how do macrophages have the capacity to digest pathogen in opsonization

It's a simple matter of ionic charge

Opsonization works because it is masking negative charge with positive charge. Phagocytosis works on positively charged things.

Your right though, the sequence seems odd.

First something is phagocytosed (by a macrophage or another monocyte-derivative, these are the APCs... but neutrophils, which are not APCs or monocyte-derivates also perform phagocytosis but they dot not have the MHC-II to be described)
then digested in endosome/lysosomal,
then presented on the MHC class II,
recognized by TCR on T-cell,
then much more complicated stuff to get to B cells to convert to plasma cells
plasma cells secrete the antibody, in order for opsonization of the pathogen to be phagocytosis more easily.

Yet it was the initial phagocytosis that led to this. A bit of a circle.

Here are three answers:

one is cytokines
another one is about how the TLR receptor mediates phagocytosis
a third is how complements act as opsonins

local presence of cytokines (ex. interleukins, interferon, TNF) from either innate or adaptive "immune system" (by "immune system" I mean immune cells other than macrophage, but also epithelium which secretes types of interferons) that lead to "signal transduction" ("signal transduction" is the intracellular chain reaction in response to the activation of the cytokine (or other ligand) binding to the receptor, too complicated for me to explain) that alters the behavior of macrophage to enhance phagocytosis.

On the other hand, PAMPs activate the TLR which could permit phagocytosis without prior activation from sources "other" than the thing being phagocytosis.

By "other" things I mean opsonins and cytokines.

PAMPs (pathogen associated molecular pattern) are things on the pathogen that are distinctively foreign to the host, like flagella or LPS [which is the outer membrane from gram (-) bacteria]

TLR is the receptor on the macrophage that recognizes PAMPs. I think that TLR simply enhances phagocytosis via signal transduction much like cytokines. As an interesting side note, the TLR is quite ancient in kingdom animalia, having it's origin in sponges  as close to the beginning as you get). Other aspects of the immune system evolved later on specifically in vertebrate. In fact the lymphocytes is unique to jawed vertebrate (aka absent in agnathans and invertebrate) and i don't know much about antibody production in non-mammals. Also in lower vertebrate and invertebrate, phagocytosis is done by hemocytes. In other words, the TLR is pretty fundamental as far as immune stuff goes, more so than cell types doing their things (ex. plasma cell making antibodies, macrophages doing phagocytosis).

But there is also complement mediated opsonization, primarily C3b but other complement proteins as well. Finally there are yet more (less important) opsonins, Mannose-binding lectin and C-reactive protein (CRP). all of these things are "Acute phase reactants" that are secreted by the liver under inflammatory conditions, mediated by cytokines. Complement is not always activated by the immunoglobulins.

Complement is activated by

classical pathway, again Fc region of antibody (IgG/IgM), just like antibody mediated opsonization. In addition, classical pathway can be activated by CRP binding to microbial polysaccharides

alternative pathway, which is the spontaneous hydrolysis of C3. Under normal (non-infected) circumstances, this is normally prevented by a variety of mechanisms.
activation by mannose binding lectin. MVL recognizes certain sugars that are found in certain positions that are unique to bacteria, fungi, viruses.

I'm saying all these things as explanations of human immune system. It's probably different in different animals, the more different the further away from human. The complement system has been discovered in primitive vertebrate (agnathans) and invertebrate (specifically in deuterostomes like protocordates and echinoderms) but there are variations.


Ni-NTA purification, problem with the chaperone protein

If chaperone proteins are not an expected binding partner to your protein/peptide fragment then you need to use imidazole in your lysis and wash buffer ranging from 1 to 10 mM depending on how stringent you want but 1 mM worked for me. Can go higher than 10 mM if the problem does not resolve but don't go too high since imidazole is also used to get the purified proteins off the nickel beads as an elution buffer!


What is the difference between vegetable and fruit?

A true fruit is a ripened ovary that usually starts ripening when it is fertilized. And vegetable is any vegetative part of the plant which is edible and contains stored food probably in the form of starch.
These definitions are not exact as there are a lot of fruits which are fruits but do not strictly follow the given definition. See Syconus, Composite fruits, Sorosis.etc

Classification is based on several different criteria, for example the mode of reproduction, arrangement and design of flowering parts and flowers and also on the basis of habitat and habit.


Relationship between lifespan and reproductive age?

The sort of thing you're talking about would be called a Life History Invariant: a dimensionless ratio between two life history traits $A$ and $B$, such that although the traits themselves vary widely between species, the ratio $\frac{A}{B}$ is relatively constant.

Eric Charnov has written a lot about this, including a book.

One of the invariants which has been suggested is the ratio of age of maturity $\alpha$ to adult lifespan $E$. Charnov claims that it is relatively invariant within taxa, but has a different value for eg. fish vs. mammals vs. birds vs. reptiles.

From Charnov and Berrigan, "Dimensionless Numbers and Life History Evolution: Age of Maturity Versus the Adult Lifespan", Evolutionary Ecology (1990).

(If the ratio $\frac{A}{B}$ is invariant, then plotting $A$ vs. $B$ for different species on a regular graph will give you a straight line passing through the origin. The slope of the line gives you the value of the invariant.

Sometimes, in looking for an invariant researchers will instead graph the quantities on a log-log plot: they then look for whether the curve is a straight line with slope 1 (whose height gives the value of the invariant), with a good fit. This method has been criticized: the fact that some quantities are just about necessarily a fraction of other quantities (eg. you can't really lay an egg bigger than yourself), together with the fact that log-log plots "squish down" variance about the regression, opens the possibility of observing artifactual yesses. I tried to give an intuitive explanation of this criticism in a quora answer. Charnov and company have dismissed it as not applying to the invariants they found, however.)

This invariant is slightly different than the one you describe, in that they deliberately ignore pre-maturity deaths. (If infant mortality were high enough then it would be possible for average lifespan to be less than the age of maturity.) Also, they measure the ratio of pre-maturity lifespan to post-maturity lifespan $(\frac{\alpha}{E})$ instead of the the ratio of pre-maturity lifespan to total lifespan $(\frac{\alpha}{\alpha+E})$. These are just two different ways of talking about the same thing, but the former has an upper bound of 1, while the latter has no upper bound.

Finally, it's important to note that even if a quantity is relatively invariant, it can't be expected to be perfect; you have to decide how much noise you want to allow while still finding an approximate invariant interesting.


Why dont "growing degree days" have units of degrees Celsius (or do they)?

Actually, the units are °C days   or °F days. The units are mostly given in the typical name, Growing Degree Days where which temperature unit is meant is understood from the context.  Much more important is knowing the base temperature ("T_base") since this value can be different in different usages, even for the same type of organism.


What is this raptor on a building in California?

It is a Red-shouldered Hawk (Buteo lineatus).

  Its breeding range spans eastern North America and along the coast of California and northern to northeastern-central Mexico.

Identifying features:

Presence of dark wings with white spots.
Presence of dark-brownish head, orangish-brown chest.


Regarding gibbons, yes. According to National Geographic:

  Gibbons are monogamous and live in family groups consisting of an adult pair and their young offspring.

There isn't a generalized answer for "family living", although specific family types are indicative of relationship type. Nuclear families (parents and children) tend to be monogamous, families with multiple males and one female tend to be polyandrous, and families with one male and multiple females tend to be polygynous. See this page on primate social structure for more information.


Explanation of the ‘cherry red spot' in Tay Sachs disease

Short answer

The fovea centralis is colored red in both the healthy retina and Tay-Sachs affected retinae. The macular region around the fovea has a yellowish hue. You are confusing fovea and macula in your question.
The reddish hue from the fovea comes from the well-vascularized choroid layer below. The choroid is not black, it is colored red due to the presence of many blood vessels. You are confusing choroid with the retinal pigment epithelium, which is indeed black.

Background
The macula includes the fovea at the center, also called the fovea centralis, which forms the very center of the retina. The macular region around the fovea includes the perifoveal and parafoveal areas. The macular region around the fovea has a slight yellowish appearance to it due to yellowish pigments present in the cone axons (Fig. 1) (Kolb, 2012).

Fig. 1. Healthy retina. The macular region is seen in the center, The parafoveal region has a slight yellow/orange hue to it. Note that the landmark yellow circle at 4 o'clock, with the vessels sprouting from it, is the optic nerve head. source: Webvision.

Below a Tay-Sachs affected retina showing the hallmark cherry red spot (Fig. 2):

Fig. 2. Tay-Sachs affected eye. The fovea centralis appears red. source: Prezi

The only normal part is the fovea centralis, appearing in its native red color, i.e. the cherry red spot.

The choroid plexus is well-perfused and is, therefore, red. You are confusing it with the pigment epithelium, which is pigmented (Fig. 3).

Fig. 3. Layers of the eye. RPE = Retinal Pigment Epithelium. source: Retina Eye Specialists

Reference
- Kolb (2012), Simple anatomy of the retina. In: Kolb et al. (eds.), Webvision. The organization of the retina and visual system. Salt Lake City, UT, Moran Eye Center


How does the sensitive plant detect vibrations?

In fact, the idea of a plant nervous system is quite serious and constantly developing; of course those are rather local, simple signal pathways rather than an "animalian" centralized global network, but they use similar mechanisms -- depolarisation waves, neurotransmitter-like compounds, specialized cells... Here is a review paper by Brenner et al.

In the case of Mimosa, there is a good paper summing up Takao Sibaoka's long research of the topic.

In short, it seems that its petioles' phloem has cells which have polarized membranes and can trigger depolarization due to a mechanical stimulation. The signal then propagates to the corresponding pulvinus by a mixture of electrical and Cl- depolarization waves.

In the pulvinus, this signal triggers a second depolarization which coordinates the pulvinus' cells to trigger water pumping responsible for the leaf drop.

The transmission to the adjacent leaves is most likely mechanical, i.e. the movement of one dropping leaf excites another.

References:

 Brenner ED, Stahlberg R, Mancuso S, Vivanco J, Baluska F, Van Volkenburgh E. 2006. Plant neurobiology: an integrated view of plant signaling. Trends in plant science 11: 413–9.
 Sibaoka T. 1991. Rapid plant movements triggered by action potentials. The Botanical Magazine Tokyo 104: 73–95.


How does mutation cause natural selection? and is it common in protists or prokaryotes?

Your question, as I understand it, concerns the relative role (compare to natural selection and drift probably) of mutation in evolution. But evolution is not one process. Mutation and natural selection are processes that influence populations in very a different manners. At first sight, it seems to me that it does not make sense to weight the important of mutation versus other processes such as selection. But again, in what term would weight these processes?


From my readings, it seems that when procaspases 8 or 10 are
  unavailable, the cell will shift to necroptosis. What makes these procaspases unavailable and why does a cell second the necropotosis?

This seems to be right.

  Mice with a conditional deletion of caspase-8 in the intestinal
  epithelium (Casp8ΔIEC) spontaneously developed inflammatory lesions in
  the terminal ileum and were highly susceptible to colitis. Casp8ΔIEC
  mice lacked Paneth cells and showed reduced numbers of goblet cells,
  indicating dysregulated antimicrobial immune cell functions of the
  intestinal epithelium. Casp8ΔIEC mice showed increased cell death in
  the Paneth cell area of small intestinal crypts. Epithelial cell death
  was induced by tumour necrosis factor (TNF)-α, was associated with
  increased expression of receptor-interacting protein 3 (Rip3; also
  known as Ripk3) and could be inhibited on blockade of necroptosis.

  Caspase-8 is a cysteine protease critically involved in regulating
  cellular apoptosis. On activation of death receptors, including
  TNF-receptor and Fas, caspase-8 is activated by limited
  autoproteolysis and the processed caspase-8 subsequently triggers the
  caspase cascade that finally leads to apoptotic cell death.
  Caspase-mediated apoptosis is important for the turnover of IECs and
  for shaping the morphology of the gastrointestinal tract 4.

2011 - Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis

  Caspase-8 has both prodeath and prosurvival roles, mediating apoptosis
  and/or preventing RIPK1-mediated necroptosis depending on cell type
  and stimulus. We found that inflammatory stimuli (LPS, lipoteichoic
  acid, or TNF-α) caused an increase in caspase-8 IETDase activity in
  primary rat microglia without inducing apoptosis. Inhibition of
  caspase-8 with either Z-VAD-fmk or IETD-fmk resulted in necrosis of
  activated microglia. Inhibition of caspases with Z-VAD-fmk did not
  kill non-activated microglia, or astrocytes and neurons in any
  condition. Necrostatin-1, a specific inhibitor of RIPK1, prevented
  microglial caspase inhibition-induced death, indicating death was by
  necroptosis.

2013 - Caspase inhibitors protect neurons by enabling selective necroptosis of inflamed microglia.

  Necrosis has long been described as a consequence of extreme
  physicochemical stress, such as heat, osmotic shock, mechanical
  stress, and freeze-thawing, which kill cells quickly and directly.
  Therefore, this cell death has been described as uncontrolled and
  accidental necrosis characterized by loss of plasmamembrane integrity
  and cellular collapse, though nuclei remain largely intact during this
  process (Krysko et al., 2008a,2008b; Vanden Berghe et al., 2010). Loss
  of membrane integrity and release of intracellular content grant
  necrotic cells the ability to induce an inflammatory response. These
  immunogenic endogenous molecules fall under the umbrella term
  ‘‘damage-associated molecular patterns’’ (DAMPs) (Garg et al., 2010;
  Kryskoet al., 2011). They include, in the case of accidental necrosis,
  HMGB1, IL-1a, uric acid, DNA fragments, mitochondrial content, and ATP
  (Tables 1and2)(Eigenbrod et al., 2008; Kono et al., 2010; Krysko et
  al., 2008a; Sauter et al., 2000). Because the nomenclature of DAMPs in
  the literature is confusing, here we define DAMPs as a family of
  molecules that are intracellular in physiological condition

2013 - Necroptosis: The Release of Damage-Associated Molecular Patterns and Its Physiological Relevance

Based on the articles above, I would say that capsase-8 is a signal that apoptosis works finely, and so the cell can kill itself whenever it wants. So if that signal is lost because of an infection, mutation or extensive cell damage, the cell has no choice, but to activate the necrotic pathway.

Figure 1 - cell survival and programmed cell death - source

  During tumorigenesis, significant loss or inactivation of lead members
  in the caspase family leads to impairing apoptosis induction, causing
  a dramatic imbalance in the growth dynamics, ultimately resulting in
  aberrant growth of human cancers. Recent exploitation of apoptosis
  pathways towards re-instating apoptosis induction via caspase
  re-activation has provided new molecular platforms for the development
  of therapeutic strategies effective against advanced prostate cancer
  as well as other solid tumors.

2012 - CASPASE CONTROL: PROTAGONISTS OF CANCER CELL APOPTOSIS

  These findings reveal that, although apoptotic/drug resistance is a
  formidable “stronghold” of cancer against chemotherapy, necroptotic
  susceptibility is an intrinsic “weak point” of cancer.

2007 - Targeting the Weak Point of Cancer by Induction of Necroptosis

  Playing a central role in cell death, caspases are targeted by
  different viruses in the aim of prolonging cell survival. For
  instance, viral IAPs (inhibitors of apoptosis) interact with and
  inhibit the processed active caspases, either by blocking the
  catalytic part of the enzymes, or through E3 ubiquitin ligase activity
  from RING domains, targeting caspases for rapid degradation via
  proteasome. Baculoviruses, asfiviruses or irridescent viruses encode
  such IAPs. Another class of caspase inhibitors frequently found among
  poxviruses include the serine proteinase inhibitors serpins:
  CrmA/SPI-2. Crma targets cysteine proteases such as host Caspase 1 and
  Caspase 8.

viralzone - Inhibition of host caspases by virus

  Pathogens specifically target both the caspase 8-dependent apoptotic
  cell death pathway and the necrotic cell death pathway that is
  dependent on receptor-interacting protein 1 (RIP1; also known as
  RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation
  of these two cell death pathways emerged when the midgestational death
  of mice deficient in FAS-associated death domain protein (FADD) or
  caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a
  far more entwined relationship than previously appreciated. Thus,
  mammals require caspase 8 activity during embryogenesis to suppress
  the kinases RIP1 and RIP3 as part of the dialogue between two distinct
  cell death processes that together fulfil reinforcing roles in the
  host defence against intracellular pathogens such as herpesviruses.

  The MCMV protein vICA prevents caspase 8 activation, and this
  sensitizes cells to death receptor-induced necroptosis. In addition,
  the MCMV protein vIRA blocks necroptosis and MCMV-induced programmed
  necrosis by inhibiting RHIM (RIP homotypic interaction
  motif)-dependent interactions.

2012 - Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways

  One potential explanation for this is that this form of death evolved
  to provide a “backup” pathway. Indeed, cowpox virus produces the
  factor CrmA, a potent apical caspase inhibitor capable of blocking
  apoptosis (Ray et al., 1992; Gagliardini et al., 1994). Several viral
  encoded genes are similarly produced to prevent apoptosis, and thus it
  is clear that inhibition of apoptosis is an important means viruses
  have exploited to avoid immune clearance. Interestingly,
  cytomegalovirus induces RIP3-mediated necroptosis via the interferon
  regulatory factor DAI (Upton et al., 2012). This virus also produces a
  protein called viRA, a protein that disrupts assembly of RIP1/RIP3
  necrosomes and consequent necroptosis. Thus, while the physiological
  function(s) of necroptosis remains to be fully elaborated, it is clear
  that this cellular process has been around for a long time during
  evolution. It is likely that necroptosis may serve as an “Achille's
  heel” in tumor cells, and thus greater understanding of the process
  may reveal novel therapies for cancer therapeutics.

2014 - Grand challenges in cell death and survival: apoptosis vs. necroptosis

It seems like there is a 3rd pathway too, it is called ferroptosis.

  TNF-induced necroptosis depends on receptor-interacting protein-1
  kinase, mitochondrial complex I and cytosolic phospholipase A2
  activities, whereas H2O2-induced necrosis requires iron-dependent
  Fenton reactions.

2009 - Necroptosis, necrosis and secondary necrosis converge on similar cellular disintegration features

  The transition metal iron is essential for life, yet potentially toxic
  iron-catalyzed reactive oxygen species (ROS) are unavoidable in an
  oxygen-rich environment. Iron and ROS are increasingly recognized as
  important initiators and mediators of cell death in a variety of
  organisms and pathological situations. Here, we review recent
  discoveries regarding the mechanism by which iron and ROS participate
  in cell death. We describe the different roles of iron in triggering
  cell death, targets of iron-dependent ROS that mediate cell death and
  a new form of iron-dependent cell death termed ferroptosis. Recent
  advances in understanding the role of iron and ROS in cell death offer
  unexpected surprises and suggest new therapeutic avenues to treat
  cancer, organ dam
  - age and degenerative disease

2013 - The role of iron and reactive oxygen species in cell death
2012 - Heme induces programmed necrosis on macrophages through autocrine TNF and ROS production

Not just a 3rd, there are many more pathways (pyroptosis, MPT-RN, parthanatos, ferroptosis, NETosis).

Figure 2 - Signalling pathways of regulated cell death.
2014 - Regulated cell death and inflammation: an auto-amplification loop causes organ failure


This is a great question.
Without going into too much detail, there is a series of studies done in northeastern US temperate forests (specifically at Great Mountain Forest in Connecticut, USA) on the growth, survival, and dispersal of canopy trees. In this particular community, light appears to be the primary limiting factor. Seedlings and saplings in low-light environments (i.e. stuck under the canopies of mature trees) grow slowly and have poor carbon balance, which makes them susceptible to mortality (probably from pathogens, although the proximal cause of death of seedlings and saplings is rarely known). Early successional tree species (in GMF, white ash/red maple/red and white oak) grow especially slowly, and hence are more likely to die, in low-light conditions; late successional (hemlock and beech) grow slowly even in high light, but are tolerant of slow growth, so are likely to survive until the adult tree above them dies and falls down.
The exact answer to "at what point do these trees die" is a little tricky, but here's a figure from Kobe et al. showing estimated survival probability for different species as a function of light availability (the assumption is of independent mortality probabilities, given light availability, at each time step, so there is no particular stage at which individuals die in the model).

Kobe, Richard K., Stephen W. Pacala, John A. Silander Jr, and Charles D. Canham. “Juvenile Tree Survivorship as a Component of Shade Tolerance.” Ecological Applications 5, no. 2 (1995): 517–532.
Pacala, Stephen W., Charles D. Canham, John Saponara, John A. Silander Jr, Richard K. Kobe, and Eric Ribbens. “Forest Models Defined by Field Measurements: Estimation, Error Analysis and Dynamics.” Ecological Monographs 66, no. 1 (1996): 1–43.
Pacala, Stephen W., Charles D. Canham, and John A. Silander Jr. “Forest Models Defined by Field Measurements: I. The Design of a Northeastern Forest Simulator.” Canadian Journal of Forest Research 23, no. 10 (1993): 1980–1988.
Pacala, Stephen W., Charles D. Canham, John A. Silander Jr, and Richard K. Kobe. “Sapling Growth as a Function of Resources in a North Temperate Forest.” Canadian Journal of Forest Research 24, no. 11 (1994): 2172–2183.


Are there human cells, apart from red blood cells and platelets, without a nucleus?

Wanted to give a one line answer some day!!

Lens fiber cells and keratinocytes.


Glen, sometimes there are many species that have same colloquial name. For e.g. frog includes hundreds of species. If you require high level of detail, you may need to look for more comprehensive lists.

There are zoology dictionaries such as this. I think it should serve your purpose.


Sugars which are Carbohydrates and vice-versa?

You need to make a distinction between polymers and monomers (or dimers).

Typically, sugars are monomers like glucose, maltose, or fructose. Sucrose (table sugar) is a dimer. These are all carbohydrates (made up of carbon, oxygen, and hydrogen).

Polymers of these sugars are also carbohydrates. For example, starch, glycogen, and cellulose.

Cellulose, which you called fibre, tends to be structural, and is only found in plants (think celery, or wood, or paper). Starch, is also synthesized by plants, and could be used for energy storage (as I recall). In animals, monomeric glucose is stored as glycogen in skeletal muscle, where it becomes available as energy for short bursts of energy.


Why do cells not spread on soft substrates?

As both @MattDMo and @WYSIWYG have already so succinctly answered this question in their comments I'm just going to attempt to expand a bit on their answers.

@MattDMo and @WYSIWYG have explained that the aforementioned paper from the question has results that are "not extensible to all cell types and environments" and "Some cells need a matrix to adhere. Adherence relays proliferative signals in these cells."

I'm just going to expand a little bit on these points... I know this addressing an erroneous assumption in the question rather than the question itself but bear with me.

Ok, so as has already been mentioned, different cell types in a multicellular eukaryote (like a mouse, or a human) only grow in certain environments and this is really important . Think about it like this, a mouse's body is made up of many different cell types all working together to create functional organs and systems and to ultimately make up the mouse. The individual cells don't know they are all coming together to make an entire animal and a cell is designed to grow and proliferate in order to make more copies of itself and spread. So why don't all cells just grow all over the place, on top of each other and spread to all parts of the body.

The reason you and the mouse aren't a formless mass of undifferentiated cells - like a big soft tumour - is because different cell types develop in such a manner that they can only grow in a restricted, structured way in a certain environment in your body. There are mechanical and chemical signals along with unique sets of growth factors that are found in different environments in the body that make it possible for certain cell types to grow in one area while not in another. It's why only blood cells can survive suspended in the blood not adhered to anything and your fibroblast cells (they make up your structured connective tissue can't, they need to adhere to a surface to grow. The different cell types only get their signal to keep growing when they are in their proper environment.

This is why when scientists are growing various mammalian cell cultures they have to be aware of what environment and growth factors the specific cell type they are working with requires in order to grow. Some mammalian (e.g. mouse) cells need a structured scaffold to grow them in culture and some can grow in soft or liquid culture.

Source: Hallmarks of Cancer: The Next Generation http://www.cell.com/cell/abstract/S0092-8674(11)00127-9?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867411001279%3Fshowall%3Dtrue [This is a classic paper that explains this far better than I can hope to - look for the section 'Sustaining Proliferative Signaling'.]


Why does blood come from mouth when people are shot in the chest area?

Substances such as blood trigger the Cough reflex, so if for any reason blood accumulates in the airways, it will be ejected this way.

If you have a look at chest anatomy, you can see how this could be caused (look at Trachea down to the lungs, aorta and the carotid arteries above the heart). A shot through the chest can peforate many large blood vessels, along with the airways, and cause leakage inside.

I would consider it quite hard to hit the aiways like that though, the bullet would have to enter the chest quite near the centre as the cough reflex is not triggered by substances in the lung itself, only in the airways. There may be other ways of blood getting into the airways, but I would assume that a scene with a shot near the breast and then blood coughing would be unrealistic.

Image source: Micheau, A (2010) ANATOMY OF THE MEDIASTINUM: ILLUSTRATIONS AND CROSS-SECTIONS. From: http://www.imaios.com/en/e-Anatomy/Thorax-Abdomen-Pelvis/Mediastinum-Illustrations


Strictly from a biological perspective, what is the functional expectation of a human being

I will start with a quote from François Jacob, a French geneticist:

  The sole ambition of a bacterium is to make two bacteria.

The same reasoning can be extended to all life on Earth, including humans.

There is no purpose to human existence, in the same way that there is no purpose for life at all. Life is there because it can. It works, chemically, physically and thermodynamically, given the physical conditions present on Earth.

Biology does not give any moral reason for our existence. It only describes what is there. Using experimental techniques we can infer the purpose of the human feet. All we need to do is to remove the feet of a human subject and see what happens. The subject will be unable to walk, and therefore we will be able to infer that the feet's purpose is to enable locomotion. In biological research, we usually remove or silence genes or proteins from an organism to infer their purpose. We then observe the phenotype. Most of the time however, such an experiment does not give any information on the purpose of the gene because its function is not obvious enough to be observed.

In the same vein, one could remove humans from the Earth and see what happens. If something changes for the worse on Earth, then we would be able to infer that our purpose was to prevent such event from happening. Obviously, such an experiment is impossible to perform, therefore we will never know what is our purpose, neither will we know whether we actually have a purpose.


First discovery of long-term depression?

The process of long-term depression (LTD) was first discovered in the cerebellum by Ito et al. in 1982:

Ito M, Kano M. Long-lasting depression of parallel fiber-Purkinje cell transmission induced by conjunctive stimulation of parallel fibers and climbing fibers in the cerebellar cortex. Neurosci Lett. 1982;33(3):253-8

Ito M, Sakurai M and Tongroach P. Climbing fibre induced depression of both mossy fibre responsiveness and glutamate sensitivity of cerebellar Purkinje cells. Journal of Physiology 1982; 324: 113–134.

Check this source.


So if siRNA appears to be just a subtype of miRNA, can we confirm
  that? Or are there any other differences that make these two molecules
  different kinds of small non-coding RNAs?

siRNA and miRNA are not identical, but similar. It's not incorrect to consider them similar phenomena in biology, but history places them apart and there exist small differences. Both are processed inside the cell by the enzyme Dicer and incorporated into the RISC complex where their target is degraded ("RNA interference"). However, there are important differences, in case you want to be absolutely correct.

siRNA is typically exogenous (introduced from outside by viruses or by engineering). It typically has 100% complimentary to its target mRNA, because we want to reduce off-target binding. If designed well, they target only the intended target and are checked to be incompatible with any other potential mRNA targets, i.e. are designed to be specific.

miRNA is endogenous (occurs naturally within cells) and is single stranded in vivo. Its complimentary is not always 100% perfect, and often has multiple targets. This is the major difference between the two. It pairs with its target mRNA imperfectly; it simply inhibits translation (protein production from the mRNA). In rare cases where it's a perfect match, it causes the cleavage and destruction of the target mRNA just like siRNA. If I remember correctly, plants miRNAs, in contrast to animal miRNAs, usually have perfect complementarity with their targets. miRNAs are also derived from shorter stemloop RNA products than siRNA.

As you probably know, both are non-coding RNAs and do not enter ribosomes for translation. They have similar effects on gene expression. If you are interested in the very first reports of either kinds of RNA, here goes:

miRNAs discovered in 1993 in worms.

siRNAs discovered in 1999 in plants.

Notice the phrase antisense RNA in both titles. Interesting!

Further reading, in case you are interested.

  Why does a cell need siRNA?

This is a very different question. Why? Probably to fine-tune the expression of its genes. Small RNA species can accumulate, aggregate, and regulate mRNA levels in ways that are probably not possible inside the nucleus at the DNA transcription level. Small RNAs are also understood to be epigenetic and function in the cytoplasm and endoplasmic reticulum!


Let's first clarify some concepts. Free fatty acids, including palmitic acid, are not present in animal tissues (or in the diet) to any large extent; they are esterified with glycerol to from triglycerides (fat), which is the storage form. This is a very important distinction, because triglycerides are chemically inert molecules that can be stored in very large amounts in cells without causing problems (adipocytes are pretty much just one big fat droplet), while free fatty acids are dangerous to organisms because they disrupt cell membranes --- fatty acids are basically soap.

When nutrition studies like the WHO report talk about dietary intake of "palmitic acid", they really mean intake of triglycerides that contain a large proportion of esterified palmitic acid as side chains. There is a large body of epidemiological studies indicating that intake of fats rich in palmitic acid correlates with cardiovascular disease and other "metabolic" disorders, although some reports show no significant effect. In clinical trials, replacing saturated with unsaturated fat seems to provide some health benefit; but there also are studies indicating that monounsaturated fat can be worse than saturated fat. So there is some evidence that too much saturated fat is problematic, although the issue is not straightforward.

The causal mechanism is to my knowledge still not clear. You are right that cells are normally perfectly capable of handling palmitic acid; it is a good substrate for beta-oxidation and a common fuel source for human cells. However, in pathological situations, free fatty acids can accumulate in cells and in the blood, probably because of excessive lipolysis. Many studies show that this can cause insulin resistance and trigger inflammatory signals, and even cell death by apoptosis. Some reports show that palmitic acid in particular causes these effects, whereas oleic acid (monounsaturated) does not, but I don't think there's any consensus on why palmitic acid is special.

My own hypothesis (if I may be so bold :) is that palmitate only appears to be special because cells have evolved to sense it as a "proxy" signal for free fatty acids in general. Since fatty acids are clearly dangerous to cells, sensing them is important, and because palmitate is the naturally most abundant fatty acid, it would be the easiest fatty acid to detect. It is known that palmitate is recognized by toll-like receptors, in particular TLR2 and TLR4, and that sensing by these receptors trigger "proinflammatory" signalling. But this alone doesn't prove my "proxy" hypothesis, of course.


what happens when you put enhancer and caat box in prokaryotes

I do not think that enchancers do anything in procaryotes since there is no
chromatin spatial organization of DNA involved.


gene duplicated on genome but is different

That sounds line one of two things. Either a sequencing or assembly error (quite likely since you're talking about scaffolds so, presumably, not a completely assembled genome) or duplication and subsequent pseudogenization.

It is relatively common for genes to be duplicated and then to be rendered inactive by a mutation event. Such genes can still be detected in the genome and are called pseudogenes. The process of their creation is, unsurprisingly, called pseudogenization. You can think of such genes as fossils. They often have significant sequence similarity to the original and can even be transcribed.

A quick search brought up a couple of articles discussing the pseudogenization of specific genes:

Pseudogenization of CCL14 in the Ochotonidae (pika) family.
Pseudogenization of sopA and sopE2 is functionally linked and contributes to virulence of Salmonella enterica serovar Typhi.

That said, is also quite possible that what you describe is a simple duplicate that has diverged without becoming a pseudogene. The details will depend on the particular sequence. Are there in-frame STOP codons? Can the gene still be transcribed? Such duplication events give rise to paralogs (note that all three of the genes you mention would be paralogs of each other, it's just that one has diverged more than the others). You can read more about those here: What is the difference between orthologs, paralogs and homologs?


What is the proper quick freezing /snap freezing protocol for pancreatic tissue?

Embed the tissue in OCT first (roughly cut to remove everything what is not needed) and the flash freeze it. Then you can cut your sections.

The first protocol describes it in detail, the second gives some additional information:

Protocol for Preparation of Frozen Tissues for Sectioning
Tissue freezing methods for cryostat sectioning


What does "local folding" means in secondary structure?

The most common examples of secondary structure in proteins are alpha helices and beta sheets, and the most important distinction between secondary and tertiary structure is that a single protein can have multiple "local structures", alpha helices and beta sheets, within its complete global structure. In contrast, a protein cannot have multiple "global structures" by definition.

In other words, a local structure can occur multiple times within a protein, while a global structure by definition can only occur once, and describes the complete shape of the protein.


Why lipophilic molecules can pass phospholipid bilayer, in spite of 2 hydrophilic layers?

Good question. This is my take.

It's not just the surface of the membrane that's polar. There is water (polar) on both sides of the membrane. In most animal cells there is also an unequal distribution of charges across the membrane. The environment outisde of the cell is typically positive due to an excess of positive ions, especially sodium. The inside of the cell is typically negative due to an excess of negative ions such as phosphate.

This means the hydrophobic molecules aren't any more at home in the environment outside, or inside, the membrane than they are at the surface. There's no reason to suppose any more repulsion at the surface. So, just due to their random kinetic motion they will find themselves at the membrane's surface, some with the necessary kinetic energy to cross.

There's another way to view this. We shouldn't think of the membrane as allowing hydrophobic substances to enter. We should think of it as NOT allowing hydrophyllic substance to enter without a proper ID check by proteins in the membrane.


I think the answer should be C because when it is submerged, cutaneous respiration takes place and hence right atrium receives more oxygenated blood.


Can solitary animals show extroverts traits?

So solitariness vs sociality in animals is a little more complex than we usually give it credit for. For example, even in species previously thought to be largely solitary except for mating, sustained observation and tracking often shows that previously assumed to be solitary individuals actually do interact and sometimes develop lasting social relationships with conspecifics, just not at times when people are observing them. This is a particularly common finding in nocturnal animals among males who are assumed to be solitary, such as buck deer who turn out to be more social than does--just primarily at night!

That Wikipedia article you cited for 'solitary animal' is actually pretty shitty when you get down to it; the list of "solitary animals" include several generic terms for animals that include common species known to have variable social systems depending on region, such as badgers, moose, jaguars, cheetahs (in whom males, often brothers usually form lasting social relationships), red fox, and devils, who actually encounter each other quite frequently over kills and scavenging sites. (Citations are listed in this Collabedit file, because Stack Exchange is yelling at me for trying to provide actual links.)

In that context, I don't think many people have done behavioral syndrome/"animal personality" work on sociality, because it's not a particularly good thing to measure--you're really measuring something more like 'aggression threshold.' People have done work on species like social spiders where sociality varies significantly between individuals, however.


What is the advantage of circular genomes for bacteria and linear genomes for other organisms?

You can package linear genomes much more efficiently than circular genomes, and bacteria simply don't require the information density to be prosperous.

To be a bit more specific, it's the torque strain put on the double-helix while it's being wound that makes the difference. Linear genomes can be wound around Histones, and these Histones can be further formed into more complex and dense patterns so that the DNA of a linear genome is condensed to a mere fraction of the size it was before. The high density allows cell division to occur much, much easier than it would otherwise happen in Eukaryotic cells.

Circular genomes cannot get rid of the torque stresses like linear genomes can. To attempt a similar packaging scheme as Eukaryotic cells would result in the DNA breaking apart at some point before you reached a high level of information density.

I'll look through my BioChem books again to find a reference later on, but hopefully you should have a solid idea of "why" from the above. For now you can do a little thought experiment: Think of all the ways you can wind a single piece of string or thread around things to make it as dense as possible. Then think of all the ways you can try to achieve the same density with a rubber band without breaking it. The string should win out in both the ease at which you can manipulate it, and the level of density you can achieve.


Is the masking effect of sound related to action potentials or to mechanical aspects of hearing?

Short answer
Both - masking occurs through neural effects, as well as via mechanical effects in the inner ear.

Background
First off, there are basically three types of masking, namely simultaneous, forward and backward masking.

Simultaneous masking experiments are the most basic and likely the most widely used. The most basic type of experiment is listening to tonal stimuli in static (white) noise. In this case, the inner ear is busy processing noise and acoustic probe stimuli (tones) are not perceived by the subject, while loud probe stimuli are noticeable. A more relevant test for everyday functioning is the speech-in-noise test, where speech stimuli are presented in noise. It appears that hearing loss causes folks to have impaired hearing in noise. The amount of impairment in speech understanding in noise exceeds by far the simple decrease in hearing sensitivity. Anyway, I'm drifting off.

Forward masking experiments present a masker before the probe.

Backward masking experiments present the probe before the masker.

To take a step back - the auditory system consists of the peripheral end organ, namely the hair cells in the inner ear (Fig. 1). Those hair cells translate acoustic physical stimuli into electrical currents. These are currents are fed to the spiral ganglion cells in the inner ear. Their axons bundle up in the auditory nerve which innervates the brain stem and ultimately the auditory cortex in the brain.

Now - forward masking experiments are generally regarded to target the peripheral structures, while backward masking experiments target the central structures at a higher level.

Peripheral masking effects occur at the level of

the basilar membrane (e.g. Zwicker (1977)
the auditory nerve (e.g. Stronks et al. (2012)

The basilar membrane is the structure that mediates the (traveling) wave that sounds generate and that traveling wave is the very basis of the frequency analysis in the cochlea, akin to a place-dependent Fourier transform. It is the basilar membrane that separates frequencies from high at the base to low frequencies in the apex due to its physical properties. Now, when the basilar membrane is busy moving in response to a masker presented at 1 kHz at 100 dB SPL, a probe tone of 1 kHz presented at hearing threshold (0 dB HL) will be totally swamped, simply because the amplitude of basilar membrane movement will be changed by next to nothing.

The auditory nerve is also an important neural site where masking occurs (e.g., Stronks (2010). This has to do with the fact that neurons fire action potentials. After a neuron has fired an action potential, there is an absolute refractory period that takes several ms to resolve. In that time, ion channels previously engaged in firing are re-opened and up and ready for the next action potential. Within the absolute refractory period, no stimulus, whatever its strength, can evoke another response in that neuron. Following that, a relative refractory period follows in which its firing threshold is increased, but strong enough stimuli can evoke a response. If a neuron is busy firing after chronic stimulation, it gets tired and a state of adaptation follows. Further stimulation results in fatigue, in which the neuron gets tired and has exhausted its resources to fire. All these processes can result in masking of simultaneously presented stimuli (simultaneous masking), but notably also in stimuli presented after the masker has subsided (forward masking).

Now, all these processes will not affect backward masking, where a short probe stimulus is swamped by a following masker (e.g., Oxenham & Moore (1995). This is caused by more central, higher-level processes that include attention processes, i.e.,

the brain

In other words, the following masker distracts the attention of the subject that in turn fails to notice the probe. It's thought to depend on central processes as peripheral processes can't be 'fooled' and faithfully transmit the stimulus to the brain, whatever comes next.

Fig. 1. The inner ear (cochlea) features hair cells that are actiovated by sound waves traveling through the basilar membrane. source: Modesto Junior College

References
- Oxenham & Moore, JASA (1995): 98; 1921
- Stronks, PhD thesis, 2010, University of Utrecht
- Stronks et al., Otol Neurotol (2012); 33: 35-42
- Zwicker, JASA (1977); 61: 1031


Here is the FTP address. Inside you will find the phase_3 folder. For other questions check this page (the link to the HelpDesk is at the bottom of the page).


Is this formula describing the loss of unfixed genes from a population accurate?

The expression is based on a real one, but missing a minus sign (EDIT: not anymore! See updated question), and the explanation is garbled. For the actual equation, see "eigenvalue effective population size" in, e.g., WJ Ewens, Mathematical Population Genetics. There should be a negative sign in the exponent: $L_T = L_0 e^{-T/2N}$. Note that you need this minus sign so that "genes" (actually heterozygosity) are lost with time rather than growing exponentially in number!

As for the errors in the explanation: $T$ should be measured in generations rather than years, and $N$ should be the number of individuals (or rather the "eigenvalue effective number") instead of the number of generations.


What is the identity of this fruit/tree found near Berkeley, California, USA?

Given that it's in central California, it's almost certainly California buckeye (Aesculus californica).  The tree is common in the Coast range and Sierra foothills of California.  It has adapted to the Mediterranean climate of the region by growing during the wet winter and spring and then dropping its leaves during the hot, dry summer.  The large seed is toxic if consumed.


I have not read the article but in general the allele frequency is pretty much the easiest statistics to compute from population genetics data.

The allele frequency $p_i$ of the allele $A_i$ is the relative frequency of this allele $A_i$ in the population. In other words, it is the counts of haplotypes having the allele $A_i$ divided by the total number of haplotypes. For the specific case of diploid organisms, this frequency is the count of allele $A_i$ divided by twice the number of individuals.

Consider for example the following data, where we have two alleles in the population, $A$ and $B$. Each individual is denoted by its two haplotypes separated by '|'. For example individual A|B is heterozygous.

A|B A|A A|A A|A B|B A|B A|B A|A A|A A|A A|A A|B A|A A|B

In this population there are $7$ Bs over 14 individuals. That makes a allele frequency for B of $\frac{7}{28} = \frac{1}{4}$.

Of course, if you have genotype frequencies, you could - making a number of assumptions - calculate the allele frequency using Hardy-Weinberg but typically from empirical data, you don't need to go through that.

More information about Hardy-Weinberg rule at the post Solving Hardy Weinberg problems.


Difference between Cary-Blair and Amies transport media for Staphylococcus and Streptococcus?

This site (no connection) states (my emphasis):

  Unlike Cary-Blair Medium, which is almost exclusively associated with enteric transport, both Stuart and Amies Medium have been widely used for the transportation of a diverse range of clinical swab samples from sites including the eye, ear, nose, throat, skin, genital tract and wounds.


Are the fossil sites in Hadar geographically separated?

Here is a map of the region where they found the Lucy skeleton.

The researchers speak of the Hadar formation at Dikika, so they are giving it an expanse of 10-15 kilometers at least.

it's quite flat as well.

Why do you want to know?


According to this article, no one knows; it's an "evolutionary mystery." As a general rule, closely related species generally have a similar number of chromosomes, and the number typically increases with the complexity of the species. However, the actual number varies wildly.

The author also points, out,

  Each egg or sperm gets 23 chromosomes (half of each pair). Which
  chromosome they get in the pair is totally random. When you do the
  math, this comes out to 10 trillion different possible combinations.
  If we had only one pair of chromosomes, the number drops to 4.


Organism-specific Kegg Pathway: Must all boxes be high-lighted/present for a reaction to occur?

Your interpretation of the pathway map is incorrect.

The boxes do not represent KOs (Kegg Orthologues) and they do not represent a protein complex. They are Enzyme Commission (EC) numbers and where there is more than one box this means that there is more than one enzyme that can catalyse the reaction.

In the case you cite the two enzymes are EC 5.3.1.9, glucose-6-phosphate isomerase, as you can see by clicking the box, and EC 5.1.3.15, glucose-6-phosphate 1-epimerase. Only one is needed to catalyse the reaction.


Blood is considered a type of connective tissue (sometimes). However, an organ is formed of multiple different tissues. Thus, blood is a tissue, not an organ.


Amine is already a reduced state and therefore the reduction part is not of the amine. In chemical process of reductive deamination the arylamine is first converted to an intermediate, usually by sulphonylation of the amine nitrogen [ref], which in turn is reduced.

$ArNH_2 + CH_3SO_2Cl \ \ \  _{\overrightarrow{pyridine}}\ \ \  ArNHSO_2CH_3 \ \ \  _{\overrightarrow{NaH+NH_2Cl}}  \ \ \ ArH$

Biochemical anaerobic reductive deamination is reported but not for amino acids (I couldn't find any). It is reported for anilines which probably proceeds via a carboxyl intermediate [1, 2].

This article says that the non-classical amino acid $ornithine\ \ $ is converted to $\delta-aminovaleric acid\ \ $ via a $\ proline\ $ intermediate but no mechanism is described.

I don't think this answers your question completely; the best solution would be to ask the author of the presentation for the exact reference.


qPCR (weird ntc curve, amplifies before templates and reaches plateau quickly)

The cause of the signal in the no template control will be contamination. It could be that the reason for the different plateau positions is the presence of reaction inhibitors, depletion of reagents, or possibly different binding efficiencies between template (and contaminating DNA) and the primers. I'm not sure about that last one but it kinda makes sense in my head: any contaminating DNA that binds to the primers probably won't bind as efficiently as the template that the primers have been designed for so the reaction is inhibited by accumulation of dsDNA faster.

Either way the cause is going to be excessive contamination. Try using more template in your samples (increasing you signal to "noise" ratio), or be more careful when preparing your samples.

There are extraordinary measures that can be taken to remove contaminating DNA (e.g. treating the water with DNase and then deactivating it) but these often aren't necessary and the added steps can actually increase contamination, it's usually best to keep it simple.


Why don't we see turbulence in the aorta even in normal situations?

Why don't we see turbulance in Aorta even in normal situations?

There are different parts of aorta where turbulence is possible and where not.

It is often said that in normal situations, we cannot see turbulence in aorta because aorta is very stiff and its surface is very smooth.
However, this is a simplification and involves an average person (middle aged) which has stiff aortic arch too.

Note that the elasticity of arcus aortae is responsible for 50% of the volume to the peripheral circulation, thus creating a nearly continuous peripheral blood flow as anongoodnurse says, see this publication.
However, not all of this blood travel to the backward direction.
It would be interesting to see how much blood is travelling backward.
This would help to understand what is the likely hood for turbulences.

Those models linked by Anongoodnurse's answer are a few models used to locate places of possible turbulences discretely but they do not seem to consider the amount of blood capable of creating turbulences, just discrete models:

Stalder et al. I do not like the first publication because it is using Reynold's number that is designed originally for laminar flow. Problem with viscosity etc. There are better ways to the same thing and consider explicitly the creation of turbulence. It does much simplifications there. Fitting the equation to the physiological ranges of some set of data is bad procedure.
Fukuda et al. I like the second publication. High velocity and turbulence and nonlinear streamlines in the ascending aorta in normal situation. In other words, high magnitude of the strain rate tensor along aortic curvatures. So we need nonlinear distribution of at least 4D (later 6D) to quantify the amount and degree of nonlinear processes in turbulences.
Lantz et al. Third publication. Linear model for nonlinear situation. I am not convinced by their Mesh selection. Only in Mechanics' journal. Very far from Medical publication or from Mathematical. Not rigorous.

In summary, there are many models and publications to answer the question where are the turbulences. However, they try to answer nonlinear problem by linear models.
I have not seen any models where they do this rigorously.
I think we should narrow this problem even more, like Fukuda et al has done.
They manage to provide some good pieces of information by just considering an intervention with least turbulence in the aorta.

Generally speaking, we can see some turbulence in arcus aortae in the diastole when blood bounces back from the aortic valve.
The walls of arcus aortae can store about 50% of left ventricular volume.
However, I do not know how much of this blood is travelling backward and reflecting back from the atrial valve and causing possibility for turbulences.

  [P]ulse pressure wave getting reflected from periphery.

Pulse pressure is systolic minus diastolic pressure.
Pulse wave is those small waves inside respiratory waves:

where vasomotor waves are controlling the big picture.

  If the pulse pressure wave is reflected during diastole and at the same time blood is being pumped forward by aorta - -.

Wrong! Blood is pumped by heart. Aorta is just a vessel for transportation.
Generally speaking, Some blood is reflected back from arcus aortae which bounches back from the aortic valve.

  [Because] windkessel effect then we have two opposite forces acting which should
  create turbulance even in normal aorta. Why doesn't this happen?

You confuse here different terms and processes.

Generally speaking.
Arcus aortae stretches during systole.
It is coils back in diastole (left atrium relaxing), blood crashing off aortic valve, possibly creating a heart sound and increasing diastolic pressure. Like anongoodnurse says, in this phase, you can see some turbulence in the aorta but little, since the wall of the aorta is very smooth and only small portion of blood is travelling backward from the walls of aorta:

where see the aorta coils part.


If bacteria with recombinant DNA molecules do not survive in gene cloning, how they can be grown into a colony after being isolated?

The question confuses too many things. The process being described, Lac Z Blue-White Screening, doesn't involve cutting the ampicillin gene, nor do the bacteria with the recombinant DNA or without the recombinant DNA die in the process of the experiment.

The plasmid contains a Lac Z gene involved in creating enzymes that break down galactose. In a test tube, the vector plasmids take up the gene of interest and the recombinant DNA is produced. The recombinant DNA is then added to the medium of bacteria, but only some of the bacteria will be transformed and take up the plasmid vector. In these bacteria, restriction enzymes will 'cut open' a space for insertion in the Lac Z gene, and DNA ligase will seal it up. The insertion of the gene in a bacterium disrupts the Lac Z gene and make it unable to produce the required enzymes to break down galactose. Then, the bacteria are applied to a Petri dish that contains growth media with a derivative of galactose, X-gal in it. When X-gal is broken down by the bacteria able to create the necessary enzymes from their functional Lac Z genes, the bacterial colony will turn blue. So, when you add these bacteria into the Petri dish, only the bacteria without the recombinant DNA will break down X-gal and turn blue, whereas bacteria with the recombinant DNA will not be able to break it down and remain white. This allows the researcher to distinguish between the bacteria with and without the recombinant DNA, and allow them to isolate for the ones with it.


What determines the influx of calcium ions in the voltage-gated ion channels?

So, let's use a neuron to neuron connection as an example.

Calcium is released into the neuron when voltage gated ion channels, specific to calcium, open. These channels can only open when there is a significant depolarisation in the axon terminal of the neuron.

Where do the calcium ions come from? The majority of them are outside of the cell by the plasma membrane and adjacent to the synaptic vesicles.

I'm not too sure what you mean when you ask what the calcium ion's "source" is. It is common for calcium ions to sit outside the cell, not just in neurons, to help maintain potential difference for example.

And yes, the influx of calcium in a neuron is determined by the opening of voltage gated calcium channels.

Sources: https://web.williams.edu/imput/synapse/pages/IIA1.htm , https://en.wikipedia.org/wiki/Calcium,  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249630/


How does shortage of oxygen halt the NADH dehydrogenase complex?

At a basic level this is quite straightforward if you look at an old-fashioned simplified diagram of the electron transport chain, such as the one below that I filched from the web.

If oxygen is absent then there will be a build up of the reduced forms of each cytochrome. Starting from the bottom, in the absence of oxygen cytochrome a is not reoxidized; if there is no oxidized cytochrome a then reduced cytochrome c cannot be reoxidized, and if there is no oxidized cytochrome c then cytochrome b cannot be reoxidized. The latter is the substrate of the NADH dehydrogenase complex — NADH-Coenzyme Q reductase in the figure — so this reaction stops for want of oxidised cytochrome b.

(Years ago I demonstrated on a standard undergraduate laboratory class using rat liver (or perhaps beef liver) mitochondria, where you inhibited different stages and detected the reduced forms by their colours in the visible spectrum.)


What does "developmentally programmed" mean?

The term could mean two things depending on the emphasis:

"developmentally programmed" would seem to emphasise the "programmed" nature of the development of something, implying that it is under specific regulation and the result of targeted energy expenditure ("Here, we describe widespread developmentally programmed nuclear destruction (PND) events that occur during yeast gametogenesis").
"developmentally programmed" would be intending to distinguish from other means of being programmed, i.e. this would go in the direction of a nature vs. nurture statement ("Hair colour is developmentally programmed and does not depend on external influences after fertilisation").

The first of the two appears to be the more common use of this phrasing if one wants to trust Google to be representative. Something along these lines might be intended in your example, though I don't see why this statement is necessary as it seems quite obvious that any organ that develops during embryogenesis is "developmentally programmed"...

I suppose the alternative ("not developmentally programmed") would imply that the development of secondary lymphoid organs is an accident which is not driven by specific mechanisms that exist for the particular purpose of developing them.

In any case, there is no magical scientific meaning to either of these two words, to me your example seems to be rather a mishap of phrasing.


Does anybody know which plant (or tree) is this?

The plant scientific name is Prosopis juliflora. It is widely found in our country (India) which is a major problem because of its impact in agricultural land. It can withstand any harsh climate also.

Initially it was introduced to our country around 1950s to be used as firewood under drought situations. But later it became a major threat, since it absorbs as much as water (approx 4 litres of water to produce 1 kg of biomass) from the soil which spoils the cultivable land and also this plant grows very fast and spreads easily as weed which also causes a major problem to the underground water table.

The government also realised its mistake later, but still this is found in most of the places in our country, particularly in the southern part of India.

You can find further details from the below links:

https://www.hort.purdue.edu/newcrop/duke_energy/Prosopis_juliflora.html
http://www.cabi.org/isc/datasheet/43942


Identification of a young tree in the alpine region of southeastern France

The tree grew its first fruits this spring, so that I could definitely identify it: it is a goat willow! This is consistent with its spontaneous sprouting in my yard, as it is a common tree in my region.


Is there any evidence of animals wanting to die?

Is it possible that an individual would benefit form being eaten?

In theory it is possible that such behaviour would evolve. An individual may improve the probability of its genes to be passed on by letting a related individual (which carries similar gene variants) to feed on it. When counting the fitness of an individual as being the sum of the fitness of all related individuals weighted by their coefficient of relatedness as inclusive fitness. We refer to the selection pressure that is due to a differential in inclusive fitness as kin selection. The field that study the evolution of altruistic behaviours is called social evolution and is an active field of research.

Example

For example, a male could much enhance the probability of survival of its offspring by being eaten by the mother. The type of cannibalism where one mate eat the other is called sexual cannibalism. A famous example of sexual cannibalism is the mantis prey. Note that it has been suggested that in natural conditions sexual cannibalism could be rarer than expected previously thought. Note also that the question of whether the male benefits from being eaten by the female in prey mantis is still controversial and could result from a sexual conflict.


Why do eyes feel overwhelmed by light when we wake up?

The reflex responsible for the phenomenon you described is called the Pupillary Light Reflex. According to the Textbook of Medical Physiology, Guyton & Hall, Elsevier, 11th edition, 2005, p. 649 (reworded by me in order to avoid direct copying):

When light reaches the retina of the eye, the optic nerves are stimulated. Most of the generated nerve impulses participate in the creation of an image in the brain etc., but a few reach an area in the brain called the pretectal nuclei. These nuclei then generate secondary impulses to another nucleus called Edinger-Westphal nucleus, which sends a signal through parasympathetic nerves to constrict the sphincter of the iris.
Conversely, in darkness, the reflex is inhibited, which results in dilation of the pupil.

To summarize, in darkness (either when you are in a dark room with your eyes open, or when you are anywhere with your eyes closed) the pupil will be dilated since stimulation by light does not occur. When stepping into the light or when opening your eyes, light immediately stimulates the optic nerve, which causes a signaling cascade that results in constriction of the pupil to a certain size, depending on the amount of light present (primarily to protect it from exposure to too much light).

Naturally, you can see this constriction happening every time you open your eyes in front of the mirror (focus on the pupil). It was also depicted rather accurately in the end of Disney's excellent rendition of the Hunchback of Notre Dame (skip to 1:22).


What are the naming conventions for mutations of proteins?

What your example is referring to is the change in the glutamic acid (E) amino acid (AA) residue, which is in position 36. This is denoted so that people/scientist would know what has been changed and usually there should be another letter after that number such as Y, which is tyrosine, to denote what it has been changed to, if it is a substitution. Then there is the delta (∆) symbol to denote deletion, and usually a number range e.g. 36-50 or just a number e.g. 70 appears after it to denote if a protein has been truncated in a certain AA range or if the entire protein from that AA is truncated, respectively. Sometimes (quite often now a days) the delta symbol is followed a protein domain name such as SH3 or RA to denote that a protein domain has been deleted and people use all sorts of naming variations for a protein that has been altered from its native sequence, which can be confusing!!

These are just some conventions, which isn't documented very well and you just figure them out when reading a few papers but I would welcome any edits for a good source for protein change annotations.

EDIT:

Since as pointed by Alan Boyd response, MalE is an E. coli gene encoding Maltose Binding Proteins, then my answer will not apply for any protein AA changes as correctly pointed out and elaborated on in Alan Boyd response.


What is PDMS used for in microfluid models?

PDMS in fact is established to be a reliable material for cell culture in many microfluidic devices.
Here are several papers (Titles) including reviews on microfluidic devices using PDMS:

Microfluidic devices for cell cultivation and proliferation Here
Adhesion patterns in the microvasculature are dependent on bifurcation angle Here (Microvascular Research)
Advantages and challenges of microfluidic cell culture in polydimethylsiloxane devices Here
A physiological model of the tumor microenvironment for screening drug delivery systems Here (Cancer Research Proceedings)
A Novel Dynamic Neonatal Blood-Brain Barrier on a Chip Here (Plos One)
A novel microfluidic assay reveals a key role for protein kinase C δ in regulating human neutrophil–endothelium interaction Here(JLB - Journal of Leukocyte Biology)

My research at Temple University is actually based on a microfluidic device to study cell-cell interaction in a real-time fashion.
Majority of established protocols are using fibronectin or collagen, and in the case of tumor cells culture, matrigel for extracellular matrix. Devices are being coated with the ECM protein and then cells can be cultured in the device.

We have shown that in our microfluidic device, human umbilical vein endothelial cells (a.k.a. HUVECs) are forming a complete 3D lumen in the channels.

It is important to note that due to the elasticity of the PDMS, cells are needed to be under physiological flow conditions. Otherwise, it was shown that the cells start to detach from the PDMS. Under such physiological conditions (flow, media, gas exchange), cells can be alive and functional up to a week or two, depending on the design. In our system, the last two publications, cells are functional up to 2 weeks and 1 week respectively.


Do Archaea have membrane-bound organelles?

A) Archaea cells contain small membrane-enclosed organelles; bacteria do not.

FALSE. As you said, Archaea and Bacteria are prokaryotes: that don't have any nucleus nor membrane-bound organelles.

B) Archaea cells contain a membrane-bound nucleus; bacteria do not.

FALSE. See comment above.

C) DNA is present in both archaea cells and bacteria cells.

TRUE. Apart from some kind of viruses, all living organisms* have DNA as the support of their genome. It confirms that other choices are false.

D) DNA is present in the mitochondria of both bacteria and archaea cells.

FALSE. See comment for answer A: neither of them have mitochondria.

More info: Archaea on Wikipedia

(*) Viruses aren't always considered living organisms.


I've never heard of such a thing, and a quick Scholar search didn't yield anything significant. In fact, artificial radio waves are used in things that usually save lives, like MRIs.

If we were truly agnostic about this, we could say that it might or might not have an effect on human survival due to the general lack of evidence or even indication of a claim, but like the orbiting teacup, it's safe to assume that given our current extensive set of knowledge of biology, radiowaves do not affect human at all, and that as it has not been observed, the claim doesn't have a scientific basis.


What animal has fat with the highest energy density?

In both humans and animals, the body fat stores appear as triglycerides, which can be composed of different fatty acids, but they all have about 9 kilocalories per gram (USDA).

There can be different amounts of fat in different fat cells, so there can be slightly different amounts of fat in 100 grams of different types of fat tissue.

Calories in 100 g of fat from different animals:

Lard = 902
Beef tallow = 902
Chicken fat = 900
Turkey fat = 900
Goose fat = 900

The fat mentioned above was white fat, which appears as a single fat droplet in a fat cell. Humans and some animals, especially rodents and bats, also have different amounts of brown fat in which the fat cells contain a lot of mitochondria and the fat is present in multiple droplets, so, logically, brown fat tissue has lower energy density.


How do minute changes in an organism, as a result of evolution, get carried over to next generation

As populations expand, generation by generation, they will inevitably
  run into limits on resources. Not all individuals in a population are
  exactly alike as some will have traits that give them an advantage in
  survival. A change in any aspect of the environment can suddenly turn
  what had been just another variation or variant into either an
  advantage or a disadvantage  If a selective pressure (i.e. change in
  the environment), acts against or upon the differences between the
  individuals in a population, you get natural selection, which, through
  time, can cause a population to evolve

http://rmitchellbioanthro.weebly.com/uploads/2/3/7/6/23767919/natselinanutshell.pdf

Evolution consists of two essential things:

Random mutagenesis (in this case a slight change that occurs in the DNA, that causes a slight change in the protein to show up)

The second stage of evolution is natural selection. After the mutagenesis event, nature rigorously selects for the mutation. If the mutation has a fitness cost to the organism, it gets removed (the organism doesn't survive). By removing all things that are more costly than beneficial, nature selects for the fittest.

Take the examples of beetels here (http://evolution.berkeley.edu/evolibrary/article/evo_25)

Very rarely does the external environment directly change the DNA code (you can argue about epigenetics, but that's a different can of worms). Changes in the environment usually dictate the survival of organisms with different traits. In fact what usually happens is a change in the DNA code occurs naturally due to mutagenesis and that change undergoes the rigours of natural selection.

So in you case what might have happened is (I am postulating here, I would recommend a literature search to verify this), your bacteria had a tubular structure that it used to inject toxins in other cells. Some bacteria (due to genetic variation in sexual reproduction) had mutations that allowed it to move this tubular structure. This allowed it to survive more efficiently, and hence reproduce more. Eventually this population of bacteria, slowly replaced the bacteria who had no locomotor control on their "tube", and hence one stage of natural selection has occurred. Now this happens again and again, till the efficiency of the locomotion is optimal.

Might I suggest you read this book ?

Bonner, John Tyler. The evolution of complexity by means of natural selection. Princeton University Press, 1988.


Is there a known glucosepane cross-link breaker?

Unfortunately at this time, there are no known glucosepane breakers which can feasibly be used in a living organism.  There is a small (very small) amount of research being done on the topic by Yale university in cooperation with the SENS foundation, but the focus is extremely early stage - nothing more than synthesis and detection of artifical glucosepane and precursors.

It is a rather frustrating situation, as there are very good arguments indicating glucosepane as an almost universal 'bad thing that should be fixed', and the molecule itself isn't particularly complicated.  It seems that this would be a low effort/high reward research area.


Heterozygosity and the Wright-Fisher model

The following borrows from Gillespie, J.H., 1998. Population Genetics: A Concise Guide. The Johns Hopkins University Press. It is a good concise guide, and reduces to some extent the mathematics.

Theorem 1.3 is used to show the decay of heterozygosity in a population due to genetic drift.

Consider alleles in a population.  Two alleles drawn at random can differ by state, meaning they have two different DNA sequences. In other words, they are different alleles. Or the randomly drawn can have the same state, meaning they are the same allele. For alleles that are identical by state, they could differ by origin, meaning they are the same allele from two different chromosomes. The two alleles in a homozygous individual differ by origin (sampled from maternal and paternal homologs) but are identical by state.  Or, two identical alleles could differ by descent, meaning they are the same because they trace ultimately back to a common ancestor.

To calculate heterozygosity, you can first account for homozygosity, the frequencies of alleles that are identical by state. First consider two alleles identical by origin.  If you draw two alleles identical by origin when t=1, the probability that the two alleles are copies of same original allele (from the same chromosome) is

$$\frac{1}{2N}$$

because there was only a single copy of that allele on that one chromosome in the population prior to the round of mating, so it is 1 out of the 2N alleles at time point 0 ($t=0$).  The probability that two alleles identical by state are not identical by origin then is

$$1-\frac{1}{2N}.$$

Therefore, total homozygosity ($G'$) in the population (identical by state) after one round of random mating is

$$G' = \frac{1}{2N} + (1-\frac{1}{2N})G,$$

where $G$ is the homozygosity prior to the round of mating.  Of course, anything not homozygous is heterozygous. So, heterozyosity ($H$) is simply,

$$H=1-G.$$

By substituting the formula for $G$ into the above equation, the equation for $H$ becomes,

$$H' = 1-G' = (1-\frac{1}{2N})H$$

where $H$ is the heterozygosity prior to the round of mating.  This formula represents the change in heterozygosity after one round of random mating.  This can now be expanded for several rounds of random mating. For example, the change from $t=0$ to $t=1$ is

$$H_1 = (1-\frac{1}{2N})H_0.$$

The change from $t=1$ to $t=2$ is,

$$H_2 = (1-\frac{1}{2N})H_1$$

Therefore, the change in heterozygosity from $t=0$ to $t=2$ is

$$H_2 = (1-\frac{1}{2N})^2H_0.$$

This can be expanded to any time $t$ with the equation,

$$H_t = (1-\frac{1}{2N})^tH_0,$$

which you will recognize as Durrett's Theorem 1.3.

In short, in the Wright-Fisher model, two alleles that have a common ancestor are by definition identical by state and so cannot contribute to heterozygosity.

I hope this helps. I was a bit rushed and have not explained this often (mostly to myself in my mind) so if I can clarify something, please let me know.


If all animals were to die, would all plants die too?

Animals are not the only organisms to respire without photosynthesizing. Fungi, many other eukaryotes and many bacteria respire too (and do not photosynthesize).

Now, if all animals were to suddenly die, there would sure cause a drastic environmental change for plants. Whether or not that would lead all plants to extinction is untestable and it is therefore impossible to give a definite answer. This type of question would be better suited for worldbuilding.SE. I personally doubt all plants would disappear.


I said that there isn't enough information to tell since the parents genotypes are unknown.

It seems like you are misreading the diagrams since you say the parent's genotypes are unknown.  All 8 individuals in the two pedigrees have the same information given for each, appearing in the eight columns directly beneath the eight individual's symbols.


What are the known energy capturing processes in biological systems?

Apart from phototrophy, there is only chemotrophy (obtaining energy from redox reactions of chemical substances) and radiotrophy (obtaining energy from ionizing radiation such as gamma rays). However, radiotrophy as of now is only known to be a supplemental mode of energy and not a primary one.
Diversity is a central theme of evolution. It would be interesting if there was a single common mechanism for all modes of energy-nutrition which is perhaps true for the case of the chemiosmotic energy generating mechanism (ATP-synthase like systems which generate energy from chemical gradients). Otherwise, diversity is expected as the organisms evolve to survive in different environments.


No, this is not possible. There are a few reasons for that, but most important are that the only thing a mosquito injects is its own saliva, while the blood is sucked into the stomach where it is digested.

To be able to infect other people HIV would need to be able to leave the gut intact and then also be able to replicate in the mosquitos which it cannot do, due to the missing of the CD4 antigen on the surface of the insect cells. These are needed as a surface receptor for the virus to bind and enter the cells. This is also true for other blood sucking insects like bed bugs or fleas.

Other pathogens can do this, examples would be Yellow fever or Malaria. In Yellow fever the virus first infects epithelial cells of the gut, then enters the blood system of the insect to finally end up in the salivary glands, where the virus is injected together with the saliva into the biten person. In Malaria the pathogen is also able to leave the gut region and mature in the salivary glands.

HIV can only be transmitted through blood (either through direct transmission, operations etc.), through semen (cum), pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, and breast milk. See reference 3.

References:

Why Mosquitoes cannot transmit AIDS
Can we get AIDS from mosquito bites?
HIV Transmission Risk:  A Summary of Evidence


Well. Science is a funny thing compared to say the Koren, the Bible or any other religious text. As Scientist learn more, the narrative in Science will change. For instance, in the 1800, there were ideas that there was free following water on Mar... channels and ditches and such. In the 1960s, Mars was considered bone dry. No water ever. A desolate waste land. In the 1990s, Mar considered to have water, but only in the distant past 3 billion years ago. No water now. Then in the 2010s it is now considered to have subsurface water ice, that may occasionally turn into free flowing water under rare conditions. And worst yet, until recently... perhaps all those features of recent running water way have been caused by out gassing of CO2... Conflict over basic interpretation.

Now in that time, religion text, while silence on the matter of Mars, has not changed much if at all. Religious text has stayed the same.

So has Science been misleading the masses on Mars? Does Mars have water? Yes or No? Science keeps flip flopping.

In some ways yes, Science has been misleading the public. It has not been on target with a singular message, unlike say a religious text book, which has been delivering the same unchanging message for a thousand years or so.

So if you are looking for a consist message, well Science way not the thing for you. Science tends to tell different stories as scientist learn more, learn new techniques, re-evaluate ideas and generally fight with among themselves. The holy men Science like to review, rewrite their holy text rather often and fight. And the common man may find that dissatisfying and perhaps worrisome. If holy men keep changing the holy text, how will the common people worship? Is the Science real? Given it changes when the holy text of many world religions have not changed in centuries or even millennia.

So back to article... the percentage similarity of human to chimp genome changes as techniques improve. If you look at the actual age of the citations used in said article.. we run from papers in the 1970s, before genome sequencing was available, and the ideas of one gene-one protein was how Science thought DNA worked, and karyotyping and chromosome banding was about the only means to make large scale chromosome comparison... to papers in the  2014. Where we know DNA does more than just encodes proteins, and non DNA coding are not junk but can encode RNA with biochemical activity (gene regulation, transcription factor regulation etc). And whole human genomes can be sequenced for less than USD 1,400 when it originally cost USD 2.7 billion.

This is nearly 50 years of change and development. Going from the time before the internet and calculators were serious business machines worth thousands of dollars to a time you can have a a 1980s super computer as a wrist watch.

So yes... the message changes. Science progresses, techniques that could only be imagined by previous generations of scientist have become routine. We have learned more.. RNA isn't just a middle man between DNA and protein. One gene can give rise to many proteins.

Have the masses been mislead?

Scientist are telling the Masses information that is to the best of their knowledge. And if the current generation of scientist (2014 scientist) say the past generation (1970s scientist) had it wrong or not quite right.... If scientist right now disagree on the best matrix... is that misleading?

A science book is not as safe as a religious text. And one of the worst offenders is biology. A biology text book book from the 1980s looks very different from 2010s, even if they are from the same series. Is that misleading or is that scientific advancement?

PS: Common genes and sequence identity is not the same. There is a bit of confusion in the article. A cat and a human may share many many genes. But those shared genes may have sequence difference between them. So you can say humans and cat share 90% (made up example) of their gene (ie both cat and human have the PTEN gene) but have only 70% (made up example) sequence identity (ie there are several DNA difference between the human PTEN gene and the cat PTEN gene). It is easy to confuse the two.

Also are you only only considering gene coding DNA? Or are you also considering the non coding DNA (which until cheap genome sequencing in the 2010s was extremely difficult to capture and sequence)


Is hydroxyproline an amino acid? (Classification question)

The other commenter answered correctly that proline is an imminoacid, not an amminoacid. But in biochemistry it is referred to as amminoacid since it basically works like every other amminoacid in any polypeptyde.

  how much can you change an amino acid and still call it an amino acid?

Have a look at:

Selenocysteine
Ornitine

As you can see there are some weird modifications of amminoacids in biology. Just like proline/hydroxyproline any amminoacid can be very well modified and be used in proteinogenesis or non-proteinogenesis. Every modification of an amminoacid is allowed, and it will still be considered an amminoacid, even if it doesn't make up a protein. The only parts which can't be changed are the COO- and NH3+ groups, obviosuly, since they give the name of the molecule: "ammino" means that it has a NH group and "acid" means it has a COO- group.


Back dimples or Dimples of Venus are created by a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic.

Source and further reading: Kumar, Kanojia & Saili (2014) - Skin dimples


The '-' means that that allele has a single base deletion.


The WHO report "Global
 prevalence of
vitamin A deficiency
in populations
 at risk
1995–2005" (page 12 of 68) puts it like this:

  Where animal source or fortified foods are minimally consumed, dietary
  adequacy must rely heavily on foods providing beta-carotene. However,
  while nutritious in many ways, a diet with modest amounts of
  vegetables and fruits as the sole source of vitamin A may not deliver
  adequate amounts, based on an intestinal carotenoid-to-retinol
  conversion ratio of 12:1 (2)  This ratio reflects a conversion
  efficiency that is about half that previously thought, leading to
  greater appreciation for why VAD may coexist in cultures that heavily
  depend on vegetables and fruits as their sole or main dietary source
  of vitamin A.

  Usually, VAD develops in an environment of ecological, social and
  economical deprivation, in which a chronically deficient dietary
  intake of vitamin A coexists with severe infections, such as measles,
  and frequent infections causing diarrhoea and respiratory diseases
  that can lower intake through depressed appetite and absorption, and
  deplete body stores of vitamin A through excessive metabolism and
  excretion (3, 4). The consequent “synergism” can result in the body’s
  liver stores becoming depleted and peripheral tissue and serum retinol
  concentrations decreasing to deficient levels, raising the risks of
  xerophthalmia, further infection, other VADD and mortality.

Just as a side note: green leaves contain heaps of beta-carotenes as well!


When was the first exception to Mendelian genetics discovered?

I would say that first exception might be White gene in Drosophila Melanogaster, described in 1910 by Thomas Hunt Morgan and Lilian Vaughan Morgan. At least, is the first exception we study in genetics since sex linkage its so fundamental. These experiments established the chromosomal theory of inheritance.

Thomas Hunt Morgan, an embryologist who had turned to research in heredity, in 1907 began to extensively breed the common fruit fly, Drosophila melanogaster. He hoped to discover large-scale mutations that would represent the emergence of new species. As it turned out, Morgan confirmed Mendelian laws of inheritance and the hypothesis that genes are located on chromosomes. He thereby inaugurated classical experimental genetics.
After breeding millions of Drosophila in his laboratory at Columbia University, in 1910 Morgan noticed one fruit fly with a distinctive characteristic: white eyes instead of red. He isolated this specimen and mated it to an ordinary red-eyed fly. Although the first generation of 1,237 offspring was all red-eyed but for three, white-eyed flies appeared in larger numbers in the second generation. Surprisingly, all white-eyed flies were male.
These results were suggestive for hypotheses of which Morgan himself was skeptical. He was at the time critical of the Mendelian theory of inheritance, mistrusted aspects of chromosomal theory, and did not believe that Darwin's concept of natural selection could account for the emergence of new species. But Morgan's discoveries with white- and red-eyed flies led him to reconsider each of these hypotheses.
In particular, Morgan began to entertain the possibility that association of eye color and sex in fruit flies had a physical and mechanistic basis in the chromosomes. The shape of one of Drosophila's four chromosome pairs was thought to be distinctive for sex determination. Males invariably possess the XY chromosome pair (Morgan used a more cumbersome notation) while flies with the XX chromosome are female. If the factor for eye color was located exclusively on the X chromosome, Morgan realized, Mendelian rules for inheritance of dominant and recessive traits could apply.
In brief, Morgan had discovered that eye color in Drosophila expressed a sex-linked trait. All first-generation offspring of a mutant white-eyed male and a normal red-eyed female would have red eyes because every chromosome pair would contain at least one copy of the X chromosome with the dominant trait. But half the females from this union would now possess a copy of the white-eyed male's recessive X chromosome. This chromosome would be transmitted, on average, to one-half of second-generation offspring—one-half of which would be male. Thus, second-generation offspring would include one-quarter with white eyes—and all of these would be male.
Intensive work led Morgan to discover more mutant traits—some two dozen between 1911 and 1914. With evidence drawn from cytology he was able to refine Mendelian laws and combine them with the theory—first suggested by Theodor Boveri and Walter Sutton—that the chromosomes carry hereditary information. In 1915, Morgan and his colleagues published The Mechanism of Mendelian Heredity. Its major tenets:
• Discrete pairs of factors located on chromosomes like beads on a string bear hereditary information. These factors—Morgan would soon call them genes—segregate in germ cells and combine during reproduction, essentially as predicted by Mendelian laws. However:
• Certain characteristics are sex-linked—that is, occur together because they arise on the same chromosome that determines gender. More generally:
• Other characteristics are also sometimes associated because, as paired chromosomes separate during germ cell development, genes proximate to one another tend to remain together. But sometimes, as a mechanistic consequence of reproduction, this linkage between genes is broken, allowing for new combinations of traits.
Morgan's experimental and theoretical work inaugurated research in genetics and promoted a revolution in biology. Evidence he adduced from embryology and cell theory pointed the way toward a synthesis of genetics with evolutionary theory. Morgan himself explored aspects of these developments in later work, including Evolution and Genetics published in 1925, and The Theory of the Gene in 1926. He received the Nobel Prize in Physiology or Medicine in 1933.

quoted from: http://www.genomenewsnetwork.org/resources/timeline/1910_Morgan.php
see more: http://www.esp.org/foundations/genetics/classical/thm-10a.pdf


Can primary tumor cells grow in 2D culture?

Short answer: Yes, this is possible, it is the way most (cancer) cell lines have been generated.

Long answer: Culturing cells from tumor tissues is done in labs, especially, if you don't want to rely on the often very old cultures used in the labs. Many of these where started in the 1970s and are strange in many ways, e.g. contain many chromosomes multiple times. I have routinely isolated new cell lines from melanoma tissues (mostly metastases from different organs), but the general procedure is the same for other tumors as well.

To isolate cells from a tumor, you first wash the tumor sample to get rid of the blood. Then you cut down the tumors into small pieces using a scalpell, before adding a mix of enzymes like Collagenase, Dispase and Hyaluronidase to dissolve the tissue further in order to get a single cell solution. After the incubation with the enzymes the suspension is passed through a cell strainer to remove all remaining bigger cell aggregates and tissues residues and centrifuge the cells down. They are resuspended in an appropriate medium for the cell type and seeded to an appropriate plate/flask. For our samples this was typically either a 35mm plate (or a 6 well plate, which has the same area per well) or a T25 flask. Most cells from such isolations grow adherent, but sometimes you can observe cells, which do not adhere to the surfaces.

The procedure itself is not very complicated, but needs optimization. Depending on your tissue, the enzyme cocktail can be varied, as well as the length of incubation and the incubation time in this step. Then different plate/flask surfaces can play an important role, also the medium composition.

When we started doing this work in the lab, about 1 in 10 attempts was successfull, after optimization we went up to 6-7 of 10. What is important to take into account is, that the cells change during incubation and adapt to it. This means you need to question yourself, how good of a model they can be and need to be. If you need our detailed protocol, let me know, I can post it somewhere.


Are gametes determined by the sex of an organism?

The gametes produced by an organism are determined by the organism's sex - Thus, that statement from Wikipedia appears correct to me. In the case of humans, males have two different sex chromosomes. Thus, males produce gametes with either a Y-chromosome or an X-chromosome (XY). Female humans also have two sex chromosomes, but they are two different X chromosomes (XX). Thus, when females produce gametes they have a single copy of one of the X chromosomes in each gamete. In most cases, a fertilized embryo results and is either XX or XY - in the case of males the embryo gets the Y from Dad and the other sex chromosome is one of the two X's from Mom. In the case of a female the embryo gets the X chromosome from Dad and one of the two X's from Mom.

Here is an image describing what I said above with a link to the page to read more:

Here is a link from a basic genetics course from Dr. Young in the UK that has a more in-depth explanation.

Here is a link to another article from Nature Education that help explain how this works in humans as well as some other organisms that are slightly different.


Could you identify which species of ant is this queen?

Although absolutely no formal criteria are visible on your photo, the general shape of the ant, especially the wide elongated head and low thorax, is typical of the ant genus Camponotus.

See ref below:

  Bolton, B., Alpert, G., Ward, P. S., & Naskrecki, P. (2006). Bolton’s
  Catalogue of Ants of the World. Massachusetts, Harvard University
  Press (CD-ROM).