Bad Study Habits To Leave In 2017

Jan 8 2018/ 1/100 days

Today was my first day back at school! I have lots of work to do already on my giant research project.It is also my first time using my bullet journal for school and I quite like it (although this weeks spread is messed up)

Can you believe it? [Twitter/Tolerance via @unofficially-nasa]

im the adoptive father of like 14 different kids because im the only out and proud trans dude at my school and all the lgbt underclassmen subconsciously flock to me

I hope I give off the vibe to all animals that I am their ally and friend

"Faggot"

STUDY STUDY STUDY- The Few Days Before Exams

My first exam (modern history) is Wednesday. Today is Sunday. For the past few days my life has been about study, study and more study. Here’s the best tips I can give you:

Start NOW

Flashcards are the best way to study- you learn while making them AND by revising

Mindmaps are also good for connecting ideas

And because they can be messy

You don’t have time to be neat and meticulous (though go ahead if it helps you)

My advice is to just make it legible enough for YOU

Remember, this is for you

Practice papers are your friend

But let’s be real, you probably don’t have time

So instead of essays do essay plans, for example

Or practice introductions, that’s useful too. It helps you come up with ideas

Take care of yourself, you’re obviously busy, but take breaks for meals at the very least

Start with the hard stuff and then do the easy stuff

For example, I have been revising history during the day and annotating books at night as part of my nighttime reading

Try and get enough sleep while you can

Don’t forget the big picture

Talk to friends & family if you’re feeling anxious

Aim for 100%- Know as much as you possibly can, even if you don’t expect to get 100

Learn the structure of your exams, it’s so much less daunting on the day

Utilise your teachers if you need them

Breathe, it’ll be okay

You got this

Don’t forget to prepare the materials you’ll need

And go ace those exams :)

things to do during winter break

- start bullet journaling

- binge watch different shows & movies

- start an exercise routine

- start learning a different language

- try cool & different restaurants

- write poems

- give yourself a makeover

- try to explore everyday

- catch up on sleep/ nap

- bake

- have a sleep over

- read a new book

- have multiple spa days

- try building a pillow fort

- clean your room

- shop for new clothes

- get a new piercing

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

Study identifies new brain death pathway in Alzheimer’s disease

Alzheimer’s disease tragically ravages the brains, memories and, ultimately, personalities of its victims. Now affecting 5 million Americans, Alzheimer’s disease is the sixth-leading cause of death in the U.S., and a cure for Alzheimer’s remains elusive, as the exact biological events that trigger it are still unknown.

In a new study, Arizona State University-Banner Health neuroscientist Salvatore Oddo and his colleagues from Phoenix’s Translational Genomics Research Institute (TGen) — as well as the University of California, Irvine, and Mount Sinai in New York — have identified a new way for brain cells to become fated to die during Alzheimer’s disease.

The research team has found the first evidence that the activation of a biological pathway called necroptosis, which causes neuronal loss, is closely linked with Alzheimer’s severity, cognitive decline and extreme loss of tissue and brain weight that are all advanced hallmarks of the disease.

“We anticipate that our findings will spur a new area of Alzheimer’s disease research focused on further detailing the role of necroptosis and developing new therapeutic strategies aimed at blocking it,” said Oddo, the lead author of this study, and scientist at the ASU-Banner Neurodegenerative Disease Research Center at the Biodesign Institute and associate professor in the School of Life Sciences.

The findings appear in the advanced online edition of Nature Neuroscience.

Necroptosis, which causes cells to burst from the inside out and die, is triggered by a triad of proteins. It has been shown to play a central role in multiple sclerosis and Lou Gehrig’s disease (amyotrophic lateral sclerosis, or ALS), and now for the first time, also in Alzheimer’s disease.

“There is no doubt that the brains of people with Alzheimer’s disease have fewer neurons,” said Oddo. “The brain is much smaller and weighs less; it shrinks because neurons are dying. That has been known for 100 years, but until now, the mechanism wasn’t understood.”

Links with Alzheimer’s

Necroptosis was first identified as a result of inflammation, a common malady in Alzheimer’s.

Three critical proteins are involved in the initiation of necroptosis, known as RIPK1, RIPK3 and MLKL. The study describes a key event in the process of necroptosis when RIPK1 and RIPK3 form a filamentous structure known as the necrosome.

The formation of the necrosome appears to jump-start the process of necroptosis. It activates MLKL, which affects the cell’s mitochondria, eventually leading to cell death.

Winnie Liang, TGen assistant professor, director of TGen Scientific Operations and director of TGen’s Collaborative Sequencing Center, said MLKL executes necroptosis to ultimately cause cell death.

“In this study, we show for the first time that necroptosis is activated in Alzheimer’s disease, providing a plausible mechanism underlying neuronal loss in this disorder,” said Liang, who contributed to the study’s gene expression analyses.

To explore necroptosis, the research team utilized multiple cohorts of human samples obtained from the Brain and Body Donation Program at the Banner Sun Health Research Institute and Mount Sinai VA Medical Center Brain Bank.

First, they measured RIPK1, RIPK3 and MLKL in a specific region of the brain that is typically ravaged by cell loss during the advance of Alzheimer’s disease — the temporal gyrus. Results showed that during necroptosis, these markers were increased in the brains of people with Alzheimer’s disease.

Next, they identified the molecular cascade of necroptosis activation, with RIPK1 activating RIPK3 by binding with it. This protein complex then binds to and activates MLKL. Analysis of mRNA and protein revealed elevated levels of both RIPK1 and MLKL in the postmortem brain tissues of patients with Alzheimer’s when compared with normal postmortem brains.  

Furthermore, they also demonstrated that necroptosis activation correlated with the protein tau. Intriguingly, necroptosis did not appear to be linked with the other chief physiological characteristic of Alzheimer’s pathology, beta-amyloid plaque.

Engines of decline

To assess the relationship between necroptotic protein levels and cognitive health, the study revisited the scores of patients whose postmortem brain tissue was evaluated for necroptosis. Results showed a significant association between RIPK1, MLKL and diminished scores on the Mini-Mental State Examination (MMSE), a widely used test measuring cognitive health.

Given the established relationship between necroptosis and Alzheimer’s pathology, including cell loss and attendant cognitive deficit, the study sought to inhibit the process to study the dynamic effects on cell death and memory loss.

With such experiments not possible in people, the team demonstrated in a mouse model of the disease that lowering the activation of the necroptosis pathway reduces cell loss and improves performance in memory-related tasks, offering new hope for human therapeutics to halt or reverse the effects of Alzheimer’s.

The results reveal that the inhibition of necroptosis activation through the blockage of RIPK1 prevents cell loss in mice. Compellingly, mice with inhibited activation of necroptosis pathways performed significantly better in tests of spatial memory involving navigation through a water maze.

New understanding, new hope

The study opens a new window on Alzheimer’s research and offers hope for therapies targeting cell loss in the brain, an inevitable and devastating outcome of Alzheimer’s progression.

Oddo stresses that RIPK1, RIPK3 and MLKL are among many potential drug targets, and others will likely follow as the links between necroptosis and Alzheimer’s become clearer. While multiple causes of the disease are likely, understanding more clearly all targets that trigger disease will offer the best hope since neuronal loss has been found in people more than a decade before any symptoms of dementia.

“One may not agree as to which molecules trigger Alzheimer’s disease, ” said Oddo, “but everybody agrees that the end result is the neuronal loss. If you can prevent that you may have a beneficial effect.”

🌿✨🧚🏼‍Lapiscat Giveaway 🧚🏼‍✨🌿

The giveaway includes: Red Jasper leather grimoire, Amethyst pendulum, Earth Power by Scott Cunningham, Ritual Loose Incense, Ritual Bath Soak, Tea drops (Citrus Ginger), Sage Smoke Cleansing set,Quartz formation, Labradorite, Rhodonite, Blue Quartz, Rose Quartz, Howlite

Rules for the giveaway:

Must be following me.

Must like and reblog this post.

Tag a friend for an extra entry

The winner will be announced March 30th, 2018!

each reblog counts as an entry, but do not spam your followers and flood their page with this post!