How to calculate apparent diffusion coefficient (ADC) with example?

Do you like R ? if so, look at this package "dcemriS4"  and its example http://www.inside-r.org/packages/cran/dcemriS4/docs/adc.lm

install.packages("dcemriS4")
install.packages("minpack.lm")
library(dcemriS4)
library(dcemriS4)

S0 <- 10
b <- c(0, 50, 400, 800)  # units?
D <- 0.7e-3              # mm^2 / sec (normal white matter)

## Signal intensities based on the (simplified) Bloch-Torry equation
dwi <- function(S0, b, D) {
  S0 * exp(-b*D)
}

set.seed(1234) # this is just to make the example reproducible
signal <- array(dwi(S0, b, D) + rnorm(length(b), sd=0.15),
                c(rep(1,3), length(b)))
ADC <- ADC.fast(signal, b, array(TRUE, rep(1,3)))
unlist(ADC) # text output
par(mfrow=c(1,1)) # graphical output
plot(b, signal, xlab="b-value", ylab="Signal intensity")
lines(seq(0,800,10), dwi(S0, seq(0,800,10), D), lwd=2, col=1)
lines(seq(0,800,10), dwi(ADC$S0, seq(0,800,10), ADC$D), lwd=2, col=2)
legend("topright", c("True","Estimated"), lwd=2, col=1:2)

Here you can see an example of the steps used for mir http://rsl.stanford.edu/moseley/tensorcalc/tensorcalc/Steps/ADCmaps/adc.html

here is to understand the math behind of its calculation
http://www.ajronline.org/doi/full/10.2214/AJR.12.9231

if you don't like R but you like Matlab, here you can use this code to calculate it in Matlab http://www.mathworks.com/matlabcentral/fileexchange/21130-dti-and-fiber-tracking/content/DTI.m one of the output is ADC for mir data


Identification of an insect from midwest US

Brown marmorated stink bug (Halyomorpha halys):

See here, here, here or here for information.

These have become hugely invasive in the Northeast and Mid-Atlantic (and slowly Southeast) portions of the U.S. as well as along the West Coast.

The brown marmorated stink bug (Halyomorpha halys) is native to Eastern Asia, and likely 1st started spreading around the U.S. in Pennsylvania in the early 2000s.

Finally, you can see an image of the life stages of H. halys here.

Update:

Just for clarification, other brown stink bugs do exist and can be easily confused with H. halys. This article from UF IFAS, for example, demonstrates how to differentiate H. halys from Euschistus servus:

See here and here for additional ID tips and further reading.


How did Shulgin take cognizance of the dosage of a new substance?

He didn't.
It was basically a matter of trial and error. Of course, having previous experience with other psychotropics of the same class helped him to have a rough estimate: in the case of MDMA, Shulgin was neither the first one to synthesize it nor the first one to use it, and he knew beforehand that the psychoactive dose was between 100 and 200 mg. Besides that, being a rational chemist, he started by what he supposed to be the smallest, safe dose.

Alexander Shulgin
For instance, regarding MDMA, Shulgin (2010) describes the following dosages (I'm copy/pasting only the start of each paragraph):

(with 100 mg) Beforehand, I was aware of a dull, uncaring tiredness that might have reflected too little sleep, and I took a modest level of MDMA to see if it might serve me as a stimulant...
(with 120 mg) I feel absolutely clean inside, and there is nothing but pure euphoria...
(with 100 mg of the "R" isomer) There were the slightest of effects noted at about an hour (a couple of paresthetic twinges) and then nothing at all...
(with 160 mg of the "R" isomer) A disturbance of baseline at about forty minutes and this lasts for about another hour...
(with 200 mg of the "R" isomer) A progression from an alert at thirty minutes to a soft and light intoxication that did not persist...
(with 60 mg of the "S" isomer) The effects began developing in a smooth, friendly way at about a half-hour....
(with 100 mg of the "S" isomer) I feel the onset is slower than with the racemate...
(with 120 mg of the "S" isomer) A rapid development, and both writing and typing are impossible before the end of the first hour...

Unfortunately, he doesn't explicitly say what was the sequence of the dosages he took... I can only assume it was the sequence of the paragraphs.
However, by far, the best example of how "blind" the chemist is regarding the adequate dosage of a unknown psychotropic is the famous case of Albert Hofmann, who invented LSD (not as a psychotropic) in 1938.

Albert Hofmann
When he decided to test LSD, in 1943, he ingested 250 micrograms... well, that's almost ten times a typical "street" dose of LSD nowadays, which is around 20 micrograms. Luckily for him, overdose of LSD (up to more than 100 times the amount he used) is not lethal.

Source: Shulgin, A. and Shulgin, A. (2010). Pihkal: A Chemical Love Story. Berkeley: Transform.


Why is there an increase of diagnoses of Lyme disease?

One of the opinions expressed on the CDC website is that the increase of diagnosis of the Lyme disease could be accounted to expansion of ticks:

  Since the late 1990s, the number of reported cases of Lyme disease in the United States has tripled and the number of counties in the northeastern and upper Midwestern United States that are considered high-risk for Lyme disease has increased by more than 300%. One explanation for this trend is that the ticks that can transmit Lyme disease have expanded their geographic range and are now being found in places they weren’t seen 20 years ago. --Rebecca Eisen, Ph.D. (source)

I have also found a report containing another possible explanation:

  Areas of patchy woods, which are very common in cities and suburban and rural areas, may have higher populations of Lyme-disease carrying ticks than forest fragments, which generally have fewer species than continuous habitat. This is because some species thrive in smaller places.

  White-footed mice, for example, are more abundant in forest fragments in some parts of the country, likely because fewer predators and competitors remain there. These mice are particularly abundant in patches smaller than about five acres, which could spell trouble for people living nearby: the mice are the main carriers of Lyme disease-causing bacteria. In the eastern and central United States, Lyme disease is contracted via blacklegged ticks that feed on infected mice, then transmit the bacteria when the ticks bite people. As a result, says biologist Felicia Keesing of Bard College in Annandale, New York, Lyme disease is concentrated in areas where people live near forests with blacklegged ticks.

  Keesing, scientist Richard Ostfeld of the Cary Institute in New York and other researchers found that smaller forest fragments had more infected ticks, which could translate to more Lyme disease. Forest patches that were smaller than three acres had an average of three times as many ticks as did larger fragments, and seven times more infected ticks. As many as 80 percent of the ticks in the smallest patches were infected, the highest rate the scientists have seen. These ticks may also be infected with other emerging diseases--Babesiosis, Anaplasmosis and Powassan encephalitis--therefore, forest fragmentation might also be contributing to other serious illnesses, Ostfeld says.

  "Our results suggest that efforts to reduce the risk of Lyme disease should be directed toward decreasing fragmentation of deciduous forests of the northeastern United States, particularly in areas with a high incidence of Lyme disease," says Keesing. "The creation of forest fragments smaller than five acres should especially be avoided."

EDIT: Another article on Vox also provides some possible explanations including the global warming, reforestation of farms and increase in the number of deers (caused by hunting protections).


Do white Australians have a distinct look?

Yes, it is possible (on some average basis, i.e. with chance better than random).

Take a look at average women faces from 41 different countries (AFAIK created with Face Research software; sadly no picture for Australia). Clearly, even from small and nearby European countries you can spot differences (which work on the average). I guess the case of Austriala vs other countries isn't an exception. Similar face averages are also on the project Face of Tomorrow.

However, when dealing with a single subjects it it may be not a reliable method to tell of his/her nationality or country of origin, as:

even within an relatively isolated group there is variance in genotype and phenotype,
people do move (especially now) and do mix (so unless you are comparing isolated islands you should't expect to have homogenous genotype).

Moreover, when identifying a person we may (even subconsciously) look at different features (including clothes, accent, behaviour, context, ...).


Could tumor cells have normal genomic profiles?

I think this is the paper about the Ampli LowPass sequencing technique. Although, I didn't read it thoroughly but from the abstract and result section titles, it appears that this technique is designed for detecting CNVs. Since it is low pass (i.e. low coverage), it may not detect substitutions and small indels accurately.

Your cells may have mutations but not big chromosomal rearrangements. It is not necessary for tumour cells to have such chromosomal aberrations. In fact a simple overexpression of an oncogene or a point mutation causing reduced/loss of activity of a tumor supressor (for e.g. p53) is enough for tumorigenesis.


This is a fascinating set of questions.  The only one I can comment on is: is KD qualitatively similar to KO?

My answer is: sometimes yes, in general no.  To understand why, I like to think of a hypothetical plot of "phenotype of interest" on the y axis, and "expression of gene" on the x axis.  You can imagine that this plot could be monotonic, i.e. that the phenotype continuously increases or decreases as expression increases.  Or it is also possible that this plot could have one or more minima or maxima in it.  One example of KD giving dissimilar results from KO is for essential genes.  If they are knocked out, they of course kill the organism.  However, there may be some levels of essential gene knockdown for which the phenotype is actually increased relative to wild-type!

I will selfishly share one of my articles where I observed something like this.  We found that ADH1 knockdown improves butanol tolerance in yeast, but that ADH1 knockout was highly detrimental to butanol tolerance.  http://dx.doi.org/10.1007/s10295-015-1713-7


Why is your taste affected due to sinuses?

The first thing which is important to note is the difference between taste and flavor.
Taste refers to the chemical sense performed by taste buds present on the tongue, and to date there have been identified 5 tastes: sweet, bitter, sour, salty and umami. Thus I understand obstructed nose and sinuses should have no significant effect on taste.
Flavor, on the other hand, is the final sensation that conveys the information about the food we're eating, and involves not only taste, but also smell, mechanical sensation (like that smooth flavor from cream) and pain and temperature pathways (hot and spicy food, like peppers). Part of the signals from all these receptors located on the mouth (and nasal) cavity ultimately converge to the same location in the brain, where they are processed to create the final flavor (I know taste and smell do converge to the same region, cannot tell the others with full certainty).
So, having obstructed sinuses and nasal cavity can interfere with the smell detection (by not allowing molecules to bind to receptors on the olfactory epithelium), and thus interfere with flavor.

You can check this site which I think explains very well what I am trying to pass on, it is very clear and covers all the physiology that I talked about, allowing you to go deeper into details if you are interested: http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/taste.html and also http://www.cardiff.ac.uk/biosi/staffinfo/jacob/teaching/sensory/olfact1.html (you have to scroll down to the main text)


How to increase the shelf life of yogurt without refrigeration?

This article gives an excellent review on yogurt manufacturing, but to summarize:

-Raw milk goes through centrifugation to remove somatic cells and other solid impurities.
-Thermalization is conducted at "60–69 °C for 20–30 s, aiming at the killing of many vegetative microorganisms and the partial inactivation of some enzymes."

After this point, the milk may be inoculated with lactic acid bacteria or other microfloras.

-Then, standardization occurs which for milk refers to the standardization of fat and solid-non-fat content (SNF).  This in short affects the fermentation process ("an increase of SNF increases the duration of the fermentation process").

-The next step is homogenization, which prevents milk fat from rising to the top of the liquid.  This has an effect on the stability of the emulsion.

-I think this step is where "sterility" comes into play, "heat treatment of milk reduces the number of pathogenic microorganisms to safe limits for the consumer’s health. Various heat treatments can be applied, which are classified based on the duration and the temperature. The most common are known as thermalization, low and high pasteurization, sterilization and UHT (Ultra Heat Treatment)."  The review goes into more detail about each type and what they eliminate or don't eliminate (spores, vegetative bacteria, etc.).

-The fermentation process is the most important one for developing flavor and texture.  The two live bacterial strains of Streptococcus salivarius subsp. thermophilus (ST) and Lactobacillus delbrueckii subsp. bulgaricus (LB) are the two most basic strains used in yogurt.  LB is what metabolizes lactose into lactic acid and LB and ST acting in synergy is what causes a decrease in milk pH.  "When the pH of the yogurt approaches 5.0, activity of ST subsides and LB gradually dominates the overall fermentation process until the target value of pH is reached and the fermentation process ceases. Normally, the fermentation period is terminated by lowering the temperature to 4 °C. At this temperature, the culture is still alive, but its activity is drastically limited to allow controlled flavor during storage and distribution."  I think to answer your question, yogurt manufacturers probably have a very sensitive gauge for pH and can control temperature fluctuations finely to maintain yogurt pH and flavor (not too sour).  "After the pH of yogurt reaches the value of 4.7–4.3, the yogurt is cooled to around 5 °C. This inhibits the growth and metabolic reaction of the starter culture and prevents the rise in acidity. Cooling of yogurt can be in one or two phases. One-phase cooling involves the rapid decrease of the coagulum temperature to less than 10 °C, where the fermentation process is inhibited leading to yogurt with low viscosity. Two-phase cooling is initiated by rapidly decreasing the temperature to less than 20 °C and then gradually reaching the storage temperature of 5 °C leading to yogurt with an increased viscosity and limited syneresis. This is quite common in the yogurt manufacture process, especially when fruits are to be added."

You can read about the other innovative methods involved in yogurt making such as: Ultra High Pressure (UHP) which inactivates pathogens and microorganisms that cause milk to spoil, High Intensity Ultrasonication and Pulsed Electric Field (PEF) which all can reduce microbial content.

Edit: Forgot to mention that some DIY yogurt instructions mention that if you ferment longer and/or in warm temperatre the more sour it will be so to reduce how sour it is, either ferment it less and/or start fermentation at a lower temperature (source).

Sfakianakis P, Tzia C. Conventional and Innovative Processing of Milk for Yogurt Manufacture; Development of Texture and Flavor: A Review. Foods. 2014; 3(1):176-193.


How to automatically obtain the "kingdom" of a species from its name?

You could try the Catalogue of Life

  The Catalogue of Life is the most comprehensive and authoritative global index of species currently available. It consists of a single integrated species checklist and taxonomic hierarchy. The Catalogue holds essential information on the names, relationships and distributions of over 1.6 million species. This figure continues to rise as information is compiled from diverse sources around the world.

You can export the search results (in the above example indicating Kingdom Plantae for search term "Prunus persica") and analyze the exported table in your program of choice.


How does one calculate the amount of oxygen produced by trees?

With detailed mechanistic models. There are a huge number of variables here, and you'll need to account for nearly all of them. Here is a similar project for crops.

You could try this model for a single tree but I don't envy trying to scale that up to entire countries.

Just to ballpark some figures, you could consider photosynthetic efficiency, average insolation, and shading effects. X amount of light falls on this country on average, and of that light .1% is converted into oxygen, so that's how much oxygen is made.

You could also approach it from the other direction and estimate how much each tree weighs. Tree dry weight is going to be mostly carbon, and necessarily nearly all of those carbon atoms were once carbon dioxide and represent one O2 molecule each. This approach has the advantage of taking into account respiration, unlike the light approach. The light approach measures total oxygen produced, but the carbon approach measures total oxygen released.


For DNA replication and transcription you need NTPs. In a dsDNA purine content will be same as pyrimidine content. I am considering that all nucleotides are synthesized de novo which would consume more ATP than getting nucleotides from the salvage pathway.

  Fig 1: Pyrimidine synthesis. Taken from Wikipedia.

  Fig 2: Purine synthesis. Taken from Wikipedia.

CTP synthesis requires one extra ATP:

UTP + Glutamine + ATP + H2O → CTP + ADP + Pi

UTP synthesis requires 2 (Step 1; Fig 1) + 1 (Step 5; Fig 1: PRPP requires 1 ATP to form) +  2 (UMP → UTP) = 5 ATPs

CTP requires 6 ATPs

GTP requires 8 ATPs (Fig 2) (ATP synthesis would also require 8 ATPs but for simplicity let us assume that ATP is already present).

Conversion of dNTP from NTP requires thioredoxin which in turn requires NADP but let us forget that.

Assuming a 50% GC content one base pair of DNA would require in an average 10 ATPs (assume a stretch of 4nt — ACTG, this would require 1+6+5+8 ATPs; i.e. 5 ATPs per nt; 10 ATP per bp)

For RNA the ATP consumption would be 5 ATPs per nt.

For protein synthesis, for every codon, the elongation factor requires one molecule of GTP and aminoacyl-tRNA synthetase requires 1 molecule of ATP. So the net consumption per amino acid would be 9 ATPs.

I am ignoring the initiation reaction that also requires ATP to phosphorylate the initiation factor. Also, I assume that amino acids are obtained from diet and are not synthesized by the organism.


Examples of things that are undefined in terms of living and non-living

People expect viruses to be alive but they are defined as non-living.

This is actually one of the most widespread misconceptions I see. I think it's just one of those interesting but dubious factoids that spreads around in dinner party conversations. There certainly are some who take that position. But, after 11+ years of formal university education in biology, I can't think of a single professor or colleague who firmly embraced the position that viruses are non-living. Most (including myself) have been firmly in the camp that viruses are, in fact, alive. And the rest are more-or-less agnostic or ambivalent on the topic.
There's an intesting mini-debate between experts on the subject found here, I'll share this quote from one of the participants below because I think it's on point.

"In many ways whether viruses are living or non-living entities is a moot philosophical point."

There isn't one single, universally accepted definition of life. So ultimately, the answer to whether viruses are living or not will depend on ones chosen definition, and that's the case with most other controversial things.
However, viruses are unquestionably classified as biological replicators. There's a review on that topic (found here). It also includes discussions of other replicators which some experts also think of as living entities (but many don't). Examples include certain genetic elements like plasmid and integrons.
One notable exception that I didn't see mentioned in that review is prions. The first virology professor I ever had strongly advocated definitions of life that were inclusive of prions, but I haven't found that position quite as common among other academics. I'm a bit more agnostic on the prion debate, because it's hard to find prion-inclusive definitions of life that arean't also inclusive of something like an inorganic crystal.
The problem is that scientists like consistent definitions that don't have lots of exceptions, or require us to split existing categories. Between viruses, plasmids, and prions, there's a lot to talk about in terms of what characteristics they share with other life forms and what they lack that makes some question their classification. It's also interesting to consider whether any of the attributes common to living things occur in silico (or if they could in the future).


How does "inheritance of methylation" of DNA and/or histones work?

Jon Wilkins has a nice introduction to imprinting.  He does a nice job of introducing the idea methylation and how these patterns are maintained during development and cell division.  Further, he links to some interesting papers on the subject.


Can someone tell me what kind of reptile is this?

My guess is that you have in your a hand a lizard of the Genus Sceloporus , and perhaps Sceloporus occidentalis longipes.

Commonly called the Great Basin fence lizard is a subspecies of the western fence lizard . It is genrally found in the western part of North America

Here is  a link to a guide of small spiny lizards .


Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?

Hospitals have certain features:

They are full of people immunocompromised in some way (old, exposed tissue, on steriods etc.)
They are full of people with pathogens
They are full of doctors who will give antibiotics to people with pathogenic infections

This is a perfect breeding ground for drug resistance in pathogens, with lots of pathogens, lots of places for them to grow (patients) and quite a lot of exposure to antibiotics.  You use Staphylococcus aureus as an example, and it is a good one.  We all have some of it on us, but it is not generally exposed to antibiotics so it does not develop resistance, and we do not generally have large areas of exposed flesh that would cause it to be pathogenic.  In hospital this is not the case, so we get it causing trouble and developing resistance.

These things do occur outside of hospitals, but it does not tend to be as common or frequent.


What is the defining characteristics of a Gap Species?

The previous answer from @Ark Lomas is true to the extent that gap-loving refers to preference of an open habitat. It was found that these species e.g. have improved flight abilities and are in general geographically more wide-spread.
Here is prove:
Ecology of Tropical Butterflies in Rainforest Gaps
J. K. Hill, K. C. Hamer, J. Tangah and M. Dawood
Oecologia
Vol. 128, No. 2 (Jul., 2001), pp. 294-302

Tropical forest gaps are ephemeral and patchily distributed within
forest areas and have very different light environments compared with
closed-canopy forest. We used fruit-baited traps to investigate if
gaps are exploited by more opportunistic butterfly species compared
with closed-canopy forest. Gaps supported a higher diversity of
butterflies in terms of species evenness but closed-canopy sites
contained species with more restricted geographical distributions.
There was little similarity between the assemblages of butterflies
trapped in the canopy and those in either gap or closed-canopy sites,
but the greater similarity was with gaps, and increased diversity in
gaps was partly due to canopy species turning up in gaps. Dispersal
rates (as measured by recapture rates) were higher in gaps and there
was evidence that butterflies in gaps had relatively larger and
broader thoraxes, indicating a flight morphology adapted for faster
flight. These results support the notion of a distinctive gap fauna
comprising more widespread, mobile species. Habitat modification that
opens up the canopy is likely to result in an increase in these
widespread species and a decline in understorey species with
restricted distributions.


Evolution of Homo Erectus to Homo Sapiens

It is not plausible that members of Homo erectus would survive and remain a separate species from Homo sapiens. For members of Homo erectus to survive implies that there wasn't significant interbreeding with Homo sapiens, which would require a significant population of Homo erectus.

There is some evidence that Homo erectus and other hominids interbred with Homo sapiens. So it is more likely that there may be some people with more genetic traits from Homo erectus than others. However, by significant interbreeding, there currently only exists a single species that may contain ancestors from multiple hominid species.


Does posture matter while drinking water?

The stomach is equipped with the pyloric valve to regulate transpyloric flow to the duodenum.
Both cold and warm drinks stimulate a pattern of motility associated with retardation of transpyloric flow.

The pyloric valve is responsible for acidifying water that you drink, and if the body's guard against amoeba's and dysentery depended on body position, it would be low survival performance, given that sedentary posture is associated with poorer health outcomes, including an increased risk of type 2 diabetes. You will benefit from minimizing time spent sitting each day, and from breaking up periods of time spent being sedentary, as often as possible. It's aperture at rest is 3mm, so it's of minimal difficulty for the stomach to hold water as required for optimal health. It's highly likely that water is kept for enough time to expose it to stomach acids, regardless of body position, and then it's transmitted.
Water doesn't flow straight through the stomach like a straight tube when it's empty.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382811/pdf/gut00528-0043.pdf


Which is the guideline to choose a molecular target to identify vertebrate hosts from arthropod bloodmeals?

I have looked about the topic and I have asked experts and the best aproximation to know the vertebrate host from arthropod blood meals is targeting mitochondrial genes because you can get clean sequence data due the fact that only one allele is present rather than two.

Within the mitochondrial genome, you should select a gene which has been widely sequenced for most vertebrate species you are likely to detect in your region, other wise you will have many unknown identities among your bloodmeals. Really, there are just two choices that match these criteria: cytochrome oxidase I (COI) gene, which has been used by the Database of Life project; and cytochrome b, for which sequences are widely available (i.e. for many vertebrate species) in GenBank. If you get a negative result for one, you can try the other. Primer sequences are widely available in the literature.

In conclusion, you must be target COI and Cytb genes to assure the host identification and prevent a unidentified match in Database of Life project or GenBank.

I give you a paper example to review the metodology: Host Preference of the Arbovirus Vector Culex erraticus (Diptera: Culicidae) at Sonso Lake, Cauca Valley Department, Colombia


How to avoid air bubbles while pipetting?

You're still pipetting too fast, you should move the piston slowly and evenly to avoid air bubbles. Also make sure that you wait a second or two for the liquid to rise before moving the tip out of the liquid reservoir.

Pipettes can also behave rather weird with any liquid that differs significantly in any physical property from water, e.g. very viscous solutions.

You can find a few more tips in this document from Eppendorf or this one from Thermo Scientific.


Snake with orange spots found in South Florida

Looks very much like a red rat snake (Pantherophis guttatus). Nonvenomous, and wonderful.


What if there are no bacteria such as Streptococcus mutans

As shigeta touched on, there's no practical way to avoid cross-contamination from other humans. Assuming by magic you delete all your mouth bacteria, there are so many paths to re-inoculation you couldn't avoid it without living in extreme isolation.

A non-exhaustive list of all the ways you could get re-inoculated:

kissing
licking
aerosolized saliva from coughing/sneezing
eating food exposed to same
Touching something contaminated then brushing your teeth
Essentially putting anything another human has touched in your mouth

Other humans get saliva on things they touch and things they breathe on. You can't breathe or eat those things without cooking them. No fresh vegetables.

Your white blood cells or your immune system in general won't help, because S. mutans is already adapted to live in your saliva and there's not (to my knowledge) any adaptive immune system components active in your saliva.


What the article is saying, is that there are several respirasomes, each of which consists of multiple other mitochondrial complexes or cytochromes. The article makes an example of three commonly observed respirasomes when it says:

  The most common supercomplexes observed are Complex I/III, Complex
  I/III/IV, and Complex III/IV.

So, the short answer to your question is that a respirasome refers to a set of multiple cytochromes, whose combined action leads to respiration.

This paper goes into more detail, and reiterates that the term "respirasome" is used to describe multiple cytochrome supercomplexes.


What is the structural/chemical difference leading to different shapes in facial/head/pubic hair?

hair shape texture is really easy. the biggest effect is the shape, size, and angle of the hair follicle. Hair with different cross sections have different properties. If hair is stiffer in one plane than other it will tend to bend along the weaker plane. Larger follicles will of course produce thicker, thus stiffer hair and the angle of the follicle can influence the hairs cross sections as mush as the follicles cross sectional shape can. Note the chart below is simplified triangular and kidney shaped cross sections also exist.


How do infants get their very first gut bacteria?

Well, the former is exclusively the answer. Humans (or other mammals, or any species in general) cannot give birth to new species (of bacteria, here); they have to be acquired from the environment at all costs. However, the environment does vary, leading to variance in gut microbiome, as will be discussed later.
First of all, gut microbiome is only a part of the total microbiome of humans (Sherwood et al, 2013). Now, usually, gut bacteria are acquired by a person within one to two years of birth (Sommer et al, 2013), while the gut of a fetus is considered as sterile. However, microbial colonization in a fetus is possible (Matamoros et al, 2013). For example, species of Lactobacillus and Bifidobacterium were found in biopsies of placenta in one study (Mueller et al, 2017).
During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer. During the first year of life, the composition of the gut flora is generally simple and it changes a great deal with time and is not the same across individuals (Sommer et al, 2013).
Now lets talk about variation in gut microbiome among individuals. The gut microbiome of an individual may vary depend mainly due to:

Age:  the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults. Much of the maturation of microbiota into an adult-like configuration happens during the three first years of life.
As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in fermentation, methanogenesis and the metabolism of arginine, glutamate, aspartate and lysine have been found. In contrast, in infant microbiomes the dominant enzymes are involved in cysteine metabolism and fermentation pathways (Yatsunenko et al, 2012).

Diet: Gut microflora is mainly composed of Prevotella, Bacteroides, and Ruminococcus. There is an association between the concentration of each microbial community and diet. Prevotella is related to carbohydrates and simple sugars, while Bacteroides is associated with proteins, amino acids, and saturated fats. Specialist microbes that break down mucin, survive on their host's carbohydrate excretions. One enterotype will dominate depending on the diet. Altering the diet will result in a corresponding change in the numbers of species (Wu et al, 2011).

Geography: In simple terms, gut microbiome composition depends on the geographic origin of populations. For example, the US population has a high representation of enzymes encoding the degradation of glutamine and enzymes involved in vitamin and lipoic acid biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of $\alpha$-amylase in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably a main determinant of gut bacterial composition (Yatsunenko et al, 2012).
Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from Florence were compared to that of children from the small rural village of Boulpon in Burkina Faso. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children was dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of gut flora in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases (de Filippo et al, 2010).

Also, as @com.prehens.ible says in comments, there are various other modes through which an infant may acquire bacteria to give rise to their gut microbiome. For more information, you can also read the Wikipedia page on Gut Flora.
References:

Sherwood, Linda; Willey, Joanne; Woolverton, Christopher (2013). Prescott's Microbiology (9th ed.). New York: McGraw Hill. pp. 713–721. ISBN 9780073402406.

Sommer F, Bäckhed F (2013). "The gut microbiota—masters of host development and physiology". Nat Rev Microbiol. 11 (4): 227–38. PMID 23435359.

Matamoros S; et al. (2013). "Development of intestinal microbiota in infants and its impact on health.". Trends Microbiol. 21 (4): 167–73. PMID 23332725. doi:10.1016/j.tim.2012.12.001.

Mueller, Noel T.; Bakacs, Elizabeth; Combellick, Joan; Grigoryan, Zoya; Dominguez-Bello, Maria G. (2017-04-08). "The infant microbiome development: mom matters". Trends in molecular medicine. 21 (2): 109–117. ISSN 1471-4914. PMC 4464665 . PMID 25578246. doi:10.1016/j.molmed.2014.12.002.

Yatsunenko, T.; Rey, F. E.; Manary, M. J.; Trehan, I.; Dominguez-Bello, M. G.; Contreras, M.; Magris, M.; Hidalgo, G.; Baldassano, R. N.; Anokhin, A. P.; Heath, A. C.; Warner, B.; Reeder, J.; Kuczynski, J.; Caporaso, J. G.; Lozupone, C. A.; Lauber, C.; Clemente, J. C.; Knights, D.; Knight, R.; Gordon, J. I. (2012). "Human gut microbiome viewed across age and geography". Nature. 486 (7402): 222–227. Bibcode:2012Natur.486..222Y. PMC 3376388 . PMID 22699611. doi:10.1038/nature11053.

Wu, G. D.; Chen, J.; Hoffmann, C.; Bittinger, K.; Chen, Y.-Y.; Keilbaugh, S. A.; Bewtra, M.; Knights, D.; Walters, W. A.; Knight, R.; Sinha, R.; Gilroy, E.; Gupta, K.; Baldassano, R.; Nessel, L.; Li, H.; Bushman, F. D.; Lewis, J. D. (2011). "Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes". Science. 334 (6052): 105–8. Bibcode:2011Sci...334..105W. PMC 3368382 . PMID 21885731. doi:10.1126/science.1208344.

De Filippo, C.; Cavalieri, D.; Di Paola, M.; Ramazzotti, M.; Poullet, J. B.; Massart, S.; Collini, S.; Pieraccini, G.; Lionetti, P. (2010). "Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa". Proc. Natl. Acad. Sci. U.S.A. 107 (33): 14691–14696. Bibcode:2010PNAS..10714691D. PMC 2930426 . PMID 20679230. doi:10.1073/pnas.1005963107.


What disease / parasite / fungi has affected the mango in the picture?

If you zoom in on your picture, you will see that the small orange blobs have legs. These are red spider mites (Tetranychus urticae), which is a very common pest species of plants world-wide. They are called spider mites as they may spin webs on the plants they are feeding off. You have quite the infestation in the picture. It will take quite a bit of pest control to get this under control. I suggest spraying with Neem oil.
The mites feed by puncturing the cells of the plant they are feeding off and sucking the cytoplasm out. This puncturing results in damage to the plant, which might cause invasion from a bacterium or fungus. In your case I would guess a fungus, probably a sooty mold. Sooty molds grow on sugary excretions from parasitic animals (like spider mites) or on secretions from the fruit itself.


To answer @RickBeeloo's comment above I decided to include an answer with some detailed code. Basically to obtain the ancestors of any Gene Ontology (GO) term using the Bioconductor package GO.db we need a call to the AnnDbBimap object for the adequate ontology. For example if we want it for Molecular Function (MF) we would use GOMFANCESTOR like in the example:

library(GO.db)

terms <- c("GO:0008022","GO:0001071")
as.list(GOMFANCESTOR[terms])

$`GO:0008022`
[1] "GO:0005515" "GO:0003674" "GO:0005488" "all"

$`GO:0001071`
[1] "GO:0003674" "all"

Similar objects can be used for Biological process (BP) and Cellular compartment (CC): GOBPANCESTOR and GOCCANCESTOR. The only limiation is that you cannot mix terms from different ontologies (i.e. all BP, MF or CC). There are similar options to obtain the children of any given GO term (e.g. GOCCCHILDREN). The description of each term can be obtained with:

Term(GOTERM[terms])
                   GO:0008022                                           GO:0001071
 "protein C-terminus binding" "nucleic acid binding transcription factor activity"

All available mappings can be listed calling GO():

GO()

Quality control information for GO:

This package has the following mappings:

GOBPANCESTOR has 28477 mapped keys (of 28477 keys)
GOBPCHILDREN has 16829 mapped keys (of 28477 keys)
GOBPOFFSPRING has 16829 mapped keys (of 28477 keys)
GOBPPARENTS has 28477 mapped keys (of 28477 keys)
GOCCANCESTOR has 3897 mapped keys (of 3897 keys)
GOCCCHILDREN has 1317 mapped keys (of 3897 keys)
GOCCOFFSPRING has 1317 mapped keys (of 3897 keys)
GOCCPARENTS has 3897 mapped keys (of 3897 keys)
GOMFANCESTOR has 10021 mapped keys (of 10021 keys)
GOMFCHILDREN has 2046 mapped keys (of 10021 keys)
GOMFOFFSPRING has 2046 mapped keys (of 10021 keys)
GOMFPARENTS has 10021 mapped keys (of 10021 keys)
GOOBSOLETE has 2012 mapped keys (of 2012 keys)
GOTERM has 42396 mapped keys (of 42396 keys)

Additional Information about this package:

DB schema: GO_DB
DB schema version: 2.1
Date for GO data: 20160305


Evidence that Attention Deficit Hyperactivity Disorder (ADHD) is caused by too much cellular ATP?

That's an interesting hypothesis - however, I am not aware of any evidence that this is the case. Importantly, there can be a lot of difference between cellular access to energy, like ATP, and the perception of "energy" or liveliness.

Here is a paper that actually suggests the opposite: that ADHD could be caused by a neuronal energy deficiency because of differences in astrocyte responses to catecholamines (astrocytes are non-neuronal cells in the brain that, among other functions, regulate metabolism in the brain including access to glucose). Importantly, though, this remains just a hypothesis, not a well-established theory.

ADHD is thought to impact the parts of the brain that are important for attentional control, inhibiting responses, and motivation. Based on that perspective, an alternative explanation for the symptoms you describe is that a sensation occurs that doesn't really require a behavorial response, and for a neurotypical individual this sensation is quickly suppressed (attentional control by not focusing on this sensation, inhibiting your response to shake your leg) without any real conscious effort. Instead, with ADHD, it is difficult to direct focus away from that sensation and mental resources need to be directed towards trying to hold still. The relief from moving around comes from letting the activity progress and not trying to suppress it any more, not because there was a literal excess of energy in the sense of ATP.

References:

Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: constructing a unifying theory of ADHD. Psychological bulletin, 121(1), 65.

Todd, R. D., & Botteron, K. N. (2001). Is attention-deficit/hyperactivity disorder an energy deficiency syndrome?. Biological Psychiatry, 50(3), 151-158.


What happens to embedded membrane proteins after a vesicle is formed?

Endosome formation.
For the sake of keeping this somewhat brief, I'm going to stay somewhat surface level.
When a vesicle is endocytosed, it is called a primary endocytic vesicle.
When multiple primary endocytic vesicles fuse together, they form a larger entity called an early endosome.
Early endosomes can also be called "sorting endosomes" because different portions of the vesicle are sorted into different destinations, including these things called "recycling endosomes."
Transmembrane proteins in endosomes
In my experience, transmembrane proteins largely get sorted into these recycling endosomes and are then re-inserted into the cell membrane.
To my knowledge and from some cursory review on the topic, this is a common outcome for transmembrane proteins; they are eventually recycled and placed back into the cell membrane via exocytosis after being sorted into a recycling endosome.
Further reading
I'm sure others can add more explanation and some of the alternative routes these proteins can take, but in the interest of brevity and clarity, I thought it best to just stick with what I've come to know as most common.
Also, if you'd like a helpful source, see if you can get access to the following paper through a school or library service: Elkin, S. R., Lakoduk, A. M., & Schmid, S. L. (2016). Endocytic pathways and endosomal trafficking: a primer. Wiener Medizinische Wochenschrift, 166(7-8), 196-204.
In a phenomenon that I think is really cool, some receptors are thought to actually keep functioning after they are endocytosed and form these things called "signalling endosomes" (search "signalling endosomes NGF and TrkA" to read more).


I've used the ThermoFisher brand of CellTrace dyes. Specifically, I co-cultured two populations of cells, one with CellTrace Far Red in the APC channel and another with CellTrace Yellow in the PE channel. My choice was in part guided by a product review by another lab touting the relatively low cytotoxicity of these products.

The protocol is quite straight forward. It's also available in CFSE and Violet, though I haven't tested those. These dyes are also optimized for lymphocytes, and so I'd recommend titrating if you're staining anything else.

The dyes are quite bright, and so there were issues with costaining APC-Cy7, for example. I ended up leaving my CellTrace dyes as the only markers on their respective lasers and stacking my phenotyping on the 355nm and 405nm lasers.

For compensation, you might just stick with cells, but in the product manual for CellTrace, however, it says:

"The CellTrace™ reagents readily diffuse into cells and bind covalently
to intracellular amines, resulting in stable, well-retained fluorescent staining that can
be fixed with aldehyde fixatives."

So if you use the ArC amine-reactive comp beads for LIVE/DEAD kits, you might be able to just make comp beads with those. I'll verify this when I'm back at work if need be, as I haven't done it myself, but it's a nice thought!


What's the name of the fibrous strands that hold the seeds in a pumpkin?

This part of the fruit is called "Endocarp". It does not become more specific as that, as far as I know.

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


Calculation of extinction coeffcient of GFP

Only the number ("n") of the aromatic amino acids Tryptophan (Trp) and Tyrosin (Tyr) in your protein contribute significantly to its absorption at 280 nm (and Cystein (Cys), albeit to a lesser extend), see also here.

You could retrieve the protein's amino acid sequence from uniprot (see GFP here). Looking through the GFP sequence, one can identify n=11 (4.6%) Tyr and n=1 (0.4%) Trp. Now you can insert those in your formula and end up with an extinction coeffient of 21'890 M^-1 * cm^-1. This formula is only valid if all Cys are reduced (GFP has n=2 Cys that could form a disulfide bridge).

If you want to avoid all the formulas I suggest you copy the sequence of GFP and paste it into ExPASy ProtParam. This way you get a nice overview of the amino acid distribution of your protein and also retrieve the extinction coefficient under oxidizing conditions, which BTW is 22'015 M^-1 * cm^-1.


What is the trigger of pollen tube formation when the pollen is on the stigma?

Germination of the pollen tube begins when the pollen grain becomes hydrated on the tip of the stigma. The pollen grain absorbs water and also exchanges signals with the stigma. Microchannels form between the pollen grain and the tip of the stigma papillae and water is transferred from the stigma to the pollen grain (Taylor 1997). cAMP, which is produced by the protein PSiP, and cytosolic free calcium can be used as signals to orient the pollen tube to grow in the proper direction (Moutinho et al 2001).

Pollen tubes can also germinate in vitro even without contacting a stigma. If you place a pollen grain in germination medium, which contains calcium and boron, among other things, the tube will germinate but it will not grow to its full length.

Often when pollen of a different species lands on the stigma, the pollen will germinate but the pollen tube growth will stop before it reaches the ovary (Ascher and Peloquin 1968). Mating barriers are very complicated, however, and there are many different mechanisms for species recognition and arrest of pollen tube growth. In some cases, the tube is halted in the style while in other cases the tube grows, but slowly and inefficiently (Swanson et al. 2004). Species recognition in some species (for example, tobacco) is related to self-incompatibility and the S-locus. Species recognition can also be unilateral: that is, the pollen of species A can fertilize the ovule of species B, but the pollen of species B cannot fertilize the ovule of species A.

I would recommend that Swanson paper if you want to read more.


Are porins on the inner or on the outer membrane of mitochondria?

This is not my field, but The Transporter Classification Database would appear to be a reliable source and states that:

  The best characterized members of the MPP family are the voltage-dependent anion-selective channel (VDAC) porins in the mitochondrial outer membrane.

Searching through the Protein Data Bank one can find a crystal structure for human voltage-dependent anion channel 1 and the associated paper also states that it is in the outer mitochondrial membrane, so you would imagine that they should know.


It's hard to judge from a single photo but it appears to be from the Family Theridiidae (cobweb spiders). Spiders in this family have long front (first legs)and much shorter third legs as the spider in your photo seems to have. But the perspective may be off. You don't mention the size which would help.

I enjoy photographing insects and spiders in my area. One thing I found when I was trying to identify spiders is colour and pattern can vary quite a bit from different locale. Sometimes two spiders of the same species could look like two completely different species.

So please bear this in mind. All I am is an arthropod enthusiast that has benefited from some more skilled and knowledgeable people helping me out. With that in mind, I wonder if your spider might be Phylloneta pictipes (syn. Theridion pictipes).

Source: http://bugguide.net/node/view/2209

I should've said but the two spiders above are the same species; male on the right and female on the left.

You can check out more spiders of this species at http://bugguide.net/node/view/49080/bgimage and see how they vary.


Parent 1 and 2 have each 5 possible genotypes (OO, AO, BB, BO and AB).

Here a Punnett square with each possibilities. I highlighted the possible parent genotypes.

The total number of possible crosses is exactly 21. Note that here A = Ia, B = Ib and O = i.

OOxBB,OOxBO,OOxAB
AOxBB,AOxBO,AOxAB
BBxOO,BBxAO,BBxBB,BBxBO,BBxAB
BOxOO,BOxBB,BOxAO,BOxBO,BOxAB
ABxOO,ABxAO,ABxBB,ABxBO,ABxAB

This is starting from the information based on your blood type only (i.e. no information about your genotype).

Some background information. Antigen expressing alleles (here referred as Ia or A and Ib or B) are dominant. Not expressing an allele is notated i or O. Being of blood type O is when you don't express both alleles so it is a recessive trait (only possible genotype is ii or OO genotype).


Never seen a spider with this pattern before

The depicted spider appears to be a European garden spider Araneus diadematus. The mottling pattern that forms a cross shape is probably one of the more distinctive features, giving these the nickname cross spiders. The distribution for your locale makes sense, based on data collected on these spp: http://srs.britishspiders.org.uk/portal.php/p/summary/s/Araneus+diadematus


Why are antibiotics prescribed with a viral infection like a cold?

In general antibiotics don't help with viruses. However, sometimes a bacterial infection may follow a cold virus, so there might be some scenarios in which antibiotics would be needed. However in many cases it could be due to people demanding antibiotics from their doctor.

You can read more here (CDC site): http://www.cdc.gov/Features/getsmart/


Yes, there are examples. First: If you want to say, that humans and monkeys evolved, than it is better to say that they evolved from a common ancestor. This makes quite a difference.

If you are looking for examples of human evolution then one of the most obvious traits under evolutionary selection is pigmentation. There is a clear correlation with lattitude (and this UV-index):

The changes in pigmentation occured - seen from a evolutionary perspective - pretty recent when humans moved out of africa and to other regions (see here).
See these papers for more details:

The evolution of human skin coloration
Colloquium paper: human skin pigmentation as an adaptation to UV
radiation.
Epidermal pigmentation in the human lineage is an adaptation to
ultraviolet radiation.

Other examples would be the tolerance for lactose (the sugar contained in the milk) in adults which arose during the last 5-10.000 years. Normally only babies can process these sugar which is contained in large amounts in the mothers milk. When they are weaned, usually the enzyme is not expressed anymore. However with the settling of the humans and the domestication of cattle this changed, so we can still drink milk and eat milk products without producing intestinal problems. See here for more details:

Genetic signatures of strong recent positive selection at the lactase
gene.
Adult-type hypolactasia and regulation of lactase expression.

A third example would be the sickle-cell anemia, which happens due to a point mutation in the human hemoglobin protein. This causes an aggregation of the hemoglobin molecules in the red blood cells which then leads to a reduced elasticity (see here for more details). It also leads to a protection against malaria (most likely by the reduction of the life span of the erythrocytes). The areas with high prevalence of the sickel cell anemia in africa correlate pretty nicely with the distribution of malaria.

An Immune Basis for Malaria Protection by the Sickle Cell Trait
Sickle Cell Anaemia and Malaria

If you look further, you will find a number of different examples, where evolution is present after humans went through a genetic bottleneck (meaning the number of humans was drastically reduced).


Lack of yolk in mammalian oocytes as compared to other vertebrates?

In oviparous animals (those that lay eggs which hatch outside the body), the eggs need to be provided nutrition for embryonic growth, which is the main function of yolk.

In placental mammals, the embryo is provided nutrition directly from the mother via the placenta.

Therefore, most mammalian oocytes do not need to develop large quantities of yolk to support the embryo in the way the eggs of most birds, reptiles, amphibians and fish do.


I'm surprised there hasn't been any answer or comments but yes, this is a fairly well known phenomena. It's quite possible that not everyone finds this to be true for them or possible they've never even noticed it. If a person doesn't need to talk for the first 15 minutes to hour, they might not realise their voice is deeper and/or raspier first thing in the morning.

Speech pathologists, voice teachers and professional singers are certainly aware of this. There's been no solid research on why that I know of. After all who's going to fund research into something that's mainly a curiosity with no medical repercussions or profits to be made? Still, there are various thoughts on why this occurs (outside of acid reflux irritating the vocal cords).

During sleep while we're in a horizontal position, a certain amount of fluid collects in our upper body (read from the neck up), so our vocal cords will swell and thicken slightly. It's why our eyes look more puffy first thing when we arise. During the night, we're not using our vocal cords either but while breathing, air is still passing over them. So while the tissues swell a little, their outer membrane dries a little. To counter the drying effect, the body secretes more mucous as a protective coat. This effect is much worse in people who are mouth breathers.

Another possible reason is what voice teachers and singers think happens, too. Vocal cords, being muscles, need to stretch and contract to vary the voice's pitch. Unused through the night, they're nit as limber and can't stretch as well as later. Vocal cords stretch to reach higher pitches. If that idea sounds far-fetched, just remember opera singers and other professional singers need to limber up before performing. They practice hours each day but before a performance, they need their voice to be at its best. Hence they'll practice singing notes up and down the scale.

Supposedly, drinking a cup of lukewarm water first thing in the morning helps, and tea or coffee is supposed to dry out the throat even more. I never drink coffee but, personally, I've found that first hot cup of tea in the morning doesn't just help my voice return to normal but wakes me up.

I've never heard of this effect lasting for a couple of hours though I haven't gone around quizzing people. :) So try either the lukewarm water or a hot drink and see if it makes a difference. You can also try singing or just talking aloud to limber your cords in the morning.

Edited June 14/17
Links (but not scientific studies) where others have noted this phenomena

Why do people's voices sound deeper in the morning? I gave greater credence to the first answer since it comes from an opera singer.

Raspy Voice In The Morning?

And from Music SE Why is my voice lower pitched when I get up in the morning


My foray into the literature suggests that mature adipocytes do not divide. See, for example:

  Lefterova, MI et al. (2009) New developments in adipogenesis. Trends in Endocrinology and Metabolism 20:107-114

In the context of looking at the possibility of stimulating the conversion of white adipose tissue to brown adipose tissue, the authors outline the way in which the expansion of adipose tissue occurs by a process in which fibroblast-like pre-adipocytes differentiate into cells capable of storing lipid droplets and responding to insulin.

It appears therefore that expansion of adipose tissue occurs by the generation of new adipocytes. Thinking of the morphology of a fully-loaded adipocyte (a lipid droplet surrounded by a narrow band of cytoplasm) it seems rather unlikely that these cells would be capable of division. The Wikipedia citation linked to by QuietThud in the comments to the OP is to a popular book on nutrition, not an authoritative source.


What is an aromatic cage and what does it do?

It refers to the structures in the PHD-finger domain and chromodomains. The aromatic amino acid residues form a cage like structure which covers and interacts with the methylated ammonium of lysine via a cation-pi interaction.

  The BPTF-PHD structures reveal the main characteristics of PHD fingers that can read H3K4me3. The binding occurs through an aromatic cage where a trimethyl ammonium group is stabilized by van der Waals and cation-–π interaction, which is similar to the ones observed in chromodomain, MBT, PWWP, and Tudor domains. This aromatic cage is composed of one Trp and three Tyr residues; and it has three faces and a 'lid' that is beyond the tip of H3K4me3. Subsequently determined structures of other fingers in complex with the H3K4me3 peptides show that the cage varies and can contain a combination of two to four aromatic and hydrophobic residues.

 Margueron et al., 2009


How to mark an ant with the least disturbance to the ant and the nest

For this purpose, people usually paint ants on top of the thorax (not on the head where it can prevent eyes and antenna to function normally, nor on the abdomen where it can block the spiracles and prevent respiration), with a bit of acrylic paint applied with a toothpick. Combination of colors are used to identify individuals.

These techniques are currently being replaced by the use of RFID tags and Flashcodes in science, to automate recordings.


What pigment is responsible for the formation of blue skin color in some animals?

Blue coloration in animals is caused by structural color rather than blue pigments. In the case of vervet monkeys and other mammals studied this is due to collagen fibers in the skin being arranged with a regular spacing that results in blue wavelengths constructively interfering while other wavelengths destructively interfere1.

This "news" article in Science discusses this phenomenon and mentions Vervet monkeys.

Reference:

1: Prum, R. O., & Torres, R. (2004). Structural colouration of mammalian skin: convergent evolution of coherently scattering dermal collagen arrays. Journal of Experimental Biology, 207(12), 2157-2172.


Its a bit confusing, but DAVID uses the term Gene List as a generic term.

Looking at Step 2, you can submit many kinds of lists to DAVID, including actual gene symbols, Ensembl or RefSeq Accessions, etc... actually nearly 30 kinds of terms including 'not sure' which probably looks at your list and tries to guess.

Affymetrix or Illumina probe set IDs are each designed to measure a gene, ideally, though its not precisely a one Probe Set to one Gene relationship.  This is because when the array is designed there may be a partial transcript RNA records which turn out later to be parts of a single gene.  There are also probe sets which may turn out to hybridize to similar sequences in more than one gene.

Its messy, but its also true that often more than one gene symbol will appear for the same gene because of historical naming conventions...


Is drinking your urine an effective way to stay hydrated in a hostile environment?

Drinking urine could help you stay hydrated a bit longer, maybe a day, but only when you are well hydrated at the start. You could get about 0.5-1 liter extra water this way. This doesn't work anymore when you start drinking urine the 2nd or 3rd day without water - the amount of urine will be very small and will be too concentrated at that time.

A man, drinking his urine has survived for 6 days under the ruins of the earthquake (Slate.com). However, people have survived for as long as 8 days without water or drinking urine: a 7 and 11 years old kids under the ruins of 2010 Haiti earthquake, and a 35 years old woman trapped in a lift.

According to Guyton and Hall Textbook of Medical Physiology:

...to excrete an average amount of waste products, let's say 600 mOsmols, your kidneys need to excrete at least 500 mL of urine, because they have a limited ability to concentrate urine.

If you drink 1 liter of urine with 600 mOsmols of waste products, you will need to excrete 500 mL of urine to excrete those 600 mOsmols and additional 500 mL to excrete 600 mOsmols from your normal metabolism. So, drinking 1 liter urine forces you to lose 1 liter of water, which means no water gain.

If you are very well hydrated at the time of first urination, your urine will be more diluted, so containing less than 600 mL of urine (minimally about 50 mOsmols/kg according to Wikipedia). Drinking such urine can provide net hydration, but your next batch of urine will be much more concentrated and will provide much less hydration. At the point when the kidneys need to excrete more water to eliminate the waste than you have drunk by urine, you will be in the negative water balance.


Would there be more amino acid residues in the extracellular or intercellular space?

Yes ,there are some patterns.
First you have to determine which group of membrane proteins you're talking about.
According to Molecular Cell Biology Lodish et al 8th ed chapter 13, there are 6 types of ER membrane proteins ( and therefore in the cell membrane)
The 6 types are type 1,type 2 ,type 3 , type 4,Tail anchored proteins ,GPI anchored proteins.
Nearly all AA residues in type 3 or  the tail-anchored type are located in the cytosolic side of the membrane ( their difference is in their N/C terminus orientation) whereas GPI anchored type has almost its entire AA residues in the exoplasmic side.
For other types there may not be a general pattern.
See E. Hartmann et al., 1989, P. Natl. Acad. Sci. USA
86:5786, and C. A. Brown and S. D. Black, 1989, J. Biol. Chem. 264:4442.
By the way , you can also think of it in another way. Antigens , Hormone Receptors , Structral proteins in exoplasmic leaflet of membrane usually have more AA in the exoplasmic side.


How to measure metabolic rates of microscopically small animals?

Metabolism in other small organisms, such as bacteria, are measured by taking the metabolism of a very large population of organisms, and then dividing that by the count of organisms in order to obtain the metabolic rate of a given individual.

In this paper on the metabolism of E. coli, they looked at the various input and output chemicals. Glucose, biomass, oxygen, and carbon dioxide were all observed. Observation of multiple variables also helps in the reduction of errors by using the stoichiometric balance to make sure that no errors have occurred in the measurements.

The methodology section of the paper had the following techniques:

  Continuous cultivations were performed at 28 °C, at a stirring speed
  of 800 r.p.m., and the pH was controlled at pH 6·6 with 2·5 mol NaOH
  l−1. The 2-l bioreactor (model SGI 7F-Set2; Setric) was equipped with
  standard measuring and control units (temperature, pH, dissolved
  oxygen, stirrer speed). A constant aeration rate of 1·33 v.v.m. was
  achieved by a mass flow controller (Brooks). Continuous cultivation
  was performed for at least eight residence times at a given dilution
  rate; steady-state conditions were verified by constant optical
  density and oxygen and carbon dioxide transfer rates. Except for
  glucose, all other substrates were in excess. The concentration of
  dissolved oxygen was always maintained above 20 % of air saturation.
  Analytical techniques.

  Culture liquid was withdrawn from the bioreactor into an ice-cooled
  beaker. Cell dry mass was determined gravimetrically after
  centrifugation of a known sample volume. The pellet was washed twice
  with 0·9 % w/v NaCl and dried at 40 °C under vacuum for 48 h.
  Elemental biomass composition was analysed with a PE 2400 II elemental
  analyser (Perkin Elmer). Glucose was measured enzymically by a YSI
  glucose analyser (model 2700; Yellow Springs Instrument Co.). Organic
  acids, i.e. acetic acid, formic acid, lactic acid and pyruvic acid,
  were analysed by HPLC using an HPX-87H Aminex ion-exclusion column
  (Bio-Rad). The column, connected to a UV detector (λ=210 nm) and RI
  detector, was eluted at 50 °C with 5 mmol H2SO4 l−1 at a flow rate of
  0·5 ml min−1.

If the tardigrades are grown in solution, an identical methodology can be used to measure respiration rate.


Why is oxygen and CO2 measured in pressure instead of mmoles/L like other ions?

As you suspected, hemoglobin is the reason why O$_2$ and CO$_2$ in blood are expressed as a pressure (mmHg) and not a concentration. Most of the oxygen in blood is bound to hemoglobin; the concentration of free oxygen in plasma is low because oxygen does not dissolve well in water (which is of course the reason why hemoglobin exists in the first place).

When the oxygen content of blood is given as a pressure, it refers to the partial pressure that a gas (air) must have in order to be in equilibrium with the blood. This might seem a bit roundabout, but it captures the effects of both solubility and hemoglobin. In essence, this pressure describes how much oxygen the blood can release, which is the critical parameter for oxygenation of tissues.

The molar concentration of free O$_2$ in plasma is proportional to the partial pressure over the liquid, a fact known as Henry's law. The proportionality constant is the solubility of oxygen in the liquid, about 1.3 10$^{-6}$ M / mmHg for plasma. So at 100mmHg, the plasma O$_2$ concentration is about 130 $\mu$M. For comparison, the O$_2$ concentration in an ideal gas at 100 mmHg is 9 mM, or 70-fold higher.

See for example this book chapter for more information.


How do liver and lung metastases cause death?

Metastasis is the spreading of cancerous cells to a new site within the body where they form a secondary tumour.  There is nothing special about how these metastases cause death, they do so in the same ways as the primary cancer eventually might:

Replacing functional cells with non-functional cancerous cells
Eroding into other tissues and disrupting normal body architecture
Causing haemorrhage
Putting pressure onto other structures

If we apply those principles to lung and liver secondary tumours, it is easy to see why they are likely to contribute significantly to mortality.

Cancerous masses in the lungs reduce the surface area available for gas exchange, reducing oxygen saturation of the patient.  The tumour may also erode into a primary bronchus, which if obstructed would cause lung collapse, or into the mediastinum.  If the mediastinum is involved then the great vessels or heart may be invaded into with significant consequences.

Liver metastases are more likely to cause problems due to the reduction of liver function as the cancer grows. This causes a plethora of problems as the liver is involved in so many pathways within the body.  Examples of serious effects would include the patient becoming coagulopathic due to a reduction in production of clotting factors, making bleeding much more severe.  The liver can begin to fail to clear toxins from the blood, leading to the risk of acidosis or hepatic encephalopathy (leading to coma and eventual death).  If the tumour were to invade the portal vein, this can cause portal hypertension, which in turn shunts pressure into the systemic venous system.  This can cause oesophageal varices which are prone to spontaneous and catastrophic bleeding. Similarly a tumour invading the common bile duct (or other part of the biliary tree) can cause obstructive jaundice and associated problems.

The reason your quote suggests that most deaths are from metastases than the primary tumour is probably because tumours in these locations have greater negative effects at a smaller size because they are in crucial tissues.

There may be another contributing factor in the form of data interpretation, however.  Tumours are often 'staged' via the TNM staging system, the last component of which is the presence of metastases.  The presence of distal metastases automatically makes colorectal cancer Stage 4.  This is often considered not to be curable, meaning a move to more palliative treatment options.  This may affect the survival curves for those with distal metastases and those without.


Could an annual plant be genetically modified to be a perennial?

Researchers at Ghent University have made a discovery that downregulation of the proteins CONSTANS 1 (SOC1) and FRUITFULL (FUL) lead to the development of many perennial traits in annual plants (in the study Arabidopsis thaliana is used) (reference).

The CONSTANS gene controls flowering in Arabidopsis thaliana (reference).

FRUITFULL (FUL) is an MADS box gene that functions early in controlling flowering time, meristem identity and cauline leaf morphology and later in carpel and fruit development in Arabidopsis thaliana (reference).

The process is complicated and would need many genes to be manipulated but this research proves that it is possible. Another article of interest.


Understanding common identifier codes (IDs) in biology databases

Common biology ID codes.

PDB: 2BIB for example. 4 letter code for a specific structure.

Uniprot: Q9NZT1 for example. A six letter combination of numbers and letters for either a TrEMBL or Swissprot record. This record contains information on domains, and Uniprot links out to lots of useful things like interaction databases, redundancy datasets etc.

Pfam: X1WG39_DANRE A uniprot ID followed by an identifier. Tightly linked with Uniprot, but with an emphasis on domains.

NCBI: NP_000108.1 For example. These IDs link to either a gene, transcript or protein in refseq. In an NCBI record there are two main distinctions in prefix of the ID code: hypothetical/automatic assertions (XM_, XR_, and XP_) and manually curated assertions (NM_, NR_, and NP_). This is followed by a 6 digit number, and sometimes followed by a "." and a number, indicating an splice isoform.

Uniprot IDs
I'm not sure where you got this output so this seems a strange concatenation of Uniprot information.
Q9NZT1 is indeed the unique Uniprot ID. This is specific to uniprot.
CALL5_HUMAN is the "gene name" or "Identifier" and often spans across different databases for that gene. It's a little more back end, but is essentially not unique due to splice isoforms.
There are many IDs in uniprot, and many types. Already below you'll notice some are swiss prot, others are Trembl. These are the main types. Swissprot are manually reviewed, whereas Trembl is an automatically compiled collection.

There are many many different accession code types with each database using it's own nomenclature that you'll come across. Unfortunately, there are too many to list here comprehensively.


How does horse extract the energy to needs from a relatively small digestive system?

The digestive system of a horse is by no means small:

They have 15 to 21 m (50 to 70 ft) of small intestine, with a capacity of 38 to 45 L.
They have a 1.2 m (4 ft) long caecum that holds 26 to 30 L.
They have 3.0 to 3.7 m (10 to 12 ft) of colon, capacity up to 76 L.
(Figures sourced from Equine Anatomy (Wikipedia))

Certainly horse stomachs are comparatively small as they are hindgut fermenters, but that is not where most energy and nutrients are absorbed. Some food passes from the stomach to the small intestines before it is fully digested, which enables more continuous eating to keep up with their energy and nutrition requirements. Most proteins, carbohydrates, and fats are absorbed in the horse's small intestine. Some nutrients are absorbed in the large intestine as well, see Is there nutrient absorption in the large intestine of hindgut fermenters?.

The hippopotamus is a pseudoruminant, having a 3 chambered stomach (unlike the 4 chambers of a cow). Hippos are therefore considered to be foregut fermenters, and are not comparable to horses. In terms its digestive tract, the hippo is much more similar to a cow than a horse.


It is a reaction to gravity, it is called geotropism or gravitropism. The roots tend to grow in the direction of the gravity (positive geotropism) and the stem is going against gravity (negative geotropism).

The mechanism works with auxins, or plant growth hormones. They are pulled by gravity toward a side of the plant and will either stimulate or inhibited growth in that area.


Why do endotherms need more food than ectotherms?

Endotherms also called warm blooded animals have the ability to regulate their body temperature by themselves.

If the endotherms are in a cold place their body increases the metabolism and generates more heat. This will compensate for the cold outside.
In a hot region the body metabolism is tuned down (this is not as efficient as the adaptation to cold region - as the metabolism can't be turned down below a certain limit - this will result in death) a little and heat generation is somewhat reduced. The second and more efficient mechanism is the heat dissipation by sweating and through skin (directly).

Ectotherms on the other hand, do not have efficient temperature regulation systems.

In warm regions when the temperature is high, the ectotherms seek shade and low-temperature areas to prevent over-heating
In cool regions they seek sunlight and expose themselves to the sunlight for warmth. For the same reason, they can also search out and stay near fire pits, campfires etc...

So when we calculate the energy demands, the ectotherms need more energy as they regulate their own metabolisms to match the need.

The increase in need for energy in hot condition maybe due to:

The extra-processes that are regulated like sweating, increased peripheral vasodilation - thereby increasing circulatory rate (increased work for heart)
This thermo-regulation inturn affects other processes and systems like electrolyte and water balance, excretory system, endocrine system, thrist, etc...

During the cold season increased metabolism itself is the main cause for increased need for energy.


Which Darwin book (and today edition) is illustrated by his own drawings?

I believe that there is only one drawing in the first edition of On the Origin of Species, and it is Darwin's.  Any good edition such as the fascimile edition with an introduction by Ernst Mayr, will include this drawing.  I'm not sure about other editions of the Origin or other books of Darwin's.  However, maybe you don't need to buy anything.  Darwin Online is a wonderful collection that includes many (all?) of Darwin's writings over the years, including images of many of them; the drawings are no doubt included.

It's possible that the History of Science and Mathematics StackExchange site would be a better place for this question.


A pathway doesn’t have substrates, only a reaction does. And therefore there’s no such thing as a direct or indirect substrate. You can perhaps ask what the precursors are for glycogen (but do you mean immediate or distal), or what the substrates are for the first reaction in the pathway (but only if it is quite clear what the first reaction i).

That’s the trouble with trick questions. They are generally badly worded and tend to lend nothing to biology education.


functional hypocholesterolemia due to very high HDL or low LDL?

Upper bound of HDL doesn't really exist. The greeks are known for their incredibly high levels of HDL and the so called mediterranean diet/genetics combination that causes this is only beneficial to health (supposedly - although never been proven that incredibly high HDL levels are beneficial, they're just not harmful).

As for too low LDL levels/cholesterol levels - that's interesting. Unfortunately it isn't possible because any mutations that caused this would be fatal, cholesterol makes up an essential part of cell membranes etc. That's why our body makes our own. A mutation preventing this would not even manifest.


The difference boils down to UnTranslated Regions. A CDS or coding sequence is the part of a transcript that is actually translated into protein. Therefore a CDS will (almost) always start with an AUG codon and stop at one of the three STOP codons (UAA,UGA,UAG).

The transcript however (note that I am referring to mature transcripts that have already been spliced so introns have been removed) will also contain the UTRs which are not actually translated into protein. A cDNA sequence is derived from the transcript by reverse transcription and will, therefore, also contain the 5' and 3' UTRs. For example, see this schematic diagram of an unspliced transcript:

The CDS of the gene depicted in image above will only contain the ATG, the STOP and the two green regions (exons). The cDNA will contain all that and, in addition, the two UTRs. Of course, both the cDNA and the CDS will not contain the introns.


Why/how does exposure to noise cause cochlear hair-cell loss?

There are a number of pathophysiological mechanisms that are thought to underlie noise-induced hearing loss:

Mechanical damage to the delicate cells and supporting structures of the organ of Corti;
Reduced blood flow to the inner ear;
Intense metabolic activity, which increases mitochondrial free radical formation.

Reactive oxygen species (ROS) are highly reactive. They are essential for mitochondrial function to generate energy. However, too many of them damage cellular lipids, proteins, and DNA, and upregulate apoptotic pathways. The observed impaired blood flow to the cochlea can enhance the toxic effects of ROS. Mechanical damage to the delicate hairs and membranes of the hair cells reduces their ability to converge acoustical energy into potential differences.

References
- Le Prell et al., Hear Res (2007); 226(1-2): 22–43
- Kurabvi et al., Hear Res (2017); 349: 129-37


What marine animals exhibit deep hibernation/aestivation?

Fish are ectothermic, and so, by definition, cannot hibernate because they cannot actively down-regulate their body temperature or their metabolic rate. However, they can experience decreased metabolic rates associated with colder environments and/or low oxygen availability (hypoxia) and can experience dormancy. For example, epaulette sharks have been known to stay dormant for long periods without oxygen (reference) Turtles in freshwater lakes have been known to hibernate by burying themselves in mud (reference). The mechanism through which turtles can experience several months of hypoxia or anoxia is explained in this paper. The Antarctic fish (Notothenia coriiceps) has been found to be able to activate and deactivate their metabolic processes independent of body temperature and hence enter a state of dormancy similar to hibernation through metabolic suppression (reference).


Peptides neither produced by the ribosome or the non-ribosomal peptide synthase complexes

One peptide that comes to mind is the metabolically important reducing tripeptide glutathione — γ-L-Glutamyl-L-cysteinylglycine:

This is synthesized from cysteine, glutamate and glycine by reactions catalysed by glutamate cysteine ligase and glutathione synthase:

Synthesis of glutathione (GSH) — two subunits of glutamate cysteine ligase (GCL) are shown

Other examples may involve amino acids not specified by the genetic code which have particular roles in metabolism. For example, taurine, which has a sulphonic — rather than a carboxylic — acid group, can be metabolized to the dipeptide γ-Glutamyltaurine which may have a role in the brain.

These two examples relate to L-amino acids, albeit with a peptide bond between the side-chain glutamyl carboxyl group rather than the α-carboxyl group. However a D-amino acid dipeptide, D-alanyl-D-alanine, synthesized in the reaction catalysed by D-alanine-D-alanine ligase, is a precursor of bacterial peptidoglycan synthesis.

All the examples given have in common the fact that the peptides are very short (di- or tri-peptides) and can be synthesized in reactions requiring one or two specialized enzymes. Bacterial antibiotics synthesized by the non-ribosomal peptide complex tend to be appreciably larger, requiring repeated formation of peptide bonds.


Insect identification: Fly with eye strip

Definitely Stratiomyidae, probably genus Odontomyia. Very widespread and species-rich genus.
Here is an example of Odontomyia - not the same species - https://www.flickr.com/photos/63075200@N07/sets/72157632905103705/.


What causes humans to be physically weak compared to animals like gorillas?

Evolutionary tools that are not needed for increased survival rate of offspring of a certain lineage deteriorate with time. The deterioration might have a form of gene expression changes or mutation accumulation. For example, gene MYH16 encodes a protein that facilitates strong jaw muscles in primates, but humans carry a mutated gene that had lost its function (Stedman et al. 2004. Nature). We cannot bite hard, but we can articulate.

With respect to muscle strength, the common ancestor of apes and humans was likely stronger than we are now. Their descendants that formed a lineage diverging towards humans increased their survival by being smarter rather than stronger than their contemporaries.


No but they can be used as part of a gene therapy to induce cellular death in cancer.

TRAIL-secreting mesenchymal stem cells promote apoptosis in heat-shock-treated liver cancer cells and inhibit tumor growth in nude mice

  Liver cancer is one of the top six leading causes of cancer-related death. Radiofrequency ablation (RFA) is an important means of treating liver cancer. Residual cancer after RFA is the most frequent cause of recurrence in cases of liver cancer. The main difference between residual cancer cells and ordinary liver cancer cells is that residual cancer cells experience heat shock. The secretable form of trimeric human tumor necrosis factor-related apoptosis-inducing ligand (stTRAIL) induces apoptosis in a variety of human cancers but not in normal tissues. It has shown potent cancer-selective killing activity and has drawn considerable attention as a possible cancer therapy. In the present work, the therapeutic potential of this stTRAIL-based gene therapy was evaluated in hepatocellular carcinoma subjected to RFA. Rat bone marrow mesenchymal stem cells (BM-MSCs) were isolated and transduced with a lentiviral vector encoding stTRAIL (stTRAIL-MSCs, T-MSCs). Cells treated with heat treatment at 43 °C for 45 min served as simulated residual cancer cells. After treatment with T-MSCs, apoptosis in heat-shock-treated liver cancer cells increased significantly, and caspase-3 was upregulated. When T-MSCs were subcutaneously injected into nude mice, they localized to the tumors and inhibited tumor growth, significantly increasing survival. Collectively, the results of the present study indicate that BM-MSC can provide a steady source of stTRAIL and may be suitable for use in the prevention of the recurrence of hepatocellular carcinoma after RFA with secretable trimeric TRAIL.


Can an attenuated virus cause infection in some rare cases?

There are two possibilities for getting the measles directly after a vaccination:

The kids where infected shortly before the immunization. Since it takes about two weeks to develop humoral immunity, it is possible that these two events overlap. The measles have an incubation period of 7 - 21 days (see reference 1), with a rash occuring around day 14. So if the kid was around day 7 of his infection, this would fit.
Since the measles vaccination is a live attenuated virus, it is possible to get a rash from it. However, these are relatively rare cases (depending on the source between 2 and 5%) and the infection is mild and not contagious. See also reference 2.

References:

Measles (from the CDC)
Measles: Questions and Answers


Europe: big fly with black/yellow striped body: I'm guessing a horse fly?

At first, because of the size and shape, I thought that it was a horsefly, but no horsefly looks like that (at least not in Luxembourg). It turns out that it was a hoverfly, just as Karl Kjer said. The species is Volucella zonaria, or the hornet mimic hoverfly. This hoverfly lives in most of Europe (including Luxembourg) and is 15-25 mm in length, consistent with your 20 mm estimate.

In this image you can see the same coloration and abdominal markings as your insect.

The markings in your photo are very difficult to see but are there.

Wikipedia page

original image source


What determines a successful protein expression in E. coli?

One important aspect when expressing a protein from a different organism in E. coli is that the codon usage of the original organism is likely different from the codon usage of the E. coli used for expression (Codon usage bias).

Though the genetic code is degenerate, not all codons are equal. They might encode for the same amino acid, but organisms tend to favor specific codons over others and the tRNAs for those codons tend to be present in different concentrations. When you now have a lot of codons in your sequence that are very rare in E. coli, the expression will suffer because the tRNA for those codons is not present in high enough concentrations to sustain the translation.

There are two ways of compensating for that, either you get your E. coli to produce more of the rare tRNAs, or you optimize your sequence to use different codons. For the first solution you can buy certain E. coli strains that contain plasmids encoding the tRNAs that are rare in E. coli, one of those strains is e.g. the Rosetta BL21 strain.

For optimizing the codon usage there are several companies offering to synthesize optimized sequences. There are also tools available online, but I have no direct experience with those.

The optimization is also not as easy as just using the most prevalent codon every time, it has been shown that optimizing the codons to match the translation speed in the original organism can enhance the expression yields. For some proteins, pause sites during the translation might be necessary to ensure proper folding. If the protein doesn't fold correctly it will be quickly degraded and your yield will suffer. This is described in the article "Heterologous Protein Expression Is Enhanced by Harmonizing the Codon Usage Frequencies of the Target Gene with those of the Expression Host" from Angov et al.

You'll find a nice overview about the whole topic in the article "You're one in a googol: optimizing genes for protein expression" from Welsh et al.


Identifying a spider from coastal Virginia

These are very likely one of the common spiders that gets called House Spider, but this variety is one of the comb-footed spiders; the Theridiidae.  They're sometimes also called Tangleweb Spiders or something along those lines.  They make those messy webs, and hang upside down just as you show.  You can tell these guys aren't Araneus or one of the other Araneid orbweavers, because they're not hanging vertically in an orbweb.  This particular spider is probably the very variable and common Parasteatoda tepidariorum, and the smaller one is, as you guessed, a male.  They will share the web for a day or so until he mates and moves on.  You should be aware that the related Black Widow has this same general body shape and habit, and may be stripy and have banded legs like you see in the photo when the females are young.  I suspect that was why TFE was asking for better photos - although you probably would have noted the red hourglass before if that was the case.  I'm inclined to go with P. tepidariorum, for two reasons: Latrodectus generally (but not always) are sensitive to disturbance, where the common House Spiders don't seem to mind, and the abdomen of the female seems to be a little more randomly patterned (as best we can see) than I would expect for a Latrodectus.
Here's a photo of P. tepidariorum with a snack:

https://bugguide.net/node/view/6919/bgimage


What is the mass of carbon dioxide absorbed by an oak tree in one year?

Re: Bryan Krause's comment, measurements per hectare are common. However, if you can just estimate average trees per hectare, then it works out. But it still likely depends on the local climate, ecology etc. It also varies across the life term of the tree.
Some estimates have been made, such as in this paper (see Table 4), for Quercus rubra and 2 other hardwood species. They estimate that for the most mature trees, Q. rubra stores ~20 Mg/hectare total biomass, of which approximately half is carbon.
This is a little more than twice the biomass of the 8-year-old tree, so if we just linearly interpolate we could say that a hectare of oak stores ~1 Mg C per year. There are some problems with this- for example, older trees are likely to store much more than that, but it is not clear exactly how much variation there is over the course of an oak's life, and also there is likely variation between the sites in the study.
It is also clear that the other species measured, e.g. American chestnut, are more effective carbon sinks than oaks as young trees.
See the paper or this pop science article on the subject for more information. THere are also a number of papers citing that paper that may be interesting, such as this, this, and this.


How loud a sound would need to be to wake someone up?

I think a SIREN sound with higher Decibel >110 will work. Because as a human being, a high pitch sound create alert signal to our brain.
Still, the sound to wake up a person will vary from person to person.
But a person will definitely react to eardrum piercing sound waves


Yes, there are well established methods for synthesizing DNA with any sequence you want. Several commercial companies will accept DNA sequence (a text file) and generate the DNA for you. Genscript for example is well known.

Synthesizing the protein can be bit more tricky, depending on what it looks like and what you want it for --- proteins are way more heterogenous than DNA. There are commercially available cell-free protein synthesis systems that might be useful if you are merely interested in a peptide. Most people express the protein of interest in cultured cells though. In either case there is some biochemistry work to purify the produced protein. Genscript provides protein synthesis services as well. (No, I'm not paid by them, just don't have the energy to google other companies :)

In most cases, this works fine, and with a bit of tweaking you can produce quite large amounts. But for some proteins that depend on posttranslational modification for their function, expression can be difficult: see Can any enzyme be produced?


Dr Karl Niklas from the Cornell University has written a book about the effects of factors that influenced the shape of early trees. He created a computer model in which he drew trees in the shape that favored particular characteristics.

  When Niklas favored plants that could gather light from the sun, they
  had non-overlapping horizontal branches. When reproductive success was
  favored, the plants grew tall, in order to spread their seeds. When
  the trait selected for was mechanical stability, the plants had few
  horizontal branches.

When he combined these three favourable traits, he noticed that most of the trees today are in a form that favors these three traits (reference).

L is light favourability, M is mechanical stability and R is the shape of trees that favor reproductive ability.

Explanations for a few shapes found commonly with examples can be found in this article.

Illustration for the common tree shapes Columnar, Pyramidal,Vase, Round, Spreading, Weeping and umbrella with a few more examples can be found in this article (reference).

Another interesting thing about trees is the way in which their shapes can be influenced for the purpose of landscaping (reference).

What you mentioned about pine cones in isolation having no definite shape at all, I would like to see a reference that this is a fact before I can elucidate on it further (I couldn't find any articles that mentioned such a phenomenon).

The reason you felt so could be because it were two completely different species of pines. Counting varieties and subspecies, the plant list of the Royal Botanic Gardens, Kew and Missouri Botanical Garden accepts 175 names of pines as current(reference). Here is a list of different pine species (reference).

Here is an article on how tree shape and light available influence yield in cherry trees.


Actually the new data set will be,

for k = 4 (k-mer value)

CGTTCT -> CGTT GTTC TTCT

or

Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874646/


The Wikipedia page you linked says that sweat is composed of a liquid similar to blood plasma. As all DNA in humans is stored in the nucleus of a cell, it seems unlikely that the sweat itself would contain any DNA.

However, when someone sweats significantly, I can't imagine that no skin cells end up in the sweat. In any case in which this occurs, then the DNA in the cell is in the sweat. Additionally, with small amounts of sweat, I can't imagine how it would be collected without getting any skin cells in it.

This source confirms that sweat contains DNA in some form. Additionally, I think the following quote from here shows that it is stored in cells:

  In every case, what is being tested is the DNA contained in cells of human tissue


What causes random long white body hairs?

Since it's been so long, I guess a rushed speculative answer might be at least an idea.

DNA gets damaged randomly all the time, and repair mechanisms are in place to fix it. When the damage is too large or of a very complex kind, permanent mutations can develop, and cause disorders such as cells proliferating without control - i.e. tumours.

I could imagine that the same mechanism could result in cells which overproduce keratin (hair) without melanin (pigment), if the associated genes are affected. Considering that trichocytes and melanocytes, the two cell populations at the base of the hair responsible for production, are among the most rapidly proliferating cell types in humans, an increased risk for mutation would not surprise me. I was able to find a few papers on keratin-associated gene clusters by a quick search, but they all seemed to be related to production of fragile hair rather than excessive length.


Stimulating an axon causes impulses to travel both ways?

Allow me to do a silly analogy: think about the electric wire going from your outlet to your computer, conducting electricity. If you make two cuts in this wire, rotate it 180 degrees and weld it again at the cutting points, what will happen? It will conduct electricity just as it did before.

The same happens to an axon (but please have in mind that this is just an analogy, an action potential is not an electric current). That is, the axon doesn't determine or influence the direction of the action potential. If you cut a piece of that axon, rotate it 180 degrees and join it back in the cutting points, it will conduct the action potential the same way.

That being said, imagine that you stimulate that axon at a given point. There will be two action potentials, going to opposite ways:

unmyelinated (A) and myelinated (B) nerve cells

In your figure (given that is a motor neuron), if you stimulate that axon in the middle, the action potential going to the neuromuscular junction, which is the normal direction, is called orthodromic (from the greek orthos, "proper", and edramon, past of "run"), while the one going to the soma (the perikaryon) is called antidromic (from the greek anti, "against").

According to Oh (2003):

  The sensory nerve conduction study measures the conduction of the nerve impulse along the sensory nerves. The routine method measures the conduction velocity of the large diameter sensory nerve fibers of the nerve being tested. There are two methods of obtaining sensory nerve action potentials (SNAP), orthodromic and antidromic. The orthodromic method includes recording of the sensory nerve action potential proximally and stimulating the nerve distally whereas in the antidromic method the location of the stimulating and recording electrodes is reversed. The latency and conduction velocities are identical with the orthodromic and antidromic methods if the recording and stimulating electrode positions are constant. (emphasis mine)

In a simplified scenario, the orthodromic impulse will reach the neuromuscular junction and stimulate the muscle contraction, while the antidromic impulse will be canceled by another orthodromic impulse or, if it can reach the dendrites, it will simply end, since there will be no neurotransmitter release.

Source: Oh, Shin J., 2002. Clinical Electromyography: Nerve Conduction Studies. Third. LWW.