. Legs have black femora; tibiae are half yellow blending into brown that exceeds to the tarsi. Black thorax (with yellow spot) and black head. Long dark antennae with broad white patch about half way along its length. Wings have a brownish tinge. Male has all dark antennae, no yellow spot to the tip of the abdomen. (emphasis mine)

It can be seen from April to July, commonly in meadows, hedgerows and woodland edge.

The adult wasp lays its eggs inside caterpillars which, after hatching,  eats the caterpillar from the inside. Hence the "parasitic" descriptor.

Further reading at Paul's Back Garden Safari
Wiki article on Ichneumonoidea


Can Biting Insects Detect Specific Places On A Host Body?

There are at least two sources that influence patterns of behavior: the individual that is doing the biting, and the individual that is being bitten.

The example of lice in one of the comments is a good example.  Three categories of lice that get on humans are: head lice, body lice, and pubic lice.  They are related species (possibly the same species in some cases - https://www.insidescience.org/content/are-head-and-body-lice-same-species/550), but each type has their own preference for habitat and feeding.  There are all kinds of reasons for a species to have a preference, and some stick to those preferences quite strongly.

As for your mosquitoes, their absolute preferences are still not known but blood seeking insects do have their senses attuned to clues such as carbon dioxide and heat (that help identify potential hosts) as well smells and other influences on their senses.  There might be something special about the side of your right knee as far as mosquito senses go, but not every individual in a species sees, smells, hears, etc. the same way.  My brother has a gene that makes broccoli taste very bitter, but I am fortunate to not have those taste buds.  Color blindness is another example of differences in perception, but even without being color blind, what you see as red is probably not how someone else sees red due to natural variations in the patterns of sensory cells in the eye.  For a consistent pattern of behavior from the mosquitoes, in spite of individual differences we still need to consider another source of variation that might lead to this mosquito preference: the host.

If the variation of individual mosquitoes is trumped by a consistent pattern of predation, perhaps the mediating factor is the host.  Your knee could have a special smell, or other sensory flag that attracts mosquitoes.  There are efforts to understand how a mosquito's perception directs who gets bitten: http://www.scientificamerican.com/video/future-repellents-mess-with-mosquit2013-12-23/ .  Not enough is known yet about the preferences of mosquitoes to say for sure what makes your knee so good.  There is also a chance that your knee is not special to the mosquito because it appears the most appetizing.

Host behavior is another possible influence.  The knee is just far enough away from the reach of your hands.  Conscious or absentminded grooming would both be limited at that distance.  The knee may also be better than an ankle or a foot, because of what is worn or because the knee moves less than the lower leg during walking and other movements.  If you are bitten on the lateral (outside) side of your knee, this would add evidence to this hypothesis of your movement influencing mosquito behavior, because the inside of your knee more frequently brushes against the other leg.  The frequency of the inside of the knee being a safe place for a meal is much lower.

As for why it's the right knee rather than the left, there is  possibility that that is also a reflection of you, rather than the pests.  Humans display preferences in dominance for both hands and feet.  One side of your body may be selected more often than another because of you being right- or left-handed, or right- or left-footed.  This could affect grooming habits (how you swat at the bugs), how your cross your legs, which side you carry items or lean against other objects which might brush against the body, influence how well you spray yourself with bug repellent or who knows what else.  (Just for curiosity's sake, ¿are you right-handed or are you left-handed?)

In short: There's a lot of evidence to collect before we could come to a definitive answer.  There are a lot of possibilities, including that your knee may not be the tastiest spot, but rather a relatively safe spot for dinner.

For more unempirical thoughts on the relationship of insects to the lower limbs, please see: http://fishboyridesagain.blogspot.com/2005/11/bugs-and-trousers.html


How do TLR1/TLR2 activate the MyD88 dependent pathway

The TLR are usually working as homodimers (Toll-like receptors), although TLR2 can cooperate with TLR1 or 6.
Upon binding of its ligand (this is called pathogen associated molecular pattern) the receptors change their conformation and allow binding of TIRAP (TIR adapter protein) to their Toll-interleukin 1 receptor (TIR) domain. TIRAP then recruits MYD88, which then recruits IRAK1 or 4. The signal is then passed down the pathway as shown in the figure below (taken from the Wikipedia article on TLR).


What is the formula to establish ec50 reproducibility with respect to dose response curves for some drug?

The different models that can be used to fit the curves do differ.  The linked paper and this website outline the differences; the discussion revolves around an R package called DRC but much of the information is generally applicable. Modelling can also be used to estimate ED50.

The parameters and models that are being used need to be consistent with the biology that is being studied. If it's appropriate, scaling the upper and lower bounds of your data can improve the consistency of ED50 estimates as this removes the requirement for the model to estimate those parameters. Something like this can be used for scaling;

(VALUE - topdrugmean)/(nodrugmean-topdrugmean)

The Akaike Information criterion can be used to measure the goodness-of-fit for different models (see the preceding links).


How can space travel affect women’s fertility?

The most obvious issue is exposure to radiation. Once you're beyond the earth's atmosphere and magnetic field you are exposed to much higher levels of radiation from cosmic rays and solar flares. It's also possible that microgravity (weightlessness) could have effects on the reproductive system, but this isn't well studied yet.

However, given the source you link to to (a nine year old article speculating on why China required female astronaut candidates to be wives and mothers), this may simply be a medical rationalization for a political decision. Radiation can damage male fertility too, and the effect of microgravity on the male reproductive system is also not well understood.


With all the research I did this is my understand of why the plant that was exposed to blue light grew taller than the plant that was exposed to white light.

The results of this experiment proves the hypothesis that the plant that was exposed to the blue light will grow taller than the  plant that was exposed to white light. Chlorophyll is a green photosynthetic pigment that is found in most plants. The chlorophylls are found around pigments in the photosystem, chlorophyll helps the plant to get the right wavelength of light. There are two types of chlorophyll a and b. Chlorophyll a absorbs red and violet wavelength best, but it absorbs very little blue light. Chlorophyll b absorbs a lot of blue light. Understanding chlorophyll  b will explain why the blue plant grew taller than the white plant. It grew taller because in both of the photosystems there were more chlorophyll b then a, therefore there was a lot of pigments that absorbed the blue light and the plant was able to use the energy to produce more ATP which in the end resulted in more growth.  There were many factors that we could not control  temperature, time exposed to light, moisture, earth/fertilizer used, size of potting. In order to get an accurate result of different light affecting the growth of plants some of these factors must be implemented.

Sources:
http://scienceline.ucsb.edu/getkey.php?key=3155

Can someone Confirm if this is right?


Which mammals cannot synthesize taurine?

It is a misconception that cats cannot synthesize taurine.

Cats can synthesize taurine, just like other mammals, but not enough of it to make up for an entirely taurine-deficient diet. Cats (and other mammalian carnivores) would have consumed a taurine-rich diet in the ancestral environment. It is only when they are fed vegetable/fruit/grain-derived foods that they show symptoms of taurine deficiency--because those foods have low quantities of taurine and other taurine precursors.

Other domesticated or captive carnivorous mammal species are at risk of taurine-deficiency if they are fed vegetable-derived foods, though members of the cat family (Felidae) are particularly susceptible.

Primary reference: This 2003 paper about taurine concentrations in animal feed, especially the 'Discussion' section.

  Taurine  is  an  essential nutrient of cats because the rate of taurine synthesis from its dietary sulphur amino acid precursors, cysteine and methionine, is much less than the extent of loss through faecal bile
  acids  and  urine  (Knopf et al.,  1978).  From  an  evolutionary  standpoint,  taurine  was plentiful  in  the  diet  of  a  true  carnivore,  as  high  concentrations  of  taurine  are  found  in muscle  tissue. However,  as  most  domesticated  felines  normally  do  not  consume  living
  prey, they are at risk to become taurine-deficient if not adequately supplied in the diet.


Are “tremors” and “ tetanic contractions” the same thing?

Tetanic contractions and tremor are different phenomena.
Tetanic contraction (or tetanus) refers to sustained contraction of a muscle subjected to high-frequency stimulation. With this high frequency, a new contraction begins before the previous one has ended. Thus the contractions get 'summed up'. You could see this interesting video for a demonstration.
Tremor is an involuntary shivering movement which is caused by alternating contractions of opposing muscle groups. The causes are many, ranging from physiologic tremor to degenerative disorders of the nervous system (such as Parkinson disease).
Note that tetanic contractions are not a symptom of Parkinson disease. In fact they are not a symptom of anything at all, inasmuch as they are a physiological property of isolated muscle. Tremor, on the other hand, is a phenomenon seen in muscle groups, and is one of the core symptoms of Parkinson disease.


Why does the olive tree produce a bitter tasting fruit?

You guessed it correctly: seed dispersal by zoochory, specially when the animal eats the fruit to spread the seeds (endozoochory), is an intimate relationship between the plant and the animal: the fruit has to be attractive to that specific animal, not attractive to you or me.

And, as you also seem to know, the same fruit will taste differently for different species. We could explain that using the concep of qualia (see my answer here), but the case here is even simpler: different species may have different receptors and different sensory perceptions (not sensations, I actually mean perception) for the same fruit. The most famous case is that one involving birds and chilli peppers, which don't taste hot to them (birds lack capsaicin receptors).

All that being said, olive (Olea europeae) fruits attract birds, which are their main dispersal agent (REY et al., 1997; Spennemann and Allen, 2000).

According to Spennemann and Allen, 2000:

  Worldwide, olives have proved to be a successful invader of disturbed lands, with birds as the principal seed vectors.

So, we can hypothesise that olives don't taste as bitter to birds... or, that birds do like a bitter taste. It really doesn't matter: what's important is that the fruit is eaten and the seed is dispersed.

A male blackcap (Sylvia) eating an olive. Source

Sources:

REY, P., GUTIERREZ, J., ALCANTARA, J. and VALERA, F. (1997). Fruit size in wild olives: implications for avian seed dispersal. Functional Ecology, 11(5), pp.611-618.
Spennemann, D. and Allen, L. (2000). The Avian Dispersal of Olives Olea europaea: Implications for Australia. Emu - Austral Ornithology, 100(4), pp.264-273.


It is a mulberry.  What isn't clear from the photos, and may not be clear without a DNA analysis, is whether it's a hybrid of the native red mulberry and the white mulberry imported from Asia in the hopes of starting a silk trade in North America (white mulberry is the main food source for silk caterpillars), or whether it's distinctly a red or white.  The berries won't always indicate this, and the leaves won't always indicate this.  At this point, our red mulberry has seen sufficient habitat loss that most new mulberry trees are hybrids.


That's a super low pH, and I kinda doubt it's real. If you used a cheap home test, it's more likely analytic error (not necessarily your fault, it's just a hard thing to measure) than a real result. 4.0 pH is lower than most plants can tolerate--it's in the range of vinegar. Most plants (I have no experience with this species) prefer a slightly acidic soil, ~6.8pH. So, if your pH is really 4.0, then that's almost certainly a problem. It messes up the cation-exchange capacity of the soil, so even if you fertilize, the plant can't access the nutrients.

You can easily amend with some lime--if you don't want to dig it up, you can just scratch it into the top of the soil, and water through it. It will leech down through the pot. Hope that helps.


Can someone help me answer or explain how to answer questions about DNA coding capabilities?

4 bases (A T C G) leads to 4 possible value per bit of information, which then leads to the formula: 4^n (n being the number of base). For the first part of your question regarding how can you have so much information, it has to do with n, as you increase the number of bases the number of different combinations increases exponentially. For a comparison, your computer stores information in a 2 value bit system (1 or 0).

If you plot the number of possibilities, you will see that DNA outpace computers very quickly, as an exponential of base 4 will go faster (2*2 = 4, 4*4 = 16, already at 2 bits you have 4 times as many possibilities)

With that in mind, you can compute the number of possibilities for any given number of bits (or bases in your case).


Genetics - Is this hybridization possible?

Flower Color

A Heterozygous (Rp) x Homozygous recessive (pp) cross can produce the distribution:

         p      p

   R    Rp     Rp  = Red, Red

   p    pp     pp  = pink, pink

Stalk Length

To me, there appears to be another allele involved or a lack of allele, and definitely Co-Dominance. The only way I could think of a way to get the ratio of stalk lengths in the question after a few minutes thought is if one of the plants are missing a gene before the cross (akin to Turner Syndrome) - the example that follows puts the missing gene on the Short-stalked parents:

SS = Short
TT = Tall
ST = Medium
SX = Short
TX = Tall
X = Missing Gene / Nothing

         S      X

   T    ST      TX = Medium, Tall

   T    ST      TX = Medium, Tall

So ultimately the cross would look like this:

        Sp     Xp

   TR   STRp   TXRp = (#3), (#1)

   Tp   STpp   TXpp = (#4), (#2)


Crossing over primarily happens because of homologous recombination (HR). From the molecular point of view, it can happen between any homologous regions and it is not necessary that an entire allele has to be crossed over. During the process of HR, a DNA double strand break occurs. This is followed by resection (exonucleolytic degradation of one of the strands — 5'→3', from the break-point) by the MRX complex which leads to formation of ssDNA ends. The length of these ssDNA ends dictate the total length of crossover region.

   Taken from: Branzei, Dana, and Marco Foiani. "Regulation of DNA repair throughout the cell cycle." Nature reviews Molecular cell biology 9.4 (2008): 297-308.

This length can be from around 1.5kb to over 10kb depending on the repair kinetics with possibly an average of 3kb (more than half the cases) [1, 2]. Therefore, the author speculates that the probability of intra-gene crossover would increase with increase in intron length. However, in my knowledge, there are no recent reports to validate this hypothesis.

Edit:

Going back to the original question. It is not necessary that entire alleles are crossed over. Generally the genome has some recombination "hotspots" flanked by what are known as LD (linkage disequilibrium) blocks. An LD block need not cover an entire gene, as observed by Twells et al. (2003)[3] :

  LD breaks down in the region LRP5 g.5257T → G–LRP5 g.28149C → T, in
  intron 1 of theLRP5 gene. A second block of very strong LD
  (‖D'‖ > 0.9) is observed, LRP5 g.28149C → T–LRP5 g.45704G → A,
  spanning 17.6 kb of intron 1 to intron 3 of the LRP5 gene.

References:

Chung, Woo-Hyun, et al. "Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting." PLoS Genet 6.5 (2010): e1000948.
Zhou, Yi, et al. "Quantitation of DNA double-strand break resection intermediates in human cells." Nucleic Acids Research (2013): gkt1309.
Twells, Rebecca CJ, et al. "Haplotype structure, LD blocks, and uneven recombination within the LRP5 gene." Genome Research 13.5 (2003): 845-855.


Do all mushrooms have the same multicellular ancestor?

All fungal species within the kingdom have the same common ancestor, which is unicellular (thought to be protistan). This common ancestor is the point at which it is thought that animals diverged, as suggested by this article.
In their words:

  It is now well established that animals share a common single-celled ancestor with fungi, and that in the two sister lineages multicellularity arose independently

A fungal phylogenetic tree is shown below, which originated from this paper.

Note: all colored areas represent different phyla of fungi.

EDIT:

I will respond to a few questions addressed in the comments.

  Is there a unique multicellular ancestor to all mushrooms?

I am rather sure (but can't explicitly confirm with a reference) that multicellularity in fungi only evolved once. If this were true, I would also hypothesize that mushroom-like characteristics also evolved only once, thus indicating that there is a multicellular ancestor to all mushrooms.

  Are there multicellular fungi outside dikarya?

No. One branch of dikarya seems to consist of only unicellular organisms, suggesting that multicellularity evolved at some point within organism under only one dikaryan branch.

  Was the common ancestor of Dykarya multicellular?

No. See previous answer.

  Are those unicellular dykaria secondary unicellular or not? Given that the both branches of dykaria show similarities in fruiting bodies, it seems to be plausible that the common ancestors of dykaria had a similar structure.

I am not exactly aware of the similarities in fruiting bodies in both branches, but if the physiology behind fruiting bodies are similar, it is very likely because the dikaryan common ancestor had a similar mechanism.


What is this microscopic image from Peter Gabriel's New Blood album cover?

This is an embryonic stem cell on the tip of a needle photographed on a scanning electron microscope (SEM). The image was taken by Steve Gschmeissner, see here for the original.


Do desulfhydrase-catalysed reactions take place in animal cells?

A desulfhydrase catalyzes the removal of hydrogen sulfide from a compound. So the answer is yes, but it's not the most-commonly annotated reaction for the enzyme cystathionine gamma-lyase.

I didn't know off-hand. Here's how I answered the question:

I searched Entrez Protein (or NCBI...whatever the thing's called) with the following terms:

(desulfhydrase) AND "Homo sapiens"[porgn:__txid9606]

And got three hits for isoforms of cystathionine gamma-lyase. I clicked on one of them and started reading. Key things I noted:

  EC_number="4.4.1.1"

  ...

  Cystathionine gamma-synthase is a PLP dependent enzyme and catalyzes
  the committed step of methionine biosynthesis. This pathway is
  unique to microorganisms and plants, rendering the enzyme an
  attractive target for the development of antimicrobials and
  herbicides.

So it's a good question because, if people normally characterize this enzyme in terms of Met biosynthesis, then we don't have a desulfhydrase. But I trusted the thing was annotated properly and that the comment above was just too medicine-oriented (as much biochemical literature is).

So to really understand the enzyme itself I searched MetaCyc for the Enzyme Commission identifier 4.4.1.1.

This let's me easily visualize the catalyzed reaction. And the annotation spells it out clearly:

  Enzyme Commission Summary: A multifunctional pyridoxal-phosphate
  protein. The enzyme cleaves a carbon-sulfur bond, releasing L-cysteine
  and an unstable enamine product that tautomerizes to an imine form,
  which undergoes a hydrolytic deamination to form 2-oxobutanoate and
  ammonia. The latter reaction, which can occur spontaneously, can also
  be catalysed by EC 3.5.99.10, 2-iminobutanoate/2-iminopropanoate
  deaminase.

  Also catalyses elimination reactions of L-homoserine to 2-oxobutanoate and ammonia, of L-cystine, producing thiocysteine,
  pyruvate and ammonia, and of L-cysteine, producing pyruvate,
  hydrogen sulfide and ammonia.


A question regarding trichomes in plants

Trichomes can serve the purpose you ask about, but certainly not only that. They also appear on a great many other, some very delicate, plants from many different habitats. Decreasing water loss is only one of a number of different functions they might serve.

But with respect to xerophytic plants, trichomes are still a projection from the leaf surface and so, by definition, increase the surface area of a leaf by a significant amount.  However, it's not the surface area per sé that leads to water loss, it's increased evapotranspiration which can be caused by and mitigated by many different factors, one of which is, indeed, trichomes.

Some trichomes, such as those on Tillandsia species, occlude or reflect light.  This reduction in incident light is primarily what protects the leaf tissue from damage and helps reduce water loss due to heat. Such trichomes may also function, as you mention in your question, by creating a insulating layer of still air around the leaf, thereby reducing diffusion of water vapor away from the leaf and creating a smaller gradient, though this is usually not their primary function.


How large an expression boost is typical from codon optimization?

I think that there is a problem with how well current codon optimization algorithms actually "optimize" protein expression. I am not aware of any algorithms that work beyond a heuristic level and so for an arbitrary protein, one cannot predict the expression boost that optimization will provide - sometimes yield is significantly decreased. This review covers some of the complexities of optimization really nicely https://doi.org/10.1016/j.molcel.2020.09.014.


From Merriam-Webster:

Definition of pore
1 :  a minute opening especially in an animal or plant; especially :  one by which matter passes through a membrane

The blastopore is a real thing, it is not imaginary. It is the point where the mouth or anus eventually develops. I'm guessing the reason your zoology class referred to it as imaginary, however, is probably because it isn't really a pore (and especially it is not a pore into the blastocoel). It sort of looks like a pore, but it's just a little indentation (and may even be considered a blastopore before the indent forms); it doesn't really become an opening until later, and the process of gastrulation doesn't actually involve anything going inside the blastopore, it's just a folding in of the cells on themselves.
In summary, I think your understanding is sound, good job, and I just wouldn't get too hung up on the "imaginary" part.


Why it is so difficult to treat leukemia?

The T315l mutation of BCR/ABL gene produce the complete resistance of CML leukemia to all currently available BCR/ABL inhibitors.

There is a idea that is not yet tested for such patients - allogenic hematopoietic transplatation.

More information:
http://www.ncbi.nlm.nih.gov/pubmed/20657522
http://www.ingentaconnect.com/content/maney/hem/pre-prints/1607845412Y.0000000050


What is the benefit of fever during infections?

Fever is a trait observed in warm and cold-blooded vertebrates that has been conserved for hundreds of millions of years (Evans, 2015).

Elevated body temperature stimulates the body's immune response against infectious viruses and bacteria. It also makes the body less favorable as a host for replicating viruses and bacteria, which are temperature sensitive (Source: Sci Am).

The innate system is stimulated by increasing the recruitment, activation and bacteriolytic activity of neutrophils. Likewise, natural killer cells' cytotoxic activity is enhanced and their recruitment is increased, including that to tumors. Macrophages and dendritic cells increase their activity in clearing up the mess associated with infection.

Also the adaptive immune response is enhanced by elevated temperatures. For example, the circulation of T cells to the lymph nodes is increased and their proliferation is stimulated.

In fact, taking pain killers that reduce fever have been shown to lead to poorer clearance of pathogens from the body (Evans, 2015). In adults, when body temperature reaches 104 oF (40 oC) it can become dangerous and fever reducing agents like aspirin are recommended (source: eMedicine)

Reference
- Evans, Nat Rev Immunol (2015); 15(6): 335–49


Can you help me identifying this spider?

I tried to identify it by your photo via Seek app and the result is "cross orbweaver / Araneus diadematus

The result seems true when it's compared to description in this site

For comparision see this image:


How does the brain train its neural network?

The answer to this question is probably Hebbian Learning.

Hebbian learning can be nicely summarised with "Cells that fire together, wire together". So basically the synapses of neurons are strengthened if they fire in sync, and weakened otherwise.

One can easily see that a) this kind of local learning mechanism makes a lot more sense for the brain then some global method like gradient descent and b) this mechanism leads to stable representations of patterns.

In artificial neural networks this kind of learning is modelled in Hopfield networks and Restricted Boltzmann Machines.

Of course this simple rule barely scratches at the surface of what goes on in the human brain, when we are learning something. A complete picture would probably involve complex feedback mechanisms of inhibitory and excitatory connections between neurons, functional modules of neurons, and different parts of the brain.

But I fear these details are not yet well understood …


What is neutral genetic differentiation?

Neutral genetic variation is variation that has no effect on fitness. I suggest reading more about neutral theory on wikipedia.

Neutral genetic differentiation is a way of talking about neutral genetic variation that follows some historical pattern, for example two populations isolated from each other for a long time will show neutral genetic differentiation even if they are individually in Hardy-Weinberg equilibrium. In other words, the two populations will have somewhat different allele frequencies from each other for no reason related to natural selection but rather because of random sampling and genetic drift over time.

It is generally thought that most genetic variation is neutral or nearly neutral. For example, most of the human genome is useless DNA or genomic parasites such as transposons. Almost all of the genetic variation that happens in those regions is not important to human fitness, in other words it is "neutral".


Increasing/decreasing signal intensity in Western blotting

There are several different places in a typical Western blotting protocol where conditions can be altered to modulate signal intensity. The first is the amount of protein loaded - more protein will give a stronger signal, less will give a weaker signal. However, too much protein can result in indistinct bands, increased background, lane distortion, and other issues.

The next condition to change is the amount of primary antibody and the incubation buffer. More primary may lead to an increased signal, but too much can give higher background. Some antibodies give a better signal when diluted in BSA, others when diluted in nonfat dry milk. Generally, milk will give you a cleaner blot, but may reduce the signal. Incubation time can also affect specificity and signal intensity - some antibodies will fully bind with a 1-2 hour incubation at room temperature, others require an overnight incubation at 4°C.

The third condition to alter is the amount and type of secondary antibody. Increasing the amount of secondary may increase signal, but again may result in increased background. There are also different types of secondaries, depending on your detection system - HRP for chemiluminescent detection, AP for colorimetric, fluorescent tags for imaging systems, etc. These have different sensitivities, but can also result in increased background, depending on the other conditions of the protocol.

Finally, the type of detection system can affect sensitivity. For example, when using standard HRP-conjugated secondaries, there are numerous different ECL substrates with widely varying sensitivities. Here is a list of different systems available from Thermo/Pierce, ranging from standard ECL to Femto.

So, while Western blotting seems like a fairly straightforward procedure, there are many places to optimize the conditions to get the results you're looking for.


Importance of Double Helix DNA Structure

The structure allows for the DNA to be tightly packed into chromosomes. It also provides an extremely stable backbone with the negatively charged phosphates pointing to the outside of the molecule. This charge aids in the attachment of other molecules to the strand of DNA.

DNA double helix allows it to be stable and it won't easily destroyed.


Can a fungus become resistant to a chemical such as Potassium Permanganate?

I don't think a fungus would develop resistance to something so quickly.
As Chris suggested in the comments, it could be because "The disinfective effect is based on the production of reactive oxygen species. The problem is that the solutions used for this purposes are not very stable." So, if fresh solution haven't been used, it may be ineffective.
As commented by @inf3rno, fungal infections could be much deeper and hence, "treating" them superficially may not help much.


Actually, nesting failure means that nesting trial fail before offspring could even leave the nest. In case of precocial species (where chicks leave nest immediately after hatching, like swans) it means that eggs was destroyed or parents abandoned nest, as @nico point out. In case of altricial birds (offspring stay in nest) nesting failure may also mean that all nestlings died before leaving nest.

for example among House wrens (Belles-Isles & Picman 1986):

  About 81%
  of nesting failures (n = 30) were due to predation (contents disappeared before the expected fledgingdate). Females abandoned seven nests, and starvation (presumably because
  of desertion by parents) accounted for one nesting failure.


If DNA is the input, what is the output?

The central dogma of molecular biology states that DNA encodes the information for building proteins, the information is copied to messenger RNA through transcription, and messenger RNA is used to build proteins through translation. DNA is also copied through replication.

So while it's true that DNA contains the information needed to build a living organism, I don't think it can described as "turing tape" If I understand turing machines correctly, you have a string of 1s or 0s, and a machine reads this string. Based on rules provided by an instruction set the machine can set positions on the tape to 1 or 0. The analogy with DNA fails because DNA does not have a separate instruction set and cannot be written to. DNA produces RNA and DNA with the help of many many proteins and other molecules, all tightly regulated to coordinate replication of the genome and to produce the right amounts of RNA and protein at the right times. DNA can mutate when replication makes an error, but this is accidental, not comparable to turing machines.

If you're interested in how DNA might be used like a computer, there are several articles on DNA Computing, though you'll have to sort through those papers because many look like they just used a computer to analyze DNA.


meaning of "usually greater than 200 base pairs"

No, similarity is not measured in base pairs. They are talking of regions of cross-over being marked by at least 200bp of highly similar sequence between the two strands involved in exchange.


Do we need to drink less water in humid weather than in dry weather?

You don't get hydrated by breathing moist air. That may at best hydrate your respiratory tract. You should drink more water in dry weather because the body gets dehydrated more.

Humid weather is not hotter, it just feels more uncomfortable. But dry heat is actually more harmful, because it dehydrates you (not in the sense of extreme heat).


Do distinctions between dry, tickly and chesty coughs have any medical basis?

If I may add to what Resonating has said, when it comes to infections, dry cough is usually associated with a viral infection, whereas wet cough is usually caused by bacteria. The two are treated very differently - dry cough is remedied with cough-supressing drugs (antivirals are rarely needed), whereas bacterial infections are medicated with antibiotics (antivirals are NOT antibiotics) and drugs that help clear the mucus from the respiratory pathway. Treating wet cough with dry cough medications is not only ineffective, it can also be dangerous. One more thing - not all bacterial infections necessitate antibiotics which should be used sparingly because the world is running out of antibiotics.


In a human, what non-germline cells have the highest/lowest mass?

Large cells: adipocytes, the cells that store fat are possible the largest in humans, because after puberty they rarely divide and just enlarge if a person gains weight. A typical adipocyte is about 0.1mm in diameter, but may be a lot larger. Another good candidate is a megakaryocyte, which is a gigantic (up to 0.1mm), cell with multiple copies of its genome producing blood platelets. Depending on your definition of a single cell, also myocytes may be considered large cells, because during development several cells fuse to form one muscular fibre. Additionally, myocytes gain weight if a person excersises and strengthens muscles.

Small cells are more common, and it is difficult to point to some consistently smallest cells. The smallest kind-of-cells are definately platelets and erythrocytes (red blood cells - they are anucleated, thus may not be considered "real" cells). Generally, the part that determines the minimum size of the cell is the nucleus, so any cells, that are more-or-less metabolically inactive may be just a tiny bit larger than the size of their nucleuses. These may be for example polar cells, the tiny cells, that carry the excess of genome during meiosis in women and die soon afterwards.

If you are interested in all kinds of strange cells inside yourself, you might start by browsing this beautiful, though longish list.


I did find an article which mentions the venom strengthening:
http://www.sciencedaily.com/releases/2012/06/120605102638.htm

It may be an evolutionary bonus. Snakes with the most potent venom may leave fewer survivors, particularly with something like humans who would hunt down a snake if they could find it. A snake which leaves fewer survivors may be better able to escape. It may also have more successful hunts which may have been what lead them to become poisonous to begin with.

Unlike the antibiotics arms race against bacteria, it's unlikely that antivenoms are the cause of more dangerous snakes.

As far as "centuries from now" we really can't hypothesize whether more potent venom will continue to be a more helpful evolutionary trait. More potent venom doesn't have an infinitely continuing effectiveness. After a certain point, whatever bitten isn't any more dead with a stronger poison.