genetics - Expression of an ancestral gene

Your updated question is still very vague, but I'm going to assume it is basically: "Why would the ancestral version of a gene be mistaken for a more recent version than the modern gene?"

If this is incorrect, please let me know and modify your question to clarify.

The simple answer to that question is that the mutations that occurred after the Ancestral gene resulted in less apparent divergence than the LCA (last common ancestor), which would cause the Ancestral gene to seemingly have more polymorphisms - and the general assumption is that the more polymorphisms (mutations) that a gene has undergone, the more recent it is.

So let's say you have the following DNA sequences:

5' - AAAT - 3' = LCA (Template)

5' - AAAG - 3' = Sample 1 : # Differences = 1 Nucleotide

5' - AACG - 3' = Sample 2 : # Differences = 2 Nucleotides

The general assumption is that the larger the difference from the LCA, the more mutations have occurred over time. So, under the general assumption, Sample 2 is probably the most recent version of the sequence.

However, and this is what I think is the answer to your question, because mutations can occur in any order and at any place in the genome, it is entirely possible for the third (from left) Nucleotide to have followed this mutation path: A -> C -> A

That would make Sample 2 appear to be more recent than it is because it essentially mutated "back" to the LCA version of the gene, despite being a linearly older version than Sample 1. In this way, an Ancestral gene can be mistaken for a more recent evolution of a gene. This is also why genomic data is never as strong as when paired with fossil records or other corroborating data that also aligns with the genomic data's proposed timeline; though the odds of a mistake being made grow exponentially less as more of the genome is compared and analyzed.

With very recent mutations; on the scale of hundreds to thousands of years, it's sometimes necessary to analyze thousands of base pairs to calculate an adequately confident answer.

metabolism - What are the differences between white and brown adipose tissue?

Not sure what you are asking, except to add to the list?

Its worth mentioning that brown adipose tissue is the only organ in the human body whose primary purpose is to generate heat. We are warm blooded, but the body temperature is regulated by other organs generating heat while they do work (like muscles or I suppose the stomach, kidney, etc).

Brown Tissue is supposed to not a juvenile attribute - doesn't show up in adults to the same extent (usually being limited to neck and upper chest.

Brown Tissue is thought to be present in only critical areas of the body - even in infants. Its found in the inner body cavity around vital organs.

The color comes from the large number of mitochondria in the cells, which is where the heat is generated via uncoupling protein 1 (UCP1).

White adipose tissue is what we more commonly call fat tissue - its primary function is to store energy in the chemical form of long chain fats. Fat tissue as it grows can inhibit the function of insulin in the body, increasing insulin resistance.

You could almost call them 'good fat' and 'bad fat'

physiology - How do the lungs act as a sieve to trap blood clots?

Just as an intro...

The heart pumps deoxygenated blood from the right ventricle, through the pulmonary arteries (pic) which then eventually split into small capillary networks that surround the alveoli. The alveoli are formed by the trachea eventually branching off. So when you breathe in, the alveoli become filled with higher levels of oxygen.

The blood then becomes oxygenated and returns to the heart via the pulmonary veins to be pumped to the rest of the body.

The deoxygenated blood becomes oxygenated because there is a difference in oxygen and carbon dioxide concentration between the capillary network (O2 low / CO2 high) and the alveoli (O2 high / CO2 low) and so gas diffuses across because of the difference in concentrations (pic).

Physiology textbooks explain these mechanisms but for blood clots in particular, you'll need to check out a pathophysiology book.

Blood clots

When a blood clot travels to the lungs, it's referred to as a pulmonary embolus or PE.

Most of the time (90%), pulmonary emboli are formed in deep veins of the lower leg. These then travel to the pulmonary circulation system.

Large emboli block larger vessels - the pulmonary arteries and their branches. The smaller ones travel further into the network.

Patients can sometimes be asymptomatic and the emboli can at times resolve on its own. The extent of the severity of a PE is determined by:

• how much blood flow is obstructed;


• how long the embolus has been there; and


• presence other underlying lung or heart disease.

There are a number of things that a PE can cause physiologically.

Reduced Gas Exchange - alveolar dead space occurs when an alveolus is ventilated, but not perfused with blood. This, along with other factors, cause varying levels of hypoxemia (lack of oxygen).

Pulmonary Infarction - in a small amount of cases loss of blood flow to lung tissue can cause tissue death. This is fairly uncommon.

Right Ventricular Failure - if there is a large enough blockage (> 50 - 60%), the pressure in the pulmonary arteries increase. Subsequently, the load on the right ventricle is higher.
So in acute cases, the ventricle hasn't had time to adapt (hypertrophy) and so the right heart can fail.

At any rate, the haemodynamic balance can be disrupted when a PE is present.

In the elderly or people with underlying disease where their lung function is already decreased, PEs can have a significantly larger effect because they can't compensate. There are many more important points related to this but hopefully this is a useful (very) basic overview.

development - How do processes of one osteocyte establish contact with processes of the adjacent cells within the mineralized matrix?

Osteocytes attach to each other by cytoplasmic extensions through gap junctions [1]. The connections between these cells are formed since they were osteoblasts and osteoid-osteocytes (type II preosteocyte) [1]. Osteoblasts have a greater volume than osteocytes and the lack of extracellular matrix favors their adhesion. As they begin to synthesize extracellular matrix, their volume is reduced and this matrix takes space between cells, but with respect to the existent intercellular junctions around which matrix forms canaliculi.

"Osteoblast Organization" by Physio Muse - I drew this figure in drawperfect, printed to .pdf, and converted to .jpg
Previously published: Not published in any form, including not used on any website. Via Wikipedia.

Osteoblasts are connected via gap junctions mediated by connexin43 protein [2]. Mature osteocytes attach to the bone matrix by integrins (alphavbeta3) [3].

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References:

1. Wikipedia contributors, "Osteocyte," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Osteocyte&oldid=618657480 (accessed July 27, 2014).


2. Civitelli R. Cell-cell communication in the osteoblast/osteocyte lineage. Arch. Biochem. Biophys. 2008 May 15;473(2):188-92. doi: 10.1016/j.abb.2008.04.005. PubMed PMID: 18424255.


3. McNamara LM, Majeska RJ, Weinbaum S, Friedrich V, Schaffler MB. Attachment of osteocyte cell processes to the bone matrix. Anat Rec (Hoboken). 2009 Mar;292(3):355-63. doi: 10.1002/ar.20869. PubMed PMID: 19248169.

genetics - How does plant grafting work?

This article analyses the exchange of DNA during the process of grafting

Exchange of Genetic Material Between Cells in Plant Tissue Grafts - Stegemann and Bock, Science 2009

Quoting from the article:

Although the grafted tissues fuse and establish vascular connections,
the stock (the lower part of the graft) and scion (the upper part,
usually supplying solely aerial parts to the graft) are thought not to
exchange their genetic materials. But grafting (whether natural or
assisted) provides a path for horizontal gene transfer. Gene transfer
is confined to the graft site and no long-distance transfer may occur.
Analyzes indicating that large DNA pieces or even entire plastid
genomes are transferred. Only plastid genes may be transferred, no
transfer of nuclear genes occur. Plant cells are connected via
plasmatic bridges called plasmodesmata, but the passage of large
macromolecules requires the action of specific plasmodesmata-widening
proteins. Whether large DNA pieces or even entire organelles can
travel through plasmodesmata requires further investigation.

Finally, although our data demonstrate the exchange of genetic
material between grafted plants, they do not lend support to the tenet
of Lysenkoism that “graft hybridization” would be analogous to sexual
hybridization. Instead, our finding that gene transfer is restricted
to the contact zone between scion and stock indicates that the changes
can become heritable only via lateral shoot formation from the graft
site. However, there is some reported evidence for heritable
alterations induced by grafting and, in light of our findings,
these cases certainly warrant detailed molecular investigation.

Creating expression template from PCR: What annealing temperature to use?

I am creating a transcription template for expression in PURExpress and was confused about the annealing temperature to use.

I have two primers with the T7 promoter and an RBS on the forward primer and a termination sequence on the reverse primer. The melting temperature of these primers are 84.4 and 83.8 degrees C. The melting temperature of the regions that are complementary to the gene of interest I want to amplify by PCR are both about 65 degrees C.

What annealing temperature should I use a h? Since at the beginning of the PCR reaction I will have mostly template that will have the complementary sequences of the primers binding to the GOI and not the 5' and 3' extensions.

Has medical progress stopped human evolution?

Keep in mind that most people live in environments where antibiotics are of limited availability and hygiene is not as rigorous as in the "western" world. Combine this with high population densities and you get, if anything, more natural selection due to the spread/proliferation of pathogens and the subsequent mortality of the patient.
Also, don't confuse natural selection for evolution. Natural selection is one of only five causes of (micro-) evolution. Mutations will continue to occur. Sexual selection continues unabated, and migration is more important now than ever. The only evolutionary factor I'd argue is being diminished is genetic drift since there are so many people today.