Cellular respiration in carnivorous animals

Your guess is correct: glucose is not the sole source of energy in the cell!

While cellular respiration is the classic mechanism for energy production (in the form of ATP) in the cell, there's another process that's equally important and a little less well-known: beta oxidation. Beta oxidation is how fats and other lipids in the cell can be broken down to produce energy. In this process, the last two carbons in the long chain are sliced off and transferred to Acetyl-CoA, which can then be used in the citric acid cycle to produce ATP.

Here's the equation describing it:

$$C_{n}acyl-CoA+FAD+NAD^{+}+H_{2}O+CoA -> C_{n-2}acyl-CoA+FADH_{2}+NADH+H^++acetylCoA$$

And here's a good diagram from the Wikipedia page that summarizes it:

Courtesy of Cruithne9 on Wikipedia [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]

This process is why fats actually have a higher energy density than sugars: 9 Cal/g, as opposed to sugar's 4. It's also why organisms tend to use fats as energy storage - while sugar and cellular respiration is great for immediate energy, fats are stable and energy dense so it's an evolutionarily favored idea to use them for long-term storage.

You're also quite correct that animals don't tend to have a lot of free sugars and carbohydrates, unlike plants. Instead, we've converted those carbs into the fat molecules via the reverse process, fatty acid synthesis. So, carnivores largely get their energy from beta oxidation and the metabolism of fats, rather than glucose.


Molds and fungi usually found on book pages: identifying and preventing further spread

Mold can grow in Extreme environments: they can live in very low water activity level, sometimes as lower as 0.71, live in refrigerator temperatures, these characteristics make it difficult to kill them thoroughly.
You can search "paper deterioration" in Google or library, then you can find lots article about this.

1) Causes

Foxing and other white, fluffy coating or light yellow powder on paper caused by: Eurotium rubrum, E. repens, Aspergillus versicolor, Penicillium solitum, and Penicillium decumbens. (Karbowska-Berent, Joanna, Joanna Jarmiłko, and Jolanta Czuczko.
Source: "Fungi in Fox Spots of a Drawing by Leon Wyczółkowski." Restaurator. International Journal for the Preservation of Library and Archival Material 35.2 (2014): 159-179.)

Black spots: Monilia, Aspergillus, Penicillium, Mucor, Stemphylium, Hormodendrum, Fusarium, Chaetomium, Byssochlamys
Source: Beckwith, Theodore Day, Wilbur Harold Swanson, and Thomas Marion Iiams. "Deterioration of paper: the cause and effect of foxing." Publ. Univ. Calif., biol Sci. 1.13 (1940): 299-356.

2) Spreading

For their spread, I think the mold can spread everywhere, but i did not find any resource about it.

3) Method that kill the mold

Drying the affected paper objects and applying 70% ethanol are the most preferred options to stop active fungal growth.
Source: Sequeira, Sílvia O., Eurico J. Cabrita, and Maria F. Macedo. "Fungal Biodeterioration of Paper: How are Paper and Book Conservators Dealing with it? An International Survey." Restaurator. International Journal for the Preservation of Library and Archival Material 35.2 (2014): 181-199.


What is the fate of NADH produced in the liver during oxidation of lactic acid?

The “best guess” in this question is incorrect and the question itself indicates a lack of understanding of the roles of NAD+ and NADH in energy metabolism. (To rectifiy this, Chapters 17 and 18 of Berg et al. are suggested.)

The production of NADH in the oxidation of carbohydrates and fats is the energetic rationale for these processes. Under aerobic conditions the re-oxidation of NADH to NAD+ via the electron transport chain in the mitochondria* generates ATP for the energetic processes of the cell.

The fate of NADH produced by the oxidation of lactate reaching the liver from the blood would be similar under conditions where it is not needed for gluconeogenesis (in the reversal of the GAPDH reaction).  In these circumstances it would be reoxidized to NAD+, generating ATP in the mitochondria*.

[Note also that pyruvate is most likely to be oxidized by the liver mitochondria to produce metabolic intermediates and ATP, rather than transferred to the blood. NADH is certainly not transferred to the blood.]

*Advanced Point: Cytoplasmic and Mitochondrial NAD

The statement above, that NADH is “reoxidized to NAD+, generating ATP in the mitochondria”, is correct, but may be taken to imply that the NADH enters the mitochondria. This is not the case becase the NADH and NAD+ cannot pass through the mitochondrial membrane (as @tomd has commented). However the electrons that represent the reduced state of NADH do pass through the membrane. They do this in the guise of other molecules which are reduced in the cytoplasm by NADH in what are known as electron shuttles. The electrons enter the electron transport chain and are finally accepted by molecular oxygen. More detail of shuttles can be found in section 18.5 of Berg et al.


From comments I understood that you need to predictions in bulk. You can use API based system of JPred. They allow you to submit more than 1000 jobs per user per day. You can go through instructions step by step from their documentation. It looks simple !

Another hit I got while searching is Phyre2. I am sure there are many such servers.


How to evolutionary explain menstrural cycles synchronization?

This is a myth which most likely came from methological flaws in the original study. It could never be reproduced. This paper ("Darwin’s Legacy: An Evolutionary View of Women’s Reproductive and Sexual Functioning") deals with it. The interesting part starts from page 30 and says (the references can be ressolved in the article):

  Critiques of MSH Studies

  Wilson (1992) and Yang and Schank (2006),
  among others, have criticized the study design, methods, and
  statistics used by McClintock (1971) and others who have claimed
  evidence of MS. For example, McClintock
  incorrectly used the Page test for ordered hypotheses with multiple
  treatments (she used the same groups of women repeatedly instead of
  independent treatments), making it impossible to evaluate the true
  level of significance of her reported findings. Likewise, reports of
  greater estrous synchrony in chimpanzees caged together than in those
  caged apart (Wallis, 1985) and synchronization of estrogen peaks in a
  sample of five golden lion tamarins (French & Stribley, 1987) are
  rendered moot by the use of unsuitable statistical tests (Schank,
  2001). Furthermore, computer simulations suggested that the null
  hypothesis of no synchronization could not be rejected in either the
  chimpanzee or tamarin samples (Schank, 2001).


Survival of the host cell is in many cases dependent on the egress strategy of the pathogen. There are many examples documented in various species. The only case I found that's somewhat relevant to human cells was were mutant Legionella pneumophila, defective in the lytic pore complex, did not produce necrosis of the host cell. However, the cells did release the bacteria after a while, probably apoptosis due to accumulation.

EDIT: I found an article documenting Cryptococcus neoformans infection.

  Cryptococcus neoformans causes disease in people with immune deficiencies such as AIDS. Upon infection, C. neoformans cells are ingested by macrophage immune cells, which provide a niche for survival and replication. After ingestion, macrophages can expel the fungi without causing harm to either cell type, a process named nonlytic exocytosis.


variation in antigen binding site of antibodies

The processes are called gene rearrangement and somatic hypermutation, and are used by maturing B-cells to generate very (very) large amounts of diversity in the antibody repertoire. If your institution has access, this great article in Annual Reviews in Immunology has all the details, or you can read about it in Janeway (slightly outdated edition). Essentially, the genes encoding the B-cell Receptor, or BCR, have many fragments of several different types in them, and through the process of gene rearrangement the final Complementarity Determining Regions, or CDRs (the antigen-binding sites), are generated into one mature sequence for each individual B-cell.

A mature IgG molecule (the soluble, secreted version of the BCR) contains four chains - 2 heavy (each of which are identical to each other) and 2 light (also identical). There are Constant or C regions in each chain that essentially don't vary much, and are not really involved in the process of antigen binding. On the "business end" are three regions (or types, from above) called V, D, and J in the heavy chain, while the light chain just has V and J. Those letters are from Variable, Diversity, and Joining, if you're interested.

Figure 4.3 from Janeway shows the number of "fragments" or gene segments of each type in humans. So, when the heavy chain is being made, 1 fragment out of 65 Vs is picked, 1 of 27 Ds, and one of 6 Js, then each is joined together in a process that can also introduce an additional amount of randomness at the joins. Combine this with an only slightly less complex process in the light chain (as there is no D region), and the fact that a single insertion/deletion of a base pair can drastically effect the resulting protein sequence, and you get a protein with a huge number of possible sequences, potentially in the range of 1011.

This process of gene rearrangement typically generates immunoglobulins with relatively low affinity for their antigens. During affinity maturation, a process called somatic hypermutation randomly changes individual base pairs (translated to amino acids) in the CDR in cells that are descendents of, and bear the same base sequence as, the original. Cells expressing antigen receptors that are of higher affinity are then positively selected and clonally expanded by the immune system, allowing your body to tailor its response to an infection or other exposure to what it sees as foreign material.


When does a chromatid become a chromosome?

If no centromere split occurs during anaphase and consequently chromatids are pulled to one daughter cell, the possible outcome is during telophase the chromatids uncoils into chromonema which in subsequent divisions become supernumerary chromosomes.


Why do neurons die so fast without oxygen and nutrients?

Neurons use lot of energy to maintain their polarized state, this is not required to other cells [1,2].

When O2 or blood flow (which is carrying the nutrients) is reduced, the neuronal ATP levels breaks down very fast, with 90% ATP depleted in less than 5 minutes. Without ATP, the neuron can not maintain the correct ion flux, so depolarization occurs causing glutamate excitotoxicity, cell swelling and finally cell death.

1] http://www.acnp.org/g4/gn401000064/ch064.html

2] http://www.scientificamerican.com/article.cfm?id=why-does-the-brain-need-s


Why do people feel shame when exposed nakedly?

Probably a cultural effect

In many tribes, people are naked. Also, the naturist movement is very popular in the western culture and they don't feel shame. In northern Europe, it is common to be naked in spas.

I would guess it is mainly a cultural effect and there is little heritability for this trait. I doubt you'll find a study on this particular question, so the best one can do is just to formulate a guess here.

If you don't quite understand why I talk about heritability here, then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is?. In layman terms and in vague terms, I meant that there is probably little role of genes to explain why we feel naked.

Yes, but let's assume it was selected for...

If we were to assume that feeling of shameful in front of nakedness had been selected for, one may hypothesize that it could be due to sexual selection, where rich and wealthy wear clothes. It could also be due the social presssure of showing off what you are worth as sexual body parts are likely under strong sexual selection as well.


The toxin is Meliatoxin, in a class of toxins called tetranortriterpenes.
I found this here.  Bold emphasis mine.
https://wagwalking.com/condition/chinaberry-tree-poisoning

What is Chinaberry Poisoning? The chinaberry tree is a member of the
mahogany family that is native to Australia, China, and India. These
deciduous trees sprout delicate light purple flowers in the spring,
which develop into yellow, berry-like fruits in the summer. They were
transported to North America in the early 1800’s as an ornamental
plant, but has escaped into the environment and is considered an
invasive species in several southern states. It produces a potent
insecticide which utilizes a tetranortriterpene neurotoxin known as
meliatoxin. This insecticide is found throughout the plant’s bark,
leaves, and flowers but is found in the highest concentrations in the
ripe fruit. If you suspect that your pet has consumed any of this
plant, contact your veterinarian immediately. The chinaberry tree, or
Melia azedarach, is a deciduous tree that produces a potent
insecticide which utilizes a neurotoxin that can prove detrimental to
your pet if ingested. Symptoms of Chinaberry Poisoning in Dogs
Symptoms of chinaberry tree poisoning occur most often from eating the
ripe fruit, however, the bark, leaves, and flowers also contain
smaller amounts of the toxic substances. Symptoms usually begin within
just two to four hours from ingestion. Abdominal pain Blood in stool
Colic Constipation Death Depression Diarrhea         Excessive
drooling Heart attack Hyperactivity Lack of coordination Loss of
appetite Muscle rigidity Seizures Slowed heart rate Stupor Vomiting
Weakness Types
The scientific name for the chinaberry tree is Melia
azedarach, and it belongs in the mahogany family.

From another source
http://www.sciencedirect.com/science/article/pii/0031942283830398

Toxic tetranortriterpenes of the fruit of Melia azedarach . .Peter >B.Oelrichs. Michael W.Hill. Peter J.Vallely. John K.MacLeod. .Tadeusz >F.Molinski
Show more https://doi.org/10.1016/0031-9422(83)83039-8Get rights and
content Abstract Four new tetranortriterpenes, meliatoxins A1, A2, B1
and B2 have been isolated and identified as toxic constituents of the
fruit of Melia azedarach L. var. australasica. Toxicity and
pathological results confirm that the meliatoxins are responsible for
most but not all of the symptoms resulting from the ingestion of whole
fruit.


When I optimized gel extraction in my hands, two factors turned out to be critical in maximizing gel extraction yield:

The pH of the eluting solution. I used to elute the final product with DEPC-treated water initially, but the yield would vary a lot as the pH of the water changed. Using buffer EB is better, since it maintains a stable pH 8.

Most importantly, *incubate the eluting solution with the column as long a possible (and also elute twice). * I incubate for about 10 min, which is longer than what they recommend but it works much better.


Is Infra Red light safe to use on your scalp?

These are entirely different devices. First off, the Anodyne product is truly far-infrared, emitting at 890 nm (infrared is above ~650-700 nm). However, the hair loss product you linked is far-red/near-infrared, with laser diodes emitting at 650 nm (which is why it glows red). If you put the Anodyne product on your skull, you'd just heat up your brain, possibly burning any hair you have left. (Well, maybe not, but it sounds kind of funny.)

I would strongly suggest you don't try regrowing your hair using an instrument designed to relax your muscles. I will give you a recommendation - read the small print very carefully. The hair product is only recommended for a certain type of hair loss called Androgenetic Alopecia. Please consult with your doctor to determine if you actually have this condition, otherwise your investment of US$600-700 will be completely wasted.


Can a single axon propagate multiple simultaneous action potentials?

When you say multiple simultaneous action potentials I assume that the stimuli for all of them are temporally overlapping. In such case a neuron can integrate the different stimuli and launch an action potential. Of the multiple stimuli some can be excitatory while others can be inhibitory. The net response would be an integration of all the signals [ref].

However, if there is a gap in the stimuli then the cell may not react as it would be in its refractory period (which results until the ions levels are back to their original state and the membrane potential is restored).

There can be long delays, which depends on various factors such as ion deficiency, ATP deficiency (ATP is needed by Na+/K+ ATPase) or neuropathological conditions. In case of nervous signaling over many neurons then synapses can suffer from synaptic fatigue, which results because of depletion of neurotransmitters.

EDIT:

Maximum AP propagation speed/Nerve conduction velocity = ~120m/s (Can't find original source. From wikipedia)

Longest myelinated axon (sciatic nerve in humans) = ~ 1m

Time required to reach synapse = ~8ms

Time required for repolarization = ~5µs

So multiple action potentials (~160), are possible (lets call it situation-X).

The squid giant axon is ~500µm. I believe it is also non-myelinated. In this case if NCV is less than 100m/s then situation-X can happen. NCV can go as low as 0.5m/s (again the reference is wikipedia as I cannot find the original source).

Having said that, situation-X can also cause synaptic fatigue if the firing rate (AP frequency) goes beyond a certain value. This value would depend on how much neurotransmitter is released per AP, how much is in storage and the uptake rate.


Looks like a papaya that isn't ripe yet. Being said, if you already cut it in half it probably isn't going to ripen any further. A ripe papaya has pink/orange flesh and the seeds turn black.


The reason for this is the oxidation of phenol residues in the banana (for example in the yellow color) which get oxidized by the enzyme Polyphenol oxidase (PPO) to melanins. The scheme (the image is from this website on food browning) looks like this (you can of course also use more complicated substrates):

For further information, see these references:

Banana Polyphenoloxidase. Preparation and Properties.
Molecular cloning and characterisation of banana fruit polyphenol
oxidase

Polyphenol oxidases are widely found in fruits and cause most of the oxidative browning. See these articles:

Polyphenol oxidases in plants and fungi: going places? A review.
Enzymatic Browning, Polyphenol Oxidase Activity, and Polyphenols in
Four Apple Cultivars: Dynamics during Fruit Development


Is there a notion of RMSD for two different molecules?

PyMOL ("align molecule1, molecule2" returns aligned structures and RMSD). TM-align (returns aligned structures and TM-score; tmalign.py is a python module for running TM-align using PyMOL).


What (if anything) about tuberculosis makes producing a highly effective vaccine difficult?

Thats an interesting and complex question. First, Mycobacteria tuberculosis is present for a long time in the human population and evolved to evade our immune system. One of the keys are glycolipids and sugars which are part of the bacterial cell wall. These either help suppressing an immune response or help the bacteria to enter host cells in which they can stay without being identified by the immune system. See references 1-3 for details on this topic.

Then most tuberculosis infections are hold of by the immune system, mostly they come up, when the carriers immune system is compromised. M. tuberculosis can successfully hide inside macrophages and multiply there and start an infection from this hiding place. See references 4 and 5 for more details here.

One of the main problems with the development of new vaccines is that this takes quite a long time from successful experiments in the lab to the availability of a usable vaccine. Tuberculosis has been neglected here for decades. Then the market for such a vaccine wasn't deemed lucrative enough from the pharma companies, as this is mostly important for poor and developing countries. For use there, the vaccine needs to be cheap and easy to administer. Additionally humans are the main host for M.tuberculosis which makes chossing appropriate animal models for research and testing not an easy task.

The development of novel vaccine candidates follow different routes. First, there are live vaccinations, which mainly consist of modified strains of the BCG vaccine strain. Then there are vaccines in the development which are supposed to support the immune answer by BCG and finally, there are vaccines which are independent of BCG and are mostly composed from proteins of the outer bacterial cell wall. For an overview about this field, I can recommend the review articles 6 and 7, if you want to go deeper in the field, also the references 8-10.

References

Mycobacterium tuberculosis Cell Wall Glycolipids Directly Inhibit
CD4+ T-Cell Activation by Interfering with Proximal T-Cell-Receptor
Signaling
Divergent Effects of Mycobacterial Cell Wall Glycolipids on
Maturation and Function of Human Monocyte-Derived Dendritic Cells
Interactions between Mycobacterium tuberculosis and host cells: are
mycobacterial sugars the key?
Annulling a dangerous liaison: vaccination strategies against AIDS
and tuberculosis
Macrophages Play a Dual Role during Pulmonary Tuberculosis in Mice
Vaccines against Tuberculosis: Where Are We and Where Do We Need to
Go?
Vaccine against tuberculosis: what’s new
Tuberculosis vaccines: past, present and future.
Childhood tuberculosis: old and new vaccines.
Exploiting the mycobacterial cell wall to design improved vaccines
against tuberculosis


Identification of black growth on onion skin

I think it is Aspergillus niger:

On the second place I'd suggest  Black Mold disease caused by Alternaria species.


Raising two legs together while lying on bed

I suspect it is just physics. Each of your legs makes up about 1/6 of body mass, leaving about 2/3 of your mass superior to your hips.

Raising one leg requires action of the hip flexors (i.e., iliopsoas complex) but also activity in the anterior abdominal wall muscles (rectus abdominis, obliques) and back muscles to stabilize your abdomen. To raise the other leg simultaneously, you recruit the ipsilateral hip flexors. But, importantly, you probably have already maximally recruited most of your abdominal and back muscles.

Imagine the body as a lever system. With one leg raised, you have 1/6 of body mass balanced against 2/3. With both legs up, you have 1/3 vs. 2/3 and with potentially increased torque, because your legs are long (a force acting at a larger distance). The muscle forces to stabilize that must be larger, but the additional muscles are not there.

I can raise both legs with difficulty (admittedly, $n=1$).


The full oxidation of TMB ( 3,5,3’,5’-tetramethylbenzidine) is 2-electron process.  The first step (one electron oxidation) gives the blue product, which is then further oxidized to a yellow product (2nd electron) that is stable in acid.  At high concentrations this might appear brown.
You might also not be fully quenching, leading to a mixture of blue and yellow products (should be more greenish though).  In this case add more stop solution.
TMB chemistry:
Josephy, P. David, Thomas Eling, and Ronald P. Mason. "The horseradish peroxidase-catalyzed oxidation of 3, 5, 3', 5'-tetramethylbenzidine. Free radical and charge-transfer complex intermediates." Journal of Biological Chemistry 257.7 (1982): 3669-3675.


I don't know if it is definitively the simplest, but the simplest organism with a nervous system that has been studied extensively is probably C. elegans, which is definitely able to learn.

Some basic learning abilities have also been shown in amoebae.

References:

Ardiel, E. L., & Rankin, C. H. (2010). An elegant mind: learning and
memory in Caenorhabditis elegans. Learning & Memory, 17(4), 191-201.
Saigusa, T., Tero, A., Nakagaki, T., & Kuramoto, Y. (2008). Amoebae
anticipate periodic events. Physical review letters, 100(1), 018101.


Does the genetic expression of specific physical traits ever correlate to behaviour?

Aldridge et al. (2011) show a correlation between facial phenotypes and autism spectrum disorders (ASD) in a sample of 8-12 year old boys.

They studied two groups of boys, 65 that had been diagnosed with ASD and 41 who had not. They collected 3D images of the faces and looked for similar patterns among the two groups. They found a significant association between some phenotypes and ASD. But, as with most studies, the results are complex; there a distinct sub-groups within the ASD group.

Keep in mind that this is an association study -- no causation is shown.


What is meant by "catalytic amount of a hormone"?

The writer obviously means “small amount”, and has chosen his words badly as hormones do not themselves catalyse reactions.

The idea he is probably trying to convey is that a few molecules of hormone binding to their receptor can cause changes to many molecules within the target cell. This often (generally?) involves catalysis within the cell produced by the receptor activating an enzyme, so one can understand the line of thought leading to the misuse of this term.


How does human body keep track of its age?

It doesn't always. Some people have an undistorted slown down aging. Jyoti Amge is over 18 and looks like an undistorted little girl. Yesterday, I saw a TV show that showed a 22 year old who looked like an undistorted 8 year old girl. There are also people who have distorted aging. People with progeria look like a distorted older person. I think nodoby has an undistorted sped up aging. Gabby Williams looked like a distorted toddler when she was 12. Nicky freeman from https://thewest.com.au/news/australia/forty-year-old-trapped-in-childs-body-ng-ya-220462 has a distorted bone structure of a ten year old boy and is all wrinkly. The girl in the YouTube video at https://www.youtube.com/watch?v=xoBetcKAxII&t=96s has the undistorted bond structure of a 13 year old girl and is all wrinkly.


Why did we evolve to control our breath?

From the abstract of MacLarnon & Hewitt, "The evolution of human speech: the role of enhanced breathing control", Am J Phys Anthropol. 1999 Jul;109(3):341-63:

  Evidence presented herein shows that modern humans and Neanderthals have an expanded thoracic vertebral canal compared with australopithecines and Homo ergaster, who had canals of the same relative size as extant nonhuman primates. Based on previously published analyses, these results demonstrate that there was an increase in thoracic innervation during human evolution. Possible explanations for this increase include postural control for bipedalism, increased difficulty of parturition, respiration for endurance running, an aquatic phase, and choking avoidance. These can all be ruled out, either because of their evolutionary timing, or because they are insufficiently demanding neurologically. The remaining possible functional cause is increased control of breathing for speech.


How do you determine the length of an annelid?

Leeches:
According to Taube (1966)$^1$:

The adults of American leeches range from about 1/4 inch to 12 inches in contracted length.

Because leeches can bloat to more than 10x their "normal" size after a meal (and can undergo up to a 300% change in length), it seems that measuring a leech at anything but their contracted state would lead to wildly too variable of measurements. Therefore, it seems likely that only contracted size would prove to be truly useful.

However, see Klemm (1982)$^2$ (or Klemm,1995 $^3$) for comments about preferred preservation for identification purposes:

[Leeches] have a soft, highly contractile body. Therefore, if leeches are dropped alive into preservatives such as 70% alcohol (ethanol)...they contract strongly and sometimes such features as the eyes, general body shape, and the genital pores become distorted and difficult for the non-specialist and occasionally even for the expert to discern. When leeches are properly anesthetized prior to fixation, there is usually less muscular contraction. the body shape remains more uniform, and there is less variability of the anatomical structures. ... The preserved leech should be straight, moderately extended and undistorted.

However, Klemm does not use body length as an identification feature in his key, and therefore his directions seem to be more concerned with preserving other anatomical features (not to ensure accurate length measurements). He does provide "average size" for species in his key but notes that "contraction during processing" can lead to variation in measured length.

Other Annelids:
Interestingly, naturewatch.ca provides the followign instructions for measuring earth worms:

1.Allow the worm to freely extend itself as if it was crawling.
2.Measure the maximum distance the earthworm covers when completely stretched out.

Similarly, a Ph.D. dissertation by Cynthia M. Hale (2004)$^4$ measured earthworms by preserving them and then

measur[ing] on the longest axis of the straightened individual.

Takeaway:
It seems as though ranges of body length are almost always provided for each species. Although this is not uncommon for any taxa, many sources (including those cited) mention that variability in preservation methods/ body orientation  can lead to variation in lengths recorded (as can age, vitality, gut content, moisture content, etc.). Klemm, in particular, suggests using numerous museum specimens to make conclusions about species because of these variability issues.
As a result of these discrepancies/inconsistencies, I would guess that you're best off citing a methodology source (e.g., Taube 1966) and explicitly indicating your measurement methods.

Lit Sources:
[1] Taube, Clarence M. 1966. Leeches. Institute for Fisheries Research Report No. 1713. http://quod.lib.umich.edu/f/fishery/AAG2862.1713.001?rgn=main;view=toc.
[2] Klemm, Donald J. 1982. Leeches (Annelida: Hirudinea) of North America. EPA-600/3-82-025. Cincinnati, OH.
[3] Klemm, Donald J. 1995. Identification guide to the freshwater leeches (Annelida: Hirudinea) of Florida and other southern states. Florida Department of Environmental Protection. Tallahassee, FL. http://publicfiles.dep.state.fl.us/dear/labs/biology/biokeys/leeches.pdf
[4] Hale, Cynthia M. 2004 Ecological consequences of exotic invaders: interactions involving European earthworms and native plant communities in hardwood forests. PhD dissertation. University of Minnesota.


Cosmid genomic library, or genomic cosmid library?

I've always used Cosmid Library but Cosmid Genomic Library is better than Genomic Cosmid Library.


S. pyogenes cultured on Blood Agar should show beta-hemolysis. B-hemolytic colonies can be further identified as S. pyogenes by the results of negative catalase (hydrogen peroxide) test, positive L-pyrrolidonyl arylamidase (PYR) reaction (1) and sensitivity to Bacitracin (2). See https://www.inkling.com/read/medical-microbiology-murray-rosenthal-pfaller-7th/chapter-19/streptococcus-pyogenes

PCR may also be used: http://www.sciencedirect.com/science/article/pii/S0923250805000215


Can you say "screening for a" in English?

"Screening" can be a verb here ("we screen for the long peptide") so your first sentence would be correct.

Even in this biological context this might still be a question better fit for the English/Learning English forums though.


What plant is this? (Found in South Thailand)

It looks like Desert Rose, commonly used for Bonsai plantings.


What is the thickness of endothelial lining in blood vessels?

I believe apart from natural fluctuations of cellular size, the size of squamous epithelial cells (the cells making up the endothelium of blood vessels) remains the same. Therefore, the thickness of the endothelium does not significantly change for any blood vessel.


Is there a limit to acceptable brightness for plants?

The wikipedia page on photosynthetic efficiency has some useful insight here:

  Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case. Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity. (5)

and

  If photosynthesis is inefficient, excess light energy must be dissipated to avoid damaging the photosynthetic apparatus. Energy can be dissipated as heat (non-photochemical quenching), or emitted as chlorophyll fluorescence.

So, briefly, yes. Too much light can harm plants.

To answer the second question: yes, there exist filters for a large variety of wavelengths of light. You could certainly filter out infrared light, just as most sunglasses filter out some UV light wavelengths. However, just filtering out infrared light would not filter out all photons that could cause damage; likewise, all wavelengths of light have the capacity to heat up what they hit, not just infrared wavelengths.


A bear usually kills its prey by biting it on the back or neck. The bear uses his forepaw to strike very hard, usually breaking the prey's spine so this is why usually his killing instinct is on the back part of a prey. Bears also bite their prey on the snout.
this information can be found at the end of this article: http://www.largecarnivores.fi/species/brown-bear/bears-diet-and-hunting-behaviour.


Does common PCR amplify genes regardless of what cells / barriers they are in?

There are many methods of DNA isolation, so it is difficult to make broad statements about all situations. Typically, though, during the DNA isolation protocol, essentially all proteins are denatured and removed, as is RNA, cell membrane components, extracellular matrix, etc. If you are using a high-quality well-validated kit from a reputable supplier, your final product should be just DNA. In your hypothetical scenario where parasites have been engulfed by macrophages (BTW, eukaryotes don't have cell walls), as long as the parasitic DNA hasn't been degraded, it will be present at some level after the purification process. As long as it is above the minimum sensitivity of the PCR reaction, any parasitic genes that are being targeted will be amplified.

During the PCR process, the heating step to 95°C completely denatures and melts all the DNA present, allowing the primers unrestricted access to their complementary sequences, where they can then base-pair during the annealing and extension step.


Yes, both tea (black tea at least, English speakers usually mean black tea when they say tea anyway) and coffee have caffeine which is addictive.

Apparently, being able to correctly reply to this question involves defining the word "addiction". My guess is that the negative connotation of the word "addiction" will cause some pressure to not use it.

Here's a recent review on caffeine addiction that says that caffeine is not addictive. I do not agree with their arguments but I'll leave it to the reader to judge.


Which statement about phenotypic plasticity is false?

I'll try to answer but I'll encounter some difficulties: first because I don't know what you mean by "plasticity". Does it mean non-reversible developmental plasticity or reversible flexibity. Then, because, I don't really like the word adaptation! Anyway'll try...

a: Plasticity  is some kind of mechanism allowing organisms to adapt to various environment. If the environment is stable and under the assumption the plasticity is associated with a intrinsic (physiological for example) cost, then a population would tend to evolve so that they always display the most optimal phenotype. I would argue that this is under the assumption that we gave enough time for the right mutations happen and under the assumptions that such mutation might exist!

b I don't really understand this statement. Does it mean that between two generations (which mean in one generation time) an adaptation cannot vary.…in what terms? in frequency? Through time any trait vary because of selection, environment, genetic drift and mutations. And to what environment is the trait under consideration adapted for? Can we accept that the environment is changing from one generation to the other in this question? What does this question has to do with plasticity? I guess that when one says that a trait is an adaptation it means (among other things) that the population has no more variance for this trait. Therefore, only mutations would bring variations if there were no environmental change making the trait not adaptive anymore.

c: Well, yes. Plasticity is an adaptation to fluctuating environment. It allows to display a rather optimal phenotype in multiple different environments.

Answer d is wrong for sure. There is variation within a population due to genetic variance and non-adaptive environmental variance (and their interactions). Variance due to plasticity is just some kind of subset of the variance du to the genetic-environnment interaction

Hope this helps a bit!


This looks to be a handmaiden moth (Syntomoides imaon) which has been observed in this part of India.

Source: India Biodiversity Portal


ImageJ is a multi platform piece of software that has a cell counter module that might be of some use, and hey its free! Its easy to use and so ludicrously crude that it is very  versatile. I remember using it in undergrad to count cells under the microscope automatically after a few image contrast tweaks. I don't see why this couldn't be reapplied to count eggs.

Download: http://rsb.info.nih.gov/ij/download.html

Cell Counter documentation: http://imagej.nih.gov/ij/plugins/cell-counter.html


How can co-dominant alleles work in flower petals?

We tend to use "incomplete dominance" to describes situation of haplo-insufficiency.  The white flower petal has two broken alleles for making pigment, and one working copy doesn't yield enough pigment to make the flower look as red as it would if it had two working red pigment alleles.

"Co-dominance" is for two functioning alleles when the effect is that you can see them each, and the result is not an intermediate blend.  Like having a working A antigen and a working B antigen. A blood will not clot when mixed with A blood.  AB blood doesn't halfway clot, it also won't clot at all, just like A blood.


Difference/similarity between adaptive radiation and species divergence?

Adaptive Radiation

A radiation refers to the process by which one species rapidly speciate into a number of different species. A radiation can be adaptive or non-adaptive. An adaptive radiation is a type of radiation when new species are formed through selection into new ecological niches. Such adaptive radiation typically occurs after the raise of a key mutation that allows for further specialization such as a mutation causing a change in the Pharyngeal jaw as observed in cichlids (Albertson et al. 1998).

You can learn much more on adaptive radiation in the book The Ecology of Adaptive Radiation by D. Schluter

Species divergence

Species divergence refers to the process by which two existing species diverge through time, either through the accumulation of neutral (or non-neutral but equally selected) mutations or by selection on different trait values.

Species Divergence and Adaptive Radiation

Because of the semantic difficulties behind the concept of species (see here), it is unclear from which point can we talk about species divergence and by which point the observed process of divergence is only divergence within a metapopulation.

Ignoring the eventual detail of the definition of species, and considering species divergence as referring to the divergence between any two lineage (whether or not in reproductive isolation), then it is clear that species divergence is part of the process of adaptive radiation.

To answer your multiple questions directly

1) On some sites, it says that adaptive radiation is a form of species divergence, while on others it says that they are different. Which one is correct?

Adaptive radiation is a little more than a form of species divergence as it includes also the event by which divergences starts.

2) Is the main difference that adaptive radiation occurs relatively rapidly and species divergence takes longer?

mmhhh... not exactly as the concept of radiation also refers to the event allowing the divergence to happen

3) Darwin's finches is used as an example for adaptive radiation, but is it also an example of species divergence?

Yes, indeed! No radiation, without species divergence. On the other hand species divergence will occur between any two existing species regardless of whether they speciated through a radiation

4) Are the finches on the galapagos islands all difference species (one species diverged into many)? Or are they all the same species, just with different characteristics (e.g size of beak)?

The Darwin's finches refers to about 15 (different) species. The different species of Darwin's finches do NOT refer to intra-species variation but to different species. In other words, there is some reproductive isolation between these different species. Again, you might want to make sure you understand the concept of species and you might want to read this post (same as the one linked above) on the subject.


What would the ploidy of a multinucleate cell be?

Ploidy is generally defined in terms of the number of chromosomes in the nucleus, rather than the number of chromosomes in the cell.

Some examples in support of this:
- A paramecium has a diploid micronucleus and polyploid macronucleus
- Muscle cells are generally considered diploid even though they have multiple nuclei
- The additional chromosomes in mitochondria and chloroplasts are not considered to make cells polyploid, even if the organelle itself may be polyploid.

Thus, I would assess a cell such as you describe to be haploid, albeit with two nuclei.


CO2 availability to phytoplankton in oceans and climate change impacts

Short Answer
I do not believe that CO2 will become less available to phytoplankton on a global scale in the foreseeable future. Instead, I believe that rates of increasing concentrations of CO2 (and resulting chemical products) will not remain sustained at their current levels.
There are two global change phenomenon occurring that are relevant :

increasing concentrations of atmospheric CO2 and
increasing global temperature.

As CO2 concentration increases in the atmosphere, diffusion will lead to higher concentrations in ocean waters as well. The rate of diffusion is related to the relative concentrations of CO2 in both air and water.
Increasing temperatures can impact this diffusion rate as well in two ways:

Increased atmospheric temperatures result in higher surface water temperatures, which leads to less mixing of water (i.e., ocean stratification). This functionally reduces the volume into which CO2 can diffuse and therefore will slow the diffusion rate. (but not decrease the amount of dissolved CO2).

Increased temperatures often decrease solubility of gasses in water, and this decreased solubility may result in offgassing of CO2. However, decreased mixing of strata may result in less upwelling and therefore less offgassing.

As long as global ocean temperatures don't get too warm and atmospheric CO2 doesn't get too low, it seems that the above will result in a net global slowing down of CO2 absorption into oceans but not a reversal (i.e., loss of CO2). In other words, I do not believe absolute CO2 availability to phytoplankton will decrease, but that only the rate of further increased availability will decrease.

Though perhaps such decreases could be experienced as local phenomena?

 Long Answer
It's not immediately clear to me what you're referring to. I'll try to react with some things that come to mind. My response is mostly biogeochemical in nature, so I invite others to address this physiologically if appropriate.
Are you sure you didn't misread something and it's really the declining CO32- that you read about?  (see here). Assuming that's not the case, read on...
Raising Temperatures may decrease the absorption rate of CO2
Alternately, maybe you read that as oceans warm, the water can absorb less CO2 (as in the rate of absorption will decline).
This is due to warm water not mixing as well with cooler lower water, so you end up with unmixing layers (called stratification). Eventually, the surface layer saturates with CO2 and can't absorb more from the atmosphere. It's not that this top layer of water has less CO2, but rather that it gets so saturated that it can't absorb any more (causing the rate of absorption to decline).

Under less warm conditions, the "layers" of water aren't so different in temperature, and so more mixing of layers can happen. As a result, all that CO2 that is being absorbed at the surface level can be exchanged to lower layers of water where it will be stored longer. In other words, with cooler surface temperatures (and therefore greater mixing of layers), the volume of water that can hold CO2 is no longer just the surface, but a much "thicker" layer of water. Result: more CO2 absorbed.

So... raising temps can cause less mixing of water due to more stratification (layering), which results in less water in the ocean available to absorb and hold the CO2. This means that as atmospheric CO2 continues to increase, the non-mixing surface layer of ocean water (which will become saturated with CO2 at some point) won't be able to keep up with more and more and more CO2 in the air. As a result, the ocean will decline (and eventually potentially fail) in its ability  to "buffer" the ever increasing CO2 in the air. This would mean that the rate of CO2 in the air will start increasing more rapidly (since less and less of it is being absorbed by the oceans).
As for the phytoplankton (which are in this top layer of water), this stratification will not directly result in less CO2 availability to them. As atmospheric CO2 increases, so will the amount in this top layer of water. The rate of increase in CO2 concentration will just slow until a saturation point is reached, but absolute levels will not decline.

Though, note, however, that phytoplankton tend to thrive in areas of high nutrients (i.e., upwelling zones). Less mixing of waters will decrease the upwelling of nutrient-rich, cooler subsurface water. So less mixing (i.e., more stratification) likely would lead to declines in phytoplankton abundance due to decreased nutrients availability. (See here). Perhaps this decreased nutrient availability (which would include loss of carbon sources) is related to what you're referring to?

Read here for some more thoughts: https://earthobservatory.nasa.gov/features/OceanCarbon
Raising Temperatures may decrease CO2 solubility
However, given all this, the solubility of CO2 in water does decline with increasing temperature (see here for raw data). This suggests that some rise in global temps may impact CO2 concentration in ocean waters.

The cause for this decreased solubility with increased temperature is due to the imbalance of an equilibrium state of free energy required for dissolving/off-gassing gasses in/out of water. Since the dissolution of CO2 into water is an exothermic reaction (i.e., one that releases heat), any addition of heat will lead to a greater favoring of the opposite endothermic reaction (release of dissolved gasses in this case). In more chemical terms, added heat to the solution provides energy to overcome attractive forces between the CO2 and the solvent (i.e., water) molecules. The result is decreased solubility. See here and here for further explanation.
(The partial pressure of gasses are also impacted with increased temperatures, so investigating Henry's Law might also be pertinent to your research. (This link I found quickly explains a bit of the phys/chem).)

However, to further complicate all of this, not all of the CO2 absorbed by ocean water remains as carbon dioxide. Much of it undergoes reactions to become carbonic acid, carbonate, etc. (see here). This means that the equilibrium state is more complex to model or understand vs simply examining these effects on CO2 in water in a controlled lab setting.

This solubility fact, in combination with the mixing of layers above, are why polar waters tend to absorb more CO2 and equatorial waters tend to give off more CO2
From http://www.carboeurope.org/education/CS_Materials/CO2solubility.pdf:

In the world oceans, the northern Atlantic and the southern Oceans act as major sinks of CO2 because they are colder. Adding to this, cold water is denser than warm water, causing it to sink. The carbon dioxide taken up in the surface can be effectively transported to the deeper waters by convection hence the CO2 is stored in the bottom layers of the ocean.

On the other hand, warm equatorial waters tend to release CO2 into the atmosphere. In these regions upwelling of CO2-rich deep waters occurs. When the water reaches the surface, it is warmed decreasing gas solubility leading to the degassing of CO2 .

However, note that if there is greater stratification of water (i.e., less mixing) as described above, such upwelling could actually decline. This would result in trapping more CO2 in cooler waters instead of warming those wters as they rise to the surface and offgassing that CO2 back into the atmosphere. (We won't even begin to discuss how ocean currents in general will be impacted by changes in temperature...).

To add even more complication, as waters warm, ice will melt leading to (at least temporary) increased mixing of ocean waters!! (see here). If temperature decline from ice melt is great enough to combat the increased surface temperature, then perhaps for some period greater mixing and offgassing could occur.

End results
What does this all mean for climate change?
Well, as atmospheric CO2 increases, it's going to make the oceans more acidic (due to carbonic acid). In other words, if we kept temperature constant, more atmospheric CO2 means more ocean CO2. (You can see that from my previous two links -- again, here (showing ocean CO2 concentration on Y axis) and here).
However, as the earth warms up, water temps will warm up. This means less mixing and therefore less net CO2 absorption. It also means that the warmest surface waters will not hold as much CO2 due to its reduced solubility, which will result in greater "off gassing" of some CO2. The combination of these two things means essentially that the rate of CO2 increase in the atmosphere will likely accelerate.
But what is the net impact on oceans? (and therefore on plankton)
Well, in regards to the oceans themselves, there is probably some calculable "tipping point"  in which the higher concentration of CO2 in the atmosphere (and therefore greater diffusion pressure) doesn't outweigh the reduced solubility of CO2 (due to higher temps and less mixing). At whatever temperature that tipping point occurs, then I assume that the CO2 in the oceans can/will decline instead of increase. In reality, though, gasses are constantly moving back and forth between atmosphere and ocean, so it's unlikely the ocean water will get so warm that there is a net movement out of the water, but probably just a decrease in the rate of further absorption.
On a more local level, if the phytoplankton are living in an especially warm region of ocean, it is possible that off-gassing of CO2 increases in those regions due to the decreased solubility as described before. However, again, if the concentration of CO2 in the atmosphere and the temperature of the atmosphere both keep increasing, then these effects would (at least partially) negate the increased offgassing from reduced CO2 solubility. Again, modelling when this would occur is much too complicated for me to figure out for this post, but I'm sure we have experts working on calculating this "tipping point" as we speak.

Again, the bigger issue for the phytoplankton is probably the reduced upwelling of nutrient-rich water due to greater climate-mediated stratification of the ocean column.

Final Thoughts
Given all of this explanation, ice-core research by Pedro, Rasmussen and van Ommen (2012)  (summarized here) suggests that after only a few hundred years of warming, CO2 concentrations seem to decline in ice cores. This may suggest that perhaps a net release of CO2 is possible within a hundred years or so. Again, this "tipping point" is likely calculable, but it's too complicated for me to figure out for a stackexchange post ;p.
Further readings:
Basu, S. and Mackey, K.R., 2018. Phytoplankton as key mediators of the biological carbon pump: Their responses to a changing climate. Sustainability, 10(3), p.869.
Hülse et al. (2017) Understanding the causes and consequences of past marine carbon cycling variability through models. Earth-science reviews, 171, pp.349-382.


Is it possible to combine live attenuated and non-live vaccines?

First let me point out that for the US, I'm not knowledgeable enough to speak for the rest of the world, you are correct.

There are no approved live attenuated vaccines mixed with componet/subunit/inactivated vaccines.

Background:

Before we go into why that's true, let's work a little to show that's true.  The FDA publishes a wonderful list of every approved vaccine for use in the US.  Of the 78 vaccines listed (and there is a lot of redundancy due to different manufacturers etc), only 16 are live attenuated (or about 20%).

Another thing to notice is that we have vaccines to both viruses and bacteria.   Technically, some of the vaccines are to bacterial toxins, not bacteria themselves, but for the sake of simplicity, we're going to group all bacterial component, subunit, and inactivated vaccine preparations together in one group.

First you will note that there is only one live attenuated vaccine for bacteria, Mycobacterium bovis (more on this exception later).  There are several reasons for this, but as a general rule, you don't want to put a foreign object capable of self replication inside a person.  Viruses cannot self replicate, they are obligate parasites by definition, so they don't fall under this rule.  One could, however engineer bacteria that were sufficiently deficient in replication that this might not be an issue.  Another safety concern with live attenuated bacteria is sepsis.  Again by choosing a delivery route that doesn't involve injections, you might be able to mitigate this risk.

I also want to be clear that I think live attenuated bacterial/fungal (yeast mostly) vaccines can work more broadly, and are likely to be used in innovative vaccine strategies.

The main obstacle to a live attenuated bacteria vaccine is that the component and subunit vaccines work.  Sometimes they work even better by only supply the part of an organism that is known to provide broad neutralization (getting rid of) of the pathogen.  And if you know that you can provide protection with out the risk of putting the live organism in a person, why would you take that risk?

Quite simply you don't.  Back to M. bovis.  For the most part, humans are not vaccinated with M. bovis (BCG) to prevent M. Bovis infection (though zoonotic infections can occur).  Instead it is to prevent M. tuberculosis (MTB) infection.  Attenuation of MTB is difficult, and not complete.  Indeed we don't have a subunit or component vaccine that has worked for MTB, and an inactivated MTB has more safety concerns than BCG.  Thus we choose a related organism, M. Bovis, which naturally doesn't cause disease in humans (or rarely), but can provide some protection against TB.  Even the product insert admits that efficacy of the vaccine is in question.

The same pattern of necessity holds true for viral live attenuated vaccines.  They are used when you need a more immunogenic vaccine, and where we haven't been able to make safe and effective, inactivated, subunit, or VLP vaccines.  Thus when you need a live attenuated vaccine, you really do need it to be alive for it work.

Answering the core question:

As @MattDMo pointed out, the storage conditions are very different for live attenuated vaccines.  Not only that, but most of the preservatives used in many inactivated vaccines cause titer loss (though there is work to find alternatives).

On the theory that a picture is worth a thousand words, I did a little experiment just for this post (and also I was cleaning out an -80).  I took a high titer stock of measles virus that has a protein tag on one of the proteins so we can easily detect it (F is Flag tagged).  Then I spiked 3 different tubes of virus in ether PBS (saline) or DTaP (an actual dose, just past expiration), and left them in the refrigerator (4oC) for 8h.  Note that Merk thinks you should toss the measles vaccine if you don't use it within 8/hours (also note their comment on preservatives).  Then I infected some cells that grow up measles, and harvested the cells in a total cell lysate.  Finally I ran equal amounts of total protein form each preparation on a gel for a western blot:

You should notice the three pairs of bands, in each case the lighter band (indicating less protein) belongs to the DTaP group.  That is to say less measles F protein (something you want to make antibodies to) came from the samples that were put into the DTaP vaccine compared to PBS.

Another serious problem is cold chain:

Again we need the virus to be "alive" when we give a person a vaccine.  This almost always means that we have to keep it frozen or at least refrigerated from the manufacturer, all the way up until moments before it goes into a person's arm.  There are many good reviews on cold chain to be found.  Quite simply, inactivated and component vaccines do not have the thermo-stability requirements that live vaccines do.  It would be a waste of energy in most cases to chill all of the vaccines which could be left at room temperature, and it would remove one of their clear advantages.

As far as the immunology is concerned, there is probably not a real limit on what the body can react to.  Indeed, as you point out, they are often administered at the same time in developed countries.  It is merely a question of how you can keep live-attenuated vaccines "alive" in the same preparation.  It is certainly possible that there is a solution to this, and vaccine stability is an active field of research.  Hopefully in 10-20 years we will be able to adjust this answer to say that such a vaccine has been made, and that it's safe enough for approval.


Why exactly does the immune system weaken with age?

We don't know.

More precisely, we know of many, many different reasons why the immune system deteriorates with age, but we don't really know which are different measures of the same thing, which are independent factors, which factors actually cause problems and which are harmless and incidental, and so on.

There are too many age-related phenomena to try to list. There's a nice recent review Aging and the immune system: An overview which spends time on

Aging and the immune cell repertoire
Cell Intrinsic defects in lymphocytes
"Inflammaging" ("an overall decrease in the ability to cope with different stressors, accompanied by a progressive increase in the organism's pro-inflammatory status")

Each of these broad topics can be broken down into dozens of sub-topics, and the molecular and evolutionary mechanisms underlying each are rarely well understood.

It's a huge area of research, and it's not possible to give a single concise answer.


Amount of carbon captured in photosynthesis by a plant

Welcome to Biology.SE! I am not entirely sure what your are asking but here are some places you might want to start:
Photosynthesis Molecular Biology
If you want to know about the number of sugar molecules created 'per photon' by photosynthesis you can explore the light-dependent and light-independent reactions used in photosynthesis. In particular you might want to look at the Calvin Cycle and how NADPH is used there and how NADP is reduced to NADPH in the light-dependent reactions.
Carbon Capture Efficiency
You might be interested in the variation between plants in carbon capture efficiency, i.e. not all plants are equally 'good' at photosynthesis. To think about this you might want to look at different photosynthesis mechanisms (C3 vs C4 and CAM; different forms or amounts of Rubisco enzyme) or you might want to look at sunlight 'capture' mechanisms (photosystem I and II and the accessory pigments like chlorophyll and carotenoids) or even at adaptations to different light environments (trichomes, leaf shape, etc).


What makes you think that the lac repressor will still be bound at the target gene?

In strains with this type of regulatory configuration (usually with DE3 in the genotype) the idea is that IPTG induction turns on expression of T7 polymerase from a lac promoter on the chromosome, and then this T7 polymerase then transcribes the target gene on the plasmid. The presence of IPTG ensures that repressor will bind at neither site.

Supplementary:

I think that I understand why you are confused now. Your picture of the way this works is based on the idea that the repressor is locked on to the operator until an inducer such as IPTG comes along. In fact there is an equilibrium between bound and unbound:

  repressor/operator <=> repressor + operator

and, in the brief periods when the repressor isn't bound, the E. coli RNA polymerase can bind and transcribe the operon. This is referred to as 'escape synthesis' and it is generally assumed that it is functionally relevant in ensuring that there are low levels of lac permease expression at all times so that lactose can be taken up. If this wasn't the case, how would the natural inducer (a derivative of lactose) ever be able to induce the lac operon?

In protein expression systems it is generally considered desirable to keep escape synthesis of the foreign protein to a minimum so that there is no selection acting on the gene to negate any deleterious effects of its expression. The use of T7 polymerase as an intermediate level of regulation helps to achieve this. Even if there is a low level of escape synthesis of T7 polymerase, the concentration of T7 polymerase will be so low in the uninduced state (compared to the endogenous RNA polymerase) that the amount of escape synthesis of the target protein due to T7 polymerase gaining productive access to the T7 promoter on the plasmid will be negligible.

Read more here.


Can animals and humans be ranked in their ability to detect moisture?

I think you simply Can't.

To design an experiment you need 2 things:

1- Something Common between Humen and Insect and can be measured.

2- Different scale to order the species.

And I Think here you just do NOT have both criteria.


Can in the case of multiple sclerosis (MS), a too high osmotic pressure in the nerve, lead to a high intracellular concentration of potassium?

Firstly, demyelination has got nothing to do with membrane integrity of the neuron. Demyelination causes the current to "leak" through the ion-channels and thus causing loss of signal.

There is an old article which reports a study on membrane integrity of RBCs of MS patients but there seems to be no connection.

It has been proven that neurons do secrete some cytokines such as IFNgamma but the signaling is mostly para/auto-crine and I dont think the cytokines will accumulate in CSF.

MS is identified by the presence of anti-myelin antibodies, which might be the exact biomarker for the disease. A general neuroinflammation is not concluded as MS.

So to answer your final question

  Is there research of this ?

There is none that exactly talks about neuron membrane dynamics in MS. The most parsimonious assumption is that there is no effect, but any hypothesis has to be proven. It might be experimentally difficult to address this question and how to design the experiment for this study would be an interesting question.


Is it possible that nearly human mammals existed before the last mass extinction dinosaurs?

Short answer

No!

Longer answer

The ancestor of all mammals lived about ~180 millions years ago (see here), so much before the Cretaceous–Paleogene extinction event (~65 millions years ago). The ancestor of all primates lived ~65 millions years ago (see here), so pretty much at the same time as the C-P extinction.

But please, don't picture the ancestor of all primates as something that is too human like. It looked more like a lemur, a tarsier or a loris, than like a human!

The first great ape lived about 14 millions years ago (see here) and the most recent ancestor of chimpanzee, bonobos and humans lived about 6 millions years ago (see here). The discovery of how to control fire happened about 1.5 millions years ago (with a pretty wide confidence interval, see the wikipedia article). The first generally considered Homo sapiens lived about 200,000 years ago (see the wikipedia article). The wheel was first invented about 5'000 years ago (see the wikipedia article).

Related: Who are humans' closest relatives, after primates?


What is the benefit for cells having the ATP production regulated in mitochondria compared to being from the nucleus?

For starters, see this thread.

My understanding is that the ancient predecessors of mitochondria were free-living unicellular organisms. Supposedly at one point, these mitochondria-like cells developed an endosymbiotic relationship with a larger cell. This relationship was advantageous for both cells: the smaller cell could focus on energy production, leaving tasks like homeostasis, nutrient collection, etc, to the larger cell. Over evolutionary time, this endosymbiosis caused the smaller cell to lose all functions unrelated to energy production, while the larger cell (as we now know it) came to rely heavily on the mitochondria for energy production.

So it's possible that at one time the nucleus encoded machinery for ATP production, but apparently the modularity and separation of function provided by this ancient symbiosis turned out to be successful.


What is the mechanism by which seeds stay alive while in storage?

Seeds are made from cells in an amorphous metastable superviscous state because the cell's cytoplasm becomes a solid matrix of hydrogenated oil and sugar. The fats also contain a lot of anti-oxidants, so that ambient oxygen that can affect the dormant cells is absorbed by buffer chemicals.
The sugars and oils in the cell cytoplasm (the inside of the cell) become hydrogenated, and change into margarine and then become solidified fat and solidified sugar. Then the consistency of the cell at that stage becomes glassy because it's so solid, which is what you can see if you try to crack a peanut or a lentil, it has a glassy surface. The cell fats can rapidly become liquid again if they absorb water and change their chemistry.
references and images
It's not very different from microbe dormancy, so it's like an ancient biological trick that cells have been doing for billions of years.
The cotyledon is the future baby leaves of the seedling, the radicle is the root and the plumule is the leaf shoots, they are all made of cells that are in a solidified dehydrated form made of fats and sugars and special chemicals that resist ambient water and oxygenation in a controlled way.


Is there a biological explanation for perceived altered cognition whilst on cannabis?

There has only been little research on the neurocognitive and neurophysiological effects of cannabis. There have been introductory neuroimaging studies in mainly non-psychotic populations, which show that cannabis does not affect gross brain anatomy. On the other hand however, it has been proved that cannabis does acutely increase cerebral blood flow (temporarily; in the right hemisphere) on the long run, exposure will cause an overall reduction in cerebral blood flow.

There have been studies with animals where they used an active cannabinol called delta-9-THC to demonstrate enhanced dopaminergic neurotransmission in brain regions which are usually associated and known to be implicated in psychosis.

In humans the delta-9-THC causes psychotic-like states and memory impairments. The effect of a CNS cannabinoid system, on humans is still tested by neuroimaging studies.
The endogenous cannabinoid system is sensitive to contact with exogenous cannabinoids such as the delta-9-THC, which is known to impair memory in humans.

In a further study is was examined what impact chronic cannabis use has on memory-related functions by examination of the subsequent memory effect (SME) of the event-related potential (ERP). The study concluded that comparing the group to the control group that chronic users of cannabis have an altered memory related brain activation in the form of dysfunctional SME production which may also go hand in hand with reduced neural efficiency.

Several investigators studied the acute effects of cannabis specifically on attentional processing. Hart et al. (2001) studied the effects of placebo, light (1.8%), and heavy (3.9%) THC cigarettes in chronic, daily cannabis users and found no significant differences in the accuracy of response to attentional tasks. However, performance on a tracking task, which requires sustained attention, was found to improve significantly after the high dose of THC, relative to the other conditions.

In one study of 37 adults with a history of light cannabis use, acute intoxication with a high dose of THC resulted in significant impairment on a measure of impulsivity (McDonald et al., 2003). Another study (Ramaekers et al., 2006) found similar impairment on a task of inhibition in intoxicated, chronic cannabis users. The results measured where in a timespan from 0-6 hours after consumption.

In another study from 2010, researchers investigated "semantic-priming".

  Under the influence of cannabis, users showed increases in both automatic semantic priming and schizotypal symptoms compared with controls. When abstinent, cannabis users exhibited hyper-priming at long SOAs.

References and further reading:

Linszen D, van Amelsvoort T. Cannabis and psychosis: An update on course and biological plausible mechanisms. Curr Opin Psychiatry. 2007;20:116–20
de la Serna E, Mayoral M, Baeza I, Arango C, Andres P, Bombin I, et al. Cognitive functioning in children and adolescents in their first episode of psychosis: Differences between previous cannabis users and nonusers. J Nerv Ment Dis. 2010;198:159–62.
Bossong MG, Niesink RJ. Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophrenia. Prog Neurobiol. 2010;92:370–85.
Battisti RA, Roodenrys S, Johnstone SJ, Respondek C, Hermens DF, Solowij N. Chronic use of cannabis and poor neural efficiency in verbal memory ability. Psychopharmacology (Berl) 2010;209:319–30.
Hart CL, van Gorp W, Haney M, Foltin RW, Fischman MW
Neuropsychopharmacology. 2001 Nov; 25(5):757-65.
McDonald J, Schleifer L, Richards JB, de Wit H
Neuropsychopharmacology. 2003 Jul; 28(7):1356-65.
Ramaekers JG, Kauert G, van Ruitenbeek P, Theunissen EL, Schneider E, Moeller MR
Neuropsychopharmacology. 2006 Oct; 31(10):2296-303.
http://druglibrary.org/schaffer/hemp/general/mjeff1.htm


Snakes have no eyelids. Each eye is covered with a single, transparent scale. These eye scales protect the eyes from mechanical damage, and prevent the eyes from drying out, just as an eye lid would do. In effect, snakes developed another solution to protect their eyes.

As a result, snakes cannot blink and they sleep with their eyes open.

A snake’s eye scales are part of its skin. This means that when a snake sheds its skin, it must also shed its eye scales. When it is time for shedding, the eye scale turns opaque, reducing vision (Fig. 1).

Fig. 1. Opaque snake eye before skin shedding. Figure source: Snakes are long blogspot

Source: Museum of Victoria


Global database for patients with rare and important injuries or disease?

The MatchMaker exchange project is a federated approach that allows clinicians to find matching cases based on genetic or phenotypic similarity, retaining patient confidentiality.


What determines whether a substance can diffuse across the blood-brain-barrier?

Short answer
The two most important factors that favor passive diffusion across the blood-brain-barrier (BBB) are:

high lipid solubility;
low molecular weight.

And to a lesser extent:

absence of charge;
low affinity for BBB proteins;
not being a substrate for the efflux pumps present in the BBB.

Background

The blood-brain-barrier (BBB) is principally formed by the endothelial cells in the capillaries of the central nervous system (CNS), as depicted in Fig. 1. Outside the CNS, the endothelial cells lining the capillaries allow for relatively free diffusion of substances from and to the blood via transcellular diffusion. In other words, substances can diffuse relatively freely to and from the blood via the extracellular space between the endothelial cells. In contrast, endothelial cells in the capillaries in the CNS are coupled via tight junctions, which prevents most compounds from diffusing into the extracellular space in between the cells (Fig. 1). Therefore, for compounds to enter the brain, they have to diffuse into the endothelial cells and back out again into the brain. This means they have to diffuse from the aqueous milieu in the blood, through the lipid-rich cell membrane and back into an aqueous solution in the extracellular space in the brain (source: University of Texas).

Blood-brain-barrier. source: RIT

Most drugs cross the blood-brain-barrier (BBB) by transmembrane diffusion, which is mainly dependent on whether the drug is able to meld into the cell membrane. A low molecular weight and high degree of lipid solubility favor this mechanism. However, a drug taken up by the membranes in the BBB must eventually dissolve into the aqueous environment of the brain's interstitial fluid to take effect. As a result, a substance that is too lipid soluble collects in the lipid portion, but is not able to leave the BBB. I.e., it enters the BBB, but doesn't cross it.

Moreover, lipid solubility also favors uptake by the peripheral tissues; this, in turn, lowers the concentration of the drug in blood.

Thus, while lipid solubility can increase transport rate across the BBB, it can also lower the amount of the drug presented to the BBB.

Factors in addition to lipid solubility include charge, tertiary structure and degree of protein binding. Chief among these secondary factors, however, is molecular weight. The best approximation of the influence of size on BBB penetration is that it is inversely related to the square route of molecular weight. Few substances over 500 Da cross the BBB. In addition, lipid-soluble substances with molecular weights over 400 Da can be substrates for P-glycoprotein, a major brain-to-blood efflux pump located at the BBB, which prevents or greatly retards a large number of small, lipid soluble molecules from entering the CNS. However, Peptides and proteins with molecular weights in excess of 600 Da are known to cross the BBB in amounts sufficient to affect CNS function, such as the enkephalins. The largest substance found to date to cross the BBB by the mechanism of transmembrane diffusion is cytokine-induced neutrophil chemoattractant-1 at 7.8 kDa (Banks, 2009).

Note that some parts of the brain do not feature a BBB, including but not limited to, the pituitary, area postrema and pineal gland. Many of these areas participate in hormonal control. These structures hence need to be in contact with the blood stream to sense the presence of hormones and other compounds (source: University of Texas).

Reference
- Banks, BMC Neurol (2009); 9(Suppl 1): S3


What causes the line patterns in the palm of the hand?

The lines on the hand are known as flexion creases, and they exist because in their absence, the skin will stretch outwards when the palm is closed due to the decreased surface area of the closed palm, causing problems with gripping.

Developmental disorders such as Down Syndrome often cause there to be only one palm line, known as the simian crease, as shown on the left.


What to look for when buying a light microscope?

Well it depends on the application. First you have to determine what it is that you want to view under the microscope e.g. an organism such as Drosophila or you want to see microscope slides? In the first case you need to by a dissecting microscope, otherwise you need to by an upright light microscope with the appropriate objective lenses, again depending on the application. If you are viewing cells in a flask/dish/plate in a cell culture setting or if viewing a haemocytometer (although not necessarily in the case of haemocytometer), you need to buy an inverted light microscope with phase contrast since you wouldn't be able to view the cells very well with an upright microscope since the goal is to reduce the distance between the objective and the sample for a better view of the samples in cases of dishes or plates. Again the choice of equipment depends on the application. But as correctly said above you need to clarify what you mean in the question.


Apparently, this is a Pollenia sp
https://forum.waarneming.nl/smf/index.php?topic=447650.0.

One of the common species from this genus, Pollenia rudis, is often found overwintering in groups in attics and is therefore known as the cluster fly or attic fly.


The genus Acesina has been revised and is now part of the genus Arhopala. The wikipedia page for Arhopala has some additional information on this genus.


An experiment to test if a bacterial resistance gene is on the plasmid or chromosome?

Based on the situation you have described, isolating the plasmid from the ampicilin-resistant strain of E. coli and allowing it to be taken up by a separate, non-resistance strain of E. coli would be the most efficient, and cost effective method of determining whether or not the AmpR gene is located on the plasmid or the bacterial chromosome itself.

In order to do this, you would need to first grow a culture of the ampicilin resistant strain, from which you could induce lysis of cells in order to obtain a solution containing free plasmids.

Several different plasmid isolation or mini-prep procedures exist that are typically quite effective, if done correctly.

Additionally, many specific "plasmid-isolation" and "plasmid-purification" kits exist that would offer the materials and instructions needed to undergo this process: Isolating your Addgene Plasmid DNA from Bacteria

After properly isolating the plasmid from your ampicilin-resistant strain, you would then need to insert that plasmid into a non-resistant E. coli strain. Bacterial transformation via electroporation is a commonly used technique that causes increased permeability of bacterial cell membranes, enabling the plasmid to enter or be taken up by the cells.

Once these cells have been allowed to "recover" they can then be grown in liquid or solid culture containing ampicilin. Growth would indicate the AmpR gene is present in the bacterial strain, and that the plasmid is responsible for carrying this resistance. Likewise, no growth would suggest that the gene must have be present on the bacterial chromosome instead.


Why do antibiotics have a special importance when taking lactulose?

From the Wikipedia article (I'm sure there's a scholarly reference, but I think this is well-known):

  Lactulose works by relieving constipation through a number of different methods. Lactulose is made up of sugar molecules and is partly broken down by the bacteria that live in the lower part of the gut.

So, certain antibiotics affect (and reduce) the intestinal flora (and neomycin especially so, which is I believe the reason why it is mainly used in ointments), leaving the lactulose undigested and not as effective in forcing the body to retain water in the colon, which is the mechanism through which the drug acts.


What is the inlet/outlet speed of air going in/out of our mouth during inhalation/exhalation

Quick clarification firstly, the main change in thoracic volume that causes inspiration is not as a result of the alveoli expanding - they have no smooth muscle lining therefore are unable to spontaneously contract.  They do have some elastic fascia however their expansion is passive. The change is mainly as a result of the diaphragm contracting to become flatter, increasing the space that the lungs can occupy.  The external intercostal muscles also raise the ribs (in adults) which further allows for inspiration.

Figure One: Inspiration and Expiration(1).  "Rib muscles" refers to the external intercostal muscles.

With that being said, the value I think you are looking for is peak expiratory flow.  Peak flow is a common medical measurement that is often taken in the management of patients with respiratory conditions, either as part of their management plan or acute assessment.  Peak flow is a measurement of the maximum speed that a person can exhale at.

As the comments on your question suggest, this varies dramatically between person to person.  Ignoring any pathologies - such as asthma, chronic obstructive pulmonary diseases (COPD) or nerve damage to the diaphragm/intercostal muscles - peak expiratory flow varies primarily with age, gender and height.  These variations are summarised in charts of expected peak flow that are used, amongst other things, to grade the severity of an asthma attack (and consequently how aggressively to manage it).  Charts resemble the following:

Figure Two: Normal values for peak expiratory flow used in UK hospitals - The EU Scale (2)

So if you pick the height, gender and age that you feel is appropriate for your question, you can then read off peak flow in litres per minute.  Then you would need, I think, to work out the area of the aperture (in your case the mouth) to get a speed in metres per second?

Medina B. Brenda's A&P eportfolio: objective 48 & 49: inhalation and exhalation [Online]. 2011 [accessed 2012 Dec 11]. Available from URL: http://blm1128.blogspot.co.uk/2011/04/objective-49-contrast-inspiration-and.html.
Häggström M. File: normal values for peak expiratory flow - EU scale.png [Online]. 2009 [accessed 2012 Dec 11]. Available from URL: http://en.wikipedia.org/wiki/File:Normal_values_for_peak_expiratory_flow_-_EU_scale.png.


Whole genome amino acid composition tool?

I have written a script that will get you started. It downloads all protein coding transcripts of the species of interest from Ensembl and prints the codon use for each codon on each transcript.

You will need to install the Bio::EnsEMBL::Registry Perl module, see here for instructions. The script also uses the Math::Round module, everything else should be installed by default with your Perl distribution. Finally, the script expects to be run from a Unix/Linux operating system.

Example run

 ensembl_get_codon_count.pl human > human.csv

Example output

Gene Name   Gene ID      Transcript ID  Ala_GCC Ala_GCC_% Ala_GCA Ala_GCA_% Ala_GCG Ala_GCG_% Ala_GCT Ala_GCT_%
CRLF2   ENSG00000205755 ENST00000400841    6       40        6      40         0       0         3       20

In the example above, the transcript ENST00000400841 of the human CRLF2 gene, contains a total of 15 Alanine residues, 6 of which are coded for by the GCC codon (40%), 6 by the GCA codon (40%) and 3 by the GCT codon (20%). The GCG codon is not used (0%).

This is a cut version of the output, the actual output lines are much longer since they include all codons and there will be one line per protein coding transcript.

This script should at least get you started since it will provide you with the raw data needed to perform your statistical analyses. If you use it in published work, I would appreciate it if you could let me know (my email is included in the script) and perhaps mention me in the acknowledgements :).


Note: This is based on literature searches I've done a while ago out of general curiosity. I'm in no way an expert on human reproduction.

If I understand you correctly you are basically asking if there are any evidence for sex biases in offspring between families, that has a heritable genetic basis. This has been an active research topic for a long time and there are a number of proposed mechanisms for how this can be achieved. Historical data sometimes shows deviations in sex ratios over time, e.g. in 20th centrury Europe after WWI and WWII (see data in Gellatly, 2009). There are also other reported/hypothesized deviations in sex ratio e.g. trends in sex ratio due to paternal age (e.g. Jacobsen et al, 1999), sex biases of offspring due to earlier insemination in the menstrual cycle, and the child rank. However, from what I've seen, the evidence hasn't been conclusive and different studies point in different directions.

As Irving et al (1999) point out, possible mechanisms for sex ratio biases can be:

deviations in X/Y-ratio of sperm
selection of sperm within the female reproductive tract
biases in implantation success and/or survival for embryos of different sex

Most evidence seems to point against explanation one, see tests in e.g. Irving et al (1999) and Graffelman et al (1999). Graffelman et al (1999) also tests for an effect of male age, but do not find support for this idea.

Another interesting study is Curtsinger et al (1983), which tries to look at vertical population transmission of sex ratio variation in Japan. They conclude that there is a marginally significant effect on the paternal side, which would support the idea that sex biases might run in families.

  An analysis of vertical transmission of sex-ratio modifying factors that excludes effects of birth order in both the parental and offspring generations has detected a marginally significant paternal effect.

However, they also conclude that the genetic variability in sex ratio is very small, if there is one. This study also does not find support for effects of e.g. paternal age or child birth order.

Gellatly (2009) provides a model of how an autocorrelation in sex ratio between generations could be explaned (while still having a stable population-level sex ratio), using an autosomal gene modifying male sex ratio. Note thought that this is a proposed model, and not empirical evidence. However, Gellatly (2009) also use genealogical/pedigree data from North America and Europe to show that there is an heritable component in the human sex ratio (an association between sex ratio in F1 and F2 generations). However, from what I can see the evidence is weak, and the models only explains 0.5% of the variance in the data. The introduction to this paper also has a useful overview of the subject with more references you might want to check out.

All in all, my perception is that there are some evidence that certain sexes can be overrepresented in families, which could potentially mean that the sex ratio in the offspring of a twin brother can contain information on the probablility that his brother will have a son or daughter. However, to me, the evidence is far from conclusive and the estimated effects seem rather weak. So as a null hypothesis, you should definately go for a 50/50 chance of a son/daughter, irrespectively of what the sex ratio of the twin brother is.

As for the general calculation of probabilities of different scenarios, you just use the product of probabilities and sometimes summation of birth orders. For instance (if assuming 50/50 sex ratio), the probability of having three sons is $0.5^3= 12.5\%$ (births: MMM) and the probability of having 2 sons and one daughter is $3*0.5^3= 37.5\%$ (births: FMM, MFM or MMF, i.e. three ways to achieve this scenario out of eight).


How to design the primer when you don't have GC?

Without the sequence information I can only give very general advice.

1) Pick a different location — primers generally work best when they have something close to 50% GC content.

2) Make sure the 3' ends of your primers aren't complementary.

There is detailed advice on how to design effective primers available online including:

from MIT
Dieffenbach, C. W., Lowe, T. M., & Dveksler, G. S. (1993). General concepts for PCR primer design. PCR methods appl, 3(3), S30-S37.


Do acetyl-CoA, acetyl-CoA carboxylase and acetyl-glutamate carry any charge?

The first compound you mention is acetyl-co-enzyme A (acetyl-CoA) (first picture, left panel). The acetyl group is uncharged, but the co-enzyme A (CoA) group (Fig. 1, right panel) does carry charge through its phosphate groups. In normal physiologic environments these phosphate groups will donate one or more protons, leaving the molecule negatively charged, as shown in Fig. 1, right panel below:

Fig. 1 Acetyl-CoA (left) and the co-enzyme A group (right).

The second compound is an enzyme, namely acetyl-CoA carboxylase. Consisting of many, many amino-acids it will carry many, many charges under physiological conditions. Some of these will be negative, some positive.

The third compound you mention is acetyl-glutamate:

Acetyl-Glutamate

This compound carries two carboxyl groups, which makes the compound acidic and negatively charged under physiological conditions, as it will donate one or two protons to the environment, dependent on the pH.

PS: For an in-depth answer on the basic chemistry and pKa values I would ask this at Chemistry.SE :)


How can skull size difference alone explain behavioral differences using evolutionary theory?

Having a large difference between the sizes of the skulls between males and females is strong sign of sexual dimorphism, particularly of males that are larger in general.  Knowing which form of sexual dimorphism there is allows you to predict several other features. In particular large males is seen almost exclusively in animals in which the males fight each other for control of a harem AKA contest competition. This means high male aggression, since they are driving away other males. Since they drive away other males they have little to no sperm competition so they also don't need competitive sperm. These species also show drastic difference in male reproductive success, males with a harem produce many offspring males without one produce few to none.

https://www.intechopen.com/books/sexual-dimorphism/the-evolution-of-sexual-dimorphism-understanding-mechanisms-of-sexual-shape-differences


How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?

Mitotic (cell division) inhibitors in plants are pretty much what a chemo therapeuticum means for cancer, i.e., rapidly dividing tissues will be affected most. Germinating seeds depend on mitosis for growth. An established plant will also be affected (it will stop growing), but it will stand its ground. To push the analogy - chemotherapy is often commenced after surgical removal or irradiation therapy to remove the tumor, and then chemo is applied to make sure any surviving tumor cell will not start to divide. Your herbicide will prevent germination (cf. cancer re-growth), but will not grossly affect established plants (cf. existing tumor).


How to find ion/water channel related genes

I think your best bet is to blast your transcripts against the TCDB which has all ion channel templates you can get in the literature. Second best would be to blast against a general protein database like UniProt.


$2.45~\rm GHz$ is well into the microwave region, which is usually defined as radio waves with a frequency of greater than $1~\rm GHz$.

Microwaves can be harmful. If you stood in front of a $1~\rm MW$ microwave dish, you would be cooked basically instantly. But that doesn't mean they are harmful in small doses: if you stand in front of a $1~\rm MW$ visible light source, you would also be cooked. You can hold your hands in front of a fire, but sticking your hands in would be bad. Like heat and visible light, microwaves aren't intrinsically harmful in moderation, but they can be deadly if you have enough of them.


Do Alzheimer's patients have spaces in their brain with low interstitial space?

It's hard to judge whether interstitial space changes are due to beta amyloid accumulation or because the Alzheimer's brain has suffered such profound cell loss and neurodegeneration as a result.

The Nedergaard paper you quote is more about a daily cycle of increase/decrease in interstitial space related to the sleep/wake cycle [Ref 1]. Specifically, that during sleep, there is more space to flush out the brain including beta-amyloid.  One interesting hypothesis from that being that perhaps the accumulation of these aggregates is actually due to inefficient sleep -> inefficient flushing of plaques which go on to give symptoms.  So even if the interstitial space in what's left of the Alzheimer's brain remained the same as a healthy brain, the problem of beta amyloid clearance could still be present.  It remains to be seen if one could restore normal clearance whether degeneration could be slowed and symptoms abated.

[Ref. 1]: Paper from Nedergaard group


Any tool to align whole genome sequence data to another genome and give exon regions a higher mark?

If you are not trying to assemble but just to align each read to the genome, you can use exonerate. On a Unix/Linux platform, once you have installed it run something like:

exonerate -m genome2genome WGS.fasta genome.fasta > out.txt

From the exonerate manual:

          genome2genome
                 This  model  is  similar  to  the  cod‐
                 ing2coding  model,  except  introns are
                 modelled on both sequences.  (not work‐
                 ing well yet)

What I would recommend though, is to align against a reference cDNA dataset, not the whole genome. In that case, you should use this instead:

exonerate -m cdna2genome genome_cdna.fasta WGS.fasta > out.txt

From the exonerate manual:

          cdna2genome
                 This   combines   properties   of   the
                 est2genome and coding2genome models, to
                 allow modeling of an whole cDNA where a
                 central coding region can be flanked by
                 non-coding UTRs.  When  the  CDS  start
                 and  end  is  known it may be specified
                 using  the  --annotation  option   (see
                 below)  to permit only the correct cod‐
                 ing region to appear in the alignemnt.


Criteria for compound action potential thresholds

Action potentials of single neurons (APs) are the building blocks of compound action potentials (CAPs). While each of the individual APs is a yes-or-no response with a clear-cut defined threshold, CAPs are not. CAPs are build up of hundreds or thousands of neuronal contributions in, e.g., the auditory nerve. Decreased responsiveness as well as desynchronization of the neuronal responses can decrease the amplitude of the CAP.

It all depends on the amount of background noise and stimulus artifacts versus the amplification factor (the gain) whether a CAP can be recorded and identified yes or no. Typically, gross-potential recordings do not allow for single APs to be measured. CAPs are therefore stochastic phenomena and hence the CAP threshold should either be defined by visual examination (subjective), or through noise-dependent threshold criteria (objective). Therefore, unlike AP thresholds, CAP thresholds are arbitrary and heavily dependent on the noise level.


I'd guess it's Nuctenea umbratica, or otherwise similar in appearance and coloration pattern, but less frequent Nuctenea silvicultrix.

At least Nuctenea umbratica was recorded in Switzerland.


It is not /Bolma rugosa/, but in fact /Angaria delphinus/, from the Indo-Pacific.

Listing on gastropods.com


The short answer is that no, a zygote doesn't express all genes simultaneously.

A zygote is like any other cell, in that it represents a distinct phenotype. And like any other cell, this phenotype is maintained by tight regulation of gene expression patterns. Check out this paper, for a nice description of the process of embryonic gene activation.

An important way in which the zygote differs from other cells, and which might be what drives your question, is that the zygote has the potential to differentiate into all the other cell types found in the body. This process of differentiation is also very tightly controlled in terms of gene expression.


How to derive the Equilibrium value $\hat F$ equation

Sign problem

When you go from

$F_t(1-(1-2m+m^2)-\frac{(1-2m+m^2)}{2N})$

to

$F_t(-2m+m^2-\frac{(1-2m+m^2)}{2N})$

You make a mistake in the sign. It should be

$F_t(2m-m^2-\frac{(1-2m+m^2)}{2N})$

Approximations

I will assume this error of sign propagate to inverse your end result. You hence should get

$F_t= \frac{1}{4Nm+1-2m} -\frac{2m}{(-4Nm)-1+2m}$

$\frac{2m}{4Nm+1+2m}$ is negligible compared to $\frac{1}{4Nm+1+2m}$, so you can indeed remove it. You get

$F_t= \frac{1}{4Nm+1-2m}$

Also, $2m$ is negligible compared to $4Nm$, so again you can remove it. You end up with

$F_t= \frac{1}{4Nm+1}$

Tadaa!


Which pair of primers should be used to amplify the ORF in PCR?

First of all, if this is a homework question, add that tag to it. And show what work you have done so far.

Secondly, primers for amplifications should lie on opposite strands. Primers are typed in 5'-to-3' direction (aka left-to-right on leading strand).

Appropriate primers will be: primer 4=GTG... and primer 5=GAA.... Note how those primers are always in 5'-3' orientation. That is how you order those.

Again, if this is homework (looks like it) it is very bad taste to just ask question without any work shown. It displays laziness and usually not respected behavior when asking for help.


Pipetting: do human experimenters need liquid class information?

In my experience it is very rare to see a protocol for humans that describes how to pipette a certain liquid, but I don't have as many years pipetting as others do.
In general, it is left to the experimenter to observe the behavior of the liquid and act accordingly. It is quite easy to determine when a liquid is leaking (e.g. ethanol) or when it is very viscous (e.g. glycerol), and determine that a change in technique is required. In this case, I would ask someone else in the lab how to deal with the situation. This is something that robots cannot do.
However, not everyone has expert help available, and although it is fairly obvious when a technique isn't working, often the solution is not intuitive. Additionally, the advice of others in the lab could be unhelpful or even inaccurate. For example, I was told to cut the tip off a pipette in order to pipette Tween-20 more easily, however in reading for this answer have discovered that this is not recommended at all! (See eppendorf FAQ linked below).
Therefore, I would say that, unless the liquid is to be pipetted in the same way as water, it is always useful to provide information for those who are not knowledgeable or do not have easy access to expert practitioners.
For some examples of the sorts of problems that experimenters come up against, and therefore which liquids especially could use instructions in protocols, see this set of FAQs from eppendorf on handling liquids.