Dear Abby: Hospital patient receives surprise anatomy lesson – Bloomington Pantagraph (blog)

Dear Abby: I recently had to spend a night in the hospital following minor surgery. One of the female techs taking care of me leaned over me to straighten out the bedding and I could see "everything" when the top of her scrubs fell open.

I'm not sure if it was on purpose or by accident. I say this because after the first time, it happened several more times. I only looked the first time out of shock. The other times, I looked away.

Other than saying, "Hey, lady, I can see your boobies when you bend over," what's the polite way to say, "Oops wardrobe malfunction"? GOT AN EYEFUL IN ILLINOIS

Dear Got An Eyeful: Since, with luck, you won't have to make another visit to the hospital, I think your question may be moot. However, the discreet way to deal with something like that would be to mention what happened to the head nurse or supervisor and say that it made you uncomfortable.

Dear Abby: I'm in my early 30s and recently met a very attractive woman my age. We are planning to get married. She wants us to be married as soon as possible because she has been divorced for the last seven years.

My problem is, she's extremely secretive about her past, especially the period between her divorce and our meeting. I have been open with her about my past, but when I ask about hers, she refuses to discuss it and says it has nothing to do with our relationship.

I have a feeling there may be something nasty she's hiding. I'm afraid I'm heading into a trap, but my love for her makes it tough to consider breaking up. Am I being too demanding? CONCERNED GUY IN THE SOUTH

Dear Concerned Guy: If your intuition is screaming that your girlfriend's desire for a hasty marriage could spell trouble in the future, you should pay close attention to it. It is not "too demanding" to want to know what one's fiancee has been doing for the last seven years. Under no circumstances should you marry this woman without first talking to a lawyer, who I am sure will suggest doing a background check and/or drafting an ironclad prenuptial agreement.

Dear Abby: I recently attended a bridal shower for my nephew's fiancee. My sister-in-law (the future mother-in-law of the bride) also attended the shower. She did not choose any gifts from the bride's registry, but decided instead to give the bride lingerie, including thong underwear. Frankly, I was shocked. I didn't think it was appropriate for either the mother or the future mother-in-law to give such intimate gifts. Am I wrong? FLUMMOXED IN FLORIDA

Dear Flummoxed: Shower guests are not restricted to items based solely upon the couple's registry. They can give whatever gift they wish to the bride and groom. Your sister-in-law chose something she thought the bride and groom would enjoy. Please try to be less judgmental and hope she was right.

Dear Abby is written by Abigail Van Buren, also known as Jeanne Phillips, and was founded by her mother, Pauline Phillips. Contact Dear Abby at http://www.DearAbby.com or P.O. Box 69440, Los Angeles, CA 90069.

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Dear Abby: Hospital patient receives surprise anatomy lesson - Bloomington Pantagraph (blog)

Anatomy of epic fail on rail offered – Maui News

In early May, on the day our Legislature adjourned, one of the newspapers summarized our Legislatures work on the Honolulu transit surcharge extension as Epic Fail on Rail. With the Federal Highway Administration poised to pull out its $1.5 billion commitment if no funding solution is firmed up, our legislators need to get their collective act together if they want to help the project get back on track.

How did we get to be in this spot? This week well retrace Senate Bill 1183 and its tortuous history through our legislative labyrinth.

SB 1183, like its companion House Bill 1442, was a six-page bill to extend permanently the current rail surcharge on general excise tax. The bill also proposed to give an unspecified percentage of the surcharge proceeds to the state Department of Transportation. The other counties were given the option to adopt their own GET surcharge beginning in 2018.

The first committees to work on the bill, the Senate committees on Transportation and Energy and Public Safety, Intergovernmental, and Military Affairs, came up with a 78-page monster containing two parts, one that would extend the surcharge permanently and another that would extend it to the year 2032. (Yes, these conflict with each other.)

Other sections of the bill would establish a tax credit for low-income taxpayers, raise the base GET rate to 4.5 percent for everyone (the surcharge would be on top of that) and contained a pages-long laundry list of mandates to the city. At the time, the Senate transportation chair explained that she wanted to keep all options open.

The Senate Ways and Means Committee took a very different tack. Its 10-page version basically said, Well take away the states 10 percent skim off the surcharge, but no extension; youre on your own. That draft unanimously passed the full Senate and went over to the House.

There, the House Transportation Committee kept the bill alive by putting blanks in it its draft extended the tax to an unspecified date, reinstated the skim but replaced the percentage with a blank percent to recover the states costs and a blank percent that would go the DOT for state highway projects.

The House Finance Committee then filled in the blanks, extending the tax for two years, and dropping the skim to 1 percent, none of which would be earmarked for the DOT.

This version went to the Conference Committee, and then surprising things started happening. First, the Senate proposed a new draft, radically different from the version that passed the Senate, which extended the surcharge for 10 years and raised the skim to 20 percent. The House came back with a draft that left the GET surcharge untouched, dropped the skim to 1 percent, and raised the hotel room tax from 9.25 percent to a hefty 12 percent.

The latter proposal, though innovative, caught the hotel industry unaware, prompting vigorous objections. Then-Senate money chair Jill Tokuda agreed to that version with tweaks a few hours later, thereby making the Final Decking deadline.

After frantic meetings through the weekend, the money chairs, apparently with some members of the hotel industry, reached a compromise involving a shorter GET extension and a lower TAT hike. Amendments were introduced on the chamber floors to implement the agreement, although another version with only a GET extension and no TAT increase, which Honolulu Mayor Kirk Caldwell supported, was circulating in the Senate. The House passed one version and jettisoned its speaker, while the Senate adopted the other version and deposed Tokuda as chair. With no agreement between the chambers, neither version can be enacted. That is where we are now.

We now seem to have a bunch of rudderless ships in the harbor banging into each other. Could the governor have brought both sides together? Was Senate President Ronald Kouchi capable of herding the 25 senators? And how about former Speaker Joe Souki, new Speaker Scott Saiki or House money chair Sylvia Luke? To what or whom should we be looking for leadership to get us out of this mess?

* Tom Yamachika is president of the Tax Foundation of Hawaii.

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Anatomy of epic fail on rail offered - Maui News

Why Fake News Goes Viral: Science Explains – Live Science

People's limited attention spans, plus the sheer overloadof information on social media may combine to make fake news and hoaxes go viral, according to a new study.

Understanding why and how fake news spreads may one day help researchers develop tools to combat its spread, the researchers said.

For example, the new research points toward curbing the use of social bots computer programs that automatically generate messages such as tweets that inundate social media with low-quality information to prevent the spread of misinformation, the researchers said. [Our Favorite Urban Legends Debunked]

However, "Detecting social bots is a very challenging task," said study co-author Filippo Menczer, a professor of informatics and computer science at the Indiana University School of Informatics and Computing.

Previous research has shown that some of people's cognitive processes may help to perpetuate the spread of misinformation such as fake news and hoaxes, according to the study, published today (June 26) in the journal Nature Human Behavior. For example, people tend to show "confirmation bias" and pay attention to and share only the information that is in line with their beliefs, while discarding information that is not in line with their beliefs. Studies show that people do this even if the information that confirms their beliefs is false.

In the new study, the researchers looked at some other potential mechanisms that may be at play in spreading misinformation. The researchers developed a computer model of meme sharing to see how individual attention and the information load that social media users are exposed to affect the popularity of low-quality versus high-quality memes. The researchers considered memes to be of higher quality if they were more original, had beautiful photos or made a claim that was true.

The investigators found that low- and high-quality memes were equally likely to be shared because social media users' attention is finite and people are simply too overloaded with information to be able to discriminate between low- and high-quality memes. This finding explains why poor-quality information such as fake news is still likely to spread despite its low quality, the researchers said.

One way to help people better discriminate between low- and high-quality information on social media would be to reduce the extent of information load that they are exposed to, the researchers said. One key way to do so could involve decreasing the volume of social media posts created by social bots that amplify information that is often false and misleading, Menczer said.

Social bots can act as followers on social media sites like Twitter, or they can be run as fake social media accounts that have their own followers. The bots can imitate human behavior online and generate their own online personas that can in turn influence real, human users of social media. [25 Medical Myths that Just Won't Go Away]

"Huge numbers" of these bots can be managed via special software, Menczer said.

"Ifsocialmedia platforms were able to detect and suspend deceptive socialbots there would be less low-quality information in the system to crowd out high-quality information," he told Live Science.

However, both detecting and suspending such bots is challenging, he said. Although machine-learning systems for detecting social bots exist, these systems are not always accurate. Socialmedia platforms have to be conservative when using such systems, because the cost of a false positive error in other words, suspending a legitimate account is generally much higher than that of missing abot, Menczer said.

More research is needed to design fast and more accurate social bot detection systems, he said.

Originally published on Live Science.

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Why Fake News Goes Viral: Science Explains - Live Science

W(h)ither the Humanities? – HuffPost

Review of Cents and Sensibility: What Economics Can Learn From the Humanities. By Gary Saul Morson and Morton Schapiro. Princeton University Press. 307 pp. $29.95

Although they make lots of mistakes, economists are in demand. By contrast, the humanities are in deep trouble. In 2014, President Obama opined that folks can make a lot more with skilled manufacturing or the trades than they might with an art history degree. A year later, Jeb Bush acknowledged that liberal arts is a great thing, only to remind potential philosophy majors to realize youre going to be working at Chick fil-A.

More and more college students seem to agree. In the late 1960s, almost twenty percent of recipients of bachelors degrees majored in in a humanities discipline; in 2010, the figure was 8 percent. Little wonder that many taxpayers and state legislators have concluded that philosophy, literature, linguistics, history, art history, anthropology, and gender studies are luxuries we can no longer afford.

In Cents and Sensibility, Gary Morson, a professor of Slavic languages and literature at Northwestern University, and Morton Schapiro, a professor of economics and the president of Northwestern, maintain that humanistic disciplines contribute essential ingredients (the role of contingency and context and the limitations of abstract one-size-fits-all models) to studies of human behavior and the complex challenges of our time. In this book, Morson and Schapiro identify concrete ways in which economists studying higher education, the family, and the development of poor countries can benefit from three fundamental humanistic capabilities: an appreciation of people as inherently cultural; stories as an essential form of explanation; and ethics in all its irreducible complexity.

Cents and Sensibility offers one argument, among many, on behalf of the humanities. Their argument is often, but not always persuasive. That said, the authors call for a dialogue between economists and humanists is welcome. Their indictment of humanists for being spectacularly inept and clueless in making the case for their disciplines is urgently necessary. As is their claim that quantitative rigor and focus on policy can and should be supplemented with the empathy, judgment and wisdom that defines the humanities at their best.

The authors use fresh and fascinating examples to bolster the oft-repeated claim that ethical considerations should be incorporated into the analysis of economists and policy makers. To bolster the standing of their institutions in the highly influential national rankings of colleges and institutions, Morson and Schapiro point out, some administrators cross ethical lines. To increase the yield (the percentage of accepted students who matriculate), they reject excellent students who they have reason to believe will go elsewhere. They count students who send in a postcard expressing interest (but dont submit essays and recommendations) as applicants. They ignore the standardized test scores of international students in English, but include scores in mathematics. They cook the books about the percentage of alumni who make an annual gift to their alma mater. Worst of all, Morson and Schapiro report that rating agencies do not fact-check the data provided by colleges and universities.

Cents and Sensibility also documents the failure of rational choice and behavioral economists and psychologists to consider the culture, traditions, and values of the people they are investigating. Although cultural evidence cannot be quantified, Morson and Schapiro show how it helps explain why such a small percentage of African-American students with high grade point averages and test scores do not attend selective colleges and universities (even when they are offered financial aid).

While acknowledging that income and family backgrounds are important variables in predicting decisions about marriage, divorce, and family planning, the authors make a compelling case that social and cultural context matters as well.

In important respects, Cents and Sensibility reminds us of the capaciousness of the humanities. A recent study, the authors reveal, found that readers of fiction did better on tests measuring empathy, social perception, and emotional intelligence. One reason, Morson and Schapiro suggest, is that fiction, more than real life, connects inner states to outward behavior, and encourages intimacy between characters and readers.

In other ways, however, Cents and Sensibility provides a rather narrow view of the humanities. Although Morson and Schapiro put culture front and center, they barely mention the discipline of history. They limit their discussion of literature to realistic novels. They do not emphasize sufficiently the unique capacity of the humanities to teach students how to analyze texts, conduct research, and write clear and persuasive essays.

Despite these caveats, Cents and Sensibility sends a powerful and timely message. The humanities, the authors conclude, if humanists will only believe in them, have a critical role to play in education, nurturing in students of all ages truths about human beings other disciplines have not attained, a respect for diverse points of view, culture, and ethics, and an escape from the prison house of self, limitations of time and place.

The humanities are in danger. Americans inside and outside the academy need to act before its too late.

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W(h)ither the Humanities? - HuffPost

Siri Needs Her Own Personal Assistant – TheStreet.com

Apple Inc (AAPL) is searching for a "Siri Event Maven" to help its digital personal assistant keep track of holidays, events and pop culture trending with people.

As Apple prepares to launch the HomePod laterthis year, it's focusing on improving Siri's understanding and strategic awareness.As of yesterday, the company is looking for a full time employee to help Siri keep track of social media trends, culture and human behavior as the Siri Event Maven.

The company said the new hire will work with engineers, analysts and designers to "provide strategic awareness of cultural happenings in the collective zeitgeist" and assist in developing responses for Siri to events original creators might have missed - Talk Like a Pirate Day, for example.

Apple stock was slightly down during midday trading.

What's Hot On TheStreet

Another bank is bullish on Alibaba: JP Morgan initiated Chinese e-commerce giant Alibaba (BABA) with an overweight rating and $190 price target in a new note Tuesday, representing more than 30% growth over Monday's closing price of $142.73. In JP Morgan's eyes, Alibaba is entering a transformation from a pure play e-commerce company to a data-driven beast that stands to power its bottom line more than most expect.

"We believe Alibaba's core commerce is expanding from traffic monetization to data monetization and such trend will quickly expand to its media/cloud businesses," writes JP Morgan analyst Alex Yao. "Such expansion not only allows Alibaba to tap into non-transaction-based corporate budget (e.g. market research, brand awareness, and customer service), but also supports our investment thesis based on sustainable revenue/earnings growth."

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Siri Needs Her Own Personal Assistant - TheStreet.com

Mice provide insight into genetics of autism spectrum disorders – Medical Xpress

June 27, 2017 by David Slipher In this mouse cortex, a mutation in the CHD8 gene caused increased brain size, or megalencephaly, a condition also present in people with autism spectrum disorder. The colored sections correspond to different layers of the developing cortex. Credit: Alex Nord/UC Davis

While the definitive causes remain unclear, several genetic and environmental factors increase the likelihood of autism spectrum disorder, or ASD, a group of conditions covering a "spectrum" of symptoms, skills and levels of disability.

Taking advantage of advances in genetic technologies, researchers led by Alex Nord, assistant professor of neurobiology, physiology and behavior with the Center for Neuroscience at the University of California, Davis, are gaining a better understanding of the role played by a specific gene involved in autism. The collaborative work appears June 26 in the journal Nature Neuroscience.

"For years, the targets of drug discovery and treatment have been based on an unknown black box of what's happening in the brain," said Nord. "Now, using genetic approaches to study the impact of specific mutations found in cases, we're trying to build a cohesive model that links genetic control of brain development with behavior and brain function."

The Nord laboratory studies how the genome encodes brain development and function, with a particular interest in understanding the genetic basis of neurological disorders.

Mouse brain models

There is no known specific genetic cause for most cases of autism, but many different genes have been linked to the disorder. In rare, specific cases of people with ASD, one copy of a gene called CHD8 is mutated and loses function. The CHD8 gene encodes a protein responsible for packaging DNA in cells throughout the body. Packaging of DNA controls how genes are turned on and off in cells during development.

Because mice and humans share on average 85 percent of similarly coded genes, mice can be used as a model to study how genetic mutations impact brain development. Changes in mouse DNA mimic changes in human DNA and vice-versa. In addition, mice exhibit behaviors that can be used as models for exploring human behavior.

Nord's laboratory at UC Davis and his collaborators have been working to characterize changes in brain development and behavior of mice carrying a mutated copy of CHD8.

"Behavioral tests with mice give us information about sociability, anxiety and cognition. From there, we can examine changes at the anatomical and cellular level to find links across dimensions," said Nord. "This is critical to understanding the biology of disorders like autism."

By inducing mutation of the CHD8 gene in mice and studying their brain development, Nord and his team have established that the mice experience cognitive impairment and have increased brain volume. Both conditions are also present in individuals with a mutated CHD8 gene.

New implications for early and lifelong brain development

Analysis of data from mouse brains reveals that CHD8 gene expression peaks during the early stages of brain development. Mutations in CHD8 lead to excessive production of dividing cells in the brain, as well as megalencephaly, an enlarged brain condition common in individuals with ASD. These findings suggest the developmental causes of increased brain size.

More surprisingly, Nord also discovered that the pathological changes in gene expression in the brains of mice with a mutated CHD8 continued through the lifetime of the mice. Genes involved in critical biological processes like synapse function were impacted by the CHD8 mutation. This suggests that CHD8 plays a role in brain function throughout life and may affect more than early brain development in autistic individuals.

While Nord's research centers on severe ASD conditions, the lessons learned may eventually help explain many cases along the autism spectrum.

Collaborating to improve understanding

Nord's work bridges disciplines and has incorporated diverse collaborators. The genetic mouse model was developed at Lawrence Berkeley National Laboratory using CRISPR editing technology, and co-authors Jacqueline Crawley and Jill Silverman of the UC Davis MIND Institute evaluated mouse behavior to characterize social interactions and cognitive impairments.

Nord also partnered with co-author Konstantinos Zarbalis of the Institute for Pediatric Regenerative Medicine at UC Davis to examine changes in cell proliferation in the brains of mice with the CHD8 mutation, and with Jason Lerch from the Mouse Imaging Centre at the Hospital for Sick Children in Toronto, Canada, to conduct magnetic resonance imaging on mouse brains.

"It's the act of collaboration that I find really satisfying," Nord said. "The science gets a lot more interesting and powerful when we combine different approaches. Together we were able to show that mutation to CHD8 causes changes to brain development, which in turn alters brain anatomy, function and behavior."

In the future, Nord hopes to identify how CHD8 packages DNA in neural cells and to determine the specific impacts to early brain development and synaptic function. Nord hopes that deep exploration of CHD8 mutations will ultimately yield greater knowledge of the general factors contributing to ASD and intellectual disability.

Explore further: Study shows connection between key autism risk genes in the human brain

More information: Andrea L Gompers et al. Germline Chd8 haploinsufficiency alters brain development in mouse, Nature Neuroscience (2017). DOI: 10.1038/nn.4592

Journal reference: Nature Neuroscience

Provided by: UC Davis

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Mice provide insight into genetics of autism spectrum disorders - Medical Xpress

Autism genetics, explained – Spectrum

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Researchers have known that genes contribute to autism since the 1970s, when a team found that identical twins often share the condition. Since then, scientists have been racking up potential genetic culprits in autism, a process that DNA-decoding technologies have accelerated in the past decade.

As this work has progressed, scientists have unearthed a variety of types of genetic changes that can underlie autism. The more scientists dig into DNA, the more intricate its contribution to autism seems to be.

Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it too. The corresponding rate for fraternal twins is around 40 percent.

However, genetics clearly does not account for all autism risk. Environmental factors also contribute to the condition although researchers disagree on the relative contributions of genes and environment. Some environmental risk factors for autism, such as exposure to a maternal immune response in the womb or complications during birth, may work with genetic factors to produce autism or intensify its features.

Genetics in motion: The secret to understanding autism lies largely in our DNA.

Not really. There are several conditions associated with autism that stem from mutations in a single gene, including fragile X and Rett syndromes. But less than 1 percent of non-syndromic cases of autism stem from mutations in any single gene. So far, at least, there is no such thing as an autism gene meaning that no gene is consistently mutated in every person with autism. There also does not seem to be any gene that causes autism every time it is mutated.

Still, the list of genes implicated in autism is growing. Researchers have tallied 65 genes they consider strongly linked to autism, and more than 200 others that have weaker ties. Many of these genes are important for communication between neurons or control the expression of other genes.

Changes, or mutations, in the DNA of these genes can lead to autism. Some mutations affect a single DNA base pair, or letter. In fact, everyone has thousands of these genetic variants. A variant that is found in 1 percent or more of the population is considered common and is called a single nucleotide polymorphism, or SNP.

Common variants typically have subtle effects and may work together to contribute to autism. Rare variants, which are found in less than 1 percent of people, tend to have stronger effects. Many of the mutations linked to autism so far have been rare. It is significantly more difficult to find common variants for autism risk, although some studies are underway.

Other changes, known as copy number variations (CNVs), show up as deletions or duplications of long stretches of DNA and often include many genes.

But mutations that contribute to autism are probably not all in genes, which make up less than 2 percent of the genome. Researchers are trying to wade into the remaining 98 percent of the genome to look for irregularities associated with autism. So far, these regions are poorly understood.

No. At the molecular level, the effects of mutations may differ, even among SNPs. Mutations can be either harmful or benign, depending on how much they alter the corresponding proteins function. A missense mutation, for example, swaps one amino acid in the protein for another. If the substitution doesnt significantly change the protein, it is likely to be benign. A nonsense mutation, on the other hand, inserts a stop sign within a gene, causing protein production to halt prematurely. The resulting protein is too short and functions poorly, if at all.

Most mutations are inherited from parents, and they can be common or rare. Mutations can also arise spontaneously in an egg or sperm, and so are found only in the child and not in her parents. Researchers can find these rare de novo mutations by comparing the DNA sequences of people who have autism with those of their unaffected family members. Spontaneous mutations that arise after conception are usually mosaic, meaning they affect only some of the cells in the body.

Perhaps. Girls with autism seem to have more mutations than do boys with the condition. And boys with autism sometimes inherit their mutations from unaffected mothers. Together, these results suggest that girls may be somehow resistant to mutations that contribute to autism and need a bigger genetic hit to have the condition.

Clinicians routinely screen the chromosomes of a developing baby to identify large chromosomal abnormalities, including CNVs. There are prenatal genetic tests for some syndromes associated with autism, such as fragile X syndrome. But even if a developing baby has these rare mutations, there is no way to know for sure whether he will later be diagnosed with autism.

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Autism genetics, explained - Spectrum

New SAFE Sens TrakStation Pricing, Software Bundle – PR Newswire (press release)

In addition, BCSI announced the availability of a stand-alone software license for TrakStation Software to monitor up to eight (8) chambers using a customer supplied Windows PC running Windows 8.0, 8.1 or 10 or Macintosh running Mac OSX 10.8 or later.

"For customers who want to reclaim their capital investment in lab computers, our software only product allows installation and use of TrakPods with those systems. Our goal is to offer affordable customized solutions for all labs who want to move to the future of pH monitoring." Aldrich said.

BCSI will be demonstrating the new enhanced ASUS tablet TrakStation and our stand alone software bundle at the European Society of Human Reproduction and Embryology (ESHRE) show at Booth G55 in Geneva, Switzerland from 2 5 July 2017.

For further details, a product demonstration or quote, please visit http://www.safesens.com, call +1 (425) 654-8445, email ph@safesens.com or contact your local distributor.

TrakStation and TrakPod are the latest generation of continuous pH monitoring laboratory instruments from BCSI. The TrakStation has the capability of monitoring and logging pH data from one (1) to eight (8) chambers simultaneously. The system provides lab managers or clinicians with assurance of a stable incubator pH environment throughout the five (5) to seven (7) day IVF cycle. In contrast to systems that spot monitor pH, this unique surrogate continuous pH monitoring approach does not require opening and closing of incubator doors, thus allowing an uninterrupted incubation cycle and promoting better outcomes for IVF procedures.

The system requires no expensive calibration or adjustments during usage. Each disposable sensor lasts the entire 7-day cycle and is replaced between cycles. A reusable QC alignment tool adjusts the instrument to factory specifications in under ten (10) seconds after each cycle is complete; the QC alignment tool is replaced annually.

About BCSI (www.safesens.com) Blood Cell Storage Inc. (BCSI), based in Seattle, Washington, is an international laboratory instrument and medical devices company. BCSI's patented technology and products benefit patients, clinicians, researchers, pathologists and doctors. In addition to IVF monitors, the company's fluorescent dyes, micro-fluidics, nucleic acid extraction capabilities and automated systems reduce healthcare costs and improve patient outcomes.BCSI is represented in over twenty (20) countries world-wide and has OEM relationships with Astec, Labotect and Esco Medical.

For more information, please contact: Russ Aldrich Blood Cell Storage, Inc. 425-654-8449 russ.aldrich@safesens.com

To view the original version on PR Newswire, visit:http://www.prnewswire.com/news-releases/new-safe-sens-trakstation-pricing-software-bundle-300480043.html

SOURCE Blood Cell Storage, Inc.

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New SAFE Sens TrakStation Pricing, Software Bundle - PR Newswire (press release)

Why do men cheat? (And the answer to every other question you have about guys) – GQ.com

Why do men cheat? It's not just a question we think you ask, it's a question we know you ask thanks to some nifty data we were given by Google. And the more we looked into the numbers, the more we realised that you ask the internet a lot of questions that begin with, "Why do men...?" From "Why do men go bald?" and "Why do men have nipples?" to "Why do men like spanking?" and "Why do men pull away when they are falling in love?" To save you the bother of scratching around questionable sources for the answers, we assembled a crack team of experts to answer every question you have about men, including a GP, qualified psychological therapist, GQ's resident sex expert and some of the finest journalists on God's green earth. Time to find out what really goes on in our heads...

Following revelations surrounding Tiger Woods' personal life in 2009, Tony Parsons offered a neat-edged summation to the mystery of male infidelity. Here is an excerpt from the piece. For the full hit, read "Why Some Men Stray" unabridged.

"Not all men stray. And some men stray for a bit and then they settle down. That is what many women find difficult to accept that sometimes a man strays not because he is a heartless, fornicating bastard but simply because he has not yet met the right girl.

As a general rule, poor men stray because of opportunity (Mavis in the stationery cupboard) and rich men stray because of a sense of entitlement (VIP areas stuffed with willing lovelies).

When Tiger Woods made his public confession after his tsunami of shagging became public knowledge, he was criticised for apologising to his corporate sponsors as well as his wife. And yet, Woods perfectly summed up why the multimillionaire alpha male can love his wife and children, and yet also love having sex with porn stars. Look beyond that sterile, stage-managed setting, and you had Woods giving the Gettysburg Address of Infidelity. "I thought I could get away with everything I wanted to," said Tiger. "I felt I had worked hard and deserved to enjoy all the temptations around me. I felt I was entitled."

He felt that he was entitled. Simple as that. Lives turned inside out, oceans of hurt and betrayal to last a lifetime, because Tiger felt they he was well within his rights to do exactly what he wanted. He summed it up perfectly. I do these things because I have earned them."

Our resident GP, Dr Alison Barwise, replies.

"It all comes down to embryology, which is the study of embryos and foetuses and how nipples develop. During weeks five to six of embryonic growth, the first stages of mammary (nipples and breasts) development occur. It is not until around week eight that a foetus starts to begin to develop male or female reproductive organs (even though the sex of a foetus is determined at the point of conception). As the foetus develops, female hormones support the development of functioning nipples whereas in a male foetus, hormones block any further development. However, as the mammary development has already occurred, the nipples simply remain anatomically present, albeit without the ability to function like the female nipples.

Men can't lactate in the same way a female can lactate because, while mens nipples may appear to look structurally up to the job, there isnt quite the same breast tissue, duct and gland network behind them or the hormones circulating in the bloodstream to support lactation.

That said, men can produce a discharge from their nipple, which is called galactorrhoea. It is always abnormal and should prompt a medical assessment. It can be caused by antidepressants, antipsychotics, cannabis, amphetamines, drugs used to treat epilepsy and blood pressure and pituitary gland tumours. So no, you can't be milked.

There is such thing as an 'extra nipple' as well. Approximately one to five per cent of men and women have an accessory nipple, like Scaramanga."

This is another one for our resident GP:

"The most common cause of baldness in men is male pattern baldness (androgenic alopecia). This condition affects up to 50 per cent of men by the time they are 50.

Androgenic alopecia is a condition caused by a genetic predisposition whereby the hair follicles in some parts of the scalp become sensitive to circulating male hormones. This causes the hair follicles to become smaller, which means that the hair is more likely to fall out.

It also results in the hairs staying in the resting phase of their growth cycle for longer than the active growing phase, which not only makes them more vulnerable to falling out, but also means the rate of hair shedding exceeds the rate of hair growth eventually leading to baldness.

Sadly, you can't prevent it from happening. Androgenic alopecia is predominantly genetically determined so there is little you can do to prevent it. There is no current evidence to support the use of dietary supplements or use of herbal remedies.

There other types of baldness that can affect you, too. Less common causes include:

Alopecia areata whereby discrete areas of baldness develop across the scalp in well demarcated patches.

Stress-related hair loss which can happen after a stressful life event and results in a diffuse thinning across the scalp.

Trichotillomania, which is a hair-pulling disorder, and can be associated with obsessive-compulsive disorder, anxiety and depression.

Scalp infections, including fungal and bacterial scalp conditions, that cause baldness often associated with patches of scaling or crusting on the head."

In researching his piece about the allure of breasts (and his resistance to the idea that bigger is better), GQ's Features Director, Jonathan Heaf, discovered:

"Historically, the idea of breasts being a turn on for men comes from the concept of signalling the greater the flesh, the riper the fruit. This is why in some parts of Cambodia, many elder tribeswomen go to great lengths to strap down, flatten with hot pebbles and generally suppress the rapidly expanding bosoms of maturing adolescent girls."

Now read the full piece, titled "Why I'm Scared Of Big Breasts".

Our resident GP replies:

"Actually, GQ, they dont. While life expectancy is increasing generally across both sexes in the UK, women are living longer than their male counterparts. Research by the Office For National Statistics, published in 2016, shows that in 2013-2015 the life expectancy at birth in the UK for men was 79.1 years and for women was 82.8 years.

So, why do women live longer than men? It's a complicated issue with many experts differing in their opinions. It is likely due to a combination of social, biological, behavioural, evolutionary and other factors that influence longevity.

Generally speaking, women have always lived longer than men, but men are closing the gap. An interesting study published in The Lancet this year by Imperial College London found that the female life expectancy advantage over men was shrinking.

It's difficult to pin down any one reason, but there are various theories including the fact that traditionally men were more likely to be exposed to industrial hazards in the workplace such as dust and fume inhalation than their female counterparts. Decreasing rates of smoking over the past 50 years may also play a part, with recent figures suggesting that, while men still generally smoke more than women, the gap between male and female cigarette consumption is closing. Men are also being encouraged through a range of national health awareness campaigns to be more proactive when it comes to their health and to seek medical advice if concerned."

We consulted with Stefan Walters on this. He's a graduate member of the British Psychological Society (BPS), a member of the British Association For Counselling And Psychotherapy (BACP) and a member of the Association For Family Therapy (AFT), so he's studied, seen and heard it all.

"There's a theory called attachment theory that states our early relationship experiences, usually with our parents, set the foundations for how we're going to respond to relationships later in life. If your parents are responsive, nurturing and safe then we learn that relationships are safe and secure. If your parents aren't very good at that; if they're busy at work, there are lots of other children around and they're too busy to give us their attention, or if they're abusive, then we might learn that relationships are unreliable.

We carry those experiences and attachments into our adult lives. If we've learned that relationships are unreliable, we learn to protect ourselves from that possible vulnerability and disappointment by putting barriers up and pushing people away because we feel vulnerable.

Attachment theory isn't specific to men, but a lot of men are brought up to show a limited range of emotions and that effects how we express our vulnerability. Lots of men are socialised to operate within two emotions positivity and anger. That then effects how you respond and communicate in relationships. If you're not allowed to show vulnerability then it limits how you can interact with someone when you're [trying to express] that emotion.

This theory largely relies on learned experiences, but there can be a biological element. You can inherit anxiety and that can mean that you're more anxious in relationships, but generally attachment styles are learned behaviours."

This one falls between our sex experts and psychologists, but we've handed over to Stefan again as BDSM is something that's tricky to unpick if you're an outsider.

"It's important to say that a lot of men have no interest in ball gags at all. But for those who do, I use the analogy of Branston Pickle. Rather than just eating cheese, for example, which is just one sensory experience, the pickle adds an extra layer even though the flavours may seem at odds. It heightens and intensifies the sensory experience. Kinks are, essentially, the same. Instead of just having sex a single pleasurable experience you're adding an experience that clashes with it like, say, pain, and that intensifies your sensory and physiological experiences.

With ball gags specifically, they limit the airways and breathing, so there's a sense of panic and being controlled. That means there's a lot of sensory experiences, psychological experiences and physical experiences mixed together, which is where the appeal lies."

Stefan replies:

"Visually, stockings trigger arousal for a lot of people because they cover up but also reveal at the same time. Visually, there's a sense of it being a bit of a tease, and the idea of teasing and wanting what you can't have is something we learn from childhood.

The same idea applies to some men's attraction to affairs with married partners. It engages a hunter's instinct, which makes men feel very predatory and want to go pursue their object of their desire. Usually, after these affairs or one-night stands, men feel less interested and ask themselves why they did it. But as long as the idea of a tease persists, as with stockings, some men can feel stimulated."

And our last reply from Stefan:

"This, again, can be related to a childhood experience. Perhaps the man was spanked and that made him feel naughty, which, in turn, made him rebellious a feeling he derided pleasure from. But it's not necessarily that simple.

For some men, it's like a therapeutic relief. Someone who has to control or discipline in their everyday life may find it therapeutic and relieving if someone else takes control. Likewise, if someone has to be polite and submissive all day, they may find a huge amount of relief in taking control and spanking. If spanking is something that a client was drawn to and it's in a consenting, controlled environment, I would advocate for that. There's nothing wrong with it."

Sex expert and GQ regular, Rebecca Newman, didn't just tell you why men like spanking, but offered a how-to guide. You can read the full piece, entitled "Happy Slapping", by following the link. The abridged reply is:

"The British live up to the stereotype: we top the global charts for watching spanking porn. Spanking is not only a fabulous act of transgression, of dominance and submission, of skill and style (involving any number of beautifully finished accessories); done right, it also confers a singularly mind-blowing sexual ecstasy whether or not it is done hard enough to 'hurt'."

The following advice is as accurate and as comprehensive as possible but it is only general advice and should not be used as a substitute for the individual advice you might receive from consulting your own doctor.

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Why do men cheat? (And the answer to every other question you have about guys) - GQ.com

What makes stem cells into perfect allrounders – Phys.Org

June 27, 2017 Just a few days old embryonic cell clusters: with functional Pramel7 (left), without the protein (right) the development of the stem cells remains stuck and the embyos die. Credit: Paolo Cinelli, USZ

Researchers from the University of Zurich and the University Hospital Zurich have discovered the protein that enables natural embryonic stem cells to form all body cells. In the case of embryonic stem cells maintained in cell cultures, this allrounder potential is limited. Scientists want to use this knowledge to treat large bone fractures with stem cells.

Stem cells are considered biological allrounders because they have the potential to develop into the various body cell types. For the majority of stem cells, however, this designation is too far-reaching. Adult stem cells, for example, can replace cells in their own tissue in case of injury, but a fat stem cell will never generate a nerve or liver cell. Scientists therefore distinguish between multipotent adult stem cells and the actual allrounders - the pluripotent embryonic stem cells.

Epigenetic marks determine potential for development

Differences exist even among the true allrounders, however. Embryonic stem cells that grow in laboratory cell cultures are in a different state than the pluripotent cells found inside the embryos in the first days of development. In a study in the journal Nature Cell Biology, researchers led by Paolo Cinelli of the University Hospital Zurich and Raffaella Santoro of the University of Zurich have now demonstrated the mechanism by which natural allrounders differ from embryonic stem cells in cultures.

At the center of their discovery is a protein called Pramel7 (for "preferentially expressed antigen in melanoma"-like 7) found in the cells of embryonic cell clusters that are just a few days old. This protein guarantees that the genetic material is freed from epigenetic marks consisting of chemical DNA tags in the form of methyl groups. "The more methyl groups are removed, the more open the Book of Life becomes," Cinelli says. Since any cell of the human body can develop from an embryonic stem cell, all genes have to be freely accessible at the beginning. The more a cell develops or differentiates, the stronger its genetic material is methylated and "sealed closed" again. In a bone cell, for example, only those genes are active that the cell requires for its function, the biochemist explains.

Protein is responsible for perfect pluripotency

Despite its short action period of just a few days, Pramel7 seems to play a vital role: When the researchers headed up by Cinelli and Santoro switched off the gene for this protein using genetic tricks, development remained stuck in the embryonic cell cluster stage. In the cultivated stem cells, on the other hand, Pramel7 is rarely found. This circumstance could also explain why the genetic material of these cells contains more methyl groups than that of natural embryonic cells - the perfect allrounders, as Cinelli calls them.

Using the stem cell function to regenerate bone tissue

His interest in stem cells lies in the hope of one day being able to help people with complex bone fractures. "Bones are great at regenerating and they are the only tissue that does not build scars," Paolo Cinelli says. The bone stumps must be touching, however, in order to grow together. When a bone breaks in multiple places and even through the skin, for example, in a motorcycle accident, the sections of bone in between are often no longer usable. For such cases, a bone replacement is required. His team is studying carrier materials that they want to populate with the body's own stem cells in the future. "For this reason, we have to know how stem cells work," Cinelli adds.

Explore further: New tools to study the origin of embryonic stem cells

More information: Urs Graf et al, Pramel7 mediates ground-state pluripotency through proteasomalepigenetic combined pathways, Nature Cell Biology (2017). DOI: 10.1038/ncb3554

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What makes stem cells into perfect allrounders - Phys.Org