How accurate is facial reconstruction in forensics? I’ve seen on tv where they reconstruct heads and faces from the remains of ancient people and I was wondering if anyone had a source that has pictures of maybe side by side of a facial reconstruction Vs. a picture of the actual person being reconstructed. I know it takes a long time to fully decompose but surely there’s been a reconstruction done of a recent person who’s been photographed

okkkk. I did a big project on this... and here's some of my research... let's hope it answers your question

Facial reconstruction (also known as craniofacial identification) is a method used in the forensic field.  Many people view facial reconstruction as an art instead of science.  Art is commonly portrayed as the expression or application of human creative skill and imagination, typically in a visual form such as painting or sculpture, producing works to be appreciated primarily for their beauty or emotional power.  Science is thought of as the intellectual and practical activity encompassing the systematic study of the structure and behavior of the physical and natural world through observation and experiment.  But where do science and art blur the lines?

WHAT CAN WE TELL FROM THE SKULL:

The skull provides clues to personal appearance. The brow ridge, the distance between the eye orbits (sockets), the shape of the nasal chamber, the shape and projection of the nasal bones, the chin's form, and the overall profile of the facial bones all influence facial features in life. Using these bones, artists and forensic anthropologists work together to reconstruct facial appearance through the process of forensic facial reconstruction.  There are many ways of telling both the approximate age, and the approximate ethnic background of the victim.  To find age, you can pay attention to the cranial suture (or the place where the cranium fuses to other bones of the skull), the size of the skull can help, as well as the teeth and the formation of the bottom jaw.  When looking for the birth gender of the victim, scientists often pay attention to the brow ridge, eye sockets, mandible, and the slant of the jaw.  Sometimes, it is impossible to tell by looking at the skull what birth gender the victim was.  In cases like this, people look to the pelvis to tell if the human has given birth, and if not, males do not have a ventral arc.  It is often very difficult to find the race of a victim if they are mixed race, or if the skull is very worn out.  However, to find the ethnic background scientists will look at the shape of the skull, the nazel root, and the space between eye orbits.

WHAT ARE THE PROCESSES OF FACIAL RECONSTRUCTION AND ARE THEY ACCURATE:

Facial reconstruction is an exacting process. The finished product approximates the actual appearance, because the skull does not reflect the details of soft tissues-eye, hair, and skin color; facial hair; the shape of the lips; or how much fat tissue covers the bone. Yet, facial reconstruction can put a name on an unidentified body in a modern forensic case, or, in an archaeological investigation, a face on history.

Today, many forensic facial reconstruction techniques are in use, including two-dimensional (drawn), three-dimensional manual and three-dimensional computer-based.  In the manual techniques, including two dimensional a cast of the skull is required, so the facial markers do not become an anomaly when analyzing the skull.  Although all of these methods are used, it is most common that a trained sculptor, who is familiar with facial anatomy, works with a forensic anthropologist and uses clay to build the facial features. The forensic anthropologist interprets skeletal features such as the subject's age, sex, and ancestry, and anatomical characteristics such as facial asymmetry, evidence of injuries (a broken nose, for example), and loss of teeth before death.

Facial reconstruction is used when the victims dental records fail to identify them, and there is no dna to pull from the body.  The process of reconstruction starts with making a mold of the unknown skull with the jaw attached and false eyes in place.  Depth markers are placed on 21 different “landmark” areas of the mold of the skull to approximate the facial tissue thickness that lay on the skull.  These tissue thicknesses are approximated from averages of other people of the same age, sex, and race as the skull is assumed to be.  Facial muscles are placed on the mold next and then the face is built up with clay to within a millimeter of the depth markers as tissue.  The nose and eye setting are very difficult to estimate due to the enormous amount of variation possible, mathematical models are used to make the approximations, the mouth is assumed to be the same width as the distance between the pupils. In facial reconstruction the eyes, nose, and mouth are mostly guess work.  Characteristics such as birthmarks, wrinkles, scars, and such are guesses at best and cannot actually be determined from the skull.  Facial reconstruction is accurate because it has been using mathematics, and calculations as such, in order to determine spaces, amounts, as well as the shapes of the face themselves.

WHY IS FACIAL RECONSTRUCTION IMPORTANT:

Facial recognition, as well as facial reconstruction is very important in the forensic field.  Both have a very important role in catching murderers, and investigating crime.  Without having a facial reconstruction, often times, you cannot identify victims.  Assuming the body is historical and for museum purposes, then without an identity it becomes very difficult to fill in large gaps of information, and time that can be crucial to history.  Also, if you can’t identify a murder victim then scientists could only look into cause of death.  Learning the identity of a deceased victim is as important to crime investigations as learning the identity of the suspect. When human remains are found, then the top priority is often to find the identity of the victim.  Police often also will look for an identity out of respect, for both the victim and the victim’s loved ones if any.  Facial reconstruction has been used ever since 1890.  Before 1890, people mostly used few facial indicators such as the shape of the frontal bone, and the remains of flesh to help identify the victim.  Facial reconstructions, can also show what injuries were sustained previous to death.

WHAT CAN WE LEARN FROM FACIAL RECONSTRUCTIONS:

Our skeleton is an extensive record of our lives. The food we eat, the rate at which we grow as a child, the injuries we sustain, whether we have given birth; all can be determined from our bones. Experts can determine sex, age, and ethnicity, relatively easily from the skeleton, with the skull and pelvis playing pivotal roles in this analysis. Later this week, we’ll be taking a more detailed look at how to determine sex and ethnicity from a skull.Teeth can reveal information about diet and a comparison between dental records of the deceased and the recovered skull is often the primary method of identification.  By looking at the scull (or any bones in fact,) you can tell childhood injuries from injuries that might have been fatal.  You can also look at bone density and other factors to tell if the victim was suffering from any diseases.  People look for the sagittal suture – the squiggly line that runs the length of the skull – If it is fully fused, the remains are likely to be of someone older than 35. After that professionals look for a second line at the front of the skull -- the coronal suture – which fully fuses by age 40. Teeth are also looked at. If they're worn down it could be a sign of a poor diet. If they're well-maintained and/or have good dental work such as fillings, they were able to afford proper dental care—another clue as to the identity of your skeleton. Oftentimes professionals consult a scientist who specializes in teeth, known as an odontologist. They can determine how old a person was at death, what kind of health they were in and what kind of diet they had.

Baby's bones begin to grow in the womb. At birth, the skeleton is partially formed. Many bones are still in "parts." The ends (epiphyses) and bony shafts (diaphyses) of long bones form separately in the womb. At birth, the ends of the long bones are mainly cartilage, with centers of bone beginning to form inside. As a child grows, the shafts get longer, and bone gradually replaces the cartilage epiphyses. Through the growing years, a layer of cartilage (the growth plate) separates each epiphyses from the bone shaft.  By paying attention to this, it is easier to tell age, and follow growth patterns to have a successful reconstruction.

Between 17 and 25 years, normal growth stops. The development and union of separate bone parts is complete. At this point, you and your skeleton are as tall as you are going to get - with many fewer bone parts than you started with.  The bones that enclose the brain grow together during childhood along lines called cranial sutures. During adulthood, bone "remodeling" may gradually erase these lines, at variable rates. Closure of cranial sutures gives general information about a person's age. It is best used with additional indicators to estimate age, or when other age indicators are unavailable.

WHAT ARE THE LIMITATIONS:

It is very hard to estimate a person’s weight and represent that with facial markers.  Since a chart of average thickness of soft tissue is used to estimate the way a person looked, if you were on the skinnier side, your head might appear a lot more overweight than usual and or skinnier.  To help determine weight, scientists look at the rest of the remains for a height.  Facial reconstruction relies on the relationships between the facial features, subcutaneous soft tissues and underlying bony structure of the skull. If there is no clue for potential identity because of impossibility to compare questioned remains with possible familiar material, in such cases one of the last chances is to recreate ante mortem appearance by face reconstruction. Many of the soft tissue thickness values are significantly different from those reported for comparable groups, suggesting that individuals from different geographical areas have unique facial features thus requiring population-specific values. This literature review attempts to throw some light on the important aspects that has to be taken into consideration while setting norms of soft tissue thickness among various populations.

Studying the unknown skeletal remains mostly becomes the only way to find out more information about individual characteristics, which could lead to identification of potential victim. If there is no clue for potential identity the most precise comparative techniques fail, because of impossibility to compare questioned remains with possible familiar material. In such cases one of the last options is to recreate ante mortem appearance by face reconstruction. Following the first introduction of reconstruction in the late 19th century, other techniques have been developed including radiography, 3D statistical model, ultrasound, MRI, CT and Cone Beam Computed Tomography (CBCT).  Facial contours were traditionally considered to be the result of positioning of underlying hard tissue followed by the soft tissue. However, current trend shows a paradigm shift from the conventional hard tissue analysis to also include both hard- and soft-tissue analysis.

IS FACIAL RECONSTRUCTION AN INTERDISCIPLINARY ART:

The skull is made up of 22 bones, 14 of those are facial and eight are cranial bones; it is a complex structure, and small variations during development and growth, together with soft tissue differences, create the enormous facial variation seen in the human population.  Artists have long been interested in the direct anatomical relationship between the skull and facial appearance.

Artist, Gaetano Guilio Zumbo (1656-1701), used facial reconstruction as an art because he believed that math and science are both forms of art.  His work can be found in the Wax Anatomical Collection at La Specola Museum, Florence, became famous for his macabre scenes depicting various stages of decomposition of the human body.  One of his most famous pieces is the head of a dead man, with facial muscles recreated in wax over a real skull.
This is the earliest surviving anatomical wax model created for didactic purposes and exhibits extraordinary anatomical precision alongside an artistic sense of horror and decay. Although we assume that Zumbo was less concerned with facial appearance than anatomical detail, he pioneered the development of scientific art and this work ranks as one of the finest examples of three-dimensional facial reconstruction.

By definition, an interdisciplinary art is relating to more than one branch of knowledge.  Facial reconstruction is often categorized as both a science and a mathematical equation.  Both science, math and art are human attempts to understand and describe the world around us. The subjects and methods have different traditions, and the intended audiences are different, think the motivations and goals, specifically for this purpose is fundamentally the same.


Hopeful Monsters in Plants? Does anyone know of any research/examples on Hopeful Monsters in Plants?

I define Hopeful Monsters as organisms of a species that have macroevolutions to prompt new speciations. These macroevolutions being themselves, prompted by smaller gradual microevolutions in the species. See this paper for more details. I'm interested in a plant based example, or any good recent example, if plants can not suffice. Ideally research that is easily read and recent, and useful for arguing the existence of themselves?

One example of what you may consider to be a macroevolutionary change is a whole-genome-duplication, or polyploidy event. These are not uncommon in plants, and can promote speciation due to a reproductive barrier arising between the polyploid progeny and the diploid parents. You can find many papers about this topic, here is one from 2009: http://www.pnas.org/content/106/33/13875.short


Why is the ingestion of salt and water beneficial to muscle cramp According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.

A lack of ATP would obviously produce cramping, as myosin requires ATP to become free from actin.

However, I have heard that potassium and sodium are useful for treating cramps and that their deficiencies can lead to cramping.

Maybe it isn't.

  The standard theory: muscle cramps are caused by loss of fluids and electrolytes, which alters fluid balance in the body and increases the excitability of nerves.

  The "new" theory: muscles cramps result from "altered neuromuscular control," which can be triggered by a variety of factors, including genetic predisposition, damaged or fatigued muscles, starting too fast, and not tapering enough -- none of which have anything to do with hydration or electrolytes. [...]

  A few years ago, researchers at North Dakota State University published a study showing that dehydrating subjects by 3% of their initial body weight didn't change their susceptibility to muscle cramps (as measured by threshold frequency). Now, in a new British Journal of Sports Medicine study, they've extended those results to a greater degree of dehydration: their 10 subjects reached an average dehydration of 4.7% (greater than 3% is "significant" dehydration, while greater than 5% is "serious") after almost four hours of exercise in very hot conditions. Crucially, they exercised only with their non-dominant limbs, while the cramp testing was performed on their dominant leg, so that muscle fatigue/damage could be eliminated as a triggering factor.

  The result: no difference in cramp susceptibility or intensity, despite an extreme dehydration protocol that saw them lose about 4 g of sodium! The researchers conclude that their data supports the "altered neuromuscular control" theory.

Even the older research that did find it more plausible that electrolytes were a cause wasn't very adamant that's the [only] cause, e.g.:

  Consumption of a carbohydrate-electrolyte beverage before and during exercise in a hot environment may delay the onset of EAMCs [Exercise-associated muscle cramps], thereby allowing participants to exercise longer. However, it appears that dehydration and electrolyte loss are not the sole causes of EAMCs, because 69% of the subjects experienced EAMCs when they were hydrated and supplemented with electrolytes.

There are a few [not very well controlled, IMO] experiments from the 1920s and 30s (three papers to be more precise) that did find a role for sodium depletion in some cases of mild cramping. The most controlled of these (published in 1936) involved sodium depletion for 10 days (daily sweating and virtually no intake), which  is hard to argue is that common in most cramp suffers. The original paper notes that the level of sodium depletion involved led to quite a few other symptoms:

  Such deprivation led to aberrations of flavour, cramps, weakness,
  lassitude, and severe cardio-respiratory distress on exertion. The nitrogen balance became negative and the blood urea rose.

And despite the severe sodium depletion, the cramps were mild but generalized:

  These muscular cramps were not of the very severe localized type which are
  said to affect stokers and miners (Moss, 1923-24), but were widespread,
  frequent, not very painful, and generally controllable. Any muscle in
  the body was liable to go into spasmodic contraction, especially if some
  little effort was demanded of it (Moss, 1923-24). “ Coughed a little
  over something, cramps round chest, mild.” * R.B.N. experienced
  occasional cramps in the muscles lining the floor of the mouth but the
  extremities were most affected, and it was possible sometimes by suitable
  movement of the toes to alternate the spasms for hours on end between
  the extensor and flexor muscles. Perhaps the most characteristic of all
  were the manual cramps. R.A.M. experienced “ constant mild cramps
  of the fingers and thumb when using forceps at the balance,” * and R.B.N.
  found that he “ cramped quickly when working, telephoning, or using
  pipettes.” *

So that's why I say these types of cramps probably have little relevance for those experienced by most people.

I'm not sure there any studies for potassium. The paper reviewing the sodium evidence notes:

  Mechanisms in heat cramping remain murky. Sodium loss contracts extracellular fluid space and may alter ion channels to make neuromuscular junctions or muscle units hyperexcitable, thus evoking
  involuntary and sustained contractions, or heat cramping. And, not all camps buy salt loss for  cramps. Bananas, for example, remain popular in some football camps, to prevent heat cramping by ‘replacing potassium’. But here, bananas are yellow herrings because little potassium is lost in sweat. The same applies to calcium and magnesium. Sweat after all, is mainly water and salt (sodium chloride).

And do note that his latter paper is written by a Gatorade consultant.

One 2009 review in clear opposition to relevance of electrolytes-water for the usual exercise-related muscle cramps notes:

  In summary, dehydration and electrolyte depletion are often considered together (and recently together with muscle fatigue) as the “triad” causing EAMC. The key components of this hypothesis (fig 1) are that electrolyte (mainly sodium) depletion through excessive sweat sodium loss together with dehydration causes EAMC. However, results from prospective cohort studies consistently show that athletes suffering from acute EAMC are not dehydrated, neither do they have disturbances in serum osmolality or serum electrolyte (notably sodium) concentrations. Furthermore, sweat sodium concentrations measured during exercise in 23 reported cases with a past history of EAMC are not higher than those reported in many other studies. Both electrolyte depletion and dehydration are systemic abnormalities, and therefore would result in systemic symptoms, as has been observed in other clinical conditions. However, in EAMC, the symptoms classically are local and are confined to the working muscle groups. Thus, the available evidence to date does not support the hypotheses that electrolyte depletion or dehydration cause EAMC — therefore an alternate hypothesis for the aetiology of EAMC has to be considered.

Suffice to say that this field is still quite contested... and plagued by conflicts of interest. Witness a 2019 paper finding that a magic electrolyte formula (contents not disclosed) from a pharma company absolutely does lower the risk of cramps after exercise compared to water. Study funded by aforementioned pharma company, of course. And the press reported this as "water after exercise increases risk of cramps" (by diluting the electrolytes in your body, of course), arguably due to the authors' summary.

And while most of the previous material was about exercise-related cramps, even for the nocturnal cramps more often experienced by the elderly, the role of electrolytes appears uncommon; according to a 2007 review:

  Muscle cramps, notably nocturnal leg cramps, are common symptoms experienced by general medical patients, particularly the elderly. Their etiology is varied; most commonly, these cramps are idiopathic. With the notable (and relatively rare) exceptions of serious electrolyte imbalances including hypokalemia, hypomagnesemia and hypocalcemia, these cramps are typically benign in nature. [...]

  The second recent study to challenge the notion that diuretics [which promote a loss of electrolytes through urine] are a common cause of muscle cramps was a cross‐sectional survey of 365 general medical patients. Although the prevalence of leg cramps in this cohort was 50%, no associations were found between these cramps and any medication except analgesics that were used to treat the cramps. [...]

  Nevertheless, a review of the Physicians' Desk Reference database (available at www.pdr.net) suggests a consistent association between diuretics and muscle cramps. [...]

  The mechanism of diuretic‐associated cramping (if such an entity truly exists) is likely related to hypokalemia, hypomagnesemia, or volume contraction (with or without metabolic alkalosis). Hypocalcemia is a possible cause during therapy with loop‐diuretics such as furosemide, but is unlikely with the hypocalciuric thiazide‐type diuretics. Interestingly, potassium‐sparing diuretics, such as amiloride, are also associated with cramping. Thus volume contraction appears to be the one mechanism that is common to all classes of diuretics.

A 2012 new large-scale investigation did point to some epidemiological associations between cramps and diuretics:

  Cramp treatment was substantially more likely in the year following introduction of LABAs [long-acting β2-agonists], potassium-sparing diuretics, or thiazide-like diuretics, and 60.3% of quinine users (individuals experiencing cramp) received at least 1 of these medications during a 13-year period. In contrast, statin and loop diuretic associations were small. Physicians should be mindful that the use of these medications may worsen symptoms in patients experiencing nocturnal leg cramps.

And they also have some comments on putative mechanisms:

  Physicians may be surprised that potassium-sparing diuretics have a stronger link to cramp treatment than loop diuretics. Yet, hyperkalemia facilitates neuronal excitation, and hypokalemia suppresses motor neuron activity. β2-Agonists are known to have a stimulatory effect on motoneurons, and β2-adrenergic receptors are found on peripheral nerves.


Effect of heat-treatment of Vitamin C When it is in the body, does it matter if vitamin C has peviously been heat-treated? Can the body still use it?

For instance, if vitamin C is added to 90 degree celsius water does it matter if you drink all of the water? Will you still gain the vitamin C?

Disclaimer: the denaturation is the process of protein unfolding from their native state. Since vitamin C is not a protein, it cannot denaturate. I think that the word you're looking for is simply "degradation".

Vitamin C can exist either in its reduced form L-ascorbic acid (L-AA) or in the oxidised form dehydroascorbic acid (DHAA). The active (antioxidant) form of vitamin C is the former; however, there are enzymes in our body that can convert DHAA back into L-AA.

In this article, the authors seek to evaluate the thermal stability of both L-AA and DHAA in broccoli. Their results are the following.

  Thermal treatments (for 15 min) of crushed broccoli at 30 to 60 degrees C resulted in conversion of l-AA to DHAA whereas treatments at 70 to 90 degrees C retained vitamin C as l-AA.

So, cooking the vitamin C does not alter its structure and your body will still be able to use it. Another reason to eat broccoli, I guess.


How do proteins and genes participate in learning? I am a computer scientist that studies biology and bioinformatics.
In the last weeks, I have been trying to study new research directions, and I would like to deepen my knowledge on the role and behavior of genes and proteins in learning.

By learning, I mean the human process: the information I is absent at time T, and present at time T+1.

I would like to study more this problem, and I am wondering: how do proteins and genes behave during learning?
I have read that proteins that participate in learning are called marker proteins. Is it true? Which role do they have?

Where could I find some resources to study this fascinating problem?

Thank you very much!

The storage of memories in cells is rarely thought of on the protein level of the cell.  Cells are usually given a developmental state, but no memory.  A cell may become a liver cell, cancerous, or diabetic, but this is not memory, but a physiological change in the cell which is usually not reversible to a previous state.

For example cancer treatments are entirely focused on identifying the cancerous cells and killing them.   Internally the genomes of cancer cells often have deletions and duplications.  They are cancerous, they have not learned to be cancerous. Though not as dramatic, it is now thought that cellular differentiation which creates different types of cells is heavily influenced by epigenetic modification of the genome; the DNA is marked by methyl groups which dictates the state of the cell by modifying the gene.  This is mediated by proteins for sure, but is quite complex and not well understood at this time. Epigenetic markers can even change gene behavior between generations of offspring as well, though that is not usually called memory.

How is information stored in the brain?  This is thought to be reflected in the organization of the neurons in the brain.  There are many kinds of neurons.  They can be distinguished by the sorts of axons and dendrites that emanate from the cell body.  They can also be distinguished by the chemical variety of neurotransmitter they use (there are a score of different molecules).  So to a great extent the type of cell and the specific proteins it chooses to use to mediate information is very important.

That being said, information is currently thought to highly related to the placement of the axons and dendrites connecting the neuron to sometimes scores of other cells, sometimes touching the cell body, other times other dendrites or neurons.  As neural activity ensues, the cells will reconfigure their connections by physically moving them.

More recently, investigators have tried to understand the genes which internally modulate the neural signals within the cells.  This nobel prize lecture discusses how the CREB/MAPK pathway can modulate Long Term Potentiation - the shape of the neuron response to a signal over time (days or hours).

Taken as a whole, you can see that memory is likely to be stored on several levels at once - the kinds of cells (dictated by differentiation) involved, structural arrangement of the neurons (axons and dendrites connecting to various cells and places on cells), as well as internal signaling circuitry that generates and modulate the electrical and chemical activity within the cell.

"Marker protein" only refers to a protein that you can follow to see some sort of activity in the cell. A typical example is Green Fluorescent Protein, which is colored, fused with a protein of interest.  It has no specific meaning regarding learning I think.


What E-value BLAST cut-off is best? What is the best cut-off for e-value in BLAST?
Some say 0.01 ,others 0.0001?
Even BLAST tutorials don't give a very clear idea about which cutoff suits which purpose?
Could some experts give me a clear idea on this.
Why are we using 0.0001 and not 0.00011?

There is no perfect cut-off. It always depends on what you're doing. The e-value is basically a measure of how many such alignments you would expect to find in a database this size by chance. Therefore, e-values greater than 1 mean that you'd expect at least one alignment similar to what you've found by chance alone.

As others have stated, the e-value is not a rigorous measure of significance. It depends on

The length of your alignment.
The alignment's bit-score score (this takes into account amino acid substitution scores based on the matrix being used, BLOSUM65 by default).
The size of the database you are searching in.

I have at different times and for different projects used e-values ranging from 10 to 1e-100 or less. You always need to take into account what you are looking for. For example, to run a tBLASTn looking for distant homologs, you'd use a relatively high e-value, say 1e-10 or even 1 or greater depending on the details. For example, the default e-value for ncbi-tBLASTn is 10.

To find extremely similar sequences in closely related species, you'd use a much smaller one. Say 1e-20 or 1e-50. Normally, you tweak these settings after seeing your results.

After running a few hundred blasts, you get the hang of it and you can have a pretty good estimate of the e-value cutoff you want to use. Until you get that experience, you will have to use trial and error. Just remember that the conclusions you can draw from your data will be heavily influenced by that e-value. Don't try to publish something claiming you've found a homolog if the supporting BLAST hit has an e-value of 45 for example.

Personally, when looking at BLAST out files, I check the e-value, the alignment's length (as a percentage of the query), the alignment's %id score and the bit score itself. Of these, the most reliable is the bit-score but, again, that too changes depending on what question you are attempting to answer.


Why can only small molecules pass through the phospholipid bilayer of the cell membrane? TO put simply: I am just wondering what mechanism or substance only enables small molecules to pass through the cell membrane. Is it cholesterol? My textbooks are not very clear.

The plasma membrane consists of a phospholipid bilayer which separates the internal environment of the cell from the external environment. It regulates the movement of substances in and out of the cell and helps keep a constantly regulated internal environment of the cell.

The plasma membrane consists of a phospholipid bilayer, which, as the name suggests, is made up of phospholipids(lipids that have a phosphate group attached to them.).
The phospholipid has two regions a hydrophilic (water-loving / has an affinity for polar molecules) and hydrophobic (water-hating / has an affinity for nonpolar molecules).

So what happens is these molecules come together and arrange themselves in such a way that it faces the least amount of repulsions. Hence, the fatty acid tails (Hydrophobic part) face inside and the polar part(Hydrophilic part) face the outside, to look something like this.

Now, what happens is that when a molecule has to enter the cell it first has to interact with the polar part of the lipid membrane and then with the inner non-polar part of the membrane to pass through, hence if it is a polar molecule it will face repulsions and will not be able to pass through without the assistance of transmembrane proteins (it doesn't matter whether it is small or large, it simply won't), but, in the case of non-polar molecules, there is no repulsion from the fatty acid part of the phospholipids and hence it can pass through the membrane. When the non-polar molecules are too big some other mechanisms may be utilized (like receptor-mediated endocytosis).

With regard to your doubt regarding the "mechanism" with which a molecule passes through the membrane, in the simplest case, it will simply slip in between the phospholipids and through the bilayer. But, this is, as I said the simplest case, there may be transmembrane proteins which create channels for diffusion (aquaporin is a good example), or as I mentioned earlier they may be taken into the cell by endocytosis, through pumps like the Na-K pump etc.

And also cholesterol acts like a buffer to ensure that the spacing between the individual phospholipids is maintained so that it stays fluid (i.e. to maintain optimum rigidity of the membrane).

This is what an actual membrane looks like in an actual cell:

Hope you got a general idea.

You can refer to Chapter 11 of Molecular Biology of the Cell (by Bruce Alberts et al) if you want a  more rigorous explanation.


How to derive Hill equation (one specific part) There is just one specific step in the derivation of the Hill equation for haemoglobin which I can't understand.

Step from: $Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$
To: $Y = \frac{(p\ce{O2})^n}{(K_d)^n + (p\ce{O2})^n}$

I don't understand where $(K_d)^n$ comes from. (I can go from this second equation to the Y/(1-Y) equation afterwards).

How I derived my equation is the following.

$\ce{Hb.(O2)_n <=> Hb + nO2}$

Hence the dissociation constant $K_d$ should be:

$K_d = \frac{[\ce{Hb}][\ce{O2}]^n}{[\ce{Hb.(O2)_n}]}$

And Y, which is the fractional $\ce{O2}$ saturation would be:

$Y = \frac{[\ce{Hb.(O2)_n}]}{[\ce{Hb.(O2)_n}] + [\ce{Hb}]}$

If you multiply the top and bottom by $K_d$, the following is obtained:

$Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$

This is where I became stuck. What am I doing wrong?

Thank you very much for your answer.

In your second step $(K_d)^n$ should be $(K_A)^n$.

Where:

$K_d$ is the apparent dissociation constant and
$K_{A}$ is the ligand concentration that results in half occupation

See for example the relevant wikipedia article.


Evolution, self organization and neuroscience I have rudimentary knowledge of evolution, and biology in general, so bear with me if this question is a bit naive.

Let's say we have a particular trait, like highly sensitive peripheral vision. There are two ways to go about explaining how this came about:

One is to say that evolution selected for it over time, because animals with a poor sensitivity to peripheral activity could easily become prey. So there is an advantage to having sensitive peripheral vision, and such a trait is adaptive. The picture I have in my mind is of an assembly line where there are randomly wired visual cortices and the best ones get selected for automatically. This seems to be the view of the field of evolutionary algorithms, at least to my mind.

Now, if we focus on the random nature of the wiring, we might see that there is an explosion of possibilities in terms of how the visual system can be wired together. After all, evolution is blind, and it doesn't know beforehand which physical signals are of interest.

I'm trying to think of a more plausible mechanistic explanation. Suppose we assume that given certain reliable properties of the physical world, like permanence of objects for example, evolution has found the optimal way to wire the visual cortex so that peripheral vision (and a host of other good-to-have features) is a natural outcome, then it would give us more focus in what environmental features and algorithms to look for. This can also be thought of as the idea that evolution, over time, has come to assume that certain things in the physical world will be a given and exploits these. (For example, objects in the peripheral areas of vision will tend to have different perceived velocities, so perhaps normalizing velocities across the field of vision automatically results in a need for higher sensitivity in that region. It just so happens that this could also be useful in detecting predators).

My question then is, is my assumption in the above paragraph valid? (Of course, the question then gets shifted to "Why normalize velocities across the visual field in the first place?").

I don't fully understand your question. I hope the following will help a bit.

I'd like to pinpoint what seems to me to be one important mistake in your text. Reading you we have the feeling that selection acts on wires so to select the best combination. If this is what you meant, then it is obviously wrong. The thing is that the change that get inherited are alleles. An allele is a variant of a gene. For example: gene codes for eyes color. A bi-allelic gene has an allele which codes for blue eyes while the other codes for brown eyes. Assuming that there is genetic variance underlying the wire connection variance in the population, then yes selection will select for the best genetic variant. This does not necessarily mean that this best genetic variant is the most optimal possible to imagine solution. The most optimal allele might have never been created just because of the randomness nature of mutations.

EDIT:

To answer:

  Do natural selection always bring a particular phenotypic (loosly speaking, phenotype = morphological) trait to its optimal state?

No! It does not.

The main reason is that the genetic variant coding for this optimal trait does not necessarily exist because of the randomness of mutational process. Also, because of the metabolic pathway bringing some variance to a trait, it is often very hard to even imagine a  mutation that would allow creating a new, more optimal, phenotypic variant. So indeed developmental biology has to be taken in account to.
Because in absence of genetic drift (infinite population), selection can only bring genotypes uphill in the fitness landscape. If a very high peak exist somewhere in the fitness landscape but in order to reach such peak, 10 mutations are needed were all of them in any other genetic background are deleterious (correspond to valleys in fitness landscape), then the optimal high will probably never be reached (except if all 10 mutations appear suddenly in the same individual).
Because selection might be weaker than genetic drift. Also, different subpopulations might be in different environments were different traits correspond to optimal traits and because of migration (gene flow) between subpopulations, it is possible that no optimal phenotypic trait can be ever seen although all the genotypic variance exist.
The seemingly most optimal trait might actually not be really optimal. For example: Peripheral vision might be limited by the brain rather than by the eye because it would be an important energy cost for the brain to process more information, a cost that might outweight the benefit of having a better peripheral vision.


What is the result of meiosis? Is the result of meiosis ONLY the sex gametes (male and female) which later meet to form a somatic cell?
Sometimes I feel as if my book is hinting towards meiosis is the process where sperm cells meet oocytes?? I'm a bit confused.

In principle, Meiosis is only the process in which the haploid egg or sperm are generated. Have a look at this figure, which shows Meiosis I and II (from the Wikipedia):

During Meiosis I homologous recombination between homologous chromosomes can happen, the chromosomes are then distributed normally among the daughter cells. In Meiosis II the cells split again and here the sister chromatids are divided and the haploid gametes form.

In the oocytes the process is in principle the same, but the cells get arrested in the so-called diplotene stage of Meiosis I (picture from here):

In the diplotene stage the chromatin is decondensated and transcriptionally active, this helps maintaining a correct chromosome structure, as the diplotene stage can last up to 50 years. When the cell receives the hormonal signal to enter the fallopian tube, Meiosis I is finished. The resulting cells are not divided symmetrical, building one big oocyte and one polar body containing the second set of chromosomes. Most vertebrate cells are arrested in this stage again until they are fertilized. Then another asymmetrical division is done, leading to a haploid cell with two polar bodies. This oocyte is then fertilized.

This process can happen almost at the same time in a lot of vertebrate species, including humans. This is probably what was meant by your textbook.

For further reading I can recommend: Meiosis and Fertilization from the NIH bookshelf.


Why can't we find a broad spectrum antiviral drug to viruses like antibiotics to bacteria? Antibiotics have a very broad spectrum because they attack the metabolism pathways many bacteria share. For example, penicillin inhibits peptidoglycan synthesis, which is vital for formation of cell wall of gram-positive bacteria, so penicillin can be used to treat gram-positive bacteria infections. Streptomycin inhibits protein synthesis of bacteria. Because all the bacteria need protein synthesis, streptomycin has a very broad spectrum.

Why doesn't such strategy work on viruses? For example, nucleos(t)ide analogues can inhibit the RNA synthesis of RdRp. Most riboviruses (except hepatitis D virus) require a viral RdRp to replicate their genome. But why can't nucleos(t)ide analogues be used as broad spectrum anti-riboviral drugs even we have found very good drugs such as Sovaldi?

One of the main issues with nucleotide analogs is that they can also affect the host replication and transcription (though they have a higher affinity to the viral polymerase), and can therefore have adverse side effects. On the other hand, the broad spectrum anti-bacterial antibiotics specifically affect prokaryotic cellular machinery.

(Note that some antibiotics like streptomycin do affect the host mitochondria and thereby cause toxicity. Ototoxicity and nephrotoxicity are known side effects of streptomycin.)

Nucleotide analogs are actually used as broad spectrum anti-virals: For example, Lamivudine is used for both HBV and HIV, which are different types of viruses.


Fate of Acetyl CoA in well fed state? When we have eaten well and take fat rich diet then in this condition Acetyl CoA produced from fatty acid breakdown will be gone to storage in adipose tissue or not? If it will go for storage then why and if not go for storage then what will be reason?

As Roland mentioned in the comments, in the well fed state, not all of the Acyl coA is converted to Acetyl coA. This picture from Harper's Biochemistry, 29th, should come handy.

It is the CPT-1 gateway that regulates the amount of acyl-coA (from FFA) that enters into the mitochondria to form acetyl-coA.

In the Fed state, the CPT gateway is shutdown (regulation by malonyl-CoA) - allowing esterification by sending them back as VLDLs. In the starved state, the gates open, leading to beta oxidation giving acetyl-CoA.

The acetyl coA then can enter the Kreb's cycle to get completely oxidised and give ATP + CO2 (this ATP the liver readily utilises). Or, the acetyl-CoA can be channeled into ketogenesis, where this energy can be used by other tissues (since liver lacks the enzyme thiolase and hence can't metabolise ketone bodies). How the liver distributes the acetyl-coA for ketogenesis/Kreb's cycle is a different story altogether.


Point mutation vs Indels DNA sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health, depending on where they occur and whether they alter the function of essential proteins.

I know that there different types of mutations.

Missense, Nonsense, Insertion, Deletion, Duplication, Silent, Frameshift indel, Repeat expansion, Inframe indel, stoploss, splicing.

Can anyone please tell me which mutations are Point mutations and which come under Indels?

Thank you

A point mutation is a mutation causing the substitution, insertion or deletion of a single nucleotide.

An indel is a change in the number of nucleotides (either through insertion or deletion hence the name). When talking about indel most people (in evolutionary biology at least) refer to the insertion or deletion of a single nucleotide but some might refer to greater changes when talking about indels.

An indel which concern the insertion or deletion of a single nucleotide is a point mutation.


What forms this pad on the side of the face? I've been trying to figure out this for the best portion of this morning, but what structures are responsible for the pad highlighted in red? (sorry for low quality of picture, was just watching the show at the time)

It's from my understanding that the zygomatic (in green) runs to the edge of the ear in a relative straight line and most muscles have their origins or insertions bellow it. I know there are some fat pads (such as the nasolabial fold in purple) on top of everything on the face, but are these all fat pads that just allign? I've seen this pad on both man and women often, although it seems more proeminent in women.

That padding is apparently from a prominent zygomatic arch also known as high chickbones (pictures).

The bones between the eye, nose and ear are: the zygomatic bone below and behind the eye, the zygomatic process of the frontal bone above/behind the eye and the zygomatic process of the temporal bone, which extends toward the ear canal. It makes sense that when the zygomatic bone is more prominent, the zygomatic processes of the connecting bones will be also more prominent and appear as high cheeks.

Image source: Wikimedia, CC license

Here's the photo of Abraham Lincoln from the Wikipedia's article about zygomatic bones:

A Youtube video The Zygomatic Bones and Ogee Curve


What percentage of the human genome hasn't been sequenced yet? If percentage estimates aren't precise, why is it difficult to estimate? What percentage of the human genome hasn't been sequenced yet? I have read different estimates, e.g.:

https://www.genome.gov/human-genome-project/Completion-FAQ (mirror): "In the April 2003 version, there are less than 400 gaps and 99 percent of the genome is finished with an accuracy rate of less than one error every 10,000 base pairs"
https://www.statnews.com/2017/06/20/human-genome-not-fully-sequenced/ (mirror):  "Church estimates 4 percent to 9 percent of the human genome hasn’t been sequenced. Miga thinks it’s 8 percent."

If there isn't a consensus on the percentage of the human genome that hasn't been sequenced yet, why is it difficult to estimate?

I answered a related question here that may be helpful.

Some initial notes:

Your first bullet point ("99%") is to my reading talking about not the total genome size but the data that they actually assembled- e.g. for 99% of nucleotides, we are 99.99% that the nucleotide at that position is not some other nucleotide, but there may be other positions not included in the denominator that are simply not in the assembly in the first place. In other words, the existence of the position in the assembly and our confidence of the accuracy of a nucleotide call for such a position are two different (though related) phenomena.
Also, you are comparing a 2003 estimate to a 2017 estimate. We learned a lot in those 14 years.

To answer the last and most specific question about why this number is hard to know, there are a variety of reasons why:

There is no single number that is the "actual" true sequenced percentage of the human genome. In this I strongly disagree with commenter Konrad Rudolph (technological change is now giving us telomere-to-telomere assemblies of human chromosomes! The question is not how much it's possible to sequence and assemble but more whether it's the worth the time and expense to do so.). No two genomes are exactly alike, and that means not only that the nucleotides are different but that the positions are different. So even if we sequence 100% of your genome, that may only include 99% of my genome. These variable regions are, as suggested in the comments, largely repetitive regions but also just big chunks that are missing; to learn more about this google "structural variation" (here is an older review on the topic).
As mentioned already, technological advances have changed how we view the linear sequence of the genome. Earlier estimates were limited by available technology of the time; now that we have 3rd-generation sequencing tech like nanopore and pacbio, we are learning more about the extent of our ignorance. In that sense, it is unsurprising that the denominator has changed/increased.
As commenter Jeppe Nielsen states, all of these are statistical estimates based on available data. As available data increase and the statistical models that we use to estimate change, thus do the estimated outcomes change.
Related to (1): Different populations have different chunks of genome that are unique. The initial sequencing project selected a small number of humans, who were not representative of all human diversity. Efforts to fully characterize the human pangenome are ongoing.
Sometimes contaminants sneak into genome assemblies, which have to be removed. So for every sequence in the human genome assembly, especially if it's fragmentary or recently added, there's a nonzero chance that it's not actually part of any human genome.


Do mosquito repellent sprays work on all insects? I would like to know the mode of action of mosquito repellent aerosols. Are these specific to mosquito or are other insects affected too?

The most common active ingredient in insect repellents is N,N-diethyl-3-methylbenzamide (other name: N,N-diethyl-m-toluamide; abbreviated DEET). It provides protection against mosquitoes and many other insects. After various interesting hypotheses, it is currently assumed that mosquitoes simply smell DEET directly and avoid it.[1]


Is the start codon regarded as part of the UTR (untranslated region)? The Wikipedia entry for Gene contains the statement:

  The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.

But the page on the Start codon says:

  The start codon is often preceded by a 5' untranslated region (5' UTR)

So is the start codon a part of the UTR?

Because the start codon is translated into methionine, it clearly can not be part of the 5'-untranslated region, as @Johnny writes in his answer.

The more contentious question would be for the stop codons and the 3'-untranslated region. Then it really is a question of semantics. One might argue that as no amino acid is inserted in response to these codons, they are not translated. However if one considers the meaning of the word ‘translate’ and its application to the genetic code, a stop codon clearly is translated — it is read and translated into information which initiates the release of the nascent peptide from the ribosome.

And so in the Wikipedia entry on Untranslated Regions it (together with the start codon) is shown in the coding sequence, and not in the untranslated region. The annotations used by GenBank also include start and stop codons in the coding sequence (CDS in their annotations) — see, for example the annotation for this insulin precursor sequence.


Can neurons become cancerous? I've been reading about brain cancer lately, and something I've noticed is that the tumors seem to start in all tissues, except neural tissue. Am I missing something, or is there an explanation?

Short answer
Neuronal tumors are rare, but they do exist. These cancers develop from neuroblast cells, a population of undifferentiated, dividing precursor cells that will eventually fully differentiate into functional neuronal cells.

Background
Most neuronal cell types have lost their ability to divide, because of their progressed state of differentiation. There are but a few regions in the brains that generate new nerve cells in adulthood, for example in the hippocampus where neuro-regeneration is believed to be involved in memory formation. Because of the rarity of cell division of neuronal cells in adulthood, neural cancers are rare.

The point where neuronal cells actively divide is during development. These cells are basically still stem cells. A prime example here are retinoblastomas. These are tumors in the photosensitive part of the eye, namely the retina. During early development stem cells actively divide to lay down a layered structure in the back of the eye eventually forming the rods and cones and other visual cells. If this division process goes out of control, tumors can develop. Retinoblasomas can now be diagnosed in utero (Paquette et al., 2012).

Tumors with a neuronal origin developing post natally are rare, but do exist. Neuroblastoma being a prime example. This is a rare cancer (prevalence of 1:100,000) most commonly found in children younger than age 5. It affects the sympathetic nervous system, which regulates involuntary bodily functions such as heart rate, blood pressure, breathing, and digestion. Neuroblastoma typically begins in the nerve tissues of the adrenal glands but may also begin in the nerves that are located anywhere along the spinal cord, including the neck, chest, or abdomen. The cancer can metastasize (spread) to other organs.

Note that both examples here are called blastomas, those are tumors caused by malignancies in precursor cells, often called blasts, these cells are dividing cells that will develop into a neuron often after a migration phase. Neuroblasts differentiate from neural stem cells and are committed to the neuronal fate. Hence, although these tumors are from a neuronal origin, they are technically not derived from (fully differentiated) neurons.

Reference
- Paquette et al., AJP Rep (2012); 2(1): 55–62


Identifying a beetle from northern California Just found this organism crawling across my wall on the second story at around 12:30 AM. We're in Sonoma County in California. Our best guess so far is a soldier beetle, but the coloration doesn't seem to match any images we can find online. It's body was about 1.5 inches long and was a uniform brownish-tan color with black eyes. It may be worth noting we're in the middle of the worst heat wave we've seen in 15 years of living here.

This is a long-horned beetle, family Cerambycidae; the site http://www.sbcollections.org/cbp/DB_Query.aspx?Field=family&Value=Cerambycidae has a list of California species, with links to pages on each species (there are 387; not all species pages feature illustrations -- those that do figure museum specimens).  From that list the first that resembled your photograph is that covering Centrodera spurca (LeConte 1856), which has been found in Sonoma County; given that I haven't gone through the entire list there are likely other possibilities.

Centrodera spurca


Do biological phenomena follow Gaussian statistics? I have recently entered the life sciences (from physics).  I am concerned about the use of p values in the life sciences literature.  For example, in this article, they test 9 - 12 rats in a control group and compare it to an experimental group.  They use p values to claim that their results are statistically significant.  This type of use of p values seems to be very common in the literature.

So here are my concerns :

Why is it so often assumed that biological measurements follow a normal distribution?  To my knowledge, this isn't known a priori.
From my physical intuition, it seems quite challenging to claim "statistically significance" when using such low sample sizes.

kmm's answer is correct; I just want to add some of my points on what kind of data should follow Gaussian distribution.

  Unless you know from observation that a process doesn't follow a
  Gaussian distribution (e.g., Poisson, binomial, etc.), then it
  probably does at least well enough for statistical purposes.

I won't fault kmm for this statement because what they said is what happens prevalently. This is practically what all biologists do, but this is an incorrect approach.

Gaussian should not be considered a default distribution. This may lead to incorrect inferences. Usually the experimenter has an idea of what kind of data they are measuring and what distribution is the data likely to follow. If you are unsure of the underlying distribution then you should go for non-parametric statistical tests.

What kind of data follow Gaussian distribution?

According to the Central Limit Theorem, the distribution of the mean (expected value) or sum of several samples of independent and identically distributed (IID) random variables would follow Gaussian distribution. The random variable itself can follow any distribution but if you measure the mean several times using repeated experimentation, then the distribution of the mean would be Gaussian.

From the Wolfram site:

  Let $X_1,X_2,...,X_N$ be a set of N independent random variates and
  each $X_i$ have an arbitrary probability distribution $P(x_1,...,x_N)$
  with mean $\mu_i$ and a finite variance $\sigma_i^2$. Then the normal
  form variate:

  $$X_{norm}=\frac{\displaystyle\sum_{i=1}^N x_i-\sum_{i=1}^N \mu_i}{\sqrt{\displaystyle\sum_{i=1}^N \sigma_i^2}}$$

  has a limiting cumulative distribution function which approaches a
  normal distribution.

The wikipedia page on CLT is also quite good. You can have a look at it too.

Usually in biological experiments we measure some property, lets say expression of some gene. When you do several replicates, and there is no specific underlying mechanism that would generate variation (i.e. the errors are purely random), then you would get normally distributed values. Note that this applies only for the sample means. In certain cases, we assume that the variation in the value of a variable is because of some random fluctuation and therefore consider these variables to be normally distributed (not their means but the values themselves); for e.g. the weights of mice which are fed and raised equally. This is just your assumption which constitutes the null hypothesis.

Another point to note is that the variable that is expected to follow normal distribution should essentially be continuous in nature. Some discrete variables can be approximated as continuous but one should have a good reasoning of doing so. For example population sizes, though discrete, can be assumed continuous if the sizes are large.

Poisson distribution is unique and is a discrete distribution. Certain kinds of phenomena result in Poisson distributed RVs. These phenomena should basically be Poisson processes. See this post for details. Poisson distribution basically models the probability of N events in a given time interval for some given rate of events ($\lambda$). This rate is also called the intensity of the distribution.

Binomial is another unique discrete distribution. Genotypes resulting because of Mendelian segregation of genes, for example, follow this distribution. It basically models the probability of N number of events in some M trials. In binomial distribution there are only two possible outcomes. Multinomial distribution is a generalization of binomial distribution with multiple outcomes.

Since both Poisson and Binomial are discrete distributions they should not be confused with normal distribution. However, under certain conditions especially when the number of trials in Binomial distribution is high and binomial probability = 0.5 then it can be approximated as a gaussian with same value of moments. Similarly, if the intensity (rate) of Poisson distribution is high or the time interval is large, the distribution of the Poisson RV can be approximated to Gaussian (with same value of moments). In these cases, the value of the mean goes up significantly, thereby allowing a continuous approximation.

Many datasets show power-law like/skewed normal distributions and people often make the mistake of assuming them to be normal. An example (from my experience) is the expression of all the genes in a cell. Very few genes have high expression and many genes have low expression. This also applies for degree distribution of nodes in some real networks such as gene regulatory network.

In summary you should assume Gaussian distribution when:

Variable is a measurement of a value which is repeated several times from identical samples
Variability is expected to be random in the control case (in t-test, when you reject null hypothesis you are actually saying that a certain variable does not follow the normal distribution assumed under the null hypothesis)
Variable is continuous, or discrete with large sample size


What animal's lower eye lid moves to upper one when closing eyes? I know cock's lower eye lids moves to meet the upper one when it closes its eye.  What other animals does this?  BTW, "cock-eyed" can mean upside down, I think.

Actaully there are quite a few animals which actually moves there lower eyelids:

Most of the birds
Reptiles(Except Snake)
Amphibians


If fever is a natural immune defense, why do people take drugs to lower it? If fever is a natural defense against pathogens, why do sick people take NSAIDs to reduce the fever?

Personal comfort is the primary answer. Quite a bit of research has gone into fevers, and the current consensus is that Fevers less than 105F (40.5C) shouldn't necessarily be treated.

The primary reason the body raises its temperature (via the Hypothalamus in this case) is that bacteria and viruses tend to optimally thrive at 98.6F, which is also your body's optimal operating temperature. By raising the body's temperature, the bacteria/viruses become less efficient, allowing your body to "catch up" since the body's immune response takes time to ramp up before it reaches its peak (which is a bit after peak viral/bacterial load). Here's an example for Hepatitis (HBxAg = the virus, Anti-HBx = antibodies against the virus):

Along with the Fever, joint inflammation (part of the Innate Immune system's primary response) is also a coinciding symptom. So when your body begins to fight an infection you get a fever (which can make the environment uncomfortably hot/cold) and the tissues around your joints swell (which makes movement and relaxation uncomfortable). NSAIDs like Ibuprofen reduce those symptoms, making the duration of the infection more bearable. They do not reduce the length of the infection by any measure (and might increase it, though the research is not particularly conclusive), but can make the day go by better if you've used up all your sick days or have a child to take care of.

Basically, people take NSAIDs to reduce fevers for the same reason most take any over-the-counter pain medications. To make life a little easier in the meantime.


Do animals also dream? By "dream", I mean:

Dreaming while sleeping.
Dreaming about their future life while being awake.

Thank you in advance.

According to this Psychology Today blogpost, it is quite likely that animals can dream.  Particularly mammals that according to the blogpost:

  All mammals share the same neural structures that are important in sleeping and dreaming.

However, for your second question, I do not think it is at all possible to know what they are dreaming about (if they indeed do dream).


Heteromaternal Superfecundation - Any known cases? Superfecundation in mammals (fertilization of two or more ova from the same cycle by sperm from separate acts of sexual intercourse) -- Is possible in nature from different fathers (Heteropaternal) as after the first zygote is formed, a second act of intercourse within a certain time span has the potential (of another ovum is present) to form a second zygote.

Has there been any cases where a naturally pregnant mammal was implanted (IVF) with a second zygote from a different set of parents?  Heteromaternal/paternal Superfecundation?

This would be termed superfetation rather than superfecundation. While this extremely rarely happens in humans, superfetation does occur naturally in some mammalian species. These pregnancies occur when the mother ovulates after she is pregnant.

Superfetation consisting of a natural pregnancy and implanted embryo has been done in cattle. In this case, 7-day embryos were successfully transferred to 14-day pregnant cows to produce superfetation. See Joel Carter's dissertation Superfetation in Beef Cattle (2002).

There have also been successful cases of superfetation in cows that were first implanted with a 7-day embryo, and then followed by natural service. See WH Hall, Bovine superfetation by natural conception secondary to an embryo transfer pregnancy, Cornell Vet. 1987 Jul;77(3):282-3.

An excellent summary of the existing literature on superfetation in many species is K Roellig et al., The concept of superfetation: a critical review on a ‘myth’ in mammalian reproduction, Biol Rev Camb Philos Soc. 2011 Feb;86(1):77-95.


I can't Identify this "bug" that seems attached to fresh cut wood I'm a very amateur entomologist (I'm actually just an old fat hippie that loves all critters).

I don't have any chops here, but I swear I've done my due diligence and tried to figure this out. I'm asking because I'm baffled. (Leg stripes are Arachnid-ish, but thorax is completely wrong ... I just dunno...)

My girlfriend sent me a pic; she swears these things were jumping out of a seasoned firewood pile and by her words "attacking".

Location:  PA Pocono mountains, circa Kunkletown, heavily wooded area.

Now granted, there was a lot of drinking going on, it was "girls weekend out", and there was a hot tub.  I wasn't there; so I cannot actually confirm what really happened... (Of course I wish I was there, but ... nevermind)

HOWEVER - here's a pic.  You can't make this up.  Or, at least, I'm not making this up ...

What is this critter?  I think it's "insect" by the leg count I can see.  But edumicate me; this is a new one to me and I'm very intrigued.

Many thanks best!

On Edit

Perhaps some sort of "wood cricket" based on rough taxonomy of the leg configuration, and it's penchant for jumping.  Pure speculation.

I think I may have it.  gOOgle terms "giant cricket wood tiger stripes" yielded very similar critters:  So-called "Camel, Cave, or Cellar Cricket."

Order Orthoptera (Ensifera), Family Rhaphidophoridae.

Genus and Species will be next to impossible unless I can capture one, but obviously one of the North American varieties that like to hang out in damp decaying wood.

From the interwebs:


Pox virus infection process How does Pox virus duplicate it's genome? Does it bring DNA polymerase or RNA polymerase into the host cell?

Poxviruses, such as variola (the causative agent of smallpox) and vaccinia (the active constituent of the vaccine that eradicated smallpox), are very large, complex DNA viruses that replicate in the cytoplasm, rather than the nucleus. Because of this, they must carry enzymes with them to accomplish tasks that occur in the nucleus of the eukaryotic cells they infect. This includes all the proteins necessary for mRNA synthesis (e.g., a DNA dependent RNA polymerase). The enzymes for DNA replication are encoded in the poxvirus genome and are transcribed and translated as part of the "early" stage, directly after adsorption and penetration.

So, yes, poxviruses bring their own preformed RNA polymerase with them. They don't bring their own DNA polymerase with them, but they do produce it shortly after infecting a cell.

You can read more about this in Murray Medical Microbiology Chapter 54.


Why do turtles ride on alligators? I often see pictures of turtles riding alligators, I even saw that in a zoo once, but why do they do that?

Is it some sort of camouflage technique for the turtles? And why doesn't the alligator get it off?

turtles will crawl onto anything to get out of the water and bask, fallen logs are common and they likely cannot tell the difference between a still alligator and a log.  It might also be possible that the turtles do know what the gator is and are hoping to tag along and pick up scraps after it strikes.

I image that for the gators thrashing around to dislodge the turtle has to high a risk of scaring off prey so they just put up with it.


Cichlid fish in Africa Are the cichlid fish in Africa an example of divergent or convergent evolution? On the one hand they have evolved similar features to each other indicating convergent evolution, but on the other, they formed as a result of an adaptive radiation which indicates divergent evolution.

Both.

Recent theoretical models, however, predict that convergence should be common within species-rich communities, such as species assemblages resulting from adaptive radiations. Here, we present the most extensive quantitative analysis to date of an adaptive radiation of cichlid fishes, discovering multiple instances of convergence in body and trophic morphology. ...

Independent adaptive radiations often produce convergent phenotypes
In Lake Tanganyika, convergent phenotypes evolved within a single adaptive radiation
These convergent morphologies are associated with adaptations to the same niche
Distantly related yet morphologically similar species coexist in the same habitat

--Convergent Evolution within an Adaptive Radiation of Cichlid Fishes


How can we measure cardiac output? I could find a way which could find it by body oxygen consumption and there is another way to measure it by injecting drugs — measuring cardiac output by the so-called “indicator dilution method,” a small amount of indicator, such as a dye, is injected into a large systemic vein or, preferably,into the right atrium.
I read about it but didn't understand it very well.

Can you explain it and Which one is mostly used in clinics to measure cardiac output?

Drs. Swan and Ganz developed a direct method of measuring cardiac output by thermodilution. They invented a multilumen catheter with a thermal resistor on the end (a Swan Ganz catheter) which could be advanced into the pulmonary artery. Through another lumen, a cold saline solution of known temperature and volume is injected into the right atrium. Using a computer model, the temperature of the blood at the catheter tip is used to determine stroke volume. Stroke volume x heart rate = cardiac output.

  The injectate mixes with the blood as it passes through the ventricle and into the pulmonary artery, thus cooling the blood. The blood temperature is measured by a thermistor at the catheter tip, which lies within the pulmonary artery, and a computer is used to acquire the thermodilution profile; that is, the computer quantifies the change in blood temperature as it flows over the thermistor surface. The cardiac output computer then calculates flow (cardiac output from the right ventricle) using the blood temperature information, and the temperature and volume of the injectate. The injection is normally repeated a few times and the cardiac output averaged.

The same principle is used with a dye study but measuring the concentration of dye downstream.

Although this is considered to be the "gold standard", because it is so invasive and carries a serious risk of complications, it has largely been replaced by echocardiography and Doppler techniques.

Measurement of blood flow by thermodilution
Measurement of Cardiac Output
Invasive and non-invasive methods for cardiac output measurement


Do I need primers if ordering from a DNA synthesis provider Do I need to design / synthesize primers for PCR if I am ordering from a DNA synthesis company and they are providing free cloning into my preferred vector backbone? Any good reason to order primers as well?

Only if you intend to subsequently amplify the DNA you've ordered. I tend to never fully trust anything I don't confirm myself so primers to sequence the insert in the construct they give you might not be a bad idea either.


On the selection coefficient I'm reading  Williams' Adaptation and Natural Selection:
A Critique of Some Current Evolutionary Thought.

In this book the author talks about selection coefficients which, if I understand it correctly, can be calculated as finiteness arithmetic means (for each allele).

My question is: should this calculation be made assuming a ceteris paribus condition?

Definition of selection coefficient

A selection coefficient is a difference in fitness between two genotypes (or haplotypes). Let the two genotypes be A and B. Let's use relative fitness and say that the fitness of A is $w_A = 1$ and the fitness of B is $w_B = 1 - s$, where $s$ is the selection coefficient. As a consequence $w_A - w_B = s$.

The question of long-term fitness is unrelated to the definition of selection coefficient, as the selection coefficient is defined as a difference in fitness. A question of importance is "What measure of fitness should one use for a population where selective pressures are changing over time and/or space".

What measure of fitness should one use for a population where selective pressures are changing over time and/or space

Roughly speaking, if changes in fitness are over space, then you should use arithmetic mean fitness and if changes in fitness are over time, then you should use the geometric mean fitness but it is not quite that easy.

The real interest is whether fitnesses are correlated among generations. In other words, do individuals within a generation tend to have a more similar fitness values than the individuals of another generation? When variation in fitness is spatial than one should not expect such correlation. When variation is temporal one should expect such correlation.

Hoping you can read a code in R, the easiest is probably to read some code that make a simulation and look at the output. So here is a code that performs simulations. The key difference between simulations with spatial and temporal variation is the line that gets fitness value (runif).

set.seed(43)

temporalVariation = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        fitnessPerIndThisGeneration = runif(1,lowestFitness, highestFitness) # All individuals have the same fitness in a specific generation
        N = N * fitnessPerIndThisGeneration
        Ns[generation] = N
    }
    return (Ns)
}

spatialVariation  = function(N, lowestFitness, highestFitness, nbgenerations)
{
    Ns = numeric(nbgenerations)
    Ns[1] = N
    for (generation in 2:nbgenerations)
    {
        FitnessOfEachIndividual = runif(N, lowestFitness, highestFitness) # Individuals differ in fitness within a generation
        N = sum(FitnessOfEachIndividual)
        Ns[generation] = N
    }
    return (Ns)
}

N = 1000
lowestFitness = 0.95
highestFitness = 1.08
nbgenerations = 200

spatialNs = spatialVariation(N, lowestFitness, highestFitness, nbgenerations)
temporalNs = temporalVariation(N, lowestFitness, highestFitness, nbgenerations)

plot(y= spatialNs, x=1:nbgenerations, col='blue', xlab = 'generation', ylab = 'N')
points(y= temporalNs, x=1:nbgenerations, col='red')

In blue is the simulation with spatial variation. In red is the simulation with temporal variation. You will note that the geometric mean is always equal or lower than the arithmetic mean.

Whether the arithmetic or geometric mean fitness matters most will affect the reproductive system that will be most successful. In this regard, you should read Ripa et al. 2009 about bet-hedging


RNA migrating slower than DNA on Formaldehyde Gel? So I ran into an interesting problem.  I'm getting a linear DNA band that is twice as long (4x bases, but as denatured probably only 2x) as an RNA band running at the same size in a formaldehyde gel.

Both sequences have been isolated an 100% confirmed.  The gel was run in MOPS buffer.  My experience, and all the publications I've found, show that if anything RNA should run faster.  Can anyone think of a reason why the DNA band and RNA band would be running the distance despite the DNA being twice as long?

I've read a lot of fun papers on drag factors in gel matrices now, but none of it leads to this confusing and repeated result.

Edit: Gel and Conditions

Gel was 1M formaldehyde, 1% agarose.  Run at 100V for 1.5h.  RNA was mixed in a RNA loading dye which contained 15.3% v/v formaldehyde, 41.3% v/v di formamide, 4.6mM EDTA, MOPS, and bromophenol blue.  We believe our RNA loading dye to be denaturing, and it ran at expected size with RNA ladder.

................(1)........................(2)............................(3)

Lane 1 is a DNA template plasmid, cut 1 location.

Lane 2 is the Template + DNase from in vitro transcription reaction w/o polymerase.

Lane 3 is the RNA + DNase from in vitro transcription reaction.

There are no other bands in the DNA lane, and it looks like if anything, the DNA is migrating much faster than expected, despite being sequence confirmed (both before the process, and gel purified out and confirmed again).

The inclusion of formaldehyde in the gel and buffer is to keep the RNA denatured (ie after heating the sample to melt the double-stranded stem-loops, just prior to loading the gel), in the hope that the RNA will migrate through the gel with an Rf proportional to its molecular weight (approximated here by its length). Therefore the correct size markers would also be made of RNA (and prepared the same way, by heating).
It is difficult to predict, a priori, how a double-stranded DNA fragment would migrate under similar conditions, without also including a lane of ds DNA size markers.
In other words I would only use DNA markers for DNA and RNA markers for RNA. By repeating this experiment (1 lane of DNA MW vs 1 lane of RNA MW) at different voltage gradients and different concentrations of agarose, you might be able to plot two standard curves that would let you predict where your DNA fragment is expected to migrate relative to the RNA transcript, but without that data I would not assume that a larger DNA fragment would run slower than its RNA transcript.
Even if the dsDNA was exactly the same length as the ssRNA (and pretending that the MW of the dNTPs and NTPs are identical), the DNA's MW would be twice as much as the RNA, but the negative charge on the DNA would also be twice as much.


Restriction enzyme type II Why can't a type II restriction enzyme cut a nucleic acid with the following base composition:

  A: 28% C: 15% G: 35% T: 22%

I suppose this is a homework, not a genuine curiosity. That being the case, I'm gonna give you two different answers here: the standard one, which is the one I believe your teacher/lecturer expects to see, and a more complicated one in the addendum.

The first thing that draws out attention in the question is the base percentages. Clearly, it doesn't follow the famous Watson-Crick pairing rule (A pairs with T, G pairs with C) and, because of that, we don't see the Chargaff's Rule in this nucleic acid.

Thus, this is not a double-stranded DNA (dsDNA), but a single-stranded DNA (ssDNA).

That being said, the answer to that question can be something along these lines:

  A Type II RE can't cut that nucleic acid because that is a ssDNA.

Addendum:

There is a complication here, which may render the previous answer questionable.

Type II Restriction Enzymes only cleave regular, that is, double-stranded DNAs. So, they cannot cleave ssDNAs, which corroborates the answer we just gave.

But the problem is that ssDNAs can form loop structures, in which there is pairing between bases in the same strand. In those structures, DNA is technically dsDNA and, as such, can be cleaved by Type II RE. For instance, have a look at this paper:
Type II restriction endonucleases cleave single-stranded DNAs in general.

That being said, Type II RE do, in fact, cleave ssDNA (in places where ssDNA form loops and structurally resembles a dsDNA), which makes the question itself meaningless.


How do PARPs counteract coronaviruses? I read that

  [SARS-CoV-2 has] a nonstructural protein called NSP3, a component of which blocks the host’s efforts to fight off the virus. In particular, this protein shuts down host enzymes called PARPs, which prevent viruses from replicating, and interferes with cellular calls for the release of virus-fighting immune proteins called interferons.

I'm somewhat acquainted with interferons, but I'm trying to better understand the part about PARPs. Alas the Wikipedia page on these does not mention an anti-viral-[replication] function. So, how do PARPs stop viruses from replicating? (Is it by triggering cell death?)

Summary
The poster’s answer to his own question focuses on the end results of the anti-viral action of poly- and mono- ADP-ribosyl transferases — PARPs. The references he provided stimulated me to read about the molecular aspects of this topic, which is where my own interests lie. The ‘answer’ emerging from this reading is somewhat extensive, but can be summarized as:

  The molecular details of the way in which PARPs act as anti-virals against
  coronaviruses, and in particular whether and how they antagonize viral
  protein NSP3, are still unknown. There is indirect evidence to
  implicate PARP9, PARP14 and PARP15, which — like NSP3 — share a
  structural feature known as a macrodomain, although their mode of
  action is complicated by the fact that PARP9 does not catalyse
  ADP-ribosylation. The viral NSP3 protein has the ability to remove
  ADP-ribose from proteins in vitro, but whether this is its mode of
  action in the cell is yet to be established.

The role of PARPs in the cell (1)
The name PARP is an acronym for poly-ADP-ribosyl transferase, although the 17 human PARPs are defined, not by this catalytic activity, but by the possession of a domain homologous the catalytic domain of the founder member, PARP1 (2). On the basis of assaying the cloned, expressed proteins for self-ribosylation activity most of these (eleven) have only mono-ADP-ribosyl transferase activity, and two (PARP1 and PARP13) are inactive — a conclusion consistent with the substitution of a key catalytic residue at the active site (3).
   One can consider three stages in the involvement of catalytically active PARPs in cellular metabolism: activation, catalytic action and effect.

A common feature of activation seems to be the response to some stress signal, which may result in increased transcription of PARP genes or activation of an inactive form, for example by combination with an accessory protein (4).
   Catalytically active PARPs covalently attach one or more ADP-ribose groups most commonly to specific glutamate residues (less frequently to asp, arg, or ser residues) of target proteins (or in some cases themselves) using NAD+ as a donor:

For those PARPs that catalyse poly-ADP ribosylation (PARP1, -2, -5a and -5b)) linear or branched chains are formed by glycosidic bonds between the 2′ and 1″ positions of ribose rings.
   Although all PARPs — by definition — contain the PARP domain, they vary considerably in the other domains they possess, and this would be expected to be the basis for different substrate specificities. However for many PARPs these substrates have not been identified — only the processes they affect, the main processes (other than anti-viral action) appearing to be DNA integrity, telomere homeostasis, RNA transcription, regulation of mRNA translation by cytoplasmic stress granules and degradation of proteins through the ubiquitin pathway. Most effort has been directed at the substrates of PARP1, which include histones H1 and H2B and  the chromatin insulator binding protein, CTCF (in response to DNA strand breakage) and the transcription factors NELF and C/EBPβ.
   The effect of modification of the substrate protein may be a change in its activity (as exemplified by the inhibition of translation EF-2 by diphtheria toxin) or more generally interaction with some other protein that recognizes the ADP-ribose moiety. One feature of this recognition — particularly significant in the context of virus–host interaction — is that it often involves a specific domain called the macrodomain (5), named after the C-terminal domain of the histone H2A variant, MacroH2A.

Macrodomain from Archaeoglobus fulgidus protein AF1521 showing binding of ADP-ribose (red)

The macrodomain is found in certain classes of enzyme responsible for the turnover of the reversible modification of proteins by ADP-ribose. These include the polyADP-ribose glycohydrolases — which cleave ribose–ribose glycosidic bonds — and MacroD1 and MacroD2 — which hydrolyse the ester bond between the amino acid and the terminal ribose.
   Also of interest is the fact that, several macrodomains are found in three PARPs: PARP9, PARP14 and PARP15.

PARPs in cellular anti-viral responses and viral anti-PARP proteins (6)
   In different classes of viruses PARPs can act in a pro-viral or anti-viral manner. In coronaviruses (human SARS-CoV has been the subject of most study) they exert an anti-viral effect, as indicated by the effect of inhibitors of PARPs. Furthermore certain PARPs (-9, -12, -13 and -14) are induced in response to interferon, itself a consequence of viral infection. As mentioned by the poster, PARP13 binds directly to viral RNA resulting in its eventual destruction. However in most cases it is unclear which PARPs are involved, what their targets are, and whether their anti-viral action is a result of their catalytic activity — clearly not in the cases of PARP9 and PARP13. This is an important proviso to what follows.
   A study of the evolutionary conservation of the all 17 PARPs in different primate species showed that five of these underwent rapid evolution, typical of proteins involved in host–viral conflict (7).
   One of these was the catalytically inactive PARP13, which before its assignment to the PARP family had been shown to have anti-retroviral properties and was termed ‘ZAP’ (Zinc-finger Antiviral Protein).  The zinc-finger domain binds directly to a long stretch of viral RNA (8), but the details of the recognition and how binding leads to the destruction of the viral RNA (is the PARP domain involved?) remain to be elucidated.
   More relevant to coronaviruses, perhaps, is the positive selection of PARP9, PARP14 and PARP15, which all contain the ADP-ribose binding macrodomain. In contrast to PARP13, the mutations in these PARPs are found throughout the proteins, including the macrodomain, where they are found distributed in surface patches, rather than in the ADP-ribose pocket. The relevance of this to anti-viral action is that there is a virulence protein, NSP3, in SARS-CoV which posses three macrodomains, one of which (MAC1) is structurally homologous to the macrodomain of the PARPs. (This macrodomain is also found in the virulence protein of hepeviruses and togaviruses.)

Structure of SARS-CoV genome and domains in gene nsp3 (from (6))

This macrodomain has been shown to bind ADP-ribose, and mutations in the macrodomain of nsp3 have been generated at key residues at the binding site. Using these mutants it has been established first, that such mutants have reduced virulence compared with the wild-type virus, but that this difference is abolished when infection was in cells with knockdowns in the gene for macrodomain-containing PARP14  (although also in PARP12 knockdowns) (9).
   It has been demonstrated that NSP3 can remove ADP-ribose from proteins in vitro, suggesting that this catalytic activity may be the basis of its virulence (6). However evidence for such action during infection is lacking.
   If indeed the continual mutation of the macrodomain of PARP9, -14 and -15 is part of an “evolutionary arms race” with NSP3, the nature of the postulated interaction or antagonism between these proteins remains to be determined.

References
   1. Gupte et al. (2020) Genes & Development 31, 101–126.
   2. Schreiber et al. (2006) Nature Reviews: Molecular Cell Biology 7, 517-528.
   3. Vyas et al. (2014) Nature Communications 5, 1–13
   4. Suskiewicz et al. (2020) Nature 579, 598–605
   5. Leung et al. (2018) PLOS Pathogens 14(3): e1006864
   6. Fehr et al. (2018) Trends in Microbiology 26 598–610
   7. Daugherty et al. (2014) PLoS Genetics 10(5): e1004403
   8. Guo et al. (2004) Journal of Virology 78, 12781-12787
   9. Grunewald et al. (2019) PLoS Pathogens 15 (5): e1007756.


Write the haplotypes of the family I'm doing old exam assignments to prepare for my finals on Monday and I've stumbled on one assignment that I'm not sure how to tackle.

A family with 2 children is examined for cataracts using PCR with 4 markers, A, B, C and D. The results are seperated on a gel and the genotypes are as follow:

Where Far = father, Mor = mother, Barn = child.

Notice that there was an error with the analysis so child 2's alleles are undetermined.

The question states: Draw a pedigree with each of their haplotypes. What is the most likely haplotype of child 2?

I don't understand exactly what it's asking. I'm not sure what a HAPLOtype is. I know what a genotype is and that is what the answer seems to indicate.

The answer for the father is: 4 3, 1 2, 11 5, 7 4. Now the only difference between these numbers and the given numbers are the re-arrangement of 5 and 11 in marker C?

Definition of Haplotype

The concept of haplotype has the default to be subject to several definiton that differs mostly by their complexity to be understood and by their specificity but different definitions also sometimes differ slightly in their meaning.

In simple terms the concept is pretty easy. A haplotype is a porte-manteau word of haploid genotype and it refers to half the genotype.

What the question is asking

The question is asking is Here is half of the genotype of the child, what do you expect the other half to be?. Note however, that for the last two markers, the first haplotype is not indicated so they are just asking for the genotypes here which makes the question slightly poorly phrased IMO.

The answer key

The answer concern the father, which is silly as the question is about the child. So the answer you stated definitely does not answer the question.

The answer

We have to look marker per marker to answer the question and then consider them all together to reconstruct the haplotype. In absence of information on the subject, we are going to assume that the markers are completely independent (unlinked, eventually on different chromosomes). We will also assume no mutation (probably negligible anyway) and we assume no crazy kind of inheritance such as some selfish elements. You will note also that information about the first child tells nothing about the second child.

Marker A

The first allele inherited necessarily comes from the mother and therefore, the second allele must comes from the father. As a consequence the second allele is either 3 or 4 with equal probability.

Marker B

The first allele inherited necessarily comes from the father and therefore, the second allele must comes from the mother. As a consequence the second allele is either 1 or 4 with equal probability.

Marker C

The four possible genotype are [5,7], [5,11], [11,7] or [11,11], that all occur with equal probability. This means that for Marker C, at one haplotype, the probability of being 5 or 7 is $\frac{1}{4}$ and the probability of being 11 is $\frac{1}{2}$.

Marker D

The four possible genotype are [4,7], [4,8], [7,7] or [7,8], that all occur with equal probability. This means that for Marker D, at one haplotype, the probability of being 4 or 8 is $\frac{1}{4}$ and the probability of being 7 is $\frac{1}{2}$.

Whole Haplotype

From the above, you can compute all possible haplotypes and calculate the most likely to occur. However, there are some ties. The most likely genotypes are (3,1,11,7), (3,4,11,7), (4,1,11,7) and (4,4,11,7) that could occur with probability $\left(\frac{1}{2}\right)^4 = \frac{1}{16}$.


why is LPL (lipoprotein-lipase) down-regulated during fasting? During fasting our body needs additional sources of energy and that's why triglycerides are broken down into fatty acids and glycerol. where fatty acids can be used to generate acetyl-coA and contribute to the citric acid cycle or build ketone bodies.

So if we are wishing to get more fatty acids why is LPL down-regulated although it's the enzyme needed to break down Triglycerides in lipoproteins?

LPL is largely expressed on tissues that metabolize or store a lot of fat, including muscle and adipose tissue, and it's regulated by a number of factors (1). This includes diet, hormones and other protein regulators. The current literature on LPL has shown that regulation of LPL is tissue-specific. The activity of LPL, like other proteins, may be controlled at the transcriptional or the post-transcriptional level. A review by Goldberg et al (2009) notes that the activity of LPL in adipose tissue during fasting is low, but high in skeletal and cardiac muscle. They also note that insulin increases transcription of LPL in adipose. So why the down-regulation? One of the proposed mechanisms for LPL down-regulation in adipose tissue is rapid inactivation by a protein inhibitor known as ANGPTL-4 (2)

ANGPTL-4 (also known as a fasting-induced adipose factor), is up-regulated in adipose tissue two to four-fold in response to glucocorticoid stimulation (3). It's commonly known that you have a cortisol spike within a few hours of fasting, which is intended to try and increase glucose availability, for example.

The idea is that ANGPTL-4 attempts to control the distribution of fatty acids (4). In a mouse study, Cushing et al. demonstrated that ANGPTL-4 in fact diverts uptake of fatty acids and triglycerides away from adipose tissues (5). And this study was published in August 2017, so the phenomenon is still under investigation. It makes sense though, right? Why does the adipose tissue need to continue to receive fats during fasting? They can be better served elsewhere like muscle, the brain or the liver. Not only so, but Catoire et al. also demonstrated in 2014 how the interplay between ANGPTL-4 and LPL between non-exercising and active skeletal muscle during exercise allows for fine-tuning of fatty acid delivery to sites that need it most (6). So the regulation extends to both inter- and intra-tissue needs.

In closing, LPL is regulated during fasting in a targeted manner, but it is not generally down-regulated. Regulation is controlled in a manner that allows the demands of tissues to be reactive to their environment.


What's the difference between a plant and an animal? Are there some living things where the distinction between plant and animal is blurry or unclear?  I wouldn't know where to put something like yeast.  I also thought of photosynthesis, but then I heard that some salamanders have photosynthetic cells.  So, what's the difference between a plant and an animal, formally?

Yeast are neither plants nor animals; they are fungi. The old classification where things were lumped into only two buckets - plants or animals - has long since broken down. In fact, even things you might think of as plants, like algae or most seaweed are no longer classified as plants. Under the old system, plants and animals were considered kingdoms, and the latest classifications now divide the Eukaryotes into six kingdoms, but even this is poorly evidenced and facing challenge.

The best method of classification is probably cladistics which is based on the evolutionary history of organisms - but even it has problems when you start considering what to do with horizontal gene transfer and endosymbiosis. Because under a cladistic view, plants and animals are defined not by their features but by their ancestors your question becomes moot, I think.


Do plants sleep under ultaviolent rays? I observed Phyllanthus reticulatus is sleeping during nights. I want to plant this species indoor under a UV device.  Do these plants sleep under ultraviolent rays?

(Sleeping means leaves are close to each other)

For this answer, I'm going to assume that by "sleep" you mean that it maintains a circadian rhythm/photoperiod. Recent unpublished research indicates that even protoplasts maintain their circadian rhythm under UV lights so the UV light isn't the problem. In order for the plant to "sleep" like you mention, the photoperiod needs to be maintained. The UV light needs to be on during the day and off at night. If you leave the UV light on all the time you would actually perturb the plant's photoperiod and it would be very unhealthy. Plant metabolism and photosynthesis requires both dark and light reactions. In summary...yes, the plant will sleep but you must maintatain the photoperiod by switching the UV light off and on.


Technique to test antibiotic resistance in a bacteria in presence of another compound so I have to 'quantitatively' assess a bacterial strain for its antibiotic resistance property (it is a specific antibiotic) in the presence and absence of another compound alongside antibiotic. What technique or protocol can be followed?

It sounds like you might employ a "Disk diffusion test" described in this Wikipedia article.  It could be done with and without the secondary adjuvant compound and be quantified by measurement of the varying diameters of the resulting zones of bacterial inhibition.

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


How do trees use Adhesion and Cohesion to move water against gravity? I have an AP Bio class where I have to name 3 properties of water and I chose adhesion and cohesion for one of them. I'm having trouble finding out how exactly trees use adhesion and cohesion to move water. There is a lot of different answers out there on the net. How do trees use adhesion and cohesion to move water against gravity?

The mechanism is called "capillary action". It requires a tube of a small diameter and happens because of the adhesion of water to the walls and the cohesion within the water (=surface tension).