a disarray of dreams, desires and aspirations ★

hey there, welcome to my personal space (◕‿◕✿)

✪ 20 year old Pakistani-American

✪ I blog about anything and everything I love, things I find interesting, and things of importance that I think need to be out there.

✪ Most posts on my blog will probably be related to football, Chelsea FC, cherry blossoms, psychology, biology, neuroscience, medicine, neuropsychology, science, neuropharmacology, animals, babies, veganism/vegetarianism, healthcare, nature, religion, food, South Korea, Japan, Michigan or the UAE.

Reblogged from deenoverduniya

punkgender:

one of the worst things about becoming educated on social issues is when people are like ‘you used to have a sense of humor’

no i used to have internalized prejudices which i’ve worked really hard to overcome and i realize now that your jokes are shitty

Reblogged from namkitten

(Source: designed-for-life)

Reblogged from colorsofmonochrome

vxpo:

Women and men should both know how to cook because neither feminism nor sexism are going to do shit for you when you’re hungry.

neurosciencestuff:

Discovery of New Drug Targets for Memory Impairment in Alzheimer’s Disease
We are now a step closer to having a drug that can cure dementia and memory loss. Research team in Korea has discovered that reactive astrocytes, which have been commonly observed in Alzheimer’s patients, aberrantly and abundantly produce the chief inhibitory neurotransmitter GABA and release it through the Best1 channel. The released GABA strongly inhibits neighboring neurons to cause impairment in synaptic transmission, plasticity and memory. This discovery will open a new chapter in the development of new drugs for treating such diseases.
Alzheimer’s disease, which is the most common cause of dementia, is fatal and currently, there is no cure. In Alzheimer’s disease, brain cells are damaged and destroyed, leading to devastating memory loss. It is reported that 1 in 8 Americans aged 65 or over have Alzheimer’s disease. In 2011, 7,600 elderly people with dementia lost their way back home and became homeless in Korea. However, to date, there has been no clear understanding of the mechanisms underlying dementia in Alzheimer’s disease. So far, neuronal death is the only proposed mechanism available in scientific literature.
The research team discovered that reactive astrocytes in the brains of Alzheimer’s disease model mice produce the inhibitory transmitter GABA by the enzyme Monoamine oxidase B(MAO-B) and release GABA through the Bestrophin-1 channel to suppress normal information flow during synaptic transmission. Based on this discovery, the team was able to reduce the production and release of GABA by inhibiting MAO-B or Bestrophin-1, and successfully ameliorate impairments in neuronal firing, synaptic transmission and memory in Alzheimer’s disease model mice.
In the behavioral test, the team used the fact that mice tend to prefer dark places. If a mouse experiences an electric shock in a dark place, it will remember this event and avoid dark places from then on. However, a mouse with modeled Alzheimer’s disease cannot remember if such shock is related to dark places and keeps going back to dark places. The team demonstrated that treating these mice with a MAO-B inhibitor fully recovered the mice’s memory. The selegiline is currently used in Parkinson’s disease as an adjunct therapy and considered as a one of best promising medicine for MAO-B inhibitor. But it has been previously shown to be less effective in Alzheimer’s disease.
The team proved that selegiline is effective for a short time, but when it is used in long term, it loses its efficacy in Alzheimer’s disease model mice. When treated for 1 week, selegiline brought the neuronal firing to a normal level. But when it was treated for 2 and 4 weeks, neuronal firing came back to the levels of untreated mice. From these results, the team proposed that there is a pressing need for a new drug that has long lasting effects.
Dr. C. Justin Lee said, “From this study, we reveal the novel mechanism of how Alzheimer’s patients might lose their memory. We also propose new therapeutic targets, which include GABA production and release mechanisms in reactive astrocytes for treatment of Alzheimer’s disease. Furthermore, we provide a stepping stone for the development of MAO-B inhibitors with long lasting efficacy.”

Reblogged from neurosciencestuff

neurosciencestuff:

Discovery of New Drug Targets for Memory Impairment in Alzheimer’s Disease

We are now a step closer to having a drug that can cure dementia and memory loss. Research team in Korea has discovered that reactive astrocytes, which have been commonly observed in Alzheimer’s patients, aberrantly and abundantly produce the chief inhibitory neurotransmitter GABA and release it through the Best1 channel. The released GABA strongly inhibits neighboring neurons to cause impairment in synaptic transmission, plasticity and memory. This discovery will open a new chapter in the development of new drugs for treating such diseases.

Alzheimer’s disease, which is the most common cause of dementia, is fatal and currently, there is no cure. In Alzheimer’s disease, brain cells are damaged and destroyed, leading to devastating memory loss. It is reported that 1 in 8 Americans aged 65 or over have Alzheimer’s disease. In 2011, 7,600 elderly people with dementia lost their way back home and became homeless in Korea. However, to date, there has been no clear understanding of the mechanisms underlying dementia in Alzheimer’s disease. So far, neuronal death is the only proposed mechanism available in scientific literature.

The research team discovered that reactive astrocytes in the brains of Alzheimer’s disease model mice produce the inhibitory transmitter GABA by the enzyme Monoamine oxidase B(MAO-B) and release GABA through the Bestrophin-1 channel to suppress normal information flow during synaptic transmission. Based on this discovery, the team was able to reduce the production and release of GABA by inhibiting MAO-B or Bestrophin-1, and successfully ameliorate impairments in neuronal firing, synaptic transmission and memory in Alzheimer’s disease model mice.

In the behavioral test, the team used the fact that mice tend to prefer dark places. If a mouse experiences an electric shock in a dark place, it will remember this event and avoid dark places from then on. However, a mouse with modeled Alzheimer’s disease cannot remember if such shock is related to dark places and keeps going back to dark places. The team demonstrated that treating these mice with a MAO-B inhibitor fully recovered the mice’s memory. The selegiline is currently used in Parkinson’s disease as an adjunct therapy and considered as a one of best promising medicine for MAO-B inhibitor. But it has been previously shown to be less effective in Alzheimer’s disease.

The team proved that selegiline is effective for a short time, but when it is used in long term, it loses its efficacy in Alzheimer’s disease model mice. When treated for 1 week, selegiline brought the neuronal firing to a normal level. But when it was treated for 2 and 4 weeks, neuronal firing came back to the levels of untreated mice. From these results, the team proposed that there is a pressing need for a new drug that has long lasting effects.

Dr. C. Justin Lee said, “From this study, we reveal the novel mechanism of how Alzheimer’s patients might lose their memory. We also propose new therapeutic targets, which include GABA production and release mechanisms in reactive astrocytes for treatment of Alzheimer’s disease. Furthermore, we provide a stepping stone for the development of MAO-B inhibitors with long lasting efficacy.”

Reblogged from itskillas

Reblogged from solitaryreflection

Reblogged from dysfunctionalmoment

thegreaterjihad:

Every time you find yourself missing someone, make dua’a for them. It’s the best way to show your love.

Reblogged from beeswaxing

mistermosher:

randomnessofskyler:

what they skylines In these cities would look like if there was no light pollution.

I legit want a world wide grid shutdown.

Reblogged from minspazz

(Source: divineopaque)

Reblogged from vuniqi

lawdhavemercy:

truth

(Source: readyokaygo)

Reblogged from kels-the-laugh

thorin-and-twerkteam:

emotional abuse is when someone does something to hurt you, and when you express your feelings, that you’re upset, they turn it around to be something you did to hurt them and they force you to apologize for it, and your feelings, like always, are rendered invalid and silenced, forever damaging the ability to trust others with your feelings because they always are used against you.

chocolateguru:

Whole Wheat Chocolate Chip Muffin

Reblogged from beroo4

chocolateguru:

Whole Wheat Chocolate Chip Muffin

Reblogged from secretariats

Reblogged from xavihernandes

cr-james:

The FIFA World Cup 2014 Statistics 

(Source: italynts)

Reblogged from myfaith-live-love-laugh