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Advancing Innovative Strategies for Change in Behavioral Health

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Ever had a bad boss?

Maybe you didn’t trust him, or she didn’t like you? Perhaps you spent more time trying to keep your job than doing your job. Maybe you also felt that other people were treated better than you, or your boss didn’t give you a fair chance to succeed.

If this sounds familiar, then you’ve experienced“low-qualityLMX.” Leader-Member Exchange Theory (LMX Theory) researchers are interested in the link between the quality of relationship people have with their boss and various outcomes. Outcomes such as…

The list of what they’ve measured goes on and on.

“High-quality LMX” is how researchers describe positive, healthy relationships between managers and employees. These relationships exhibit feelings of trust, feelings that you both are on the same side, a belief that the boss cares about the employee and wants the best for them.

You can probably guess the effects of high-quality LMX on team members. Studies show that individual performance is higher, turnover rates (and intention) is lower, commitment to the company and the work is higher, politics are lower, etc. Many goodthings flow out of your vital relationship with each team member.

First, see your role differently. Your job is less about telling people what to do, or even “just getting out of the way,” and more about building those key relationships.

Second, recognize that you have two sub-groups within your team. LMX Theory calls this your “in-group” and “out-group.” Your in-group are the ones closest to you, who enjoy a better relationship with you and the benefits that flow from that. These are people who you probably have high-quality LMX with.

Your out-group is everyone who’s not in your in-group. These are the folks who are most at risk to leave, who are more likely to have poor performance and be dissatisfied with their pay. People didn’t choose which group to join, and you didn’t put them there intentionally, but those groups do exist on your team.

You may not have seen these two groups before, so It’s worth taking a few minutes and evaluating which group each team member is in.

Third, consider how you can invite your out-group to come closer to you. Think about how you can give more feedback to them, use your 1:1 meetings to build trust, and learn to listen more and talk less. When you make these invitations to have a better relationship, it shows your team you care and that you’re on their side.

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Where other technical coaches focus on process or tools, I focus on the human aspects of your Programmer to Manager transition. I help you hire the right people, create the right culture, and setup the right process which achieves your goals. Managing your team isn't something you learned in college. In fact, my clients often tell me "I never prepared for this role, I always focused on doing the work". If you're ready to improve your leadership, process and team, find out how I can help you .

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Original Research
Alexander Strobbe , Tom Adriaenssens , Johan Bennett , Christophe Dubois , Walter Desmet , Keir McCutcheon , Johan Van Cleemput , Peter R Sinnaeve
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Journal of the American Heart Association. 2017; 6: e007598
Alexander Strobbe
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium
Tom Adriaenssens
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium Department of Cardiovascular Sciences , University of Leuven , Belgium
Johan Bennett
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium
Christophe Dubois
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium Department of Cardiovascular Sciences , University of Leuven , Belgium
Walter Desmet
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium Department of Cardiovascular Sciences , University of Leuven , Belgium
Keir McCutcheon
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium
Johan Van Cleemput
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium Department of Cardiovascular Sciences , University of Leuven , Belgium
Peter R Sinnaeve
Department of Cardiovascular Medicine , University Hospitals Leuven , Belgium Department of Cardiovascular Sciences , University of Leuven , Belgium

Background Pericardial effusions can be caused by a variety of disorders. The frequency of the underlying diseases varies with patient population; therefore, previously reported series are not necessarily representative of other populations. Our purpose was to examine the etiology of pericardial effusions and the survival of patients requiring pericardiocentesis at a tertiary center.

Methods and Results We performed a retrospective observational study of 269 consecutive patients who underwent percutaneous pericardiocentesis at our university hospital between 2006 and 2016 and had prospective follow‐up for up to 10years. The most frequent etiologies were idiopathic (26%), malignancy (25%), and iatrogenicity (20%), whereas bacterial causes were very rare. The most frequent malignancies originated from the lung (53%) or breast (18%). A new cancer was diagnosed with malignant pericardial effusion as the presenting complaint for 9% of patients, whereas the pericardium was the first metastatic site of a known malignancy in 4% of patients. Survival was significantly poorer in malignancy‐related versus non–malignancy‐related effusions (<0.001) and in cytology‐positive versus cytology‐negative effusions in the overall cohort (<0.001). Among cancer‐only patients, however, there was no significant difference in long‐term survival between cytology‐positive and ‐negative effusions.

Conclusions In this contemporary tertiary‐center cohort, pericardial effusions often represent the primary instance of a new malignancy, underscoring the importance of cytological analyses of noniatrogenic effusions in patients without known cancer, as survival is significantly worse. In cancer patients, however, the presence of pericardial malignant cytology does not appear to affect outcome significantly.

What Is New?

Malignancy‐associated effusion, representing the most frequent etiology among tertiary care patients undergoing pericardiocentesis and often the primary instance of cancer, is associated with a significantly worse survival than nonmalignant effusion, but the presence of malignant pericardial cells does not significantly affect outcome among cancer patients.

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By Dana Smith / Gladstone News / April 9, 2018
Yadong Huang and his team discovered how to erase the damage in human brain cells caused by apoE4, the primary genetic risk factor for Alzheimer’s disease

Using human brain cells, scientists at the Gladstone Institutes discovered the cause of—and a potential solution for—the primary genetic risk factor for Alzheimer’s disease, a gene called apoE4.

Having one copy of the apoE4 gene more than doubles a person’s likelihood of developing Alzheimer’s disease, and having two copies of the gene increases the risk by 12-fold, as compared to the most common version of the gene, apoE3.

The apoE4 gene creates a protein of the same name. The apoE4 protein differs from the apoE3 protein at only one point, but that single change is enough to alter its main structure and, thus, its function. Scientists have been unclear about why apoE4 is so much more damaging to brain cells than other versions of the protein.

In a new study published in , researchers revealed how apoE4 confers its risk for Alzheimer’s disease in human brain cells. What’s more, they were able to erase the damage caused by apoE4 by changing it, with a small molecule, into a harmless apoE3-like version.

A Better Model

Most Alzheimer’s research and drug development are done in mouse models of the disease. However, a succession of clinical trial failures has spurred scientists to turn to other models.

“Drug development for Alzheimer’s disease has been largely a disappointment over the past 10 years,” says lead author adidas Consortium Men Ultraboost Lux White/Vintage White/Chocolate Brown Vintage White Chocolate Brown T3gJ2Duy
a senior investigator and director of the Center for Translational Advancement at Gladstone.

“Many drugs work beautifully in a mouse model, but so far they’ve all failed in clinical trials. One concern within the field has been how poorly these mouse models really mimic human disease.”

Instead, Huang decided to use human cells to model the disease and test new drugs. Thanks to induced pluripotent stem cell technology, his team was able to examine, for the first time, the effect of apoE4 on human brain cells. To do so, the researchers created neurons from skin cells donated by Alzheimer’s patients with two copies of the apoE4 gene, as well as from healthy individuals who had two copies of the apoE3 gene.

The researchers confirmed that, in human neurons, the misshapen apoE4 protein cannot function properly and is broken down into disease-causing fragments in the cells. This process results in a number of problems commonly found in Alzheimer’s disease, including the accumulation of the protein tau and of amyloid peptides.

Notably, the presence of apoE4 does not change the production of amyloid beta in mouse neurons. But in human cells, scientists noticed apoE4 has a very clear effect on increasing amyloid beta production, which highlights the species difference in the way apoE4 controls amyloid beta metabolism.

“There’s an important species difference in the effect of apoE4 on amyloid beta,” says Chengzhong Wang, PhD, the first author on the paper and former research scientist at Gladstone. “Increased amyloid beta production is not seen in mouse neurons and could potentially explain some of the discrepancies between mice and humans regarding drug efficacy. This will be very important information for future drug development.”

Fixing a Toxic Protein

Once the scientists confirmed that apoE4 does, indeed, cause damage in human cells related to Alzheimer’s disease, a key question remained: how does the presence of apoE4 lead to cell damage? Is the presence of apoE4 resulting in a loss of normal apoE3 function, or does the addition of apoE4 cause the toxic effects?

“It’s fundamentally important to address this question because it changes how you treat the problem,” explains Huang, who is also a professor of neurology and pathology at UC San Francisco. “If the damage is caused due to the loss of a protein’s function, you would want to increase protein levels to supplement those functions. But if the accumulation of a protein leads to a toxic function, you want to lower production of the protein to block its detrimental effect.”

To answer this question, the researchers examined brain cells that did not produce either form of the apoE protein, and the neurons looked and functioned just like cells with apoE3. However, if the researchers added apoE4, the cells became riddled with pathologies related to Alzheimer’s disease. This discovery indicates that the presence of apoE4—and not the absence of apoE3—promotes the disease.

Finally, the researchers looked for ways to repair the abnormalities caused by apoE4. In earlier work, Huang and his collaborators developed a class of compounds that can change the structure of the harmful apoE4 protein so it resembles the innocuous apoE3 protein, referred to as apoE4 “structure correctors”.

Treating human apoE4 neurons with a structure corrector eliminated the signs of Alzheimer’s disease, restored normal function to the cells, and improved cell survival. Huang is now working with his collaborators in academia and the pharmaceutical industry to improve the compounds so they can be tested in human patients in the future.

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Posted on Feb 2, 2018

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