Transfer of antibodies from mother to fetus My questions: When does fetus begins to acquire antibodies from mother? Does it continue throughout the pregnancy?

From Wikipedia: http://en.wikipedia.org/wiki/Passive_immunity

  This occurs around the third month of gestation.

From Helena Curtis Biology :

  During the last month of pregnancy , the baby usually begins to acquire antibodies from its mother,....

I believe that both these sources are reliable but they contradict when the transfer of antibodies starts.

Both are technically correct.  Here's a review that goes into some detail about the process: IgG Placental Transfer in Healthy and Pathological Pregnancies.  It's worth a read if you're interested in the subject.  In particular, it cites a study of immunoglobulin transport which:

  demonstrated a continuous rise in IgG levels in the fetal circulation between 17 and 41 weeks of gestation. Fetal IgG concentrations were only 5%–10% of the maternal levels at weeks 17–22 but reached 50% of the maternal concentrations at weeks 28–32. The majority of IgG is acquired by the fetus during the last 4 weeks of pregnancy, and fetal IgG concentrations usually exceed maternal ones by 20%–30% at full term.

So it begins a wee bit before week 17, so definitely within the second trimester, but it is only by the third that concentrations begin to be truly meaningful.  However, most of the antibody acquired, going above the maternal level, is done in the last month.


Book-recommendation: Biochemistry I need to have a book which covers following topics two may also be fine:

(a) Structure and role of carbohydrates, fats, fatty acids and cholesterol, proteins and amino-acids, nucleic acids. Bioenergetics.

b) Glycolysis and the Krebs cycle, oxidation and reduction, oxidative phosphorylation, energy conservation and release, ATP cycle, cyclic AMP – its structure and role.

(c) Hormone classification (steroid and peptide hormones), biosynthesis and functions.

(d) Enzymes: types and mechanisms of action.

(e) Vitamins and co-enzymes

(f) Immunoglobulin and immunity.

Lehninger Principles of Biochemistry by Nelson and Cox is quite popular and covers everything you listed in great detail except for immunology.

I don't really have a recommendation for an immunology book; I think pretty well any of them will cover immunoglobulins (they're pretty integral). My university uses Kuby Immunology by Kindt et al. Molecular Biology of the Cell by Alberts et al. has a couple chapters (some 115 pages) on the subject. As a bonus, it's an amazing reference for cell biology (which you'll need, at least someday, if you're pursuing biochemistry).


Removing DNA from a cell Stupid question perhaps but what does happen if one completely removes DNA from a single cell organism? As far as I know DNA is only needed for propagating information to descendants doing it's removed from a grown up cell and put some artificial source of protein there will it just lose ability to mate or will it die immediately?

That depends on the status and activity of the cell. Red blood cells purge their nuclei and DNA contents and continue to perform their function quite well, though they lose their ability to split and form new cells (i.e. are terminally differentiated). Most cells, however, require the genome to transcribe and translate genetic information into protein to maintain their metabolic and functional activities. As you say, DNA would also be required to divide and build new cells, so that would be one major downside of removing all DNA. Adding exogenous proteins or amino acids will not help with ensuring correct protein production and maintenance, because proteins are coded for by mRNA which act as mobile transcripts of DNA. They are dependent on DNA transcription, without which they cannot exist. Proteins do not spontaneously form. Long story short, DNA is almost always absolutely essential, and it is the case that if you removed the nucleus from most cells, they would die very shortly thereafter.


How is silica transported to the leaves of genus Dendrocnide trees to form stinging needles for toxin delivery? I just read the NYTimes' This Tree’s Leaves Look Soft and Inviting. Please Don’t Touch Them. which mentions the genus Dendrocnide and that Wikipedia section begins with:

Contact with the leaves or twigs causes the hollow, silica-tipped hairs to break off, penetrate the skin and inject the toxins.10 The hairs cause an extremely painful stinging sensation that could last from several hours to 1–2 days, recurring to a lessening degree for several months or more whenever the area is touched, exposed to water, or subjected to temperature change. The injured area becomes covered with small, red spots joining together to form a red, swollen welt. The hairs are also believed to be released to the air when the plant is cut or cleared in large areas. Workers without respiratory protection have reported sneezing, runny noses, mild nasal bleeding and throat irritation while cutting or clearing.
10Hurley, Marina. "'The worst kind of pain you can imagine' – what it's like to be stung by a stinging tree". The Conversation. Retrieved 2020-03-08.

and that article says:

The stinging hair structure is complex and consists of a tip, shaft and bulb composed of silica, calcium carbonate and calcium phosphate.

Reference 5 in Neurotoxic peptides from the venom of the giant Australian stinging tree (open access in Science) is Stinging hair morphology and wall biomineralization across five plant families: Conserved morphology versus divergent cell wall composition and this article contains a lot of information, for example following Figure 2:

Biomineralization
Notable differences were found in the mineralization of stinging hairs. Three zones of the stinging hairs could be distinguished based on their mineralization patterns. The tip regions were generally strongly mineralized with highly concentrated silica or calcium phosphate, except for Cnidoscolus stinging trichomes, which were completely nonmineralized. The shafts were usually mineralized with calcium carbonate, but in some cases with calcium phosphate or silica besides calcium carbonate. Trichome bases showed more irregular mineralization, mainly with calcium carbonate and often additional silica deposits (Fig. 2K, L), or they were not yet completely mineralized (Fig. 2M).

This article primarily addresses structure and morphology, but I'm interested in how silica actually makes its way into a leaf structure. Unlike calcium and phosphorous, neither elemental silicon nor SiO2 readily dissolve in water, so I'd like to ask the following:
Question: Presumably it comes from minerals in the soil, but is it transported as particles of silica, or molecules of SiO2, or by other chemical forms containing silicon and reformed as silica on site, or something else?

Biosilicification is a good search term to use.
The silicic acid present around the roots can be actively transported into roots, and later into specific cells or cell compartments. It is deposited preferentially onto lignin or polysaccharide surfaces.
For free articles giving an overview there is:
Nawaz, Muhammad Amjad et al. “Phytolith Formation in Plants: From Soil to Cell.” Plants (Basel, Switzerland) vol. 8,8 249. 26 Jul. 2019, doi:10.3390/plants8080249
found at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6724085/
and:
"From biosilicification to tailored materials: Optimizing hydrophobic domains and resistance to protonation of polyamines"
David J. Belton, Siddharth V. Patwardhan, Vadim V. Annenkov, Elena N. Danilovtseva, and Carole C. Perry
PNAS April 22, 2008 105 (16) 5963-5968; first published April 17, 2008 https://doi.org/10.1073/pnas.0710809105
found at:
https://www.pnas.org/content/pnas/105/16/5963.full.pdf
Keywords silaffins, frustulins, pleuralins (used by diatoms) silicatein (used by sponges)


Can a broken thumb/finger bone not require realignment of the bone? Is it possible that a finger/thumb bone fracture is so superficial, that the doctor does not need to realign (re-set) the bone before applying the cast? Or does it always require for even a finger/thumb broken bone to be put back in place before applying the cast?

Yes. You can figure that yourself if you look a bit at the types of fractures on Wikipedia, the Bone Fracture page:

  Other considerations in fracture care are displacement (fracture gap) and angulation. If angulation or displacement is large, reduction (manipulation) of the bone may be required and, in adults, frequently requires surgical care.

  [...]

  Other types of fracture are:

  Complete fracture: A fracture in which bone fragments separate completely.
  Incomplete fracture: A fracture in which the bone fragments are still partially joined. In such cases, there is a crack in the osseous tissue that does not completely traverse the width of the bone.
  [...]

Incomplete fractures and fractures with less or no displacement may heal correctly in some situations without needing realignment.


How can E. coli proliferate so rapidly? The E. coli has a genome with approximately 5×106 bp. The main DNA polymerase involved in its chromosome duplication (DNA pol III , the one with highest processivity) can polymerize ~103 nucleotides per second.
By a simple calculation, we would conclude that the whole chromosome duplication would take ~ 5000 seconds ( about 80 minutes, so more than an hour). The whole cell duplication would probably take much more than that, considering not only DNA Pol III is involved.
However, in optimal conditions, E. coli can actually duplicate in ~30 minutes.
How could that be possible?

OBS.: all the numbers used here are aproximate, but sufficient to account for the correct orders of magnitude.

Though Escherichia coli has only one origin of replication (oriC), replication proceeds in both directions from it. Thus, based on your calculations, DNA replication takes 40 minutes (which is still too long if the doubling time is 30 minutes). The solution is to start replication again before the previous round has completed, and here's some research which shows just that:

Yoshikawa H, O'Sulliven A, Sueoka N. 1964. Sequential replication of the Bacillus subtilis chromosome. Prod Nat Acad Sci 52:973-980

  Obviously, dichotomous replication is advantageous for bacterial growth because the bacteria can replicate chromosomes faster than by having one replication point. With one replication point, the replication time, and consequently the cell generation time, would be limited by the maximal rate of DNA polymerase.

Cooper S, Helmstetter CE. 1968. Chromosome replication and the division cycle of Escherichia coli B/r. J Mol Bio 31(3):519-540

  …cells growing faster than 40 minutes per doubling must initiate new replication points prior to the completion of DNA synthesis at the previous points; in other words, there should be multiple forks.

Skarstad K, Boye E, Steen HB. 1986. Timing of initiation of chromosome replication in individual Escherichia coli cells. EMBO J 5(7):1711-1717

  In rapidly growing cultures, with parallel replication of several chromosomes, cells will end up with 2n (n = 1, 2, 3) chromosomes if initiation occurs simultaneously at all origins. A culture with asynchronous initiation may in addition contain cells with irregular numbers (not equal to 2n) of chromosomes. The frequency of cells with irregular numbers of chromosomes is a measure of the degree of asynchrony of initiation.

Fossum S, Crooke E, Skarstad K. 2007. Organization of sister origins and replisomes during multifork DNA replication in Escherichia coli. EMBO J 26(21):4514-4522

  …initiation occurs at two origins in the ‘mother' cell. It can even occur in the ‘grandmother' cell at four origins if the time it takes to replicate and segregate the chromosome exceeds two generations.

This last image is interesting because you actually see the multiple replication origins in single cells by fluorescence microscopy.


Natural Toxins and Medicine How are natural venoms and toxins (e.g. spider and snake venoms) used to make antidotes? In other words, what is in that venom that is part of a harmful substance but, when used correctly, can actually help us, and why can these molecules help or harm in different situations?
Also, why are we looking to natural toxins to produce new medicines instead of synthetic chemicals we could make or already have?

You are probably thinking about antivenom using immune serum.
You give the venom to a host animal to induce an immune response, and then purify (to the extent possible) antibodies collected in serum from that animal, and then inject these to the patient to neutralize the venom. You don't use the venom directly.
Isolating components of venom could also allow for screening for molecules that will bind to them strongly and possibly block their action, though I'm not aware of specific antidotes that have been produced this way.


When do kinetochores attach? I am really confused as to when kinetochores are attached to centromeres. Are they attached soon after replication or after condensation ?

Kinetochore (KT) is a multilayer protein complex. It's main function is to link chromosomes to the positive ends of the spindle microtubules. Also it plays role in the formation of heterogenic region at and around the centromer. The attachment of the KT is not uniform among living species. According to this paper on KT assembly in yeast:

  .  ...  KTs  remain attached to the MTs throughout the cell cycle in this organism. However, a temporary detachment of chromosomes  from  MTs  occurs  (for  1–2 min)  at  the  time of CEN DNA replication in S phase in S.cerevisiae (Kitamura et al. , 2007). After completion of CEN replication, a KT reassembles and reestablishes its attachment with  MTs.

source:http://femsle.oxfordjournals.org/content/femsle/338/2/107.full.pdf
(CEN - centromere, MT- (spindle)microtubules)

Thus the exact time of kinetochore attachment depends on the organism, though I must note that S. cerevisiae has somewhat different mitosis than us.


Is every flower on a plant unique? I've noticed on my dahlia plants that sometimes there's a flower which looks completely different then the rest . Either color or structural.  I dig these bulbs up each fall and keep inside to replant.  So my question is are these simply mutations, or caused by environmental factors or? I would assume the dna should be identical to the mother plant ? Thanks

Dahlia cultivars are known to undergo somatic mutations, e.g. mutations that occur during growth that can lead to different flowers. See for example this old paper.

So it would be very possible that your bulbs yield somatic mutations that crop up as you regrow them each year. This could be the case even if your bulb has not undergone the mutation, because the mutation possibly is occurring in the meristem of the plant as it makes new shoots or inflorescences from the bulb.

Other possibilities would include epigenetic changes which do not actually modify DNA but can possibly lead to modifications of the expression of genes. These can occur due to changes in environment, but they are a bit more difficult to demonstrate as such.


Where are the evolutionary "inbetweeners"? The problem I've always had with evolution is the actual lack of variation between animals. More specifically, the lack of observable gradual change between species.

Take for example the hammerhead shark. It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right? As far as I understand, evolution works by random mutation in a child being somehow slightly beneficial to that animal so it get's to live longer and reproduce more, eventually resulting in it's genetic material in dominating the inferior ones before it. But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now? On the other hand, if it wasn't beneficial, how come the hammerhead still exists?

Furthermore, I feel like some characteristics of a certain animal can't really have gradual benefits. There's a lizard that shoots blood out of it's eyes. The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life. So for it to actually become beneficial, it seems to me that there had to be a ton of lizards that had a disadvantage of bleeding slightly. In fact, there had to be so many that they evolved even further in the same direction and kept doing that until they bled so much it's an actual benefit (sorry for this turning so gross). So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

More specifically, the lack of observable gradual change between species.

Most significant phenotype differences occur over several thousand generations, which means several thousand years on up. While we certainly can create experiments where a controlled form of evolution occurs within a very small time-frame, I'm going to assume that you're not interested in closed laboratory experiments given the nature of your question.

  It obviously has a strong connection with a normal shark, but where's the "half-hammerhead" shark? Where's the species that only has a SLIGHTLY wider head?

The data below does answer you question, but in reverse. Hammerheads are much older than most of their relatives; so their cousins have actually grown smaller heads... but there are certainly intermediates.

From Andrew Martin (1993 - mtDNA data) via Elasmo-research.org:
*The circles represent the head-width vs. body-length ratio.

Martin's conclusion: "...the hammer appeared rather suddenly and fully formed, and was later optimized along different lines to suit various selection pressures."

  I really doubt that a single mutation on a normal shark resulted in a head shaped like that, it had to happen gradually. Right?

Not necessarily. Single Nucleotide Polymorphisms (a.k.a. - "SNPs" - a change in one nucleotide) can have pretty wide-ranging effects.

The vast majority of humans, for instance, are lactose intolerant in adulthood. However, lactose tolerance evolved twice from two different SNPs in two different human populations: One European and one African. One gene. One regulatory mechanism change. Massive benefits (essentially opening up a whole new resource in adulthood).

Significant differences in phenotypes (the physical appearance of something) can require more gene mutations, or not. It depends on where the mutation is in the genome and what the gene does.

  But if it was for whatever reason beneficial to have a slightly wider head, why don't all the sharks have slightly wider heads now?

The simple answer is because either there wasn't enough selective pressure that the rest of the shark phenotypes succumbed to that the hammerhead avoided, or that the hammerhead design doesn't give enough of an advantage to completely dominate the gene pool. An alternate, but more abstract answer, is that there simply hasn't been enough time for the hammerhead design to dominate the shark phenotype. Remember, evolution works by generations - not years. It would take unknown thousands of generations for a weakly-advantageous design to dominate an entire niche - if it ever would.

Also, it is worth it to point out that evolution doesn't only select for advantageous mutations. Mutations that aren't very detrimental can still exist within a population as long as the detriment doesn't prevent resource exploitation and offspring production. Think Huntington's Disease which severely restricts a person's survivability, but only after their mid-30's (in general) - plenty of time for the person to have sex and raise a kid into semi-adulthood. It is a genetic defect which sticks around only because it allows humans to reproduce before it seriously affects them.

  The original ancestor certainly didn't, and I'm sure that if it's child only bled slightly from it's eyes it wouldn't really help if much in life.

Maybe, maybe not. Maybe it shot something else before blood, and then a mutation caused it to shoot blood instead - but the overall effect (deterring predators) was the same so it doesn't really matter.

You're correct that some traits might appear very awkward if they had evolved gradually, but the question then becomes: Did they evolve gradually? Sometimes we simply do not know.

  So why did the inbetweeners survive long enough to evolve even more, and why did they THEN die out?

Like I said above, just because a trait is detrimental doesn't necessarily mean it will be eliminated. As long as the being can survive long enough to reproduce successfully with the trait, the trait might not be eliminated for a very, very long time- if ever.

As for in-betweeners dying out - it's difficult to think of it like that. You're talking bout LCAs ("Last Common Ancestors") of extant (currently-living) species. While some LCAs just die out for some reason or another, it's more common that the LCA simply continued to evolve and become a genetic relative due to some sort of isolation.

Think of it like the in-betweeners coming to a fork in the road. Some choose right, some choose left. There isn't anybody left behind - merely two populations that are changing over time that were once one group until they don't really mate between each other anymore (or can't). Heck, even Biologists have trouble deciding at what point a population is considered a different "species" because of discoveries in the last 50 years - so right now a firm answer like "It takes 15% of the genome to change for a new species to emerge" isn't possible as it doesn't really work like that.

We'll get to it eventually, but for the time-being, it might be easier to say that everything currently living on Earth is an in-betweener of something else in the future. Everything in its current iteration will eventually die off, but not before something else emerges from our offspring which may or may not be significantly different from us due to however many genetic mutations our offspring have from us. It could be one that opens up a whole new realm of possibilities (like lactose tolerance) or an accumulation due to selective pressures (like Phoemelanin production and pale skin in humans [Redheads] to produce more Vitamin D3 at higher latitudes).


Protocol to dilute DNA step ladder? I need to run gels that are of not the "most" importance. So I do not want to waste alot of money on step ladder. How do I dilute DNA step ladder? Is there a general procedure, for I have tried googling for one, but I get varying answers, such as a 1:4  dilution, and so on.

This is the information on the Step ladder, by Promega, posted as an image, since copy and pasting would mess up readability.

EDIT:

Even though I awarded the bounty because it gave me the same concept; what I had actually did was to assume I would use $60ul$ of ladder combined with $1$x dye.

Therefore since I started with $1ml$ of $6$x loading dye, $100ul$ of DNA step ladder, and available nuclease free $\ce{H2O}$, and I desired a 5:1 ratio of solution(dye and $\ce{H2O}$)  to ladder.

I would then use $12ul$ of stock to the $60ul$ total.

To make the dye $1$x, I would add $10ul$ of the $6$x dye to make the final concenetration of dye $1$x.

Then I would add up to $38ul$ with nuclease free $\ce{H2O}$.

So, sorry if this was worded redundantly, but It helps me to read, therefore in summary:

$$  +10ul  \text{ of 6x dye}$$
$$  +12ul \text{ of stock 100bp DNA step Ladder}$$
$$+ 38ul  \text{ Nuclease Free } \ce{H2O} $$
$$ \text{__________________________________}$$

$$\sum{60ul} \text{ of ladder & dye} (1 \text{x}) $$

of which total I can aliquot out to my hearts desire.

EDIT2:
The ladder turned out successful.

You'll probably have to titrate it down yourself. You might be able to estimate: The detection limit for ethidium bromide staining is about $1 ng$ per band. The insert says it's at "1 $\mu g/ \mu l$", but that's for all 40 bands and they're clearly not all at the same concentration. Depending on which bands you care about (1600 and below are dim), you might be able to get away with $(\frac{1}{25})^{th}$ their recommended concentration (1 $\mu g / 40$ bands = 25 $ng$) -- but I would titrate a small amount and see what works.


Does the Enzyme Monoamine Oxidase, Isoenzyme A have an allosteric modulatory site? Does the Enzyme Monoamine Oxidase, Isoenzyme A (MAO-A) have an allosteric modulatory site? I ask because I would like to know if it is possible, in theory at least, for a positive allosteric modulator of MAO-A to be developed.

I think an allosteric modulatory site has already been found, but it's not specific to Isoenzyme A, if that's what you were looking for.

See these papers:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564771/

http://www.jbc.org/content/270/17/9856.full


How does Tylenol relieve pain without making me drowsy? So I have a crown that popped out and has been killing me, I've lived on a steady diet of Tylenol since it popped out. I've noticed that aside from killing most of the pain from the tooth, the tylenol hasn't made me particularly drowsy, which to my understanding was how most pain killers work. If it doesn't just put me to sleep, how does tylenol work to numb pain?

Opiate pain killers or pain killers that act on opioid receptors have a different mechanism of action than NSAIDs. They tend to act as receptor agonists which exert their effect on the CNS (oxycodone as an example). Opioid receptors are associated with analgesia, CNS depression, sedation, etc. Tylenol on the other hand is thought to exert its effect by downmodulating cyclooxygenase, and therefore inhibiting the production of prostaglandins like H2, which is a precursor to lots of pro-inflammatory compounds.


What's the (or some of the) minimum(s) amount of atmospheric carbon dioxide needed by plants? We currently have a problem of increasing $\ce{CO2}$ in the atmosphere.  But assuming we find a way to carbon sink it, what is the minimum $\ce{CO2}$ we need to leave in the atmosphere to provide a source for plants to photosynthesize?  I'm assuming this may vary per plant, and that we could choke plants so they're less productive - but at some point they will starve to death if we remove too much $\ce{CO2}$.

Where does this point lie?

Approximations, or a specific data point (say for one plant, or one type of plant) would be an adequate place to start.

Current atmosphere composition is $\pu{0.035\%}$ carbon dioxide.  In the past it has been higher (has it ever been lower?), which in theory has resulted in higher plant growth - but I've seen some contradictory statements about higher Carbon Dioxide.

(related: What is the effect of a pure-oxygen environment on a plant?)

The values provided in the other answer are actually related to the minimum values experienced by land plants in the past, not the theoretical minimum possible concentration of CO2 capable of maintaining plant life.

According to Gerhart and Ward (2010):

  During the Last Glacial Maximum (LGM; 18 000–20 000 yr ago) and previous
  glacial periods, atmospheric [CO2] dropped to 180–190 ppm, which is among the
  lowest concentrations that occurred during the evolution of land plants.

Thus, what is the theoretical minimum possible concentration of CO2 capable of maintaining plant life?

According to the same paper (Gerhart and Ward, 2010), there has been several experimental studies focusing in low concentration of CO2:

  In the mid-1990s, a later phase of technology was introduced at the Grassland, Soil, and Water Research Laboratory (USDA-Agricultural Research Service) that involves an outdoor tunnel system, whereby plants are grown across a continuum of modern to low [CO2] (Mayeux et al., 1993; Fig. 3b,c). During the day, air of known [CO2] is pumped into one end of the tunnel where plants experience relatively high [CO2]. Plants near the end of the tunnel, on the other hand, experience low [CO2] (similar to glacial values) as a result of photosynthetic removal of CO2 from air as it moves progressively through the tunnel. At night, airflow is reversed while plants are solely respiring, and this serves to equalize [CO2] throughout the tunnel.

Despite those studies not focusing explicitly on what's the minimum possible concentration, we can still draw some conclusions based on them. For instance, in Fig.4 (ibidem):

As you can see, those vertical lines represent the minimum concentration experienced in the past. However, we still observe CO2 assimilation (photosynthesis) below those values. Unfortunately we cannot simply get the value where the line touches the x axis, because those values are intracellular CO2 concentration.

That being said, the answer depends on other concept: CO2 compensation point. For a C3 plant, carbon dioxide compensation point is around 50ppm (Tolbert, Benker and Beck, 1995).

Thus, we can say that, as a rough estimate, the value you want lies between 50ppm and 170ppm (probably closer to 170ppm than to 50ppm).

Of course, that minimum possible value depends on several factors, as the species of the plant, the type of photosynthesis (C3, C4, CAM), temperature, humidity etc.

Sources:

Gerhart, L. and Ward, J. (2010). Plant responses to low [CO2] of the past. New Phytologist, 188(3), pp.674-695.
Tolbert, N., Benker, C. and Beck, E. (1995). The oxygen and carbon dioxide compensation points of C3 plants: possible role in regulating atmospheric oxygen. Proceedings of the National Academy of Sciences, 92(24), pp.11230-11233.


Help with preparing Congo Red TSA So I want to make Congo Red TSA. My instructor gave some hints but I still have some questions:

I start by making two stock solutions: 20 mg/ml of congo red and coomassie in two different falcon tubes. To prepare 30 ml of each, would I dissolve 600 mg in sterile water?
The final concentation in a 500 ml TSA solution needs to be 40 μl/mL of CR and 20 μg/mL of coomassie. How do I calculate the amount of solution needed for the TSA?

1) Yes, that's correct.

2) This is just a simple matter of applying the equation $C_1V_1=C_2V_2$. For congo red:

$C_1=20\frac{mg}{mL}$
$C_2=0.04\frac{mg}{mL}$
$V_2=500\ mL$

I'm sure you and a calculator can figure the rest out.


What is the diameter of the measles virus? I have searched countless studies. None have given this number. In fact there seems to be no details of any kind about the measles virus.

I believe this paper answers your question or at least comes very close to it: https://www.ncbi.nlm.nih.gov/pubmed/6540797
I'll reproduce the abstract here, with emphasis mine to indicate the relevant portion:

The molecular length of measles virus RNA and the structural organization of measles nucleocapsids.
Full-length measles virus RNA molecules isolated from purified virions or nucleocapsids and examined by electron microscopy were 5.12(+/- 0.12) micron in length, corresponding to a molecular weight of 5.2 (+/- 0.1) X 10(6). Purified virions examined by negative staining in the electron microscope exhibited a pleomorphic range of particle sizes varying in diameter between 300 nm and 1000 nm. Purified nucleocapsids had dimensions of 21 nm (diameter) X 1254(+/- 7) nm (length) and a central core of diameter about 5 nm. Full-length nucleocapsids were composed of 204 (+/- 3) protein discs. The pitch of the nucleocapsid helix was calculated to be 6.1 nm and the helix angle, alpha, to be 8 degrees 16'. Approximate volume calculations indicate that each enveloped virus particle contains multiple nucleocapsids.

In case of unfamiliarity with the term "virion", see: https://www.britannica.com/science/virion
In case of unfamiliarity with the adjective "pleomorphic", see: https://en.wikipedia.org/wiki/Pleomorphism_(microbiology)


Does myopia tend to decrease the risk for later hyperopia? It seems like being nearsighted for much of your life due to elongated eyes would make it easier in general to focus on near objects rather than far since the lens would not have to change much. Since in old age we lose the ability to focus close images due to a hardening of the lens over time, wouldn't having eyes shaped more for near images be helpful in maintaining the ability to see close up, and thus nearsighted, or myopic people, would be less likely to develop farsightedness, or hyperopia, with age? It seems then that nearsightedness is more of an adaptation that occurs at a young age, so that these people can work up close for longer periods of time both in the the short term(studying) and long term(age). I'd love to hear if any research has been done on this subject, and any other input you have.

It is generally understood that we tend to become hyperopic as we age (reference). As to whether this aids in decreasing myopia is stated as marginal in papers. One paper titled "Is there a hyperopic shift in myopic eyes during the presbyopic years?" states that

  it was found that almost all hyperopic and emmetropic eyes showed an
  age-related hyperopic shift; but only a small proportion of myopic
  eyes shifted toward hyperopia, with others remaining relatively stable
  and still others increasing in myopia.

In a second study titled "Age-Related Decreases in the Prevalence of Myopia: Longitudinal Change or Cohort Effect?", it was found that there is a decline in the prevalence of myopia in older adults.

Some people in personal experiences have stated that their myopia has decreased (reference) while others found themselves wearing bifocals (reference). In closing, I would say that this is something that your Ophthalmologist may be able to predict better but it is not a given that your myopia would decrease. It may or may not be so with many factors like your eye shape coming into play.


Why doesn't telomerase activity cause DNA to get longer each time a cell undergoes DNA replication? Telomerase extends the ends of the lagging strands in order for all of DNA to be be copied. Doesn't this also mean that DNA gets progressively longer each time it undergoes replication? Why is this not the case?

I will assume that you are referring to humans, though much of the research to elucidate telomerase function was performed in yeast.

The first reason is that only a small subset of somatic cells express telomerase. Most somatic cells are terminally differentiated and mitotically inactive, so they are not called upon to replicate their DNA and divide. And when they do, their telomeres get shorter due to the 3' end replication problem.

The end replication problem arises due to the biochemical limitations of DNA Polymerase. Pol requires a primer, 5' to 3', in order to bind to the template strand and begin to catalyze the elongation reaction. So when DNA Polymerase gets to the 3' end of the template strand, it is unable to catalyze the reaction because it doesn't have a free 3' hydroxyl. When the end RNA primer that was used to catalyze the Okazaki fragment just before the 3' end is removed, there is no place left on the template strand to prime, so there is no 3' hydroxyl to begin the elongation reaction and you are left with a 3' overhang of single-stranded DNA.

On the 5' end of the Template Strand, even though the polymerase is able to catalyze the reaction all the way to the end, the end of the chromosome is processed and nucleotides are removed to make a single-stranded 3' overhang on this end. The overhangs are necessary to do strand invasion to form the T-Loops of the telomeres. So every time a chromosome in a cell that has inactive telomerase replicates, it gets shorter.

For the cell types that have telomerase actively express, such as lymphocytes, partially-differentiated stem cells, and the precursor cells to sperm, there is a negative feedback loop based on the length of the telomeres, which in turn regulates the activity of telomerase. Telomerase maintains the ends of the chromosomes, especially in these mitotically active cells, but it will only elongate them to a certain point.

  It has long been known that telomere length is regulated by a negative feedback loop (reviewed in Smogorzewska and de Lange, 2004). Long telomeres contain more negative regulators that limit further telomere elongation by telomerase. Because of this, the enzyme preferentially acts on the shortest telomeres in the cell (Hemann et al., 2001; Zhu et al., 1998).
  - Loayza, et. al.; Cell; Volume 117, Issue 3 30 April 2004


Presence of Aromatase enzyme in males : Result of Natural Selection Males have increased chances of getting cardiovascular diseases than females ; one of the reasons might be less level of oestrogen ( which decreases deposition of low density lipoprotein LDL in blood vessels).

I know that Aromatase enzyme is produced by sertoli cells in males. It converts androgen into oestrogen.

Now ,
today my teacher said that the presence of Aromatase enzyme in males is the result of natural selection against increased chances of heart attack in males.

My question is-

1. Is the amount of oestrogen produced significant to decrease cardiovascular diseases that it can lead to natural selection?

2. Are there any evidences for the same? please enlist them.

Any help is appreciated.  Thank you!  :)

Estrogen has other functions in males; it is very misleading to attribute the ability in males to synthesize estrogen to effects on heart attack chances. The relationship between estrogen and cardiovascular disease risk is also very complicated, and current guidelines do not suggest estrogen replacement as a preventative treatment for heart disease.

A better explanation for increased male risk of heart attack might be the increased levels of testosterone, but the data on that are mixed as well.


Can lysozyme also lyse gram-negative bacteria and if yes, how fast? Lysozyme attacks peptidoglycan, which are found in Gram-positive bacteria. I know someone who uses lysozyme to lyse Escherichia coli, which is Gram-negative. How is that possible? Can lysozyme lyse all bacteria, independently of their Gram status? Does anybody have information on how long I should leave lysozyme in a bacterial solution for it to be effective?

Gram-negative bacteria also have peptidoglycan which can be degraded by lysozyme. However they have an outer membrane lying outside the peptidoglycan layer and this will block lysozyme action.

Because of this if you intend to treat Gram-negative bacteria with lysozyme it is necessary to add something that will disrupt the outer membrane—the usual choice is EDTA since removal of magnesium ions by chelation will destabilise the outer membrane.


What is the defining characteristics of a Gap Species? For the following competitive exam question: A road is constructed through a tropical rain forest, following which a population of a species of butterflies declines. Which of the following is NOT  a possible explanation for the road causing a decline in the forest butterfly population?
The answer: The Road facilitates immigration of gap-loving species which compete with the forest species
What is the defining characteristics of a 'gap' species?

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

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


Why not surgically resect the tumor before CAR-T cell therapy? Won't that be more efficient? If CAR-T cell therapies suffer from tumor antigenic escape, why not just resect the tumor via surgery, leaving behind a small number of cancerous cells, and then wipe them out with CAR-T cells? The small number of cancerous cells may reduce the chance of too many cancerous cells escaping CAR-T cell cytotoxic killing that may cause tumor regrowth.

CAR-T cell therapy (Chimeric Antigen Receptor-T cell Therapy) is most effective in treating hematological malignancies. Hematological malignancies (known as blood cancers in common parlance) mean the cancers produced due to over-proliferation of hematopoietic stem cells and the liberation of the immature cells into the circulation . Till now all clinical trials of CAR-T cell therapy has seen more and more success. With the development of second, third and fourth generation (also called TRUCK T cells) CAR-T cells the percentage of remission is increasing. But  almost all these advances are in hematological malignancies.

Clinical trials on solid tumors has shown that the "efficacy is not as remarkable as in the case of hematological malignancies".

The question asked was about resection of the tumor before treating with CAR-T cell therapy. This question is valid only in case of solid tumors (you can't resect blood as it is liquid). As I already said this therapy is only used for blood cancer till now, so there is no question of surgery before the therapy.

I think I could answer your query above. If you want to gain more knowledge, then read below -

The best use of this therapy in blood cancers is after hemato-poietic stem cell transplantation (note that it is not surgical resection)
If you ask, why this therapy was not successful in solid tumors, I would recommend to read the review published in Springer with the title "Hurdles of CAR-T cell-based cancer immunotherapy directed against solid tumors".

Recently however there are new developments that are helping to apply this immunotherapeutic procedure in case of solid tumors also and in that case it is usually given after surgical resection.


How do you obtain specific mRNA transcript levels for comparison from a Hi-Seq dataset? I have HiSeq data from mice exposed to two conditions. I would like to answer the following question: "Is there a significant difference in mRNA transcript levels when comparing condition A to condition B?"

To answer this question, do I have to map my HiSeq reads to the reference genome to determine expression values or is it acceptable to use a small set of reference sequences of interest (approx. 50)? These particular sequences are not annotated on the reference genome. What are the downsides to not mapping to the genome?

It's going to be hard for you to generate an RPKM or RPM value without % aligning to the genome, or the transcriptome.  Your read counts will have no context.


What are the ecological effects of moderately high and prolonged concentrations of nitrogen deposition on an ecosystem? There are many sources of nitrogen which eventually get deposited out of the atmosphere and onto the land/surface.  Typically higher levels of nitrogen compounds are emitted near urban and roadway locations, raising the levels of nitrogen deposited on the nearby landscape.  What are the ecological effects of moderately high (at least double background) and prolonged concentrations (10+ years) of nitrogen deposition on an ecosystem?  Please be specific about which type of ecosystem your comments are intended.

Too much nitrogen can run off during rain and collect in ponds, leading to eutriphication, find more here: https://en.wikipedia.org/wiki/Eutrophication

It's probably also responsible for dead zones: https://en.wikipedia.org/wiki/Dead_zone_%28ecology%29

This is an important question because we've more than doubled the amount of bioavailable nitrogen on Earth in the last 100 years simply because of the haber process and man made fertilizers. This amount of nitrogen has never been available before.


What does these $\Delta \Delta G$ numbers signify? I was reading a paper and came across this table showing  $ \Delta \Delta G$ numbers of different nucleotide sequences in DNA/RNA. I know that $\Delta G$ is free energy and $ \Delta \Delta G$ is relative free energy with respect to L. variegatus 5 S RNA gene. What does this numbers signify actually?

Very basically, what they've done in the paper was incubate different DNA sequences with histone octamers which were then separated on a gel. From this they could measure the ratio between nucleosomal and free DNA, which represents an equilibrium constant. This can then be expressed as a change in free energy ($\Delta G=-RTln(K)$), which is what the table shows. A lower (more negative) free energy change corresponds to a higher equilibrium constant which represents a greater proportion of DNA bound to histones. In other words, the free energy change quantifies the propensity of these different DNA sequences to form nucleosomes.


Application of Latin names for Taxonomy The current taxonomy has family names like Canidae and Felidae. But Felidae has sub families like Felinae and Pantherinae. Roaring cats and non-roaring cats. My question is based on the fact that we can have common words for these families based in Latin: Felines, Canines, Pantherines. Can every family in the taxonomy be represented by this latter form? Is Pantherine a valid name? Is was created by dropping the a from the subfamily but caninine was created by dropping the da from the main family and replacing with in.

Is "Pantherine" a valid vernacular name for this group in English? Sure, although "panther" is much clearer ("Pantherine" in English would mean "like a panther", not "a panther"). Also, many family names are fairly obscure: even a pretty well-known group, like Apidae, would become "Apinine" in your scheme, which is less clear to me than "a family of bees".

Is it a valid family name? No. The International Code of Zoological Nomenclature (ICZN Code), which governs all scientific names for animals, says:

  Article 29.2. Suffixes for family-group names. The suffix -OIDEA is used for a superfamily name, -IDAE for a family name, -INAE for a subfamily name, -INI for the name of a tribe, and -INA for the name of a subtribe. These suffixes must not be used at other family-group ranks. The suffixes of names for taxa at other ranks in the family-group are not regulated. [emphasis mine]

Family names that don't have an "-idae" suffix need to be corrected (ICZN Code Article 32.5.3.1).

Note that the ICZN Code doesn't cover other ranks in the family-group or above.


Term for timespan between generations Is there a terminology for the average timespan between generations, like ΔG ?
I mean by that the time from the parental generation being mature to the filial generation being mature.

You mean generation time?

There are several definitions in use, but one is "the average difference in age between parent and offspring" (or "age at which members of a given cohort are expected to reproduce") which would be the same as the time period you're asking about.

(The difference between these two depends whether the population is at equilibrium or not.)

The two above are 'shortest generation time'; a third definition (which is the first in the link) is a little more complex but is more useful where individuals reproduce over a prolonged period.


Why does air from the nasal cavity not go into the oesophagus? When we ingest food, the epiglottis covers the trachea and the uvula covers the nasal passage. But what happens when we breathe? Why does the air go into our trachea and not the oesophagus?

Swallowing food requires muscle strength to force the food down the oesophagus, which is a soft tube that collapses when empty, simply because the body is very crowded (space-efficient) and empty spaces collapse unless forced open. Only when you swallow, the oesophageal muscles force space to be made for food coming through.

In contrast, the trachea and bronchi are covered in almost-circular or C-shaped cartilage which holds them open and stable for air to flow through. You can see it here: http://en.wikipedia.org/wiki/Bronchi.

Concluding, air does not enter the oesophagus because it is always closed. Additionally, when the chest expands for breathing, the lungs expand and create suction down the trachea and not into the stomach (simply because this is where they connect).

The exception of course is if air is trapped in the swallowing motion with (or without) food. In this case it will enter the oesophagus and cause you to burp.


Breathing water vapour Normal air consist of oxygen, CO₂ and nitrogen, with traces of water etc.

Now imagine displacing all gasses except oxygen with water vapour. By water vapour I don't mean hot steam or fog. Just gaseous water.

The question is would it be beneficial or harmful to human, and how much so?
And assuming it's not deadly, in which circumstances could it be useful?

One thing I am wondering in particular is deep dive and high altitude applications. Having no/low content of nitrogen in such an artificial air mixture would help to avoid decompression sickness. And one would think water vapour is at least cheaper than pure oxygen (also might be safer and have less side effects).

Just because you have removed the Nitrogen and CO₂ won't help you keep a higher vapour pressure of H₂O in the air. You Could REMOVE all the other gasses and just have O₂ at its normal partial pressure at 1/5 bar total pressure and breath fine, but there would be a fire risk in this environment due to no non O₂ molecules to quench excited O₂.

The only way to have a high enough vapour pressure of H₂O for something like diving would be to heat it, but I don't think a lungful of very hot water vapour would be terribly good for you.

You can't just pressurise water vapour to any pressure you feel like; it will condense fairly easily.

To avoid Nitrogen's toxic effects, divers often use Helium to replace it as pure Oxygen is deadly at high pressures.


Help to identify larva found in sink? I need some help in identifying this critter. It was found in southeast Georgia in a home I am renovating. There were several around the sink and toilet bowl.

Approximately 5 millimeters long. Stripes black/dark gray. Tapered end seems to be moving as though it was the head. Bulbous end has two extrusions like antennae?

Thanks in advance.

Found it!

Seems to actually be the pupae phase of the common drain fly - psychoda spp.

Looks like I'm going to be routing or replacing the pipes in that house.

Thanks.


Does natural selection apply to entire populations as it does to individual organisms? The context: the other day I was reading an article about a peculiar species of ant that when threatened by a predator would “explode” in order to help protect the rest of the colony, although it kills the individual ant. I was wondering how this kind of behavior could evolve via natural selection if it only picks out the individual organisms best suited for the environment - because it seems like a self-destruct type of behavior wouldn’t be helpful to the ants that are trying to survive and reproduce. Though it would make sense if natural selection also applies to entire populations as it does to individual organisms - picking out entire populations that are best suited for the environment. It would make sense because populations that have individuals willing to explode to help protect the other individuals would have an advantage over the ones that don’t.

The question: does natural selection apply to entire populations as it does to individual organisms or have I made a mistake somewhere in my logic - and if so, where?

Unit of selection

Your question is about the concept of unit of selection. Selection acts on any populations of things that have heritable features which explain at least part of the fitness variance in this population. The "things" can be genes, cells, organisms, groups of organisms, species, lineages, etc...

The standard is to view selection acting on population of individuals. But of course, selection can also act on populations of groups of individuals (or populations of populations if you prefer) or populations of species. When talking about selection on a population of groups of individuals, we talk about group selection (a concept very related to kin selection) When talk about selection on a population of species, we talk about species selection (or lineage selection).

Social evolution and altruism

An altruistic phenotype is defined as being a phenotype that is causing a decrease in the fitness of the carrier of the phenotype coupled with an increase in the fitness of one or more recipient individuals. Altruism can evolve at a level, only by selection applying at levels above it.

Imagine for example a population of individuals. If one individual mutates and as a result display a behaviour of donating food to the others. The cost for this individual is -0.5 and the benefit for the recipient is say 0.7. In absence of reciprocity, this mutation will not be passed on on future generations because  this individual carrying it have lower fitness. Therefore altruism should not evolve in this population. Imagine however if there are many populations and that some populations are altruistic and other aren't. Then, the altruistic population will likely outcompete the non-altruistic populations and therefore over time only the altruistic populations will remain.

It is by the way the existence of an altruistic behaviour that brought to wonder about the level at which selection can act.

The field that studies the evolution of such social phenotypes is called social evolution


$S_{0.5}$ vs $K_m$ values in enzyme kinetics What is the difference between $S_{0.5}$ values and $K_m$ values in enzyme kinetics?

This expands my comment on the question to an answer.

If an enzyme exhibits Michaelis-Menten kinetics, then it is valid to define a KM and this equates to the substrate concentration when reaction velocity is 0.5 * Vmax.

However, many enzymes do not exhibit Michaelis-Menten kinetics. One example is when the enzyme shows a co-operative response to substrate concentration. In these circumstances the substrate concentration when reaction velocity is 0.5 * Vmax is still a useful parameter, but there is no KM.

See this paper for a discussion of the kinetic properties of the glucokinase of pancreatic β cells, which acts as the glucose sensor. This enzyme shows positive co-operativity with respect to its substrate glucose, and the authors develop a kinetic analysis in terms of various parameters. These include an S0.5 value for glucose, but a KM value for ATP (presumably because the kinetics with respect to ATP are simple Michaelis-Menten).


Comparison between Transmission Electron Microscope (TEM) to Scanning Electron Microscope (SEM) Can someone state the advantages of Transmission Electron Microscope (TEM) over Scanning Electron Microscope (SEM) and vice versa?

Well, the main difference between them is that with SEM you get information about the surface using scattered electrons whereas with TEM you get information about the inner structure with transmitted electrons. TEM has higher resolution, but SEM is simpler because you do not need a thin sample.

I recommend these videos about SEM and TEM. Short description of both can be also found at this webpage and in the material for students by ThermoFisher Scientific.


help identify this fish I came across this washed up fish in Panama City, Florida in November 2015. I'm guessing it's a puffer fish but I can't find anything like it online.

Thanks.

This is a kind of trunkfish. (They have different names, this could be a smooth or spotted trunkfish.). It's really a lovely and comical little fish when observed alive in coral reefs. It has the ability to change its coloration depending on whether it's excited or calm, or to minimize its contrast to the background. It is related to puffer fish.

It has a boxy, triangular body shape, and propels itself with relatively tiny, delicate fins. Like pufferfish, they are toxin producers.

In death, the body shape and coloration are different, of course. Never saw a dead one before; sad. The juveniles are adorable:

  Members of this family occur in a variety of different colors, and are notable for the hexagonal or "honeycomb" patterns on their skin. - Wikipedia


Salt Bridge for Microbial Fuel Cell: Full or Partly Full? I'm making a microbial fuel cell out of benthic mud and salt water in containers. My salt bridge will be made of agar and table salt solidified in PVC pipes. Does the salt bridge connecting the anode (benthic mud) and cathode (salt water) have to be full of the agar-salt solution, or can it be partly full?

Main function of the salt bridge is to conduct electrons. It should be in such a way that the agar within the PVC pipe from both end should be in contact with anode and cathode. so I would say keep it completely filled for better conduction.


Cutting dna using restriction endonuclease Genomic dna is digested with alu 1 which is a four base pair cutter. What is the frequency with wich it will cut the dna assuming a normal distribution of bases.

(this is not a homework)

Welcome to Biology.SE. I think this question would be better on-topic on math.SE.

Assuming the chromosome is either 4 bases long or infinitely long, then the answer is simply $\left(\frac{1}{4}\right)^4$. However, chromosomes are not infinitely long so the result should be (negligibly) lower than $\left(\frac{1}{4}\right)^4$. If chromosomes are only 3 nucleotide long, then of course, the probability will be $0$. If it is 4 bases long the probability is $\left(\frac{1}{4}\right)^4$. If it is 5 bases long the probability is $\frac{2}{4^5} = \frac{1}{2}\left(\frac{1}{4}\right)^4$.

Consider this numerical approximation, to ensure the result is correct with this simple one liner in R

n = 1e7
length(gregexpr('abcd', paste(letters[sample(1:4,n,replace=TRUE)], collapse=""), perl=TRUE)[[1]])/n
[1] 0.0039041

which is really close to $\left(\frac{1}{4}\right)^4 ≈ 0.00390625$.

So, in a genome of 3 giga bases, that represents an expected $\frac{3\cdot 10^9}{4^4} = 11,718,750$ (or ~11 millions) such locations where Alu 1 can cut.


Curious about Brazzein What is in compound "Brazzein" that it makes it 2000 times more sweeter than sugar?
Can anyone please explain the science behind it?

Brazzein is not even a sugar - its a protein that comes from Oubli, a West African climbing plant.

While I think nearly every living thing from bacteria up to large animals can perceive some carbohydrates as a food source, the mechanisms vary over the tree of life.

Because of this the taste of sweetness in animals varies a lot.  Aspartame, a non carbohydrate sweetener does not register as sweet in all the primates.  Brazzein and aspartame as capable of activating one or more of the human taste receptors.  Receptors are just proteins which sense a stimulus.  They can be activated by other compounds - this is how most pharmaceuticals work.  Sweeteners which are not glucose/sucrose can bind more tightly or affect the structure of the receptors, causing them to send a sweetness signal. Often these compounds also register with other sense receptors and so the sweetness is accompanied by other tastes as well.  It sounds like Brazzein is a clean taste, less likely to have such side effects.

I've not dug fully into this - its clear that some human sweetness receptors are known, but I'm not sure they are all known.


Why do ion concentrations change with different secretion rates in pancreatic juice? Why is it that when secretory rate increases in the pancreas the concentration of chloride ions decreases, and the concentration of bicarbonate increases in the production of isotonic NaCl secretion?

The modification that goes on in the duct of the acinus is dependent on flow. If the flow is faster, then less ions can be reabsorbed from the primary secretion. In the pancreas, chloride ions are removed, so surely their concentration should go up as the flow increases?

Bicarbonate on the other hand is added to the primary secretion in the duct. So shouldn't its concentration in the secretion stay the same or even increase as flow increases?

An interesting question!

I am attaching the picture from Boron & Boulpaep, Medical Physiology, 2nd Ed, p921 here to clarify the details left out in the hand drawn picture.

The flow of the digestive pancreatic enzymes increase mainly during food consumption. This is brought about by a number of redundant systems. The fasting secretion of pancreatic enzymes depends on the MMC (migrating motor complex).

Bicarbonate ions are exchanged with chlorine ions in the apical membrane of the acinar cells through a Chloride Bicarbonate Exchanger. This process is driven by:

Secretin - most important humoral factor - Increases secretion
ACh through muscarinic receptors - Increases secretion
GRP (Gastrin Releasing Peptide) - Increases secretion
Substance P - Decreases secretion

Mechanism of action of secretin seems to be through activation of cAMP. However even small amounts of secretin which do not raise the cAMP levels measurably can stimulate bicarbonate secretion. This suggests secretin response may be by

Unmeasurably small amount of increase in cAMP
Raise in cAMP levels in localised compartments
Activation of alternative second messenger pathways

In case of GRP the second messenger is not known.

The answer to your question is that when secretin is secreted, the Bicarbonate-Chloride transporter is accelerated to achieve the result displayed. This mainly happens when food enters the small intestine so as to neutralize the acid permitting the digestive enzymes to function at the optimal pH.

The Chloride-Bicarobonate Transporter is an exchange transporter which explains why there is a sharp fall in the chloride levels.


Insect making continuous sound in summers In deciduous to tropical-deciduous forests and residential places with such vegetation I have found this insect to make continuous sounds all through the day (even in nights sometimes) during the summers. Average summer temperature > 30 C around noon and ~ 28-29 around nights with high humidity.

I want to know what is the reason they make this sound ?

Recently, I found several of them dead near light poles etc..., and some sit very close to windows of air-conditioned rooms. I think they want some cool environment.

These are Cicadas, of the superfamily Cicadoidea of the order Hemiptera.

These sounds are made by the males to attract mates. There are a lot of species, each making there own specific sound to attract the right mate. However, to the human ear, these sounds don't sound different. Cicadas are also able to produce other sounds, in distress or during courtship and mating, but the continuous sound during night and day is to attract mates.


What happens after the purification step in Hi-C sequencing? I am a statistician reading an article on Hi-C, and I am trying to better understand one of the steps in the DNA isolation and sequencing process.

Since I'm a statistician, please try to avoid too much jargon in your answers, and if you must use jargon, please define/explain it.

Specifically, I am confused about the isolation and shearing step.  To explain myself, I will make reference to the following images, labeled 1 through 4.

Image 1)

Image 2)

(source: nature.com)

Image 3)

(source: babraham.ac.uk)

Image 4)

(source: nature.com)

I understand that the DNA is cut up with restriction enzymes, producing a cloud of DNA fragments, some crosslinked and other not. When these pieces are attached with biotin and ligated in a dilute mixture, it is highly likely that these pieces will ligate with themselves, resulting in either; 1) a ring from strands that were NOT crosslinked (as in the third drawing in Image 3 marked "self-ligation"), or 2) figure-eights from strands that ARE crosslinked (as in the fourth drawing in Image 1).

Now, the following is what I find confusing:

The pull-down step draws down the rings containing biotin, but Image 1 and Image 4 make it seem as though only the crosslinked bits are pulled down, and not the solo rings. Don't both have biotin?  And thus would both be drawn into the pulled-down sample?  Or does the pull-down process rely on a molecule having 2 biotins?  If not, can one discern whether a pulled-down piece of DNA is the result of a cross-linked or solo piece of DNA?
Why aren't all of the loose ends of the DNA ligated in Image 2?  Incomplete digestion?  Does this affect the biotin linkage?
My next question.  Assuming that the pull-down process only selects the figure-eights that are crosslinked, then purified (i.e. the cross-linking protein or formaldehyde is removed) forming a ring that is composed of two strands of ligated DNA (as in the upper-right corner of Image 4).  The process then records a genome-wide contact matrix $m_{ij}$, the number of "ligation products" between locus $i$ and locus $j$.  What is a "ligation product"?

Sorry, I know the above is a lot, but I want to understand the nature of the data before I analyze it.  Thank you for your help.

So, after the restriction digestion, the sample consists of DNA fragments with 5' overhangs. These are filled in by Klenow DNA polymerase, adding biotin-dCTP to both ends of each fragment. Then the fragments are ligated under conditions (ie low DNA concentration) such that ligation between non-crosslinked DNA is less likely. This reduced ligation efficiency (which is already lessened by the use of blunt end fragments) means that all crosslinked fragments may not be ligated, which I imagine is what they are showing in Image 2. Any two molecules which become joined by this reaction are called ligation products (ie they are the products of the ligation reaction).

After this step, the sample is treated with T4 DNA polymerase which, as well as having polymerase activity (obviously), also has 3'->5' exonuclease activity. Thus, any free DNA ends which have not been ligated will be trimmed, removing the biotin. After this step, biotin will mostly be present at ligation junctions, and these molecules can be selectively pulled down by the beads. I say mostly because some of these so-called dangling ends will still retain biotin, but these can be distinguished during mapping (see image below).

As for self circles: because they have been ligated, they will contain biotin and be pulled down with the crosslinked DNA. However, since this DNA is from the same genomic locus, they can also be distinguished from valid interacting pairs during mapping:

[source]

Finally, a quick note on the pull-down mechanism. The beads are coated with a protein called streptavidin (or avidin), which just binds to biotin very tightly. Only one biotin need be attached to any molecule (such as DNA) for it to be captured.


Betaine HCl stomach pH It seems betaine HCL is often recommended for those suffering from "low stomach acid" -- which, as I understand, is having too high stomach pH for proper digestion (especially for proteolysis via pepsin). However, I have a few questions then -- though I'm not sure if my reasoning is correct here:

Understandably, one wouldn't want to drink pure or highly concentrated HCl by itself to increase stomach acid! But then, what role does the betaine play?

I'm guessing betaine HCl probably does not dissolve in water to give the same pH as just straight (or concentrated) hydrochloric acid -- since then it would seem just as dangerous as drinking plain HCl!

In that case, if it doesn't decrease the pH as much, making it safe for oral consumption, what value does it bring for "lowering stomach pH" anyway? I mean, one could just drink a little vinegar or citric acid for the same effect?

Or, perhaps, is betaine-HCl just a means of some "delayed release" of HCl to lower stomach pH without hurting the mouth and esophagus during its initial consumption? Betaine may just be a useful carrier here, given it's quaternary ammonium and carboxylic acid groups (e.g., a zwitterionic carrier)

Alternatively, could the value of betaine HCl simply be in providing a source of Cl- anions, possibly for increased pepsin activity? (I'm not sure if pepsin requires merely low pH or specifically also needs Cl- anions as well) Betaine-HCl does seem to be often formulated with additional pepsin enzyme(s) as well...

Betaine HCl (trimethylglycine) was present in over the counter "stomach acidifiers" but the US FDA says there is no evidence for its efficacy and has banned its use for this indication (source: US FDA) - it may be freely available elsewhere, I am unaware of the regulatory status in other jurisdictions.

There is no biological reason to expect the "HCl" portion for most drugs to have any substantial effect on stomach acid. Lots of drugs are packaged in an acidic form as "drug HCl" - this is usually because the acidic form of the drug is more soluble. Drug doses are commonly in the microgram to milligram range (though obviously this varies for different drugs) - at those concentrations, the stomach acid is much too concentrated to be affected by the small amount of acid added from the drug.

The catch with Betaine HCl is it looks like websites are advocating for taking several grams to provide enough HCl to affect stomach acid. I suspect that supplement makers suggesting these high doses is what led the FDA to ban the drug OTC in the first place. Although betaine is produced as part of normal metabolism, there are some side effects reported, mostly mild.

Note that anhydrous betaine is prescribed (and approved by US FDA) for homocystinuria, and used as a supplement to animal feed, but neither application is related to stomach acidification (and the anhydrous form is not acidified).

One recent study supports use of Betaine HCl with patients who are being treated with acid-suppressing drugs such as proton-pump inhibitors, to be given along with other drugs that require an acidic environment to function/be absorbed. However, it is important to note that this study was in fasted patients: they consumed nothing but a little water with the betaine HCl. In this circumstance, the little bit of HCl in a moderate to large dose of betaine was sufficient to lower stomach pH. However, the results likely would have been very different if the patients had eaten a recent meal.


Is there a complete connectome of a cortical minicolumn? I know that there are projects that try to map brain connectivity. Given that a cortical microcolumn has only around a hundred neurons I wonder whether there is a dataset available with the complete connectivity of just a single minicolumn of the neocortex. Doesn't have to be human.

I posed this question on cognitive science stackexchange already, but it doesn't seem to be happening.

Perhaps the first place to look would be the Allen Brain Atlas
 (for mice, this is a paper about it), and also [this paper].(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169118/)


How good is the reproducibility of preclinical models? Unofficially, biology researchers always complain how frequently fail to replicate results others have achieved. But of course, such failed experiments are underreported.

Is there data, or at least well-reasoned guesses, on what is the success rate of experiment replication in preclinical models? I don't mean translational research and the impossibility to replicate a mouse result in a human. My question is about failing to reproduce the results within the same model system, replicated at the detail level available in the original publication (e.g. same animal strain, same drug dosages, etc.)

The Cochrane Collaboration has a great deal of this type of analysis. One of my favourite features of a Cochrane Review is the routine use of Funnel Plots, where there are sufficient data to produce them. Sensible interpretation of funnel plots can give some fairly strong hints about the reproducibility of published literature.

Funnel plots show datapoints of individual published studies which investigated the effectiveness of a technique when used for a specific purpose. The datapoints are plotted by estimated effect size (on the x axis) and an assessment of the quality of the trial, incorporating things like sample size and experimental design (on the y axis). A study with a small sample size and/or poor design (low on the y axis) would be expected to provide a relatively inaccurate estimate of the method's true effect size. As sample sizes increase and experimental methodology gets better (travelling up the y axis), you expect the studies to zero in on the true effect size, giving a pyramid or 'funnel' shape to the overall plot.

The reproducibility of trials affects where the points are in the pyramid in a couple of ways.

If there were a bunch of studies which looked for an effect of the method, and didn't find one, they might not be published because null results are considered boring by journal editors - the so-called 'file-drawer effect'. This would show up in a funnel plot as a pyramid that has a suspiciously low number of datapoints on the side of the pyramid that is close to the zero effect-size. The 'missing' datapoints are an indicator that this technique probably did not always reproduce an effect size as strong as the published effect sizes.

The other way that funnel plots can inform on the reproducibility of published studies is simply by looking at the width of the base of the pyramid. If it's wide, then with the experimental design methods of the studies at the bottom, the results aren't highly reproducible - different studies give very different results when looking at the same question.

It's a big job to synthesise this into a global assessment of 'the reproducibility of pre-clinical trials', but if you're interested, I'd recommend you spend some time trawling the Cochrane Library to get a hang of the sorts of variance you're dealing with.


What is a suicide plasmid? What is a suicide plasmid?

Example: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2737453/ mentions a "suicide vector". See also http://www.sci.sdsu.edu/~smaloy/MicrobialGenetics/topics/plasmids/allele-exchange.html which also mentions them.

As can be inferred from the Shanks et al. paper linked in the question: In molecular biology, "suicide plasmid" is a term that refers to a plasmid which is replication incompetent.*

Plasmids normally bear a sequence called "origin of replication" Ori which marks the plasmid for replication by the host cell. Plasmids that lack this Ori will not be replicated during cell division, and will become diluted away and/or degraded after a few generations. Hence the name: The plasmid will "commit suicide" by promptly becoming eliminated from the population of DNA molecules inside each cell.

Note that because not all Oris are universal, the same exact plasmid may be a normal vector in one species (eg. E. coli) and a suicide vector in another species (eg. P. aeruginosa) - which is logical: If a vector can't replicate in any species at all, how do you produce this vector in the first place? (there are ways, but they are laborious)

*: I am unable to find an authoritative source for this definition. The other two paragraphs are common knowledge.


What's the mechanism for pain-induced swoon? Is it true that people will pass out when subject to pain too much to bear, or there's no such threshold? What's the reason for passing out under acute pain, even if no physical injuries occur (e.g, loss of blood, etc.)?

Swooning, fainting otherwise termed Syncope or Primary shock (Triggered by pain or any unpleasant stimuli through the vaso vagal effect), is due to generalised vasodilation. The capillaries loose their tone and dilate resulting in an increase in volume capacity of the vascular system. This results in draining of blood to the dependent areas due to gravity thus hindering blood supply to the brain which shuts down and results in collapse (fainting) of the individual. This is a safety mechanism. Once the patient is in the lying down position the blood supply to the brain returns and the patient recovers. An individual who has fainted should not be propped up as this may result in seizures or worse.


Electron transport in granal stacks See paper for distribution of PS-I and PS-II within grana

As explained in the above paper, the PS-I complex is primarily located within non-appressed thylakoid region and stroma lamella, while PS-II in the appressed regions. Now since non-cyclic electron transfer (non-cyclic photophosphorylation) requires both the photosystems, wouldn't their distribution within grana far from one another hamper their ability to carry out non-cyclic electron transport. Although there are mobile untis to account for the electron transport between marginal PS-I and the PS-II immediately below, but the electron transport to the PS-II units deep in the granal core would still be unaccounted for.

First a clarification: the mobile units are no so "mobile". Due to (1) the high protein:lipid ratio of the thylakoid membrane and (2) the packing of protein complexes, the rapid diffusion of components along the membrane is hindered.

It has been proposed the existence of small local PQ diffusion microdomains, based upon the percolation theory:

  From the percolation theory, above a critical density, immobile or slowly moving transmembrane proteins are, indeed, expected to form flexible 2D networks of closed compartments preventing long range movement of small molecules. (Kirchhoff, H et al. (2000) Biochim. Biophys. Acta 1459, 148–168)

For this reason the PQ are confined, on a short time scale, within these domains, preventing their "dispersion".

In addition of the low diffusion of mobile carriers, the geometry of the granal stacks mantains the contact area between the PSII of the appressed grana and the PSI in the margin annulus domains relatively large, enabling effective linear electron transport in microdomains.

Figure 2b of the paper cited below shows the geometrical organization of the stacked grana and its description says:

  The circular border between the appressed domain and the margin annulus (ring) allows a large contact area between the PSII and the PSI domains and efficient linear electron transport from PSII via plastoquinone (PQ), plastocyanin and cytochrome b6f to PSI at a short distance of ~30–60 nm in local domain.

Further informations can be found in Albertsson, P-Å. (2001) Trends Plant Sci. 6, 349–354.


What does "delineate" mean in this context? I was reading a Scientific American story, “Controversial Spewed Iron Experiment Succeeds as Carbon Sink” (by David Biello), when I came across this sentence:

  “The problem for scientists is that oceanic waters tend to mix, which
  makes monitoring and delineating an experiment in the ocean
  challenging.”

I'm wondering what “delineate” means in this context. I think I grasp the general idea of this sentence, but it is the exact meaning of the word that has been troubling me.

Could someone kindly enlighten me on this?

Thanks!

To delineate an experiment is to describe precisely the conditions and the states of all the parameters.

So in your sentence it probably means a scientist might struggle to keep track of all the confounding factors (changing salinity, composition, dissolved gases, particulates, pH, temp, etc.) which might affect an experiment in such a dynamic system as the ocean.


What is allelic effect sizes and direction? In a paper, Berkley, C. A., and C. Lexer. 2008. Admixture as the basis for genetic mapping. Trends in Ecology & Evolution 23:686–694, the definition of Genetic architecture is given. It says:

  Genetic architecture: the number and genomic location of loci that
  contribute to variation in a trait, as well as the allelic effect
  sizes and direction, the genotypic effects (additivity and dominance)
  and the extent of epistatic interactions among loci.

What is the allelic effect sizes and direction?

I found that allelic effect sizes is the same thing as penetrance. But the direction?

These two concepts are different from penetrance.

Allelic effect size

An allelic effect size is the magnitude of the effect of an allele on a phenotype.

The detailed definition seems a little bit trickier than it sounds I think (and I would love confirmation by other users on what follows and or a reference). For example, a phenotypic trait might be influenced by 20 QTL. At one such QTL (say QTL8), you may observe two alleles in the population: QTL8_A and QTL8_B. The effect size is the absolute phenotypic difference between two individuals differing exclusively at QTL8. I suppose it is also possible to define an allelic effect size as the average difference between the phenotype of QTL8_A and QTL8_B over all possible genetic background (eventually weighted by the average frequency of each background in the population at a given instant). In the case of a QTL that contains more than two alleles, then the allelic effect size can be defined either between each pair of alleles or between one allele and the average effects of all the others. Strong epistasis make the whole thing more complicated if one wants to average over all possible genetic backgrounds.

Direction of an allelic effect

The direction of an allelic effect is the direction (add or subtract) that an allele has on a phenotype.

Talking about direction makes sense only in the absence of sign epistasis.


Firstly, Spider ID? Also possible relation to ~100+ serious bite reactions in past 1-2yrs Might have been occuring since day 1 in new residence about 2 years ago. Bites are painful to touch, when fresh, very odd sort of void filled with black stuff under skin which regularly shows fang type trackmarks.(golf ball size swelling, pussing, twin &/or parallel punctures wounds, black(necrotic?) Substance under hardened skin cap as healing, long term healing) Spider found in nightstand drawer, maybe stranded in bottom of SS can cooler.
I have many pics of the live spider in a jar. Thankyou...;)>!

It is a wolf spider. It grows from about 1cm to 5cm long. Wolf spiders are usually gray with brown to dark gray markings. It does not spin webs, instead it actively hunts it's prey. Wolf spiders are agile, robust and have excellent eyesight$^1$. That is why you have noticed that it is quite aware of your movements.
Hogna radiata:

Alopecosa Kochi:

The bite of this spider leaves prominent marks$^2$.

In severe cases, the surrounding area may develop redness, swelling, and even ulcers that spread beyond just the bite location. Allergic reactions may cause even more severe symptoms in some people$^2$.

Since the wolf spider is not poisonous its bite can be treated by cleaning the area with soap and water and then placing a bandage over it$^2$.
Note:
I am unable to identify the exact genus of the spider. I believe it could be Hogna or Alopecia. Someone more knowledgeable could inform me.
References:
1.Wikepedia
2.Healthline


Can anyone tell me what type of fish this is? Notice the reflective patterns on its underside.  I think it must be a deep water fish.  It was found washed up on the ocean sand in Myrtle Beach, South Carolina (USA) after a hurricane.

Not an expert, but an online search for bioluminscent fish led me to a bioluminescent toadfish called Porichthys porosissimus. The ventral angle of your specimen looks a lot like the photos I could find...

 Source: Robertson, R on Fishbase

Like many midshipman fish, P. porosissimus have photophores (those dots in your specimen) that glow to attract prey:

 Source: W. Ward (Rutgers Center for Research and Education in Bioluminescence and Biotechnology)


What is cognate miRNA? I understand what miRNA are, but I'm unsure of what cognate means. Looking at this post, it seems that a cognate miRNA is a known miRNA vs. a recently discovered/possible miRNA. Is this thinking on the right track?

The use of the word cognate in molecular biology reflects adjectival definition 2 from Lexico:

2 formal Related; connected.
‘cognate subjects such as physics and chemistry’

The example given shows that this can be used in the most general sense of related, so that there is no requirement for some common antecedent as a surrogate for a human mother or ancestor.

Specifically there is no implication of the involvement of a common DNA sequence, as in the answer from @Dirigible, nor that of a common origin as invoked in an earlier answer on this topic.

This is quite clear if one considers the much earlier usage of cognate in molecular biology in relation to an mRNA codon and the tRNA anticodons that can recognize it, or a tRNA and an aminoacyl tRNA synthetase that can aminoacylate it.

As far as the usage with microRNAs is concerned, a cognate mRNA is one with which the miRNA can interact by base-pairing — no more, no less.


Why will happen if plant phloem does not contain sieve plates? What are the primary functions of the sieve plates that make them so crucial? I've done a bit of reading online and found
"Sieve plates are perforated end walls separating the component cells (sieve elements) that make up the phloem sieve tubes in vascular plants. The perforations permit the flow of water and dissolved organic solutes along the tube and are lined with callose."
However, wouldn't the flow of water or organic diluted be faster without the extra sieve plates obstructing the flow? Or is there some other functions of the sieve tubes?

First of all, phloem sieve cells (opposing to xylem vessels) are live cells. In the phloem, a transport occurs not like in water pipes (with free movement of liquids) but through cells transport structures, particularly through plasmodesmata. As live cells, sieve elements need all standard structures, including cell wall, to sustain functionality.

Moreover, the phloem transport is (at least partially) an active process. I.e. to transport something you have to spend some energy. Today the most supported hypothesis of phloem transport is Pressure Flow Hypothesis . According to Wikipedia:

  While movement of water and minerals through the xylem is driven by
  negative pressures (tension) most of the time, movement through the
  phloem is driven by positive hydrostatic pressure. This process is
  termed translocation, and is accomplished by a process called phloem
  loading and unloading. Cells in a sugar source "load" a sieve-tube
  element by actively transporting solute molecules into it. This causes
  water to move into the sieve-tube element by osmosis, creating
  pressure that pushes the sap down the tube. In sugar sinks, cells
  actively transport solutes out of the sieve-tube elements, producing
  the exactly opposite effect. The gradient of sugar from source to sink
  causes pressure flow through the sieve tube toward the sink.

So, a plant needs live cells to support such mechanism.

Here we come to sieve plates. In plants, live cells interacts by means of plasmodesmata. In simple words, they are extensions of endoplasmatic reticulum which connect the cytoplasm of two cells and act as transport channels. And sive plates are simply places of highly hypertrophied plasmodesmata region.

So in conclusion:

Phloem transport is a partially active transport which occurs with
an involvement of cells transport structures like plasmodesmata.
The region of hyper-developed plasmodesmata on sieve elements wall
appears as sieve plate.
That is why an absence of such structure will not provide any gains in conductivity.

UPD. In response to Jim Young comment.
Damage protection is not a major role of sieve plates. Again, sieve plates are areas where plasmodesmata penetrate cell wall. Plasmodesmata act as the main vector of intercellular transport. So, the transport is the main purpose (or a reason) of sieve plates.  The damage protection is an additional property and not an aim of these structures. As to tyloses, yes it is a common mechanism of vertical transport prevention in xylem. But xylem vessels consist of dead cells. They are literally pipes. Therefore it is possible to cork up xylem vessels by simply inserting packs of fibre. BTW, that is why cavitation in vessels can cause embolization.  In contrast, phloem cells are live cells (with cytoplasm and EPR). They conduct water and sugars not by free flaw but with an involvement of intercellular mechanisms. That is why mechanical embolization is not a case for phloem cells.


What color is the hemolymph of the Japanese giant hornet? This is a random and very specific question that's been nagging me for quite some time. I've tried asking on other websites with no luck, and am hoping that somebody here can either give me an answer or redirect me to somebody/somewhere where I can get my answer. I guess it isn't required but I'd also prefer to know, if you can give me an answer, how you got your knowledge on it. Thank you in advanced!

I was able to figure this out for myself by watching videos of the hornets being eaten by other insects. The answer is that the hemolymph is a pale yellow color, like I've heard other wasps and some bees have as well.


What are the advantages of forgetting? How  forgetting things is helpful for the brain or the human body  biologically? This web page

After some moment of being rude, selfish, or weak, either we are able to put it behind us, or the person who suffered at the result of our imperfection moves on. The reason for this is our ability to forget about it. We forget not because we have an imperfect hippocampus (our brain’s memory organ); it's actually an evolved solution. The ability to lose information allows new information to come in that is more relevant, more pertinent to an ongoing reality. Forgetting allows us to update.

and this Huffington post article

According to a study in Nature, our awareness is limited to only three or four objects at any given time. To be able to think at your highest level, you therefore must be very efficient at filtering out all of the background noise: Your racing thoughts, the ringing phone, your neighbor’s barking dog, and the list goes on.
The Nature study found that when participants were asked to “hold in mind” certain objects while ignoring others, there are significant variations in how well each of us can keep irrelevant objects out of our awareness.
The researchers concluded that our memory capacity is therefore not simply about storage space, but rather “how efficiently irrelevant information is excluded from using up vital storage capacity.”

provide some backgrounds.

Short answer
It has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.

Background
First off all, there are many types of memories, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental.

Beneficial effects of loosing memories
Long-term memory is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that detect (anterior cingulate cortex) and resolve (dorsolateral and ventrolateral prefrontal cortex) mnemonic competition (Kuhl et al., 2007). The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones (Shea & Right, 1991).
Inherently volatile memory
Short-term working memory is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (which objects depicted here match the colors you just saw?). If all these memories would be retained, tasks dependent on working memory would not be possible. Sensory memory an ultra-short term memory that is kept only for very short amounts of time, allowing people to, e.g., track a light and make a symbol or letter out of it before the information is funneled to the short term-memory.
Neutral effects of loss of neural function: a side track off memory lane
However, forgetting may be simply another example of the use it or lose it principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the plasticity of the cortex. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated (Stronks et al, 2015). In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available per se. Hence, 'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever, barred a minority of studies that showed a slight benefit of being blind in auditory tasks (Stronks et al., 2015).
Pathological memory loss - not so good:
However, forgetting of memories may also be pathological; think of the impaired short-term memory of Alzheimer's patients, or amnesia due to stroke. Forgetting is not always beneficial.

References
- Kuhl et al., Nature Neurosci (2007); 10: 908-14
- Shea & Right, Res Quarterly Exercise Sport (1991); 62(3)
- Stronks et al., Brain Res (2015); 1624: 140–52


What does the immune system do to stop pathogens that aren't killed by macrophages? For instance, say a host is infected with salmonella where the pathogen can enter into a macrophage without the macrophage destroying it. How does the body then fight off an infection that is capable of surviving the mechanism by which pathogens are destroyed?

There are two broad types of infection classified by their persistence: acute and chronic infections.

I find that most courses on immunology nicely cover acute infections and their detection, and resolution. In the case of S. typhi, which has the ability to invade host cells such as phagocytes and inhibit their ability to properly function, the case isn't so pretty (1). The same can be said for some viruses like HepC and HIV, or other bacteria like Mycobacterium.

Salmonella spp. have a number of virulence factors. The flagellum of the bacteria actually acts as a TLR agonist that activates phagocytes like monocytes/macrophages and neutrophils, which are often first-responders. Then, the bacteria can facilitate the injection of some of its own proteins into the host cell which does a number of things like modulate vessicle trafficking, suppress cellular functions, induce apoptosis and promote overall survival of the bacterium inside the phagocytes (2).

So normally, and referring to the below figure, the overall reponse to a Salmonella infection is adaptive in nature, presumably because your innate effectors have been stunted:

SRC

You can see in healthy phagocytes that through one of two pathways, protein antigens end up displayed on HLA molecules for cellular immunity to take over. Option B is that another cell like a macrophage detects distress signals from the infected cell and induces cell death in it through receptors or oxidative burst. In the case of Salmonella, HLA expression is down-regulated and oxidative burst can be inhibited so localized, infected antigen-presenting cells cant mount an effective response.

That's not to say everything is de-regulated early on. If you succeed in antigen presentation or innate killing (perhaps a non-pathogenic strain), you will resolve the infection as seen in the above figure: a combination of T-mediated killing, B-mediated killing, NK-mediated killing, and generalized inflammation.

In the chronic case, the pathogen will have escaped the primary immune response, but the system will attempt to continue to resolve the infection. This can lead to a number of things: cellular anergy, cellular hyperactivity, sequestration (see granuloma), chronic inflammation & tissue damage, and so forth. The following diagram is predicated upon viral infections but the immunology is largely similar:

SRC

There are changes to the system that are a result of over-exposure to antigen, and an inability to clear that stimulation. The best way to explain it is that chronic stimulation leads to both hyperactivity and suppression. The constant presence of effector molecules like TNF-a leads to a persistent state of tissue inflammation, which is bad for the tissue, but taken together with the persistent presence of antigen, this may lead to dysfunctional responses by lymphocytes (3).

A particularly virulent infection may be impossible for your immune system to clear without assistance, then, requiring the intervention of gram-negative antibiotics, for example.