A high ranking employee for the Pennsylvania Department of Corrections went viral on social media Thursday after he posted a tweet suggesting "there is a genetic component to crime."

Bret Bucklen, the director for the DOC's Office of Research and Statistics, was engaged on May 1 in a political debate on Twitter that appears to have been based on the new Republican health care bill.

"There are those who are unfortunate. There are many more who made bad choices," Bucklen said. "Why can't liberals come to terms with that."

The debate took a turn, though, when Bucklen suggested crime was genetic.

One Twitter user responded, writing that "this could go toward a racist fallacy really quick and I hope it doesnt." To which Bucklen replied, "You doubt that there is a genetic component to crime?"

Race and crime have been scientifically linked with racists promoting the idea that Blacks and other ethnic minorities are genetically disposed to criminality, are less intelligent and lack work ethic to justify white superiority.

The ideas also go along with eugenics, a strain of thought from the early 20th century and adopted by the Nazi regime of Adolf Hltler that believed controlled breeding could improve the human race.

In recent years though, linking criminality and genetics has become more acceptable in science and a New York Times article from 2011 about it said researchers estimate about 100 studies showed a link between genes and crime.

But with nearly 2,000 retweets by Thursday afternoon, including one from new era civil rights activist Deray McKesson, Bucklen's comments were looked at through a racial lens by many social media users.

Secretary of Corrections John Wetzel noted the limits of social media in an email that was sent through a spokesperson to The Tribune.

"Complex subjects rarely are adequately defined in 140 characters," Wetzel said. "Department of Corrections employees have the right to freedom of expression on their personal social media accounts on their own time.

"With that being said, we recognize the sensitivity to a subject like this given the historic connotation of race in criminal justice policy," he added. "I have spoken to Dr. Bucklen, our Director of Planning, Research and Statistics, and that was not the intent of his remark and he should have used better judgment in his word choice and lack of context for his comments.

"That said," Wetzel said, "Dr. Bucklen has been a leader on my team in reducing biased and unjust policies in Pennsylvanias criminal justice system, including criminal justice reforms through the Justice Reinvestment Initiative and leading the fight against new mandatory minimums."

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Official's tweet causes flap in linking crime, genetics - The Philadelphia Tribune

Scientists from University College London and Imperial College London in the United Kingdom have identified new genetic locations that might make some people more prone to developing type 2 diabetes.

Type 2 diabetes affects hundreds of millions of people worldwide, and the numbers have skyrocketed in recent years. According to the World Health Organization (WHO), the number of people with diabetes has almost quadrupled in the past few decades, from 108 million in 1980 to 422 million in 2014.

In the United States, 29 million people currently have diabetes, and 86 million are thought to have prediabetes.

Until now, researchers were aware of 76 chromosomal locations, or "loci," that underlie this metabolic disease. However, new research analyzed the human genome further and found an additional 111.

The new study - published in the American Journal of Human Genetics - was co-led by Dr. Nikolas Maniatis of University College London's (UCL) Genetics, Evolution, and Environment department, together with Dr. Toby Andrew of Imperial College London's Department of Genomics of Common Disease.

Using a UCL-developed method of genetic mapping, Maniatis and team examined large samples of European and African American people, summarizing 5,800 cases of type 2 diabetes and almost 9,700 healthy controls.

They found that the new loci - together with the ones previously identified - control the expression of more than 266 genes surrounding the genetic location of the disease.

Most of the newly discovered loci were found outside of the coding regions of these genes, but within so-called hotspots that change the expression of these genes in body fat.

Of the newly identified 111 loci, 93 (or 84 percent) were found in both European and African American population samples.

After identifying genetic loci, the next step was to use deep sequence analysis to try to determine the genetic mutations responsible for the disease.

Maniatis and colleagues used deep sequencing to further examine three of the cross-population loci with the aim of identifying the genetic mutations. They then investigated a different sample of 94 Europeans with type 2 diabetes, as well as 94 healthy controls.

The researches found that the three loci coincided with chromosomal regions that regulate gene expression, contain epigenetic markers, and present genetic mutations that have been suggested to cause type 2 diabetes.

Dr. Winston Lau, of UCL's Genetics, Evolution, and Environment department, explains the significance of these findings:

"Our results mean that we can now target the remaining loci on the genetic maps with deep sequencing to try and find the causal mutations within them. We are also very excited that most of the identified disease loci appear to confer risk of disease in diverse populations such as African Americans, implying our findings are likely to be universally applicable and not just confined to Europeans."

Dr. Maniatis also highlights the contribution their study brings to the research community:

"No disease with a genetic predisposition has been more intensely investigated than type 2 diabetes. We have proven the benefits of gene mapping to identify hundreds of locations where causal mutations might be across many populations, including African Americans. This provides a larger number of characterized loci for scientists to study and will allow us to build a more detailed picture of the genetic architecture of type 2 diabetes," says the lead author.

Dr. Andrew also adds, "Before we can conduct the functional studies required in order to better understand the molecular basis of this disease, we first need to identify as many plausible candidate loci as possible. Genetic maps are key to this task, by integrating the cross-platform genomic data in a biologically meaningful way."

Learn how gene discovery could yield new treatments for type 2 diabetes.

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Scientists find new genetic locations for type 2 diabetes - Medical ... - Medical News Today

The lost function of two genes prevents infant laboratory mice from developing motor skills as they mature into adults, a new study from Cincinnati Childrens Hospital Medical Center and the City University of New York School of Medicine reports. Researchers also suggest in the study that people with certain motor development disabilities be tested to see if they have altered forms of the same genes.

The study demonstrates that neural circuits between the brains motor cortex region and the spinal cord did not properly reorganize in maturing mice. The circuits are part of the cortical spinal network, which coordinates the activation of muscles in limbs.

Researchers bred the mice to lack molecular signaling from the Bax/Bak genetic pathway. Investigators demonstrated in a variety of experiments how Bax/Baks downstream molecular targets are vital to developing appropriately sophisticated connections between the motor cortex, spinal circuits and opposing extensor/flexor muscle groups in the animals.

Lead author Yutaka Yoshida, PhD, of the Division of Developmental Biology at Cincinnati Childrens, said:

If mutations in the Bax/Bak pathway are found in human patients with developmental motor disabilities, these findings could be very translational to possible medical application. Our goal is for future studies to determine whether disruptions in Bax/Bak pathway are implicated in some people with skilled motor disabilities and whether it also regulates reorganization of other circuits in the mammalian central nervous system.

The researchers stress that because the study was conducted with mice, additional research is required before it can be confirmed whether the data apply directly to human health.

Young postnatal mammals, including human babies, can perform only basic unskilled motor tasks. Citing a number of previous studies on this point, the authors of the paper write one reason for this is that infantile neural circuitry is wired to activate antagonistic (or opposing) muscles at the same time.

As humans and mammals age beyond infancy, and try repeatedly to perform skilled movements, neural circuit connections between the motor cortex of the brain and spinal cord reorganize. Connections to the spine and to opposing muscle groups become more sophisticated.

This enables antagonistic muscle pairs to be activated reciprocally when certain tasks call for it.

An estimated six percent of children worldwide suffer from developmental motor disabilities that affect skilled motor control, according to Yoshida. A significant number of these individuals maintain an immature pattern of co-activating opposite muscle pairs into adulthood, which impedes skilled movements and manual dexterity.

One lifelong disorder is dyspraxia, also called developmental coordination disorder (DCD). According to the National Institute of Neurological Disorders and Stroke, developmental dyspraxia is characterized by an impaired ability to plan and carry out sensory and motor tasks.

People with the disorder may appear out of sync with their environment and symptoms can vary, including: poor balance and coordination, clumsiness, vision problems, perception difficulties, emotional and behavioral problems, difficulty with reading, writing, and speaking, poor social skills, poor posture, and poor short-term memory.

Although people with the disorder can be of average or above average intelligence, they may move their limbs immaturely.

To explore connections between corticospinal neurons in the mouse brains motor cortex and muscles and to identify genetic pathways involved in their development scientists in the study used trans-synaptic viral and electrophysiological assays. This allowed them to observe and trace how these connections develop in maturing mice.

Yoshida and colleagues point to earlier studies showing that the initial formation of prenatal motor circuits are determined genetically by the effects of transcription factors (which turn genes on and off in a cells control center, the nucleus). This control in turn triggers molecular processes that influence the development of never fibers, which transmit impulses.

Knowledge is limited about how initial motor circuits are reorganized after birth to become more sophisticated in adulthood. Even less is known about why this organization fails to occur as mammals mature, according to the researchers.

But trans-synaptic tracing in the current study highlighted how the presence of Bax/Bak signaling resulted in sophisticated circuity as mice matured. It also triggered the development of circuits that allowed opposing muscle groups to activate reciprocally.

The absence of Bax/Bak signaling resulted in continued formation of inappropriate circuitry that did not allow reciprocal activation of these muscles.

In skilled motor tests involving adult Bax/Bak mutant mice, the animals exhibited abnormal co-activation of opposing extensor and flexor muscle pairs. Although they demonstrated normal reaching and retrieval behaviors when given mouse chow, the mice had deficits in skilled grasping.

Mice lacking the Bax/Bak pathway signaling also had difficulty with walking tests on a balance bar and metal grid as measured by the number of foot slips.

Image: Cincinnati Childrens

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Genetics May Underlie Impaired Skilled Movements - ReliaWire

Its Star Wars Day, and thats got everyone celebrating the awesome lore and amazing detail of the Star Wars universe. So, lets talk about one question thats never really been explained: How exactly does the ability to use the Force get passed on in the Star Wars universe?

Helix, a personal genomics company, hastaken a closer look at that question. And theyve used science to come up with some possibleanswers

We have theorized that based on the lineage of the Skywalker-Solo clan, theres abundant evidence that Force-sensitivity is genetic. This is due to the similarity in traits between Skywalker family members raised in isolation from one another, and in totally separate environments (with the exception of Ben Solo who was raised with his mother and trained by his uncle). Luke and Leia grew up on entirely different planets. Neither knew their father (until later in life), and Leia was raised as galactic rebel royalty, whereas Luke was a simple moisture farmer bullseyeing womp rats in his T-16.

The experts at Helix have come up with a number of other fun science-y theories about how the Force is inherited in the Star Wars universe:

Its okay if you dont understand the genetics terminology. What this actually means is that the Force is a trait which parents pass on to their kids who pass them onto their kids. You see the trait in every single generation, just like the Skywalkerfamily.

Now, without getting too technical, this is a special type of genetic mutation which can have repeating effects. In some cases, repeat mutations can increase with each generation, and when the number of repeats exceeds a certain number, resulting traits can appear. So, for example, Shmi Skywalker may have had a repeat number just below the threshold, but it expanded in Anakin to the point where it appeared as if he had suddenly inherited the Force.

Of course, Star Wars is a fantasy and science doesnt necessarily apply, especially to things as mystical as the Force. But its fun to think about.

Want to know more?Read the full story on Helix.

Would you like to be part of the Fandom team? Join our Fan Contributor Program and share your voice on Fandom.com!

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How Do the Genetics of the Force Work in Star Wars? - Fandom (blog)

What happened

Shares of genetic-testing pioneer Myriad Genetics (NASDAQ: MYGN) received a much-needed boost today, rising as much as 16%, after the company announced fiscal third-quarter 2017 financial results. The stock has witnessed a 42% decline in the last year, although it is now up roughly 28% year to date, as investors see signs of life for the company's most important revenue machine and are holding out hope for a pipeline of promising growth products.

The strong performance in the most recent quarter prompted management to raise its full-year fiscal 2017 financial guidance for revenue and narrow the range for earnings per share. As of 12:45 p.m. EDT, the stock had settled to a 15.5% gain.

Image source: Getty Images.

There were reasons for optimism and pessimism in the financial update. Consider how the most important products fared compared to last year's fiscal third quarter:

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Hereditary-diagnostic-testing revenue

$140.8 million

$156.3 million

(10%)

GeneSight testing revenue

$23.9 million

N/A

N/A

Vectra DA testing revenue

$11.2 million

$12.3 million

(9%)

Prolaris testing revenue

$3.4 million

$5.2 million

(35%)

EndoPredict testing revenue

$2.3 million

$1.1 million

109%

Other revenue

$3.6 million

$2.5 million

44%

Data source: Myriad Genetics.

A 10% year-over-year drop in revenue from hereditary diagnostic testing may not seem like much reason to celebrate, but it marks the second consecutive sequential gain for Myriad Genetics after many quarters of decline. It's a silver lining investors aren't willing to overlook.

Of course, the array of promising growth products is turning in more mixed results. Products excluding GeneSight combined for a year-over-year drop in revenue of $1.7 million. In fact, if not for GeneSight, Myriad Genetics' total revenue would have declined. It's a major reason for the updated revenue guidance -- and investors should be happy to have GeneSight growing into a significant contributor to the overall business and performing well against offerings from competitors.

Metric

Fiscal Q3 2017

Fiscal Q3 2016

% Change

Total revenue

$196.9 million

$190.5 million

3%

Operating expenses

$139.7 million

$107.7 million

30%

Net income

$4.2 million

$34.5 million

(88%)

Data source: Myriad Genetics.

Efforts to rapidly scale new products and services have resulted in a large increase in operating expenses in recent quarters, eating away at net income. Last quarter was no different, but the increase in operating expenses is a necessary evil for investors looking for the company to turn the page long-term.

The company now expects full-year fiscal 2017 revenue to fall between $763 million and $765 million, compared to $754 million in fiscal 2016. Meanwhile, diluted earnings per share are expected to fall between $0.23 and $0.25, compared to $1.71 in fiscal 2016.

Investors are aware that Myriad Genetics is a company in transition, turning away from proprietary testing products (driven by price) and toward cheaper, larger-scale, and more flexible services such as GeneSight (driven by volume) that are in high demand from patients and clinicians. Viewed through that lens, there were no major surprises in the most recent quarter. The company continues to work toward its long-term goals.

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Here's Why Myriad Genetics Rose as Much as 16% This Morning - Madison.com