Daily Archives: March 26, 2016

Okay, A Bit Peeved This Morning…..

Job Hunting with Bipolar Disorder
Job Hunting with Bipolar Disorder

I honestly do not understand people who try to help me put a positive spin on the Mack truck sized whole in my work history. They always tell me things like say you were a homemaker (that was true for about 2 years out of 4 years of marriage), say you got married and didn’t need to work ( I have been divorced for 3 of the 9 year employment gap.) All of these things to say would be lies; do you honestly want to start a new job having told lies during the interview? At some point, the Bipolar disorder will rear it’s ugly head.

I know people mean well when they offer these bits of advice on how to handle a really ugly work history deficit., but I do not feel comfortable just straight out lying about the reason I have been out of the workforce. I would rather say something to the effect of “I suffered an illness, and I have spent the last few years recovering. I am recovered now, and ready to rejoin the workforce.” That isn’t a lie. It is all true; I am just leaving out the Bipolar part. Once hired, I am covered by the ADA. I have, however, been feeling mostly normal for a while now. I am really not liking staying home, but the last time I went job hunting, I applied for about 20 positions and got 3 calls, and no return calls after revealing that I had been recuperating from an illness, and that I was fine to work.

All the job sites I have read recommend facing the problem head on, and being honest about what and why you were out of the workforce for so long. I do not like lying, so this seems to me to be the logical path to take. Besides, if you lie, you have to remember the lie, you have to live the lie, and you certainly cannot reveal the real reason you haven’t been working. It just doesn’t work for me all the way around. If an illness can return, then the employer needs to know about it so they can provide reasonable accommodations.

Filed under: “Disability”, “normal”?, work related, Working Tagged: Bipolar I disorder, Job hunting

#FeatureFriday: Natasha Tracy in the house!

Originally posted on Our Lived Experience:
Interview by the Blahpolar *passes Natasha a glass of water* How would you describe yourself, if you weren’t allowed to mention bipolar? I would describe myself as a writer, speaker and social media consultant. I would also say I’m an ex-skydiver, techie geek and avid cook. What is your…

Alex Kipman: The dawn of the age of holograms

Alex Kipman: The dawn of the age of holograms
https://go.ted.com/Cyu2

This Ted Talk astonished me.  Watch for the mushrooms 🍄

And be sure to stick around to see how eloquently Alex, who is clearly very solidly “on the (Autistic) Spectrum,” answers the stuffy Ted host’s questions at the end of his show.

Unlike most Ted Talks, this is not merely an inspirational speech about triumph over an apparently insurmountable hardship, or even about saving humanity by means of understanding and innovation.

It’s about a way of life that is hurtling toward us at the speed of light.

Watch, enjoy, and let me know how you feel about this!


Alex Kipman: The dawn of the age of holograms

Alex Kipman: The dawn of the age of holograms
https://go.ted.com/Cyu2

This Ted Talk astonished me.  Watch for the mushrooms 🍄

And be sure to stick around to see how eloquently Alex, who is clearly very solidly “on the (Autistic) Spectrum,” answers the stuffy Ted host’s questions at the end of his show.

Unlike most Ted Talks, this is not merely an inspirational speech about triumph over an apparently insurmountable hardship, or even about saving humanity by means of understanding and innovation.

It’s about a way of life that is hurtling toward us at the speed of light.

Watch, enjoy, and let me know how you feel about this!


Alex Kipman: The dawn of the age of holograms

Alex Kipman: The dawn of the age of holograms
https://go.ted.com/Cyu2

This Ted Talk astonished me.  Watch for the mushrooms 🍄

And be sure to stick around to see how eloquently Alex, who is clearly very solidly “on the (Autistic) Spectrum,” answers the stuffy Ted host’s questions at the end of his show.

Unlike most Ted Talks, this is not merely an inspirational speech about triumph over an apparently insurmountable hardship, or even about saving humanity by means of understanding and innovation.

It’s about a way of life that is hurtling toward us at the speed of light.

Watch, enjoy, and let me know how you feel about this!


Editing HIV out of our genome with CRISPR

crispr-pathwayThis is very cool! CRISPR is the system that excises foreign DNA out of bacterial genomes. It’s the equivalent of a bacterial immune system. Where we have a very complicated and extensive immune system that protects us from foreign pathogens (viruses, bacteria and others), it protects us even form poison, venom, foreign things and it is instrumental in healing us when we get cut or injured in some way. For a long time it was thought that bacteria had no such defense mechanism, then surprisingly CRISPR was found! It is the system that protects bacteria form bacteriophages, which are viruses that infect bacteria. If a virus successfully inserts its DNA into the chromosome of a bacterium, it will use the bacterial enzyme systems to make millions of copies of it self, eventually lysing and killing the bacterium to release all those copies of virus, and these viruses will then infect other bacteria. Bacteriophages are viruses that infect bacteria. There are other viruses which infect animals or people, such as the chicken pox virus, aka varicella, the AIDS virus aka HIV (human immunodeficiency virus,) Herpes virus, Hepatitis virus, many many viruses. Retroviruses such as the HIV (AIDS) virus also incorporate themselves into the DNA of in this case T cells, and they incapacitate T cells which are part of our immune system. Thereby we get acquired immunodeficiency or AIDS. Now researchers have developed a new technique using CRISPR, the bacterial “immune system” to excise the HIV virus out of the DNA of human cells that it had infected. Although at this time, this technique can only be used in vitro, CRISPR isn’t specific enough to use in humans. It can cut large regions of DNA in cells, in a nonspecific manner. So CRISPR has to be made more specific before it can be used as a therapy, for HIV or anything else.

Read the article, it is really cool!

http://www.umassmed.edu/news/news-archives/2015/04/editing-hiv-out-of-our-genome-with-crispr/

The virus that causes AIDS is an efficient and crafty retrovirus. Once HIV inserts its DNA into the genome of its host cells, it has a long incubation period, and can remain dormant and hidden for years. And while physicians can mix a cocktail from a variety of antiretroviral drugs to keep it in check, the virus can reactivate if treatment is stopped.

In an attempt to render latent HIV completely harmless, UMass Medical School researchers are using CRISPR/Cas9, a powerful gene editing tool, to develop a novel technology that can potentially cut the DNA of the latent virus out of an infected cell.

“On the simplest level, we’re employing a very precise pair of scissors to go in and clip out all, or part of, the HIV genome and reattach the severed ends of the human genome,” said principal co-investigator Scot Wolfe, PhD, associate professor of molecular, cell & cancer biology. “If we could do that, the hope is that this would be a step on the road to getting a functional cure for HIV.”

CRISPR is a component of the immune system found in normal bacteria. In its natural state, it protects bacteria from viral invasion. Since its discovery, researchers have been seeking ways to program this system to quickly and selectively edit specific genetic sequences for study.

For all its versatility, applications for the CRISPR system remain confined to the lab. Despite recent advances showing that CRISPR/Cas9 can edit HIV from an infected cell in culture, this technique remains too imprecise to be used clinically because of its tendency to cut into random regions of the genome, producing deleterious, off-target effects.

To improve the fidelity and precision of the CRISPR/Cas9 gene editing system for this project, Dr. Wolfe has proposed fusing it with an additional domain that improves its specificity. This would conceivably allow the CRISPR system to edit out only the HIV DNA without the potential for stray cuts in the human genome.

The other hurdle to using current CRISPR/Cas9 technology against HIV is that while researchers have some notions where the virus might be hiding, they still don’t know how to find the virus in latently infected cells.

“Cells that are infected with HIV are permanent carriers of the viral genome. They are a kind of time bomb that can be reactive at any time if a patient stops taking their antiretroviral treatment,” said principal co-investigator Jeremy Luban, MD, the David J. Freelander Professor in AIDS Research and professor of molecular medicine. “In order to attack the virus in its latent state, we really need to understand where the virus lives and what it needs to survive.”

Dr. Luban and Wolfe will use a combination of innovative technologies to describe and model HIV DNA integrated into the genome of reservoir cells, also known as provirus. Characterizing the genomic landscape of these latently infected cells will allow the researchers to identify vulnerable and accessible genetic sequences that can be potentially cut out of the HIV virus to make it permanently inactive.

“Many scientists are looking for tools that will activate the virus so it will be visible to the immune system or drugs. We’ve chosen a different approach that looks to isolate and excise the provirus directly from resting cells,” said Luban.

With a model of the latently infected cells’ genome from which to work, Wolfe hopes to use his precise gene editing tool to excise the latent virus from cells. Part of the project will be to assess whether the precision of the system has improved enough to allow for selected removal of the HIV genome in humanized mouse models and cells from infected patients without causing collateral damage to the human genome.

“The underlying premise of this project that Scot has pushed forward using new technologies that he has developed, is to genetically engineer a system that can potentially remove the HIV genome from infected cells,” said Luban. “The hope is that one might develop the tools to deliver these agents to cells of the human immune system and actually eliminate the virus from where it is hiding.”

Joining Luban and Wolfe on the five-year, $4.6 million National Institute of Allergy and Infectious Diseases funded project are Dale Greiner, PhD, the Dr. Eileen L. Berman and Stanley I. Berman Foundation Chair in Biomedical Research and professor of molecular medicine; Oliver J. Rando, MD, PhD, professor of biochemistry & molecular pharmacology; Job Dekker, PhD, professor of biochemistry & molecular pharmacology; and Manuel Garber, PhD, associate professor of molecular medicine. Each will lend their respective expertise in developing humanized mouse models; mapping chromatin structure; modeling 3D chromosome organization; and computational biology. Additionally, Katherine Luzuriaga, MD, professor of molecular medicine, pediatrics and medicine, and Thomas C Greenough, MD, assistant professor of medicine, will provide clinical expertise on the project.

“We’ve assembled a team of researchers here at UMass Medical School with the goal of better understanding the intricate structure of the latent HIV virus when integrated into immune cells because we believe that will allow us to better target it with CRISPR for gene editing,” Wolfe explained.


Prozac in the Water Makes Fighting Fish More Mellow (What?!?!?!)

http://blogs.discovermagazine.com/inkfish/2016/03/23/prozac-water-makes-fighting-fish-mellow/#.VvXXTYwrLpA

Siamese Fighting Fish

Prozac in the Water Makes Fighting Fish More Mellow

By Elizabeth Preston | March 23, 2016 2:00 pm 156

Had Teresa Dzieweczynski chosen to publish her recent findings as an updated children’s classic, rather than as a research paper, she could have titled it If You Give a Fish an Antidepressant. The book would probably be less charming than If You Give a Mouse a Cookie. But it would also be, unfortunately, more realistic. Our pharmaceuticals are steadily trickling into the homes of fish and other animals. And—as the hero of the original book could have told us, his house in disarray after fulfilling the whims of a hungry rodent—there are consequences.

Dzieweczynski, a psychologist at the University of New England, looked at just one of the drugs that’s crept into American waterways: fluoxetine, better known as Prozac. It’s an antidepressant that makes the hormone serotonin linger in the brain for a longer time. Antidepressants of this type are commonly prescribed, and they commonly get into the water as a result. They’ve turned up in wastewater, drinking water, and other aquatic environments.

She tested fluoxetine on male Siamese fighting fish, or Betta splendens. No one knows how much Prozac is in the water in Thailand, where these fish live naturally. But they make a good model, Dzieweczynski explains, because scientists already understand a lot about their brains, behavior and hormones.

Dzieweczynski and her coauthors put the fighting fish into three different lab environments. Some of the fish swam in tanks with clean water. Others swam in water with a low concentration of fluoxetine—0.5 micrograms per liter, which is at the higher end of what’s been found in U.S. waterways. The third group of fish swam in a stronger dose of fluoxetine, 5 micrograms per liter.

The researchers gave the fish behavioral tests to see how bold they were. In one test, they put a fish into a big empty tank and watched how far it roamed. In another test, they dropped a fish into a tank with rocks and artificial plants it had never seen before, and observed it again. How much did the fish explore? Was it curious about its new environment, or cautious and still? Finally, researchers put a fish into a clear tank adjacent to one that held three other fighting fish. Did the subject approach the strangers, or stay at the opposite end of its tank?

After getting baseline behavioral scores for all their fish, the researchers started dosing them with fluoxetine. They retested the fish after a day of drug exposure. After a week of drug exposure, they tested them again. Then they put all the fish into clean water for a week and tested them a final time.

Across all the behavioral tests, fish exposed to the antidepressant were less bold. They stayed in one place, explored their environment less, and were more hesitant to approach other fish. Their behavior was also more erratic. A higher dose of the drug caused a more dramatic effect.

“Perhaps most importantly and alarmingly,” the authors write, they could still see these effects after the fluoxetine was gone. Even after a week of swimming in clean water, drugged fish behaved less boldly than normal.

In an earlier study, Dzieweczynski drugged female fighting fish with fluoxetine and saw similar results. The effect was a bit stronger in male fish, she says—maybe because they have higher levels of serotonin or testosterone to begin with.

Dzieweczynski didn’t test her “fighting” fish to see how much they actually fought each other. She says other studies have shown that fluoxetine makes them less aggressive. When the fish in this study approached strange fish from across their tank, they may have been seeking a fight, a potential mate, or just safety in numbers.

But no matter what the fishes’ intentions, acting less boldly could hurt their odds of survival in the wild. If fish are less eager to explore their environments, they might have trouble searching for food. Shyer behavior could also make it harder for fish to defend their environments, migrate, or escape predators.

That means letting our drugs get into the water could have a cascade of consequences throughout an ecosystem. And if even temporary drug exposures can have lasting effects, it might be hard to turn the story back to page one. (Can someone bring that mouse back now?