Researchers create ‘mini-brains’ in lab to study neurological diseases

Neurons (stock illustration).
Credit: © ktsdesign / Fotolia

Researchers at the Johns Hopkins Bloomberg School of Public Health say they have developed tiny “mini-brains” made up of many of the neurons and cells of the human brain — and even some of its functionality — and which can be replicated on a large scale.

The researchers say that the creation of these “mini-brains,” which will be discussed at the American Association for the Advancement of Science conference in Washington, DC on Feb. 12 at a press briefing and in a session on Feb. 13, could dramatically change how new drugs are tested for effectiveness and safety, taking the place of the hundreds of thousands of animals used for neurological scientific research in the United States. Performing research using these three-dimensional “mini-brains” — balls of brain cells that grow and form brain-like structures on their own over the course of eight weeks — should be superior to studying mice and rats because they are derived from human cells instead of rodents, they say.

“Ninety-five percent of drugs that look promising when tested in animal models fail once they are tested in humans at great expense of time and money,” says study leader Thomas Hartung, MD, PhD, the Doerenkamp-Zbinden Professor and Chair for Evidence-based Toxicology at the Bloomberg School. “While rodent models have been useful, we are not 150-pound rats. And even though we are not balls of cells either, you can often get much better information from these balls of cells than from rodents.

“We believe that the future of brain research will include less reliance on animals, more reliance on human, cell-based models.”

Hartung and his colleagues created the brains using what are known as induced pluripotent stem cells (iPSCs). These are adult cells that have been genetically reprogrammed to an embryonic stem cell-like state and then are stimulated to grow into brain cells. Cells from the skin of several healthy adults were used to create the mini-brains, but Hartung says that cells from people with certain genetic traits or certain diseases can be used to create brains to study various types of pharmaceuticals. He says the brains can be used to study Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and even autism. Projects to study viral infections, trauma and stroke have been started.

Hartung’s mini-brains are very small — at 350 micrometers in diameter, or about the size of the eye of a housefly, they are just visible to the human eye — and hundreds to thousands of exact copies can be produced in each batch. One hundred of them can grow easily in the same petri dish in the lab. After cultivating the mini-brains for about two months, the brains developed four types of neurons and two types of support cells: astrocytes and oligodendrocytes, the latter of which go on to create myelin, which insulates the neuron’s axons and allows them to communicate faster.

The researchers could watch the myelin developing and could see it begin to sheath the axons. The brains even showed spontaneous electrophysiological activity, which could be recorded with electrodes, similar to an electroencephalogram, also known as EEG. To test them, the researchers placed a mini-brain on an array of electrodes and listened to the spontaneous electrical communication of the neurons as test drugs were added.

“We don’t have the first brain model nor are we claiming to have the best one,” says Hartung, who also directs the School’s Center for Alternatives to Animal Testing.

“But this is the most standardized one. And when testing drugs, it is imperative that the cells being studied are as similar as possible to ensure the most comparable and accurate results.”

Hartung is applying for a patent for the mini-brains and is also developing a commercial entity called ORGANOME to produce them. He hopes production can begin in 2016. He says they are easily reproducible and hopes to see them used by scientists in as many labs as possible. “Only when we can have brain models like this in any lab at any time will we be able to replace animal testing on a large scale,” he says.

The work was supported by the National Institutes of Health’s National Center for Advancing Translational Sciences (U18TR000547), the Alternatives Research & Development Foundation and the Bart McLean Fund for Neuroimmunology Research/Project Restore.

Other researchers involved in the project include David Pamies; Paula Barreras, Katharina Block; Georgia Makri; Anupama Kumar; Daphne Wiersma; Lena Smirnova; Che Zang; Joseph Bressler; Kimberly M. Christian; Georgina Harris; Guo-li Ming; Cindy J. Berlincke; Kelly Kyro; Hongjun Song; Carlos Pardo; Thomas Hartung and Helena T. Hogberg.

[“source -cncb”]

Half the world to be short-sighted by 2050

Boy with glasses (stock image). The number with vision loss from high myopia is expected to increase seven-fold from 2000 to 2050, with myopia to become a leading cause of permanent blindness worldwide.
Credit: © gamelover / Fotolia

Half the world’s population (nearly 5 billion) will be short-sighted (myopic) by 2050, with up to one-fifth of them (1 billion) at a significantly increased risk of blindness if current trends continue, says a study published in the journal Ophthalmology.

The number with vision loss from high myopia is expected to increase seven-fold from 2000 to 2050, with myopia to become a leading cause of permanent blindness worldwide.

The rapid increase in the prevalence of myopia globally is attributed to, “environmental factors (nurture), principally lifestyle changes resulting from a combination of decreased time outdoors and increased near work activities, among other factors,” say the authors from Brien Holden Vision Institute, University of New South Wales Australia and Singapore Eye Research Institute.

The findings point to a major public health problem, with the authors suggesting that planning for comprehensive eye care services are needed to manage the rapid increase in high myopes (a five-fold increase from 2000), along with the development of treatments to control the progression of myopia and prevent people from becoming highly myopic.

“We also need to ensure our children receive a regular eye examination from an optometrist or ophthalmologist, preferably each year, so that preventative strategies can be employed if they are at risk,” said co-author Professor Kovin Naidoo, CEO of Brien Holden Vision Institute. “These strategies may include increased time outdoors and reduced time spent on near based activities including electronic devices that require constant focussing up close.

“Furthermore there are other options such as specially designed spectacle lenses and contact lenses or drug interventions but increased investment in research is needed to improve the efficacy and access of such interventions.”

Story Source:

The above post is reprinted from materials provided by Brien Holden Vision Institute. Note: Materials may be edited for content and length.

Journal Reference:

  1. Brien A. Holden, Timothy R. Fricke, David A. Wilson, Monica Jong, Kovin S. Naidoo, Padmaja Sankaridurg, Tien Y. Wong, Thomas J. Naduvilath, Serge Resnikoff. Global Prevalence of Myopia and High Myopia and Temporal Trends from 2000 through 2050. Ophthalmology, 2016; DOI:10.1016/j.ophtha.2016.01.006
  2. [“source -cncb”]

Obamacare is main roadblock to cancer ‘moonshot’

President Barack Obama has promised a “moonshot” to cure cancer, but the biggest obstacle to that goal could be his major healthcare achievement – The Patient Care and Affordable Care Act.

Obama said in his final State of the Union speech that vice presidentJoe Biden will push researchers to cure cancer within five years. It’s a worthy ambition. The American Cancer Society estimates that 1.69 million Americans will be diagnosed with cancer in 2016 and 596,000 U.S. people will die of it. Only heart disease kills more Americans.

President Barack Obama delivering the State of the Union address on January 12, 2016 in Washington.

Ricky Carioti | The Washington Post | Getty Images
President Barack Obama delivering the State of the Union address on January 12, 2016 in Washington.

There is, however, no single, silver bullet that will cure cancer. Cancer encompasses more than 200 diseases that are best cured by innovative precision medicine strategies.

The good news is that last year Obama embraced personalized medicine with a $215 million initiative. In his 2015 State of the Union speech, Obama announced “a new precision medicine initiative” that promises a “new era of medicine, one that delivers the right treatment at the right time, every time, to the right person.”

Unfortunately, the Affordable Care Act works against advancing personalized medicine to cure cancer because it forces doctors to employ one-size-fits-all, “evidence-based” generic therapies. That approach promotes interventions that may only be effective for patients similar to those in research studies – and that is the exact opposite of personalized medicine.

Precision medicine methods, beyond cancer therapies, include measuring unique biomarkers, and monitoring trends within an individual over time, taking into account genetics, lifestyle, and family history. Treatment models that have developed under The Affordable Care Act encourage significantly fewer tests. For instance, women who want mammograms before the age of 50 might have to pay more than before because of updated guidelines.

And genetic testing is permitted only for rare cases. The result is that the wealthy get the tests and treatments they need while middle and lower class Americans might only get the most basic of tests, which will not reveal the dangers already lurking in their body or in their genetics.

The modern war on cancer began in 1971 with President Richard Nixon’s National Cancer Act. Scientists embarked on two paths. The first approach was to identify and kill cancers; the second path was to better understand cancer at the genetic and molecular level.

Advances in understanding cancer, prompted Andrew von Eschenbach, then the director of the National Cancer Institute, to pledge in 2003 to “eliminate suffering and death from cancer by 2015.” His bold promise would only be realized through personalized medicine, he said.

“Genomics, proteomics, and emerging technologies are enabling us to profile not only diseases but the persons who bear those diseases. We can thus understand the genetic and molecular differences so that we can begin to personalize intervention strategies,” von Eschenbach said in a 2005 speech to the Center for Medical Progress.

[“source -cncb”]

All you need to know about the Maruti Suzuki Vitara Brezza

All you need to know about the Maruti Suzuki Vitara Brezza

The newly launched Vitara Brezza is quite a crucial product for Maruti Suzuki. We say crucial because it has been designed and developed in India using one of Suzuki’s global platforms and unlike Maruti’s previous launches (Read: S-Cross and Baleno) which are limited to the brand’s Nexa premium dealerships, the Brezza is available across Maruti’s entire dealer network.

The Vitara Brezza boasts of a bold new look, thanks to a high-riding stance, chunky chrome grille and ‘bull horn’ shaped LED lights along with the projector headlamps. The overall length and width are rated at 3995mm and 1790mm respectively while the 1640mm of height is commanding enough for a crossover. What’s unique to this car is the dual colour scheme with floating roof effect. The rear end, however, looks a bit flat in comparison though there are some nice looking bits in the form of the silver accents to the bumper and the taillights.

Besides the usual assortment of features including fog lights, alloy wheels, climate control and the lot, Maruti is offering unique shaped LED lights, a large touchscreen infotainment system and instrumentation with multiple themes as interesting features. Safety-wise, a driver’s side airbag is standard across all trims while dual airbags and ABS with EBD are available on higher trims.

The Vitara Brezza, as we know, is being offered only as a diesel vehicle. This means it gets the familiar 1.3-litre Fiat-sourced turbo diesel engine under the hood. In the DDiS 200 trim, this engine develops 89bhp of power at 4,000rpm and 200Nm of torque at 1750rpm. As for the gearbox, Maruti is offering a 5-speed unit which sends power to the front wheels. Now the power output may not impress everyone but the fuel efficiency certainly will. Maruti, in fact, is claiming a class-leading efficiency of 24.3kmpl.

The Vitara Brezza weighs in between 1170kg and 1195kg, depending on the trim. That makes it significantly lighter than the competition including the Ford EcoSport and the heavyweight i.e. Mahindra’s TUV300.

While the Vitara Brezza is being offered in single tone colours across most trim levels, the ZDI+ trim gets dual-tone paint with red-black, blue-white and yellow-white combinations.

Priced between Rs 6.99 lakh and Rs 9.68 lakh depending on the trim, the Vitara Brezza is noticeably cheaper than the competition and offers a lot of equipment. Add Maruti’s trusted after-sales support into the mix and this new addition could be the real game changer in the compact SUV segment.

[“source -cncb”]

‘Angry Birds’ maker Rovio to change CEO

Rovio, maker of hit mobile phone game Angry Birds, said on Wednesday chief executive Pekka Rantala would step down after just a year in the role, which included deep job cuts and restructuring at the Finnish company.

Rovio, which in October cut 213 jobs after forecasting falling profits for this year, said chief legal officer Kati Levoranta would take over as new CEO from the beginning of 2016.

More independence will be given to the company’s two main units, games and media. The media unit will be led by Mikael Hed, former Rovio CEO, while Wilhelm Taht, currently head of external products, will take the helm of the games business.

“We used to have a corporate model with centralized decisions, but that resulted into too slow reacting in very competitive markets,” chairman and main owner Kaj Hed told Reuters in an interview.

“As the CEO will not be so hands-on anymore, he (Rantala) felt that it wasn’t for him anymore.”

Hed also said an initial public offer was not currently on the agenda for Rovio, but added the European gaming industry needed to consolidate and that Rovio could play a role.

Angry Birds, launched in 2009, is the most downloaded mobile app of all time, and Rovio has capitalised on the brand by licensing its use on a string of consumer products.

But that business has recently slowed down, and now the company is pinning its hopes on an Angry Birds 3D movie, due for release in May 2016 and which the company believes will yield new licensing deals.

[“source -pcworld”]

New research clarifies how stem cells get activated to produce new hair

Stem cells residing in hair follicles are held in an inactive state for long periods of time. A new study shows that these quiescent periods are essential for maintaining the cells’ rejuvenating activity over time, and clarifies the mechanisms that bring the cells in and out of quiescence.

Hair follicle stem cells lacking the protein FOXC1 can only retain one old bulge in their hair follicles, while normal stem cells can keep up to four.
Credit: The Laboratory of Mammalian Cell Biology and Development at Rockefeller University/PNAS

Adult stem cells provide the body with a reservoir from which damaged or used up tissues can be replenished. In organs like the intestines and skin, which need constant rejuvenating, these stem cells are dividing frequently. But in other body structures, including the hair follicles, they are held in a quiescent state–one in which they don’t reproduce until they receive signals from their surroundings that it’s time to regenerate.

It makes intuitive sense that stem cells, being such a valuable resource, would be used sparingly. Yet scientists have limited understanding of how their quiescence is regulated, and are even unsure of its precise biological function. In a study published recently in PNAS, Elaine Fuchs, Rebecca C. Lancefield Professor and head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development, and Kenneth Lay, a graduate student in her lab, report on new insights into the biological signals that make hair follicle stem cells oscillate between states of quiescence and regenerative activity.

“In an earlier study, my lab showed that when mice age, the old fat in their skin produces higher levels of a secreted signal, called BMP,” Fuchs says. “This signal acts as a molecular brake on the hair follicle stem cells, causing them to spend much longer times in quiescence.”

In the present study, Lay identified a stem cell gene that is activated by BMP signaling, and showed that when this gene is missing, the stem cells grow hairs with dramatically shorter intervals. “We thought initially that the key to hair growth might be the fountain of youth,” Fuchs says, “but the mice’s hair coat surprisingly thinned and greyed precociously.”

More growth and fewer bulges

Usually the stem cells then create a new bulge along with the new hair, while ensuring that the old bulge and the old hair stay put in the hair follicle. Only the new bulge can make another new hair, but the old bulge is kept in place to maintain a thick and lush coat. In mice, hair follicles can accumulate up to four of these bulges.

When Lay and Fuchs created mice that lack FOXC1–by disabling or “knocking out” the gene that produces this protein–they observed that the animals’ hair follicle stem cells spent more time growing hairs and less time in quiescence. Over the course of nine months, while hair follicles from normal mice grew four new hairs, those from the FOXC1 knockout mice had already made new hairs seven times. “The knockout stem cells enter an overactive state in which they can’t establish quiescence adequately,” explains Lay.

The researchers also found that in the absence of FOXC1, hair follicles always had only one hair despite having made new hairs seven times. This is because these hair follicles could not retain their old bulges, though they generated a new bulge without a problem. As the stem cells started proliferating more, they became less able to stick together. As a result, their old bulges did not stay properly tethered to the hair follicle when the newly growing hair pushed past it. And since the bulge emits quiescence signals, its loss activated the remaining stem cells even faster.

Going grey and going bald

While the hair follicle stem cells of FOXC1-deficient mice produce hairs at a relatively breakneck pace, this profligate growth seems to wear them out. Older knockout mice had sparser, greyer coats, and they could not regenerate their fur as quickly as their normal age-matched or younger peers. A similar phenomenon has been described in mouse hematopoietic stem cells, which give rise to blood cells–those stem cells that are more active in young animals appear to become exhausted as the animals grow older.

“Hair follicle stem cells influence the behavior of melanocyte stem cells, which co-inhabit the bulge niche,” explains Fuchs. “Thus, when the numbers of hair follicle stem cells declined with age, so too did the numbers of melanocyte stem cells, resulting in premature greying of whatever hairs were left.” Not much is known about naturally occurring hair loss with age, but these balding knockout mice may provide a model to study it.

[“source -pcworld”]

Samsung Galaxy S7 camera to protrude just 0.8mm

Seasoned leakster OnLeaks has outed a couple of schemanics, which show that Samsung has made subtle changes to the back design of the Galaxy S7 compared to the Galaxy Note5. Both phones have slightly curved backs, but whereas the Galaxy Note5 sports curves only on the left and right sides, the Galaxy S7 will sport them from each side on every edge of the back.

Additionally, another schematics snapshot shows that the Galaxy S7 will have a camera bump, but not the same as the Galaxy S6. Samsung has tried to reduce the bump on the back and for the Galaxy S7 it’s believed to be 0.8mm compared to the 1.7mm of the Galaxy S6’s camera.

Yesterday, @evleaks leaked an alleged press photo of the Galaxy S7’s back.

Previous leaks have suggested the phone will have four versions: Galaxy S7, Galaxy S7 Plus, Galaxy S7 edge, and Galaxy S7 edge Plus. In terms of specifications, expect a choice between the Exynos 8890 and Snapdragon 820 chipsets. Other rumors point a brand new 12MP 1/2.0″ sensor.

Samsung will reveal the Galaxy S7 on Sunday, February 21 in Barcelona. That’s just a day before MWC 2016 officially kicks off.

[“source -pcworld”]

Three easy ways to paste plain text into Word

Formatting is easily one of the biggest annoyances when copying text from the web into a local document. That’s not a problem if you’re using a plain text editor like Sublime Text, but it becomes a big hassle in programs like Microsoft Word.

Here are several ways you can make sure you get plain text and not words in bold, italics, or a different font every time you paste text.

Word 2013 and 2016

If you’re running a newer version of Word, Microsoft offers a built-in solution to strip text of its original formatting. When you right-click to add text to your document you’ll see three options: paste with the formatting from the source, paste with the formatting of your document, and paste in plain text only.

The last option is the easiest to use, but if you want to keep hyperlinks, bold, or italics choose the merge formatting option so it blends in with your document’s text.

To set your paste options so it automatically pastes plain text only click on File > Options > Advanced, and then under the Cut, copy, and paste subheading choose the paste options you want.

Browser add-ons

Copy Plain Text 2 add-on for Firefox

Another option is to have your text automatically stripped from the site through the magic of web browser extensions. Firefox users can try Copy Plain Text 2. Once it’s downloaded and installed typeabout:addons in the URL bar.

Find the entry for the add-on and click Options. Under Behavior, check the box that says “Make as default Copy action.” That way everything you copy will be automatically stripped of text.

Google Chrome users can try Copy as plain text. Unlike the Firefox option which works behind the scenes, this browser extension adds a new option

Copy as plain text

to the context menu for copying in plain text as pictured here.

[“source -pcworld”]

Study examines intent of glaucoma patients to use marijuana for treatment in a city with legalized medical use

A survey of patients with glaucoma in Washington, D.C., showed that the perception of the legality and acceptability of marijuana use was significantly associated with intentions to use marijuana for the treatment of glaucoma, even though research has indicated it is of limited benefit, according to a study published online by JAMA Ophthalmology.

It is estimated that 2.2 million adults in the United States are affected by glaucoma. Alternative therapies are being explored but have not shown promise, including marijuana. Previous research has shown several limitations associated with its use as a treatment for glaucoma. Driven mainly by public support, 21 states and the District of Columbia have legalized the medical use of marijuana, citing mainly the 1999 Institute of Medicine report that found possible therapeutic benefits for the use of marijuana in various debilitating medical conditions, including glaucoma. Given these legal changes, glaucoma physicians are approached with patient inquiries about treatment of their glaucoma with this alternative therapy.

David A. Belyea, M.D., M.B.A., of the George Washington University School of Medicine and Health Sciences, Washington, D.C., and colleagues examined factors associated with intentions by patients to use marijuana as a treatment for glaucoma. The study included a survey of patients with glaucoma or suspected to have glaucoma at a clinic in Washington, D.C., between February and July 2013. The survey assessed demographics, perceived severity of glaucoma, prior knowledge about marijuana use in glaucoma, past marijuana use, perceptions toward marijuana use (legality, systemic adverse effects, safety and effectiveness, and false beliefs), satisfaction with current glaucoma management, relevance of treatment costs, and intentions to use marijuana for glaucoma.

Of the 334 patients who were invited to participate in the study, 204 (61 percent) completed the survey. Analysis of responses indicated that perceptions of legality of marijuana use, false beliefs regarding marijuana, satisfaction with current glaucoma care, and relevance of marijuana and glaucoma treatment costs were significantly associated with intentions to use marijuana for glaucoma treatment.

“This study contributes to filling the gap in our knowledge about patients’ perceptions toward using marijuana for glaucoma and their intentions to seek this therapeutic alternative. Understanding these intentions will become even more important as states continue to legalize marijuana for recreational use (currently Washington, D.C., and 4 other states), as patients with glaucoma will then have access to marijuana without the need for a physician to prescribe this drug,” the authors write.

“Our findings suggest a need for more education on this topic to protect patients with glaucoma against the increased acceptability among the public toward using marijuana based on false perceptions of its therapeutic value in glaucoma therapy”

Commentary: Shaping Patients’ Perspective of Medical Marijuana for Glaucoma Treatment

Belyea and colleagues have identified an intricate web of factors that influence the perception held by patients with glaucoma about medical marijuana, write Eve J. Higginbotham, S.M., M.D., of the University of Pennsylvania, Philadelphia, and Lenora A. Higginbotham, M.D., of Johns Hopkins Hospital, Baltimore, in an accompanying commentary.

“Altering this complex web of beliefs, misconceptions, satisfaction, and discontent requires an equally intricate patient-centered approach if physicians who treat patients with glaucoma are to effectively influence patient perception and transcend the clash between scientific evidence and popular culture.”


An Introduction to Apoptosis

In normal tissues there is a balance between the generation of new cells via cell division and the loss of cells via cell death. Old cells become damaged over time and are eliminated.  This is an essential form of renewal.  Examples include shedding of skin cells and the replacement of the cells lining our digestive tract.  Like cell division, cell death is also tightly controlled.   Cells frequently die by a process termed programmed cell death or apoptosis. (1) Apoptosis is the cellular equivalent of a “self destruct” button.

Apoptosis is a very orderly process during which the genome of the cell is broken down, the cell is fragmented into smaller pieces and the debris is consumed by nearby cells (phagocytes) that clean up the cell fragments. Besides getting rid of damaged, potentially dangerous cells, apoptosis is crucial for embryological development and neurologic pruning. The term “apoptosis” comes from the Greek words apo (from) and ptosis (falling) and it was used to describe leaves falling from a tree. (2)

There are two distinct phases in apoptosis, the initiation phase and the execution phase. The initiation phase involves many different proteins and it is quite complex. It is started by various “stresses” from either outside the cell (extracellular) or inside the cell (intracellular). (3) Some examples of extracellular signals that trigger apoptosis include loss of growth factors, low oxygen levels (hypoxia), and radiation. Intracellular signals include DNA damage, the damage caused by chemotherapydrugs, telomere malfunction, and infection with viruses. The initiation phase triggers the execution phase.  The execution phase involves the activation of specialized enzymes (caspases and others) that directly result in cell death. (3)

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References for this page:

  1. Vo TT, Letai A. BH3-only proteins and their effects on cancer. Adv Exp Med Biol. 2010;687:49-63. [PUBMED]
  2. Wong RS. Apoptosis in cancer: from pathogenesis to treatment. J Exp Clin Cancer Res. 2011 Sep 26;30:87 [PUBMED]
  3. Bender T, Martinou JC. Where killers meet–permeabilization of the outer mitochondrial membrane during apoptosis. Cold Spring Harb Perspect Biol. 2013 Jan 1;5(1):a011106 [PUBMED]
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