In my spare time, I enjoy picking up random books and drinking tea on my balcony. I am very quickly becoming a more studious person than I have ever been before in hopes to obtain the best possible chances for medical school.
I have had a very adverse personal history, but I've overcome many obstacles and have already come so far in life. I only hope that this increases with time and that I make an impact in the scientific field before I pass away.
For the Love of Knowledge.
A brief history of microscopy by i-heart-histo
c2000 BC
The Chinese use water microscopes made of a lens and a water filled tube to better visualize smaller objects.
1590
Hans Jansen and his son Zacharias Jansen invent the compound microscope.
1609
Galileo Galilei develops a compound microscope with a convex and concave lens. Calling it the occhiolino - the little eye.
1625
The term ‘microscope’ is coined by Giovanni Faber of Bamberg, an anology with the word ‘telescope’
1665
Robert Hooke publishes Micrographia and coins the word ‘cell’ after his examination of cork bark.
1674
Anton van Leuwenhoek develops the compound microscope to optimize it for observing biological specimens.
1860s
Ernst Abbe discovers the Abbe sine condition for manipulating the axis of optical systems to improving sharpess of images. This breakthrough in microscope design was exploited by microscope manufacturers Zeiss and Leitz resulting in a microscope boom.
1920
Olympus manufacture their first microscope - the Asahi.
1957
The Olympus DF Biological Microscope becomes the first microscope to feature an attached light source rather than a mirror that reflects light on the specimen.
1976
The popular CH series of Olympus microscopes appear in universities and colleges around the world. Chances are your college still uses these lab teaching scopes (or the slightly newer CH2 version).
1993
Introduction of a unique Y-shaped design for the microscope body for enhancing optics.
2004
Confocal and virtual microscopy are now common place.
(via scientificthought)
7313:
I’ve been staring at this for days. It’s beautiful.
I AM SCREAMING BUT IT IS ALSO REALLY FASCINATING AND KIND OF BEAUTIFUL.
look at those freaking amazing tendons! tendons of extensor digitorum.
beautiful.
(Source: ultrasadism, via a-freudian-slip-of-the-mind)
“Kiera Wilmot made an honest mistake, but the police were trying to throw away her life with a felony. After the community stood up for the girl, the charges were dropped, and she was allowed to move on with her life. Well, her greatness is really starting to shine, as she was recently granted several extraordinary opportunities through scholarship offers she has received.
Dr. Christopher Emdin, a professor of education at Columbia University, says that the schools are now very similar to prisons in terms of how they are structured, and how the inhabitants are treated. Kiera overcame her situation, but there are thousands of kids across the country who aren’t so lucky. Maybe it’s time to attack the system that is attacking us.
Check this out from Gawker:
“Kiera Wilmot, the 16-year-old honor student expelled from her high school after she allegedly ignited a chemical explosion on school property, received a full scholarship to the U.S. Space Academy, courtesy of a NASA veteran who, as a teenager, was accused of starting a forest fire during a science experiment.”
The lessons here are simple: Black kids have potential, and we can’t allow this system to destroy them. Also, hard work always pays off, especially when it comes to education. Dr. Boyce Watkins and Minister Louis Farrakhan recently held a forum called “Wealth, Education, Family and Community: A New Paradigm for Black America.” In the forum, Dr. Watkins and Min. Farrakhan both agree that African Americans are going to have to think differently when it comes to deciding what it means for your kids to be educated.”
Just when I feel like all hope is lost :) may she grow up to become another awesome woc scientist, we need more of those too.
(via fudgesmonkey)
Long exposure picture of a Lightning Bolt hitting a Tree!
holy shit
God dammit Azula
Look at those colours…
Is this Swanqueen magic I see before me?
(via saucybastards)
Fake forest converts sunlight into chemical energy
Mimicking photosynthesis, these nanowire trees absorb light to generate oxygen and hydrogen.
(via scientificthought)
Thymus Teaches Immune Cells to Tolerate Gut Bacteria
The thymus, the immune organ nestled near the heart, “educates” T-lymphocytes (T cells), which are critical cells of the adaptive immune system.
Researchers at the Center for Biotechnology and Genomic Medicine at the Medical College of Georgia at Georgia Regents University show that the regulatory T cells, or Tregs, teach the immune system to ignore the essential foreign bacteria in the gut that helps you digest and absorb food. Their study is published in the journal Nature.
When immune cells recognize essential gut bacteria as foreign, inflammatory bowel disease such as ulcerative colitis and Crohn’s disease can result.
(via numantinecitizen)
“Books are the perfect entertainment: no commercials, no batteries, hours of enjoyment for each dollar spent. What I wonder is why everybody doesn’t carry a book around for those inevitable dead spots in life.”
-Stephen King
I just can’t not reblog this
is that an aloe plant eating your face
(via infinitum-ultra)
Science and Space Posters by Ron Guyatt
Part of a series for spacevidcast.com to help inspire and spread the Good Word of Science! Prints available at etsy.
(via likeaphysicist)
This has been one rolled coaster of a week. I found out some pretty devastating news yesterday at work and could hardly keep my emotions in check to finish my shift, but I did it. Dinner with my aunt and uncle made things seem less scary, and today has followed up with news that a couple of my Australian friends are coming to America in September, so we’re going to meet up in NYC. I’m very excited to go on a mini vacation to reconnect with the place I miss the most in those people, and also to see my sister. I suppose we have to take the good with the bad.
Bright Explosion Seen on the Moon
For the past eight years, NASA astronomers have been monitoring the Moon for signs of explosions caused by meteoroids hitting the lunar surface. “Lunar meteor showers” have turned out to be more common than anyone expected, with hundreds of detectable impacts occurring every year.
They’ve just seen the biggest explosion in the history of the program. “On March 17, 2013, an object about the size of a small boulder hit the lunar surface in Mare Imbrium,” says Bill Cooke of NASA’s Meteoroid Environment Office. “It exploded in a flash nearly 10 times as bright as anything we’ve ever seen before.”
Read more: http://www.laboratoryequipment.com/videos/2013/05/bright-explosion-seen-moon
(via numantinecitizen)
▶ Reversing Obesity: http://is.gd/SpQwKM
▶ Stem Cell Cloning: http://is.gd/c9dVfC
▶ 3D-Printed Solar Panels: http://is.gd/PbD97i
▶ Brain Shocks: http://is.gd/6JnDAz
▶ Lunar Crash: http://is.gd/XoRoeS
▶ Bacterial Circuits: http://is.gd/hyEeSF
Science Days
▶ May 17, World Information Society Day
▶ May 18, World AIDS Vaccine Day
Scientists’ Birthdays
▶ May 13, 1857 - English pathologist, Ronald Ross
▶ May 14, 1686 - Daniel Gabriel Fahrenheit
▶ May 14, 1946 - Surgeon & inventor, Robert Jarvik
▶ May 15, 1859 - French Physicist, Pierre Curie
▶ May 16, 1950 - German Physicist, Johannes Bednorz
▶ May 17, 1940 - American Scientist, Alan Kay
▶ May 18, 1901 - Biochemist, Vincent du Vigneaud
Enlarge This Graphic : http://is.gd/RA5uDo
More Science Graphics On My Flickr Page : http://is.gd/kO94brStem cells: http://bit.ly/12vsvqh
Climate change: http://bit.ly/17RcMX9
Fungi: http://bit.ly/115CdeJ
Butterflies: http://bit.ly/12chvw6
Fossils: http://bit.ly/10OCG68
Depression: http://bit.ly/10dgnHh
(via numantinecitizen)
Teen’s invention could charge your phone in 20 seconds
(Photo: Intel)
Waiting hours for a cellphone to charge may become a thing of the past, thanks to an 18-year-old high-school student’s invention. She won a $50,000 prize Friday at an international science fair for creating an energy storage device that can be fully juiced in 20 to 30 seconds.
Everybody, remember this face.
Remember this name.
If this becomes a commonly used & highly lauded discovery, at some point a White guy is going to take credit, even if he has to word it like “Improved upon a previous…”
No no no
Fuck that guy.
Remember this brown girl.
Remeeeemmmmmberrrrr
(via fudgesmonkey)
Study finds that sleep apnea and Alzheimer’s are linked
A new study looking at sleep-disordered breathing (SDB) and markers for Alzheimer’s disease (AD) risk in cerebrospinal fluid (CSF) and neuroimaging adds to the growing body of research linking the two.
But this latest study also poses an interesting question: Could AD in its “preclinical stages” also lead to SDB and explain the increased prevalence of SDB in the elderly?
The study will be presented at the ATS 2013 International Conference.
“It’s really a chicken and egg story,” said Ricardo S. Osorio, MD, a research assistant professor at NYU School of Medicine who led the study. “Our study did not determine the direction of the causality, and, in fact, didn’t uncover a significant association between the two, until we broke out the data on lean and obese patients.”
When the researchers did consider body mass, they found that lean patients (defined as having a body mass index <25) with SDB did possess several specific and non-specific biomarkers of AD risk (increased P-Tau and T-Tau in CSF, hippocampal atrophy using structural MRI, and glucose hypometabolism using FDG-PET in several AD-vulnerable regions). Among obese patients (BMI >25), glucose hypometabolism was also found in the medial temporal lobe, but was not significant in other AD-vulnerable regions.
“We know that about 10 to 20 percent of middle-aged adults in the United States have SDB [defined as an apnea-hypopnea index greater than 5] and that the number jumps dramatically in those over the age of 65,” said Dr. Osorio, noting that studies put the percentage of people over the age of 65 with SDB between 30 and 60 percent. “We don’t know why it becomes so prevalent, but one factor may be that some of these patients are in the earliest preclinical stages of AD.”
According to Dr. Osorio, the biochemical harbingers of AD are present 15 to 20 years before any of its currently recognized symptoms become apparent.
The NYU study enrolled 68 cognitively normal elderly patients (mean age 71.4±5.6, range 64-87) who underwent two nights of home monitoring for SDB and were tested for at least one diagnostic indicator of AD. The researchers looked at P-Tau, T-Tau and Aβ42 in CSF, FDG-PET (to measure glucose metabolism), Pittsburgh compound B (PiB) PET to measure amyloid load, and/or structural MRI to measure hippocampal volume. Reduced glucose metabolism in AD-vulnerable regions, decreased hippocampal volume, changes in P-Tau, T-Tau and Aβ42, and increased binding of PiB-PET are recognized as markers of risk for AD and have been reported to be abnormal in healthy subjects before the disease onset.
Biomarkers for AD risk were found only among lean study participants with SDB. These patients showed a linear association between the severity of SDB and CSF levels of the biomarker P-Tau (F = 5.83, t=2.41, β=0.47; p< 0.05) and between SDB and glucose hypometabolism using FDG-PET, in the medial temporal lobe (F=6.34, t=-2.52, β=-0.57,p<0.05), the posterior cingulate cortex/precuneus (F=11.62, t=-3.41, β=-0.69, p<0.01) and a composite score of all AD-vulnerable regions (F=4.48, t=-2.11, β=-0.51, p<0.05). Lean SDB patients also showed smaller hippocampi when compared to lean controls (F=4.2, p<0.05), but no differences were found in measures of amyloid burden such as decreased Aβ42 in CSF or PiB positive scans.
Dr. Osorio and his colleagues are planning to test their hypothesis that very early stage preclinical AD brain injury that associates with these biomarkers can lead to SDB. They have proposed a two-year longitudinal study that would enroll 200 cognitively normal subjects, include AD biomarkers and treat those patients with moderate to severe SDB with continuous positive airway pressure, or CPAP, over time.
The purpose of the new study would be to determine the “direction” of causality between SDB and preclinical AD in elderly patients. After an initial assessment, the patients would be given CPAP to treat their sleep apnea. After six months, they would be evaluated again for biomarker evidence of AD.
“If the biomarkers change, it may indicate that SDB is causing AD,” explained Dr. Osorio. “If they don’t change, the probable conclusion is that these patients are going to develop AD with or without CPAP, and that AD may either be causing the apneas or may simply coexist with SDB as part of aging.”
Either way, Dr. Osorio believes the relationship between SDB and AD deserves further study.
“Sleep apnea skyrockets in the elderly, and this fact hasn’t been given the attention it deserves by the sleep world or the Alzheimer’s world,” Dr. Osorio said. “Sleep particularly suffers from an outmoded perception that it is an inactive physiological process, when, in reality, it is a very active part of the day for the brain.”





![neuromorphogenesis:
Study finds that sleep apnea and Alzheimer’s are linked
A new study looking at sleep-disordered breathing (SDB) and markers for Alzheimer’s disease (AD) risk in cerebrospinal fluid (CSF) and neuroimaging adds to the growing body of research linking the two.
But this latest study also poses an interesting question: Could AD in its “preclinical stages” also lead to SDB and explain the increased prevalence of SDB in the elderly?
The study will be presented at the ATS 2013 International Conference.
“It’s really a chicken and egg story,” said Ricardo S. Osorio, MD, a research assistant professor at NYU School of Medicine who led the study. “Our study did not determine the direction of the causality, and, in fact, didn’t uncover a significant association between the two, until we broke out the data on lean and obese patients.”
When the researchers did consider body mass, they found that lean patients (defined as having a body mass index <25) with SDB did possess several specific and non-specific biomarkers of AD risk (increased P-Tau and T-Tau in CSF, hippocampal atrophy using structural MRI, and glucose hypometabolism using FDG-PET in several AD-vulnerable regions). Among obese patients (BMI >25), glucose hypometabolism was also found in the medial temporal lobe, but was not significant in other AD-vulnerable regions.
“We know that about 10 to 20 percent of middle-aged adults in the United States have SDB [defined as an apnea-hypopnea index greater than 5] and that the number jumps dramatically in those over the age of 65,” said Dr. Osorio, noting that studies put the percentage of people over the age of 65 with SDB between 30 and 60 percent. “We don’t know why it becomes so prevalent, but one factor may be that some of these patients are in the earliest preclinical stages of AD.”
According to Dr. Osorio, the biochemical harbingers of AD are present 15 to 20 years before any of its currently recognized symptoms become apparent.
The NYU study enrolled 68 cognitively normal elderly patients (mean age 71.4±5.6, range 64-87) who underwent two nights of home monitoring for SDB and were tested for at least one diagnostic indicator of AD. The researchers looked at P-Tau, T-Tau and Aβ42 in CSF, FDG-PET (to measure glucose metabolism), Pittsburgh compound B (PiB) PET to measure amyloid load, and/or structural MRI to measure hippocampal volume. Reduced glucose metabolism in AD-vulnerable regions, decreased hippocampal volume, changes in P-Tau, T-Tau and Aβ42, and increased binding of PiB-PET are recognized as markers of risk for AD and have been reported to be abnormal in healthy subjects before the disease onset.
Biomarkers for AD risk were found only among lean study participants with SDB. These patients showed a linear association between the severity of SDB and CSF levels of the biomarker P-Tau (F = 5.83, t=2.41, β=0.47; p< 0.05) and between SDB and glucose hypometabolism using FDG-PET, in the medial temporal lobe (F=6.34, t=-2.52, β=-0.57,p<0.05), the posterior cingulate cortex/precuneus (F=11.62, t=-3.41, β=-0.69, p<0.01) and a composite score of all AD-vulnerable regions (F=4.48, t=-2.11, β=-0.51, p<0.05). Lean SDB patients also showed smaller hippocampi when compared to lean controls (F=4.2, p<0.05), but no differences were found in measures of amyloid burden such as decreased Aβ42 in CSF or PiB positive scans.
Dr. Osorio and his colleagues are planning to test their hypothesis that very early stage preclinical AD brain injury that associates with these biomarkers can lead to SDB. They have proposed a two-year longitudinal study that would enroll 200 cognitively normal subjects, include AD biomarkers and treat those patients with moderate to severe SDB with continuous positive airway pressure, or CPAP, over time.
The purpose of the new study would be to determine the “direction” of causality between SDB and preclinical AD in elderly patients. After an initial assessment, the patients would be given CPAP to treat their sleep apnea. After six months, they would be evaluated again for biomarker evidence of AD.
“If the biomarkers change, it may indicate that SDB is causing AD,” explained Dr. Osorio. “If they don’t change, the probable conclusion is that these patients are going to develop AD with or without CPAP, and that AD may either be causing the apneas or may simply coexist with SDB as part of aging.”
Either way, Dr. Osorio believes the relationship between SDB and AD deserves further study.
“Sleep apnea skyrockets in the elderly, and this fact hasn’t been given the attention it deserves by the sleep world or the Alzheimer’s world,” Dr. Osorio said. “Sleep particularly suffers from an outmoded perception that it is an inactive physiological process, when, in reality, it is a very active part of the day for the brain.”](http://25.media.tumblr.com/862b5766d9e5d3b53f61d08300959cca/tumblr_mn2si0EMgp1qhejy8o1_1280.jpg)