Honestly I Know Its Cool To Stay Up Late, But Sleep Is So Incredibly Important To Learning And Understanding

english essays would be way cooler if they’d teach us to be just, super critical of classic literature 

imagine if the standard teaching approach to essays was more along the lines of “here’s an outdated written work by a member of the ruling class of a society that was conspicuously more prejudiced than ours. use textual examples to demonstrate why it would be hella inappropriate and probably quite shitty to publish-glorify today.

Thank you so much for tagging me @studyingdayandnight

Things that make me happy are:

1. Listening to music

2. Rain in general

3. Learning about things that I find interesting

4. Working lights or management on a show

5. Drawing

Thank you all so much!!!!!

I'm tagging @studyign @studywithinspo @emmastudies @mattystudies @tbhstudying

Pass the happy! 💛 When you get this, reply with 5 things that make you happy and send this to the last 10 people in your notifications! 😊

Thank you!! So 5 things that make me happy…1.Reading 2Listening to music3.Going out with Family4.Talking/chatting with (online)/ rl friends5.(ridiculous but does make me happy) watching YOI or reading about it (Victuuri) very sweet can’t help itOk so for tagging here it is: @bujo-ie @lightbeanvibes @i-actually-study-a-lot @studyblr @interiorsthetic @elkstudies @nehrdist @notesworthtea @way-to-study @studydiaryofamedstudent

REBLOG IF YOU'RE A STUDYBLR.

I wanna see how many of us are there cx

Please support this project.

I reorganized my desk today!

[ 3 / 100 Days of Productivity ]

05.17.18 | 🎶 civil war - andy grammer

just finished with my biology honors symposium 😊 and i feel like i did really well. i just took some quick ( and unfinished ) spanish notes on the present progressive.

MoonAlchemy’s 2018 Beltane inspired Giveaway! 

This giveaway is in no affiliated with Tumblr. 

Hello, everyone! I have been waiting for the right time to begin this giveaway, and today is that day! I have collected some Beltane inspired items that are just begging to fin a place on someone’s altar. 

RULES: 

You MUST be following me.

Think of something you are grateful for in your life. (feel free to send it to me in a message, or tell someone you care about!)

Only reblogs count.

DO NOT tag as a giveaway.

Extra entry: Favorite my Etsy shop, or an item if you already do! (message me your username on here!)

No giveaway accounts, and please don’t spam your followers!

Only open to U.S. residents, sorry!

Winner chosen on April 25, 2018! 

What you can win:

Three chime candles (red, yellow and green)

One succulent tea light. 

One Quartz point.

One piece of Rose Quartz

One piece of natural Citrine

A super awesome full sized chalice

Faux Dahlias

Large Vials of Rosemary, Basil, and Rose Petals 

Handmade necklace with faux florals inside. 

One full Celtic Cross tarot card reading from me! 

Thank you for your continued support and have fun!

They can flip off this country all they want considering the fact it was theirs first.

you can like both humanities and STEM.

you don’t have to “pick a side” and completely discard the other field after choosing your major.

you can like both science and art, and none is better than the other.

Study identifies new target to preserve nerve function

Scientists in the Vollum Institute at OHSU have identified an enzyme that plays a crucial role in the degeneration of axons, the threadlike portions of a nerve cell that transmit signals within the nervous system. Axon loss occurs in all neurodegenerative diseases, so this discovery could open new pathways to treating or preventing a wide array of brain diseases.

The research team discovered a new role of the enzyme Axundead - or Axed - in promoting the self-destruction of axons. They found that when Axed function was blocked, injured axons not only maintained their integrity but remained capable of transmitting signals within the brain’s complex circuitry for weeks. Their research was published July 5 in the journal Neuron.

“If you target this pathway, you have a really good chance of preserving the functional aspects of neurons after a variety of types of trauma or injury,” said senior author Marc Freeman, Ph.D., director of the Vollum Institute at OHSU. “It’s a very attractive therapeutic target.”

Freeman conducted the work in the Department of Neurobiology at the University of Massachusetts Medical School. He has since been recruited to head the Vollum Institute, which conducts cutting-edge basic research into how the nervous system works at a molecular level.

Severing axons, or axotomy, is a simple way to study the molecular basis of neurodegeneration as it leads to the activation of explosive axonal degeneration. In the laboratory, researchers using this technique can identify pro-degenerative genes with great specificity, especially when using sophisticated genetic approaches in the fruit fly Drosophila, Freeman’s primary research model organism. Drosophila shares these same pathways with humans. Previous work by Freeman’s lab identified another enzyme, a gene called SARM, which was the first shown to activate a process that causes axons to disintegrate when damaged.

In the current study, Freeman and colleagues identified Axed, showed that it functions downstream of SARM to execute axonal degeneration, and, surprisingly, that the protection afforded by blocking Axed was even stronger than SARM.

“There was really nothing we could do to kill axons where Axed function was blocked,” Freeman said.

From an evolutionary perspective, Freeman said SARM and Axed function are likely important in the peripheral nervous system after injury because programmed axon death allows for efficient packaging of damaged cellular materials for removal by immune cells. This process thereby clears the pathway for new neuronal processes to regrow, reinnervate tissues, and recover function.

From a therapeutic perspective, the goal of the work is to understand at the molecular level how axons degenerate, and block those pathways in patients to preserve nervous system function. In many nervous system injuries axons are not severed but become stretched or crushed, which activates the SARM-dependent death program and drives axon loss. In those cases, it’s imperative to block SARM and Axed signaling to preserve axon integrity, and in turn neuronal function. At the same time, Freeman and others have shown that SARM-dependent signaling pathways also drive axon loss in neurodegenerative conditions including glaucoma, traumatic brain injury and peripheral neuropathy. This suggests the notion of an ancient and conserved axon death signaling pathway that is widely activated to drive axon loss. Since axon loss is a universal feature of neurodegenerative diseases, it seems likely that blocking this pathway could have enormous therapeutic benefit.

“If we can find ways to block it, maybe we can preserve function in a wide array of patients who have lost axons through neurodegenerative diseases or other neural trauma,” Freeman said.