Reshared post from +Akinola Emmanuel

How do gut pathologies arise and why is our immune system unable to prevent it? I am happy to say that our lab at The University of Chicago believes that the answer is the abnormal activation of an ancient pathway and its effector protein Beta-Catenin.

The Wnt/Beta-Catenin pathway is highly evolutionarily conserved and has roles in everything from embryonic development to cel-cell communication. There's a good chance that if you look at any human cancers, the Wnt/Beta-Catenin pathway is negatively affected.

Our research, spearheaded by lead author Dr. Shilpa Keerthivasan, has shown that in patients with colitis or colon cancer, Beta-Catenin is highly expressed compared to healthy patients.

Incredibly, she worked out on the cellular level that this activation corrupts the function of T-cells that regulate the immune system (Tregs). Instead of suppressing the activation of the immune system, these Tregs instead cause inflammation. What makes matters worse is that the other T cells that become activated can no longer be shut down. In the gut, activation of T cells is fairly common because T cells are constantly coming in contact with bacteria (as can be seen in the image below). The gut has the highest concentration of immune cells so you can imagine that improper activation of these cells can have catastrophic effects. This is why it's really crucial to have normally functioning Tregs. Once these Tregs become corrupted, activation of the immune system spirals out of control. In fact, if you transfer these corrupted Tregs to healthy mice, they also develop gut inflammation.

These findings are huge because now we have a good idea as to how colitis and colon cancer can seemingly develop sporadically. The next step is finding out what activates this pathway in people. Don't worry, we're on it!

The press release (less jargon) can be found here: http://www.eurekalert.org/pub_releases/2014-02/uocm-bat022414.php
The article can be found here (unfortunately, it's behind a paywall) http://stm.sciencemag.org/content/6/225/225ra28.short?rss=1
Photo credits: http://scicasts.com/disease-processes/6438-location-in-the-body-where-immune-cells-reach-maturity-is-important-for-their-later-function/

#scienceeveryday  

How do gut pathologies arise and why is our immune system unable to prevent it? I am happy to say that our lab at The University of Chicago believes that the answer is the abnormal activation of an ancient pathway and its effector protein Beta-Catenin.

The Wnt/Beta-Catenin pathway is highly evolutionarily conserved and has roles in everything from embryonic development to cel-cell communication. There’s a good chance that if you look at any human cancers, the Wnt/Beta-Catenin pathway is negatively affected.

Our research, spearheaded by lead author Dr. Shilpa Keerthivasan, has shown that in patients with colitis or colon cancer, Beta-Catenin is highly expressed compared to healthy patients.

Incredibly, she worked out on the cellular level that this activation corrupts the function of T-cells that regulate the immune system (Tregs). Instead of suppressing the activation of the immune system, these Tregs instead cause inflammation. What makes matters worse is that the other T cells that become activated can no longer be shut down. In the gut, activation of T cells is fairly common because T cells are constantly coming in contact with bacteria (as can be seen in the image below). The gut has the highest concentration of immune cells so you can imagine that improper activation of these cells can have catastrophic effects. This is why it’s really crucial to have normally functioning Tregs. Once these Tregs become corrupted, activation of the immune system spirals out of control. In fact, if you transfer these corrupted Tregs to healthy mice, they also develop gut inflammation.

These findings are huge because now we have a good idea as to how colitis and colon cancer can seemingly develop sporadically. The next step is finding out what activates this pathway in people. Don’t worry, we’re on it!

The press release (less jargon) can be found here: http://www.eurekalert.org/pub_releases/2014-02/uocm-bat022414.php
The article can be found here (unfortunately, it’s behind a paywall) http://stm.sciencemag.org/content/6/225/225ra28.short?rss=1
Photo credits: http://scicasts.com/disease-processes/6438-location-in-the-body-where-immune-cells-reach-maturity-is-important-for-their-later-function/

#scienceeveryday  

Google+: View post on Google+

Reshared post from +Yonatan Zunger

Jupiter and the Sun are the two largest objects in our Solar System, and as they orbit around one another, they create regions where their gravity roughly cancels out. These are the Lagrangian points, created whenever two objects orbit one another: places where gravity is such that another small object can follow along in the orbit without being pulled in or out. And since things aren't getting pulled out of there, they get stuck in there as well: and so we have two large clumps of asteroids (and miscellaneous smaller space debris) in Jupiter's orbit. These are called the Trojan Asteroids; the group ahead of Jupiter is known as the Greek Camp, and the group behind it the Trojan Camp, with the asteroids in each camp being named after famous people in that war. Together, these two camps have as many asteroids as the Asteroid Belt.

Other stable patterns are possible, too: another one is what's called a 3:2 resonance pattern, asteroids whose motion gets confined to a basically triangular shape by the combined pull of Jupiter and the Sun. This group (for Jupiter) is called the Hilda Family, and their route forms a triangle with its three points at the two Lagrange points and at the point on Jupiter's orbit directly opposite it from the Sun. 

None of these orbits are perfectly stable, because each of these asteroids is subject to pulling from everything in the Solar System; as a result, an asteroid can shift from the Lagrange points to the Hilda family, and from the Hilda family to the Asteroid Belt (not shown), especially if it runs into something and changes its course. 

The reason that Pluto was demoted from planet to dwarf planet is that we realized that these things are not only numerous, but some of them are quite big. Some things we formerly called asteroids are actually bigger than Pluto, so the naming started to seem a little silly. So our Solar System has, in decreasing order of size, four gas giant planets (Jupiter, Saturn, Neptune and Uranus); four rocky planets (Earth, Venus, Mars, and Mercury); five officially recognized dwarf planets (Eris, Pluto, Haumea, Makemake, and Ceres); and a tremendous number of asteroids. (We suspect that there are actually about 100 dwarf planets, but the job of classifying what's an asteroid and what's actually a planet is still in progress — see the "dwarf planet" link below if you want to know the details)

Ceres orbits in the Asteroid Belt, about halfway between Mars and Jupiter, just inside the triangle of the Hilda Family; Pluto and Haumea are both in the distant Kuiper Belt, outside the orbit of Neptune but shepherded by its orbit in much the same way that the Hildas are shepherded by Jupiter; Makemake is what's called a "cubewano," living in the Kuiper Belt but unshepherded, orbiting independently; and Eris is part of the Scattered Disc, the even more distant objects whose orbits don't sit nicely in the plane of the Solar System at all, having been kicked out of that plane by (we believe) scattering off large bodies like Jupiter.

But mostly, I wanted to share this to show you how things orbit. This picture comes from the amazing archive at http://sajri.astronomy.cz/asteroidgroups/groups.htm, which has many other such pictures, and comes to me via +Max Rubenacker. 

More information about all of these things:
http://en.wikipedia.org/wiki/Lagrangian_point
http://en.wikipedia.org/wiki/Trojan_(astronomy)
http://en.wikipedia.org/wiki/Hilda_family
http://en.wikipedia.org/wiki/Dwarf_planet
http://en.wikipedia.org/wiki/Kuiper_belt
http://en.wikipedia.org/wiki/Scattered_disc

#ScienceEveryDay

Google+: Reshared 14 times
Google+: View post on Google+