FSU #39;s Jimbo Fisher Sheds Light on Jameis Winston Suspension
Jimbo Fisher addresses the media about how his team was able to persevere without their suspended quarterback in Florida State #39;s 23-17 win over #22 Clemson. SUBSCRIBE: http://bit.ly/Oqg3iE...
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By Dexter R. Matilla |Philippine Daily Inquirer
FEU Theater Guild PHOTOS BY DEXTER R. MATILLA
An exciting title that explores these characters is Moymoy Lulumboy: Ang Batang Aswang, by Segundo Matias Jr.
Launched during the 35th Manila International Book Fair recently by Lampara Publishing House Inc., Moymoy Lulumboy has the potential to be a popular series with the possibility of crossing over to film and on stage as proven by the Far Eastern University Theater Guild whose short performance of the storys prologue had guests clamoring for more.
Moymoy is from the world of the enchanted or Gabun but circumstances force the tibaro Montar to leave him as an infant in the care of a human named Tracy, who works as a bookstore staffer in a Makati mall. Montar says that the future of Gabun rests in the safety of the child and that he will be back to retrieve him when the time is right.
There will understandably be comparisons with a certain boy wizard from the West and Matias Jr. recognizes this. He says that it is one of his biggest obstacles when he was writing the storywhich was how to make it not similar to any preexisting text.
Its difficult he admits but any such similarities end there as Moymoy has much to learn about his past and future while embracing his role in Gabun, a once-peaceful place that has been cursed by the gods due to the actions of one greedy tibaro.
Illustrating the book is Jomike Tejido, an architect who finished his studies at University of Santo Tomas and who has done work as both writer and artist in almost 70 childrens books, including Tagu-Taguan (Best Reads 2010); Pundido (Golden Book 2002)l Ma-Me-Mi-Mumu!; Foldabots Toy Books; and the Jepoy Dyip series.
Jomike Tejido
Tejido is also a painter; his paintings on banig have been exhibited in solo shows in Manila and in group shows in Tokyo, Paris and US. Through his works, he aims to showcase the richness of Filipino culture. His banig paintings were featured in the Lampara book, Mabuting Pilipino, written by singer-songwriter Noel Cabangon.
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Moymoy Lulumboy sheds new light on the aswang
Mumbai, Sept 22:
The Sensex and the Nifty ended the session marginally in the green amid weak European cues.
The 30-share BSE index Sensex rose 116.32 points or 0.43 per cent at 27,206.74 and the 50-share NSE index Nifty gained 24.85 points or 0.31 per cent at 8,146.30.
Rajesh Agarwal, Head-Research, Eastern Financiers, in a report said: "Going forward, the Sensex earnings multiple at 17 times FY15 earnings looks a bit stretched, and investors would be better off being cautious as the near term upside looks a little difficult. Some reforms have taken place but the quantum of impact on the bottom-line of corporates needs to be seen. Hot money, lower crude prices, monsoon not turning out to be as bad as was earlier expected, are some of the factors that are driving the markets. While we believe that markets could witness correction in short-term, earnings expansion, government initiatives towards infrastructure and strengthening economic data, provide comfort on the medium-term. We strongly believe that the Governments pro-growth approach will aid the revival in the economy and would in turn boost equity markets."
Among BSE sectoral indices, consumer durables, FMCG, auto and oil & gas indices were the star-performers and were up 3.12 per cent, 1.9 per cent, 1.1 per cent and 0.88 per cent, respectively. On the other hand, metal index fell the most by 1.22 per cent, followed by healthcare 0.89 per cent and India infrastructure 0.87 per cent.
Tata Motors, ONGC, ITC, Hero MotoCorp and SBIN were the major Sensex gainers, while the major losers were Cipla, BHEL, Tata Steel, Hindalco and Infosys.
Concerns over a slowdown in China hammered stocks and commodities on Monday, while signs of differences between major economic powers on the need to stimulate growth further clouded the outlook.
Asian shares fell as investors worried a key measure of Chinese manufacturing, due on Tuesday, could indicate activity was contracting.
The slide was carried over into Europe, where fears over Chinese demand hit miners' shares. A further profit warning from British supermarket Tesco, whose shares fell 8 per cent, also took its toll.
Adding to the sense of gloom in markets, Group of 20 finance ministers and central bank chiefs meeting in Australia at the weekend said they were close to adding $2 trillion to the global economy, though there were signs of disagreement.
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Sensex sheds 167 points in early trade
Burlington, VT (PRWEB) September 22, 2014
Everyone is talking about Hillary Clinton. But who is Bernie Sanders the fist-pumping, Democratic Socialist Vermont senator who may challenge her in the Democratic primary? For more than four decades, the politician known simply as Bernie has often inspired, sometimes irritated and nearly always captivated Vermonters with his trademark economic populism and, yes, that Brooklyn accent.
As Sen. Sanders publicly weighs a 2016 presidential campaign, Americans will want to get to know him as well as Vermonters do. Thats why Seven Days Vermonts award-winning independent weekly has launched Bernie Beat (Berniebeat.com), a digital guide to Sanders colorful political career, from his eight years as mayor of the Peoples Republic of Burlington to that 8 12 hour speech against Bush-era tax rates on the floor of the Senate.
Seven Days dug up a treasure trove of mostly pre-digital resources including hard-hitting articles and original source video from more than 30 years of local Bernie-watching, to create a multimedia timeline that tells the real story of the outsider who would be president. The micro-site, which also features Bernie singing tunes from a long-forgotten 1987 album entitled We Shall Overcome, is a ready-made archive of inside information that is essential to understanding one of the nations most iconic public servants.
Find it at Berniebeat.com.
Independently owned Seven Days was founded in 1995. In 2013, Editor & Publisher selected it for inclusion in its annual feature 10 Newspapers That Do It Right.
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Bernie Beat Sheds Local Light on Sanders Vermont Roots
By Rick Nauert PhD Senior News Editor Reviewed by John M. Grohol, Psy.D. on September 22, 2014
New research suggests the quest to understand the mechanism by which Alzheimers disease impacts memory and cognition may be more complicated than previously understood.
University of Wisconsin researchers, including lead study author Sigan Hartley, Ph.D.,and Brad Christian, Ph.D., looked at the role of the brain protein amyloid-beta in adults living with Down syndrome, a genetic condition that leaves people more susceptible to developing Alzheimers.
As published in the journal Brain, their findings reveal more information about the earliest stages of the neurodegenerative disease.
Our hope is to better understand the role of this protein in memory and cognitive function, said Hartley.
With this information we hope to better understand the earliest stages in the development of this disease and gain information to guide prevention and treatment efforts.
However, the findings of their study not only may help scientists better understand the condition as it impacts those living with Down syndrome, but they are also relevant to adults without the genetic syndrome.
There are many unanswered questions about at what point amyloid-beta, together with other brain changes, begins to take a toll on memory and cognition and why certain individuals may be more resistant than others, says Hartley.
The University of Wisconsin, Madison scientists, along with collaborators at the University of Pittsburgh, studied 63 healthy adults with Down syndrome, aged 30 to 53, who did not exhibit clinical signs of Alzheimers or other forms of dementia.
They found that many adults with Down syndrome had high levels of amyloid-beta protein but did not suffer the expected negative consequences of the elevated protein.
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Speaking of the high cost of living in Manhattan, the Census Bureaus American Community Survey finds that the top 5 percent of households earned $864,394, or 88 times as much as the poorest 20 percent in NYC last year. The median income is up to $52,223 from $52,640, though still lower than the $55,307 from 2008. Non-Hispanic Whites have the highest median income at $75,145 and Hispanics have the lowest with $36,196.About 1.7 million New Yorkers live below the poverty line.
According toThe New York Times,the disparity is caused by the resurgence of the financial industry, with hedge funds and investment banks surging in the recovery after dipping low during the worst of the Great Recession.
At least we have a small decline in the poverty level, which was 14.5 percent in 2013, down from 15 percent. Still, those living at or below the poverty line is 45 million.For Hispanics nationwide, themedian income has gone up 3.5 percent in the last year.
A disproportionate number of African Americans nationwide live in poverty, however. There are so many in the Black population mired in poverty that getting out is incredibly difficult. And a third of all the poor are children. That increase in the median income for Hispanics has a big impact on the number of children in poverty as four in 10 are of Hispanic origin.
Nationwide, the media income is just under $52,000, about where it was in 2012 and eight percent lower than it was in 2008. The median income for women is $39,000 versus $50,000 for men. So women on average are making 78 percent of what men are.
Long story short, there are various kinds of income inequality in this country. And its time we try to tackle all of them.
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New Census Survey Sheds Light On Income & Poverty In The US
if you could read my mind - Two Sheds Jackson
from the album "memory lane"
By: twoshedsjacksonmusic
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if you could read my mind - Two Sheds Jackson - Video
gettin #39; high - Two Sheds Jackson
from the album "memory lane"
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gettin' high - Two Sheds Jackson - Video
Metal Sheds Rialto CA 92376 | 877-689-0730 Call Now! | Storage Sheds Outlet
For more on Metal Sheds visit- http://www.storageshedsoutlet.com or Call- 1-877-689-0730 Storage Sheds Outlet, leading providers of top quality outdoor stora...
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Newswise (SALT LAKE CITY)A new study by researchers at the University of Utah School of Medicine sheds light on a longstanding question about the role of mitochondria in debilitating and fatal motor neuron diseases and resulted in a new mouse model to study such illnesses.
Researchers led by Janet Shaw, Ph.D., professor of biochemistry, found that when healthy, functioning mitochondria was prevented from moving along axons nerve fibers that conduct electricity away from neurons mice developed symptoms of neurodegenerative diseases. In a study in the Proceedings of the National Academy of Sciences, Shaw and her research colleagues said their findings indicate that motor neuron diseases might result from poor distribution of mitochondria along the spinal cord and axons. First author Tammy T. Nguyen, is a student in the U medical schools M.D./Ph.D. program, which aims to produce physicians with outstanding clinical skills and rigorous scientific training to bridge the worlds of clinical medicine and basic research to improve health care.
Weve known for a long time of the link between mitochondrial function and distribution and neural disease, Shaw says. But we havent been able to tell if the defect occurs because mitochondria arent getting to the right place or because theyre not functioning correctly.
Mitochondria are organelles compartments contained inside cells that serve several functions, including making ATP, a nucleotide that cells convert into chemical energy to stay alive. For this reason mitochondria often are called cellular power plants. They also play a critical role in preventing too much calcium from building up in cells, which can cause apoptosis, or cell death.
For mitochondria to perform its functions, it must be distributed to cells throughout the body, which is accomplished with the help of small protein motors that transport the organelles along axons. For the motors to transport mitochondria, enzymes known as Mitochondrial Rho (Miro1) GTPases act to attach mitochondria to the motors. To study how the movement of mitochondria is related to motor neuron disease, Nguyen developed two mouse models in which the gene that makes Miro1 was knocked out. In one model, mice lacked Miro1 during the embryonic stage. A second model lacked the enzyme in the cerebral cortex, spinal cord and hippocampus.
The researchers observed that mice lacking Miro1 during the embryonic stage had motor neuron defects that prevented them from taking a single breath once born. After examining the mice, Nguyen, Shaw and their colleagues discovered that neurons required for breathing after birth were missing from the upper half of the mices brain stems. The phrenic nerve, also important for breathing, was not fully developed, either.
We believe the physical difficulties in the mice indicated there were motor neuron defects, Shaw says.
Conversely, the mice without Miro1 in their brain and spinal cord were fine at birth but soon developed signs of neurological problems, such as hunched spines, difficulty moving and clasping their hind paws together, and died around 35 days after birth. Those symptoms appeared similar to motor neuron disease, according to Shaw.
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Mouse Model Sheds Light Mitochondria's Role in Neurodegenerative Diseases