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Online Graduate Programs / Online Psychology Programs
Online Master's in Psychology ProgramsOnline Master's in Psychology ProgramsOnline Master's in Psychology Programs
Pepperdine Graduate School of Education and PsychologyPepperdine Graduate School of Education and PsychologyPepperdine Graduate School of Education and Psychology
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Become a Catalyst for Inspiration and Change
Since its founding in 1971, the Pepperdine University Graduate School of Education and Psychology (GSEP) has been an innovative learning community where faculty and students of diverse cultures and perspectives work collaboratively to foster academic excellence, social purpose, and meaningful service.
Today, that innovative learning community is available to students all over the globe through our research-backed, top-tier online psychology programs. We invite you to learn more about our programs, designed to prepare students everywhere to enrich lives in their organizations and communities.
Best Online College for ROI
for master's in marriage and family therapy programs1
for master's in counseling programs2
GSEP by the Numbers
Students in our online and on-campus programs inspire real change.
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The final deadline for the April 2023 cohort is February 10, 2023. Request information by completing the brief form.
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Find Your Online Psychology Master's Degree Program
We offer three online degree programs, each with specialized areas of interest.
Online Master of Science in Applied Behavior Analysis (ABA)
Our online ABA program prepares students to develop a deep understanding of behavior analysis and the modern techniques used to recognize, assess, and treat human behaviors. Our ABAI-verified course sequence features concepts and principles of ABA, assessment procedures, and applications of ABA for behavior change. The program can be completed in as few as 15–21 months.
Explore the master's in ABA program.
Online Master of Arts in Clinical Psychology
Our online Master of Arts in Clinical Psychology program is designed for students who want to serve individuals, couples, and families as a counselor or marriage and family therapist. Graduates will be prepared to pursue a licensed professional counselor (LPC) or a licensed marriage and family therapist (LMFT) upon graduation. The program can be completed in as few as 27 months.
Explore the master's in clinical psychology program.
Online Master of Arts in Psychology
Our Master of Arts in Psychology program is designed for students who want to gain a thorough understanding of human behavior and psychological principles. Students are prepared to take the next step in a human services field, advance in a related field, or pursue doctoral study in psychology. The program can be completed in as few as 18–24 months.
Explore the master's in psychology program
Learn more about our on-campus psychology programs.
Antiracism and Antidiscrimination Statement
The online psychology programs and the GSEP Psychology Division stand in solidarity against racial inequities and injustice and other forms of discrimination and oppression. We are committed to fostering an inclusive learning environment that is enriched and strengthened by diversity, including but not limited to race, ethnicity and national origin, gender and gender identity, sexuality, class, age, ability status, and religion. GSEP also encourages all community members to engage in critical learning and reflection to strengthen our capacity for being effective, active, and outspoken against all forms of racism and intersectional oppression.
Our Faculty: Passionate and Purpose-Driven
GSEP faculty members are renowned practitioners in their fields who are passionate about their work and their students. Our professors teach because they want to—not because they have to—and they see sharing knowledge, mentoring students, and enriching lives as not just work, but a noble pursuit and responsibility.
Dr. Thema Bryant-Davis
Dr. Thema Bryant-Davis, associate professor, ordained minister, psychologist, author, host of the Homecoming podcast, and recipient of the Sarah Allen Research on the Status of Black Women Award.
Learn more about GSEP leaders on the Meet Our Faculty page.
Prepare for What's Next
At GSEP, we work closely with our current students and alumni as they pursue meaningful career outcomes. Students have access to a number of Pepperdine career resources, including:
One-on-one advising with an executive coach.
Student and alumni job boards.
The PeppConnect online alumni community.
Virtual and in-person networking events.
Experiential and Online
We've combined our values-based approach to education with 21st-century learning best practices to create an online experience that promotes deep thinking, purposeful reflection, and meaningful connection. As a student, you'll benefit from:
Weekly live classes that encourage discussion.
Collaborative tools and small-group activities.
Interactive course work including modules, video lectures, and case studies.
On-Campus Psychology Master's Programs
The psychology master's programs at Pepperdine GSEP empower you for personal growth and service. Change lives as a marriage and family therapist, clinical psychologist, or applied behavior analyst. Extensive practicum experience is offered through a scholar-practitioner model. Whether you're looking for a full-time program or need flexibility as a working professional, our on-campus programs offer a degree for you.
Visit our on-campus site to learn more and apply to on-campus programs. Note that on-campus and online psychology program applications are separate. Access the online psychology programs application here.
Clinical Training in Your Community
Clinical training is an essential component of our online ABA and online master's in clinical psychology programs. Our dedicated placement team will work with you to find and secure Pepperdine-approved practicum and internship opportunities, where you can observe professionals in the field and gain direct experience working with clients in or near your own community.
Serving the Greater Good for More Than 50 Years
For the last 50 years, Pepperdine has empowered students to transform themselves, and others, into the best possible expression of themselves. That legacy is alive today more than ever, as we help students all over the globe gain the skills they need to achieve personal fulfillment, lead with purpose, and make a lasting impact in the lives and communities they serve.
We look forward to the next 50 years of psychology education the Pepperdine way:
with purpose, service, and leadership.
Join us—we're just getting started.
1 2020 Best Online Master's in Counseling Degrees (March 9, 2020). Retrieved from OnlineU Nov. 9, 2020, from https://www.onlineu.com/degrees/masters-marriage-and-family-therapy arrow_upwardReturn to footnote reference
2 2020 Best Online Master's in Counseling Degrees (March 9, 2020). Retrieved from OnlineU Nov. 9, 2020, from https://www.onlineu.com/degrees/masters-counseling arrow_upwardReturn to footnote reference


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Investigative Treatment for Pulmonary Arterial Hypertension Fails to Meet Top Goal in Phase 2 Study
by Patricia Silva PhD
Gilead Sciences reported that selonsertib (also known as GS-4997), an investigational treatment for pulmonary arterial hypertension (PAH), did not achieve the primary endpoint in an analysis of ARROW, a Phase 2 clinical trial (NCT02234141) evaluating the drug's efficacy, safety and tolerability.
The company also reported top-line data from two other Phase 2 clinical trials assessing selonsertib, one in people with nonalcoholic steatohepatitis (NASH), and the other in diabetic kidney disease (DKD) patients.
Selonsertib is an orally bioavailable inhibitor of apoptosis signal-regulating kinase 1 (ASK1), a protein that promotes inflammation, apoptosis (cell death), and fibrosis in settings of oxidative stress. It is being tested in Phase 2 trials as a therapy for PAH, NASH and DKD.
The ongoing, 24-week, randomized, dose-ranging ARROW trial compared the efficacy, safety, and tolerability of three doses (2 mg, 6 mg, or 18 mg once daily) of selonsertib to placebo in 151 patients with PAH (WHO Group 1).
Based on an analysis, Gilead reported that the trial did not achieve its primary endpoint. At week 24, treatment with selonsertib did not result in statistically significant changes from baseline in pulmonary vascular resistance (PVR), as measured by right heart catheterization (RHC). RHC is the most accurate test to measure pulmonary artery pressure and to officially diagnose PAH.
Due to the lack of efficacy evidence, the company said it will not move the drug into Phase 3 studies in PAH.
Separately, selonsertib showed anti-fibrotic activity in an open-label Phase 2 (NCT02466516) study in patients with NASH and moderate to severe (F2-F3) liver fibrosis. In this trial, 72 people were treated with selonsertib (6 mg or 18 mg, orally once daily) alone or in combination with simtuzumab (SIM; a monoclonal antibody by Gilead being investigated for the treatment of fibrosis), or SIM alone (125 mg via subcutaneous injections) for 24 weeks. Results showed that treatment with selonsertib improved fibrosis compared to SIM alone, and reduced progression to cirrhosis (fibrotic liver). Selonsertib was generally well-tolerated, with no major treatment-related adverse events observed.
The results will be presented at The Liver Meeting, set for Nov. 11–15 in Boston.
"We are committed to advancing our pipeline of investigational molecules that separately target metabolic dysfunction, inflammation and/or fibrosis associated with NASH," Norbert Bischofberger, PhD, executive vice president, Research and Development, and chief scientific officer, Gilead Sciences, said in a press release. "We are encouraged by these data demonstrating the anti-fibrotic effect of GS-4997 in patients with NASH after only 24 weeks of treatment, and look forward to sharing the complete results with the hepatology community. Additionally, pending discussions with regulatory agencies, we plan to initiate a Phase 3 clinical trial program of GS-4997 in patients with NASH."
Gilead also reported that, based on a preliminary analysis of a Phase 2 study (NCT02177786) on patients with DKD, selonsertib did not achieve its primary endpoint. As in ARROW, due to the lack of efficacy evidence, Gilead said it does not plan to move the drug into Phase 3 trials for DKD at this time.
Patricia Silva PhD
Patrícia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.
Tagged ARROW, clinical trial, diabetic kidney disease, DKD, fibrosis, Gilead Sciences, GS-4997, NASH, nonalcoholic steatohepatitis, pulmonary vascular resistance, Selonsertib.
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WASHINGTON (Reuters) – The U.S. Treasury sanctioned three Russian individuals and five entities on Monday over malicious cyber activities including providing material and technological support to Russia's intelligence service, according to a statement.
"The entities designated today have directly contributed to improving Russia's cyber and underwater capabilities through their work with the FSB and therefore jeopardize the safety and security of the United States and our allies," said Treasury Secretary Steven T. Mnuchin said in a statement, using an acronym for the Russian Federal Security Services.
This entry was posted in National Security and tagged Russia, Sanctions, Steven Mnuchin. Bookmark the permalink.


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How To: Zero your Rifle with Iron Sights and Optics
Posted by Monte Long on Sep 23rd 2022
Welcome to September in Texas! Y'all know what that means, right? If you guessed "Hot as hades," then you're right. But it also means that you should be getting ready for hunting season 'cause it's only about two months away.
By getting ready, I mean making sure you're scouting your hunting area, ensuring your feeders are working, and getting your rifle(s) zeroed and ready to go.
For those that might be new to firearms, zeroing a firearm is the process of getting your sighting system set up so that, provided you do your job right as the shooter, your bullets go where you want them to go. There are many thought processes regarding what distance you should zero a rifle.
We'll talk about some of them, and I'll walk you through zeroing a couple of rifles I will be working with between now and the end of whitetail season (assuming I get the opportunity to get out and hunt a bit).
At what distance should I zero my hunting rifle?
Once your sighting system is installed and bore sighted, the next order of business is to decide what distance to zero at. Figuring that out is entirely up to you, the shooter, and how you plan to hunt with the rifle.
For this article, I'm working with two rifles – a Marlin 1894 in .357 Magnum and a Ruger Gunsite Scout Rifle in .308 Winchester. Let's discuss my thoughts on the differences in how I will zero these two rifles.
The Marlin is primarily intended as a quick, handy carbine while I'm out wandering around on my parents' land. It's a nice mix of open pasture, creeks, and heavy underbrush. The Marlin is dedicated to walking around on the other side of the creek – lots of brush and not a lot of distance that you can see. I've typically got a scoped carbine if I'm working in the pastures feeding horses, working on fences, or running the brush hog.
I lucked into a decent amount of Speer .357 Magnum 125-grain Gold Dots to feed it. Out of that little 16" barrel, it's cooking –my LabRadar tells me the bullets are heading down range at 2,300 feet per second. Between the velocity and the sights being close to the bore, a 50-yard zero looks like the way to go. From the muzzle to 90 yards, the point of impact will be within an inch of my point of aim. At 100 yards, the point of impact will only be about 1.25" low. That should work just fine for the intended purpose.
The Ruger Gunsite I zeroed with Federal 150 grain PowerShok jacketed soft point hunting ammo. For the iron sights, I settled on a 100-yard zero. It's simple, easy, and will work fine to 150 or so yards, just in case the scope fails. For the Leupold Scout Scope, I did a bit more thinking.
The chronograph told me the bullets started at 2,650 feet per second. A little work with a ballistics calculator, and I settled on a 150-yard zero. With a 150-yard zero, the bullet should be within 3 inches of point of aim to about 200 yards and within 4 inches of point of aim to about 250 yards. With a 2.5 power scout scope, I don't want to take a shot on a game animal much beyond 200 yards, but if I decide to, I should be able to hold the center of the thoracic cavity and get an acceptable hit in the heart, lungs, or all three.
Simple Math: Zeroing your Rifle Sights
Once I decided on zeroing distances, it was time to do some math! Hold on! I know math wasn't my favorite subject either, but this is pretty straightforward.
I don't like wasting ammo (especially in this economy!), so doing some prep work should help me save some ammo once I get to the range.
Before heading to the range, I wanted a reasonable idea of how much POI would move for a given adjustment of the rear sight. To get that info, we need three numbers. We'll need to know zero distance, sight radius, and how much the rear sight moves for a full revolution of the aperture.
The sight radius is pretty simple – measure the distance between the front and rear sight.
In the case of the 1894, it comes out to 20".
Zero distance is also pretty easy. As I mentioned above, I decided on a 50-yard zero. The only hiccup is for the POI change formula, and I'll need that information in inches. That's a relatively straightforward task of multiplying 50 (the yards) by 36 (the number of inches per yard), reaching 1,800.
The XS Ghost Rings have both windage and elevation adjustments. The aperture threads up or down to adjust elevation, and the screws that lock it in place are used to adjust the windage.
Zeroing the Marlin 1894
Let's start with the Marlin 1894. We need to know how much the aperture moves in a full rotation to determine how much the POI will shift at a given distance. To do that, we need to know the thread pitch of the aperture. All XS apertures have a 64 thread per inch (TPI) pitch. That means that, for an inch of movement, there are 64 threads. To determine how much movement we get out of a single revolution of the aperture, we'll need to divide 1 (the inch moved by 64 revolutions) by 64 (the thread pitch). That comes out to .015625 inches of movement in a complete revolution. Since both the aperture and the dovetail slide that it threads into have tolerances, and since I'm not always so good with math, we'll round that to .016" per full revolution.
Next up, we'll need to determine what that translates to in shift of impact. We'll start by dividing .016 (the movement of the rear sight) by 20 (the sight radius of the rifle), which comes out to .0008. Next, we multiply that by the distance we're zeroing at, which is 1,800. That number comes up as 1.44". So, for every full revolution of the aperture, the point of impact will move about 1.5" (again, tolerances on both parts and math without a calculator are not always my strong suit, so I'm rounding to make life easy at the range). That also means there should be about a .75" shift in POI for a half-turn on the rear sight.
For windage, the screws are a 40 TPI. So, for one full revolution, the screw is moving .025". Dividing that by 20 and multiplying that by 1,800 gives us the result of a 2.25" shift in impact per full revolution of the windage screw.
Zeroing the Ruger Gunsite Scout Rifle
The Ruger Gunsite Scout also uses an aperture with threads at 64 TPI and, coincidentally, has a 20" sight radius. However, I zeroed it at 100 yards. That means that every revolution is going to move the POI by 2.88" [(.016/20)(3600)=2.88].
Windage is also different.
The windage screws on the Gunsite Scout are 32 threads per inch. That works out to a 5.6" shift per full revolution [(1/32)/20)*(3600)=5.6].
With that figured out, it was time for the range.
How to Zero your Rifle with Iron Sights
I fired the first group out of the Marlin and had a group that was about 10.25" high (I was holding at 6 o'clock on the bullseye to put the group as close to 6 o'clock as possible – I wanted the group to impact at the top edge of my front sight, and that's the easiest way for me to keep a consistent hold).
The rear sight only had three full revolutions of downward movement, which works out to 4.5", which wasn't enough. That meant I could save ammo – I knew I couldn't zero the rifle with the front sight I had installed. It happens occasionally.
Working the formula from above backward (10.25" of POI shift divided by 1,800 comes out to .005694 multiplied by 20) tells me that the front sight needs to be about .114" taller to zero correctly. That was a bummer, but saving the ammo was nice. Once I was back in the office, I swapped the front sight for one that was taller and was ready to go for the next time.
For round 2, the first group was centered for windage but impacted about 2.5" high:
I screwed the aperture in 1.5 revolutions (1.5 revolutions * 1.5 inches per revolution =2.25" total shift in impact) and fired again:
Not my best group, and definitely not one to stop on. I settled back in behind the carbine, remembered the fundamentals, and put three more rounds down range:
That wasn't too bad.
The group is a touch high, but a half revolution on the rear aperture would have put me just under my point of aim. If I can't get the exact zero, I prefer to be just a little high rather than low.
How to Zero your Rifle with Iron Sights and an Optic
Now it was time to get the Ruger squared away. I started with the irons. While the optic is mounted in Leupold QRW rings that, in my experience, tend to return to zero pretty well, I'd prefer not to install and remove the optic and expect it to return to zero. Surprisingly, the irons were on with the first group (sorry, I didn't get a photo of the target).
With the optic installed, I had previously run the ballistics and determined that at 100 yards, I needed to be about .75" high at 100 yards for a 150-yard zero. I benched the rifle and shot the first group at 100 yards holding on the red dot in the center of the Shoot-N-C target:
Not too bad. The center of the group was about ½ inch high.
I dialed up one increment (on the Leupold, the adjustments are ¼ MOA) and fired again:
For shooting at 100 yards, that's sufficient. The next step should be shooting at a true 150 yards.
Unfortunately, the range was pretty busy that day, so I didn't have the opportunity to set up a target at 150 yards and get a true 150-yard zero. Before I get out in the field with the rifle, I will want to do that. The ballistics programs that are available now are very, very good, but nothing trumps actually shooting at the intended distance.
Hopefully, you'll find this info helpful when you get out to zero your rifles. Get out there, get them zeroed, and prepare for hunting season!
About XS Sights: XS Sights is known for making the fastest sights in any light. For more than 25 years, the XS team has created some of the most innovative sights on the market today for pistols, rifles, and shotguns. Whether used for personal defense or hunting, these sights are designed and built to be the absolute best for their specific purpose. American Made. Texas Proud. 2A Strong.
#Range
#How to
#Rifle
#Carbine
#Rifle Sights


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Injection improves vision in a form of childhood blindness
PHILADELPHIA — A new treatment for patients with a form of congenital retinal blindness has shown success in improving vision, according to results published today in Nature Medicine led by researchers at the Scheie Eye Institute in the Perelman School of Medicine at the University of Pennsylvania.
The treatment was designed for patients with CEP290 mutations and a diagnosis of Leber congenital amaurosis (LCA). CEP290 acts as a gate between two compartments of photoreceptor cells – a type of sensory neuron in the retina that converts light into signals that provide vision. Primary photoreceptor blindnesses – such as those caused by CEP290 mutations – are the most common form of LCA and they are currently not treatable.
In this clinical study at sites in the United States and Europe, participants received an intraocular injection of an oligonucleotide – a short RNA molecule – created to reduce the mutant CEP290 protein levels in the photoreceptors and restore retinal function.
"It was very dramatic to see one of the patients improve from only being able to differentiate light or dark to reading many letters on an eye chart at two months following the first injection," said lead author Artur V. Cideciyan, PhD, a research professor of Ophthalmology. "So, we performed a thorough interim analysis of all results from all patients."
Ten patients received at least one injection into their worst-seeing eye. At three months after the first injection, half of the patients showed improvements in visual acuity, measured by the ability to either read letters, or distinguish direction of black and white bars.
The most basic functions of photoreceptors are to receive and then signal light. This aspect of vision was tested in patients by presenting flashes of light in the dark and measuring the dimmest flash intensity detected. Treated eyes could detect on average more than six-fold dimmer lights three months after the injections compared to before. The results were highly statistically significant. Evaluations with two colors of flashes suggested that it was the cone photoreceptors used for daytime vision that were improving with the treatment.
"This therapy to repair the genetic defect in LCA10 is a breakthrough in treatment strategy and will open the door for clinical trials in other patients with this condition and other similar conditions that are currently untreatable," said Samuel G. Jacobson, MD, PhD, a professor of ophthalmology and co-lead author of the study.
All patients enrolled so far into the study had two different CEP290 mutations. The p.Cys998X mutation causing a splicing defect was common in all patients and was specifically targeted by the oligonucleotide.
"We performed an extreme form of personalized medicine where we targeted not just a specific gene but a specific mutation in a gene," said Cideciyan. "It is gratifying to see clinical evidence supporting the action of this oligo predicted from basic science. In the future, we hope to evaluate patients carrying two identical splicing mutations to determine whether the efficacy of the injection might be even greater."
The authors note that the clinical trial is ongoing to measure safety and efficacy of the injections long-term and the effects of further doses.
Additional Penn authors include Jason Charng, Alexandra V. Garafalo, Alejandro J. Roman, and Alexander Sumaroka. Other authors include Arlene V. Drack, Ian C. Han, Maria D. Hochstedler, Wanda L. Pfeifer, Elliott H. Sohn and Stephen R. Russell from Carver College of Medicine, University of Iowa; Allen C. Ho from Wills Eye Hospital, Thomas Jefferson University; Magali Taiel, Michael R. Schwartz, Patricia Biasutto, Wilma de Wit, Peter Adamson, David M. Rodman, Gerard Platenburg, and Maria D. Tome from ProQR Therapeutics; Michael E. Cheetham from UCL Institute of Ophthalmology, and Irina Balikova, Fanny Nerinckx, Julie De Zaeytijd, Caroline Van Cauwenbergh, and Bart P. Leroy from Ghent University.
The trial is being funded by ProQR Therapeutics.
Penn Medicine is one of the world's leading academic medical centers, dedicated to the related missions of medical education, biomedical research, and excellence in patient care. Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System, which together form a $7.8 billion enterprise.
The Perelman School of Medicine has been ranked among the top medical schools in the United States for more than 20 years, according to U.S. News & World Report's survey of research-oriented medical schools. The School is consistently among the nation's top recipients of funding from the National Institutes of Health, with $405 million awarded in the 2017 fiscal year.
The University of Pennsylvania Health System's patient care facilities include: The Hospital of the University of Pennsylvania and Penn Presbyterian Medical Center — which are recognized as one of the nation's top "Honor Roll" hospitals by U.S. News & World Report — Chester County Hospital; Lancaster General Health; Penn Medicine Princeton Health; Penn Wissahickon Hospice; and Pennsylvania Hospital – the nation's first hospital, founded in 1751. Additional affiliated inpatient care facilities and services throughout the Philadelphia region include Good Shepherd Penn Partners, a partnership between Good Shepherd Rehabilitation Network and Penn Medicine, and Princeton House Behavioral Health, a leading provider of highly skilled and compassionate behavioral healthcare.
Greg Richter
https://www.pennmedicine.org/news/news-releases/2018/december/injection-improves-vision-in-a-form-of-childhood-blindness
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As a big fan of Warhammer Underworlds: Shadespire I was pleased with the news last year of a second Underworld location….the Nightvault. Not an entirely unique locale the Nightvault is deep within the heart of the Mirrored City, Shadespire. More importantly though…more warbands!
Continuing my recent post on Games Workshop's new competitive title – Warhammer Underworlds Shadespire – here's a picture of the Bloodreaver portion of the base box painted up after conversion.


The association community is full of bright, optimistic professionals whose minds are sparking with promising and innovative ideas. But, ideas aren't worth much unless you put them into action. The biggest barriers to association innovation are the people, processes, and practices that make up your organizational culture.
Take a tough look at your organizational culture to see whether you're tolerating these barriers to innovation. You know what they say… the first step to solving a problem is knowing you have a problem.
Sometimes, outdated or ill-fitting technology holds an association back from pursuing change, but usually people are to blame. Or, more accurately, the organizational culture is causing dysfunction.
Dysfunction rules when departments compete for resources, and are more concerned with their own agendas than organizational priorities. Silent turf wars result when one department sees another department's project encroaching on their territory or staff time.
Turn this warped perspective around by planning more cross-departmental projects involving staff at different levels. You may not be able to eliminate silos, but you can connect them. Encourage communication and knowledge sharing between departments so staff understand what's going on and why.
Help staff keep their eyes on the prize—larger organizational goals. Spell out expectations: when an innovation project is approved to go forward, all departments are expected to support their colleagues. All for one and one for all.
What happens to employees who question the way you've always done it? What about the ones who go out on a limb by suggesting a process or practice change? Are they putting their reputation, raise, promotion, or job at risk?
• Suggesting and trying out new ideas for improvements and changes—no matter the result.
• Making an effort to increase their skills and knowledge.
• Working with others to achieve organizational goals.
Employees who try to do the right thing shouldn't be punished for coming up short.
The human ego craves safety—it's our survival instinct at work. That's why so many organizational cultures are rooted in the past—it's what they know.
Innovation can be threatening to staff and members who are invested in legacy programs and processes. A change to their way of doing things could make them feel dishonored or incompetent.
Include all stakeholders in innovation projects, especially those who are tied to the old way of doing things. They need to feel like they're an important part of the change, plus they have knowledge to share. You don't want them to feel threatened by change, and get defensive or obstructive as a result.
Nurture a forward-thinking, change-receptive culture by supporting cross-departmental ideation sessions where colleagues can tackle problems and opportunities together. Have a process for collecting and reviewing new ideas, and for bringing new perspectives to the planning table.
Innovation isn't for the privileged few. You shouldn't have to occupy a certain level in the org chart, work in a favored department, have seniority, or be part of an office clique to contribute your thoughts and ideas. When you always invite the same people to meetings and ask the same people for their opinion, you're missing out on valuable perspectives. Innovation conversations must be intentionally inclusive, not exclusive.
Give everyone on staff the permission and responsibility to help solve problems and explore new opportunities, especially those who have the most contact with members and customers. Create a safe space or process for new ideas to emerge without fear or consequence. Encourage those who normally don't have a voice to share their thoughts in a way that's most comfortable for them. Listen up and down the org chart and across generations.
People make internal cost/benefit analyses when it comes to change because time is a non-renewable, limited resource. When you're swamped with work, it's easy to keep doing something the same old familiar way because it takes less time.
Change is stressful. It means you have to find time to attend project meetings, set up new processes, and figure out something new. Who has that kind of time? Because innovation projects pile on to an already full plate, work with staff to delegate or put tasks on hold so the project doesn't become overly burdensome.
Time-starved employees aren't likely to come up with innovative ideas in the first place. It takes time to better understand your members and market. It takes time to read, think, and learn. Give staff time to slow down and think. Create meeting-free blocks in everyone's schedules. Set aside time every week for professional development. Dedicate 20 minutes in weekly meetings to pie-in-the-sky innovation discussions so everyone has a chance to contribute.
Association staff with ideas for innovation often have to work with an overtaxed IT department who's more likely to say "No" than "Maybe" or "Yes." Staff should see their IT colleagues as partners who help them explore new ideas and plan innovation projects, not as buzzkills.
If your IT team is spending most of their time on network management or help desk requests, they don't have the bandwidth to be technology advisors to other departments. It's better to outsource IT operational tasks so they can focus on more strategic and meaningful work.
Staff shouldn't have to spend time and energy making the case for investing in innovation. Associations need an innovation budget along with a process for approving and prioritizing new projects.
Resources are best invested in projects that further the mission and improve the membership experience. When staff have a good understanding of organizational goals and strategies, they're less likely to propose ideas that are out of alignment with the mission.
Staff must have a sense of which ideas align with strategic goals and which don't. Rejection is demoralizing. It dampens the will for sticking your neck out. If your idea has been rejected once, you're less likely to try again—unless the organizational culture encourages you to do so. Seeing your fall from grace, colleagues will be hesitant to follow your example.
Ideas are great, but you need to act on them. Some organizations are aware of the disrupters in their changing market, but don't do anything about them. You need people on staff who constantly scan the horizon for signals of disruption and change, and a process that takes their "intel" and turns it into a topic for discussion, evaluation, and action.
But don't just rely on these "scouts." Everyone on staff must understand the process for submitting an idea, and the criteria used for evaluating their idea.
Agility takes practice. Start with small pilot projects. For a greater chance of success, make sure you have people on staff with project management expertise who can guide these projects. Test, evaluate, tweak, and try again. Know when to move forward and when to walk away with lessons learned.
Innovation doesn't have to be a large undertaking. You can improve a process so it provides a better user experience. Maybe next you try repurposing content to create a micro-credential, or creating a blended learning experience in conjunction with your annual conference. Cultivate an innovation mindset in your staff, scrutinize your organizational culture for innovation barriers, and start flexing your innovation muscle.


Consider what others are wanting when they are searching for videos.
Most people are looking for something entertaining as well as informative. If you are explaining how to do something, use inflections as you talk and give information that others may not know. It is also beneficial to show how to do something while talking.
When you are making a video, do not focus on what it looks like. Many times you will not get a great return on a very large investment. Even large corporations, like Dell, have been successful with simple demos made by employees.
This entry was posted in Marketing and tagged Marketing on May 3, 2018 by ScottyF.


> to do this (via make.conf).
> > consequence is that new CONFLICTS checking routines are required.
> > accomplish. If you want to do this `just because it can be done' -  yes.
> files and such around.
> on, but I won't since it'd start to get off-topic.
> utility called showpath that can be used to set paths programatically.
> archmaster) and then distributed out to clients.
> about FreeBSD lacking xhier before they even come up.
> "./configure --prefix=/software/packagename" usually does the trick.
> you a full day for Solaris."
> package tarball across to be installed with pkgadd).
compatable fasion using the pkgviews concept.


This 6 minute segment is not merely smart and hysterical, it is littered with stomach turning truths and prescient commentary on the reality of printed news. The "Aged News" exchange about 3 minutes in is a brilliant reporter/subject exchange that is almost unbelievable to watch.
← Rocket camping near Cape Canaveral, Fl.


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The formation of a tubular organ, such as the heart, requires the communication of positional and polarity signals between migratory cells. Key to this process is the establishment of a new luminal domain on the cell surface, generally from the apical domain of a migratory cell. This domain will also acquire basal properties, as it will produce a luminal extracellular matrix. Integrin receptors are the primary means of cell adhesion and adhesion signaling with the extracellular matrix. Here we characterise the requirement of Integrins in a genetic model of vasculogenesis, the formation of the heart in Drosophila.
As with vertebrates, the Drosophila heart arises from lateral mesoderm that migrates medially to meet their contralateral partners, to then assemble a midline vessel. During migration, Integrins are among the first proteins restricted to the presumptive luminal domain of cardioblasts. Integrins are required for normal levels of leading edge membrane motility. Apical accumulation of Integrins is enhanced by Robo, and reciprocally, apicalisation of luminal factors like Slit and Robo requires Integrin function. Integrins may provide a template for the formation of a lumen by stabilising lumen factors like Robo. Subsequent to migration, Integrin is required for normal cardioblast alignment and lumen formation. This phenotype is most readily modified by other mutations that affect adhesion, such as Talin and extracellular matrix ligands.
Our findings reveal an instructive role for Integrins in communicating polarising information to cells during migration, and during transition to an epithelial tube structure.
Vascular endothelia are characterised by a polarised cell architecture, wherein Cadherin based cell junctions establish the integrity of the vessel walls, while the lumen of the vessel is defined by Integrins and an extracellular matrix (ECM) [1, 2]. When these vessels first form, grow or are remodeled, the progenitor cells must be less polarised, as they will change neighbours, migrate through other tissues, and respond to local growth cues. During vessel formation, progenitors may have a more mesenchymal organisation, while the differentiated vessel must have stable epithelial polarisation of membrane domains. Vasculogenesis, therefore, can be interpreted in the framework of mesenchymal to epithelial transition .
Integrins are transmembrane receptors comprised of pairs of α and β subunits, which link the ECM to the cell cytoskeleton, and mediate cell locomotion, adhesion and signals that affect differentiation and survival [4, 5]. There are at least 7 different Integrin dimers expressed in the vascular system, implicated in vascular cell migration, and subsequently in lumen formation . Reduced B1-Integrin function in endothelia, by B1-Integrin antibody in quail embryos  or by knockout of B1-Integrin function restricted to mouse endothelia  result in a reduced or lost vascular lumen. In other contexts, reduced Integrin function is not sufficient to prevent lumen formation, possibly due to the contributions of other ECM factors .
During mesenchymal to epithelial transition, Integrins are thought to regulate migration by activation of intracellular cell polarity signals that modify submembrane protein scaffolds and regulate intracellular protein traffic . The same network of polarising signals, including Rho family GTPases Cdc42 and Rac1, Pak kinase and the Par3-Par6-aPKC complex are also linked to lumen formation in vitro models of lumen formation, such as Madin-Darby Canine Kidney Cells and Human Umbilical Vein Endothelial Cells [9–11]. Therefore, Integrins may play a central role during lumen formation.
Drosophila affords multiple models of lumen formation, such as the salivary gland, trachea and dorsal vessel (heart) that enable a genetic dissection of these signal pathways [12–14]. Here we focus on the role of Integrins in the formation of the lumen of the Drosophila heart. Despite its relative simplicity, the Drosophila heart shares conserved mechanisms of cell fate determination and differentiation with vertebrates, reviewed extensively [15, 16]. The Drosophila homologues of genes associated with 34 different heart disease genes have been identified, including ones associated with cardiomyopathies, conduction failure, hypertension, atherosclerosis and vascular malformations [17, 18].
As with vertebrates, the Drosophila heart precursors arise from lateral mesoderm, which migrate medially after specification to meet their contralateral partners, and then assemble a midline vessel [13, 19]. The regulators of this collective cell migration event have not been characterised, however genetic and developmental studies illustrate that the precursors (called myocardial cells or cardioblasts, CBs) maintain a close association with the migrating ectodermal cells that provide the inductive signals that establish cardiac fate. The inductive signals are Pyramus, a ligand for the FGF receptor Heartless, and Decapentaplegic, a ligand for the BMP receptor Thickveins [20, 21]. Reduced Cadherin function does not affect CB alignment or migration, but the sole Integrin dimer expressed by the CBs (αPS3, βPS), and ligand (Laminin) are required for CB alignment [19, 22]. Significantly, the timely migration and alignment of CBs requires the Slit morphogen and Robo receptor, a requirement that interacts genetically with the αPS3 gene scb, and the Laminin genes LanA and wing blister [23–25]. Furthermore, the subsequent formation of a lumen in the Drosophila heart requires Slit pathway genes, as well as E-cadherin, Dystroglycan, Syndecan and NetrinB [19, 26–28]. These observations suggest that the integrated function of all these cell surface signals are required to complete cell polarisation and establish the luminal ECM. Previous studies suggest that Robo signals establish the luminal domain by excluding Cadherin adhesion [27, 29]. Syndecan, recognised as a co-receptor for Slit, is required together with Robo to establish a lumen . However, it is not clear whether Integrins function upstream to apicalise the migrating CBs, or as co-factors with Robo, to help assemble the luminal ECM. Here we characterise changes in CB polarisation and heart morphogenesis subsequent to genetically altered Integrin function. We identify a role for the αPS3, βPS1 Integrin dimer in both the early establishment of the apical, pre-luminal domain, as well as a requirement upon Robo for maintained apicalisation of proteins required for lumen formation. This suggests that Robo dependent lumen formation acts downstream of other cell polarising signals.
The Drosophila heart vessel is formed by the dorsal and medial migration of lateral somatic mesodermal cardioblasts (CBs). The migration of this mesoderm is linked to dorsal closure, which is the tandem dorsal migration of lateral ectoderm to envelop the gut, which also replaces a transient embryonic tissue, the amnioserosa on the dorsal surface of the embryo . Previous studies have established a role for the αPS3/βPS1 Integrin dimer in the displacement and involution of the amnioserosa, as well as the assembly of the heart vessel . Involution of the amnioserosa, and dorsal closure is incomplete in embryos lacking zygotic function of either αPS3 (scb) or βPS1 (mys), complicating an assessment of heart morphogenesis. We have assessed the mutant heart in two manners: in zygotic mutants, and after dsRNA mediated reduction of Integrin levels. Zygotic mutants for the amorph scb 2 had complete dorsal closure of abdominal segments 6 to 8, which contains most of the heart chamber, so our analysis focused on these segments. In wildtype embryos, and embryos heterozygous for scb 2 , two rows of CB were aligned across the midline, and the morphogen, Slit was restricted to the heart lumen (Figure 1A). Embryos mutant for αPS3 (scb 2 ), in contrast, revealed less regular alignment of CB nuclei, with displaced CBs forming blisters across or beside the midline being a common feature (Figure 1D). Levels of Slit were reduced, and were not concentrated apically. Similarly, zygotic mutants for βPS1 (mys 1 ) had blisters and gaps in the CBs, and reduced Slit accumulation (Figure 1J, Table 1), although apicalisation was better preserved.
We found that βPS1 Integrin was concentrated in the luminal domain of wildtype stage 17 hearts (Figure 1B, arrow) with lower levels on the basal surface of the CBs. In the absence of α Integrin, β Integrin is not properly targeted to the cell surface . Accordingly, in scb mutants, levels of βPS1 were reduced, with relatively more immunolabel outside the luminal domain (Figure 1E). βPS1 antigen was not detected on CBs of zygotic mys 1 mutants (Figure 1K).
Pericardin is a collagen-like protein secreted by the pericardial cells, which concentrates at the CB-pericardial cell interface . In wildtype, Pericardin labeling marked a continuous structure at the base of the CBs (Figure 1C). In scb mutants, Pericardin label more frequently surrounded the pericardial cell (arrowhead, Figure 1F), and was distributed discontinuously on the CB surface. Embryos mutant for mys have Pericardin distributed irregularly over the pericardial cell surface, and pericardial cells were displaced towards the midline (asterisk, Figure 1L).
As an independent approach to assessing Integrin function in the CB, we have reduced αPS3 and βPS1 protein levels in the mesoderm, with targeted expression of dsRNA (in dMEF2-GAL4/UAS- scbRNAi embryos in Figure 1G-I, and in dMEF2-GAL4/UAS- mysRNAi embryos in Figure 1M-O). We obtained qualitatively similar results with 2 scbRNAi strains and 2 mysRNAi strains (see Methods). Dorsal closure was normal after Integrin knockdown in the mesoderm, and CBs from all segments met their contralateral partners. However, small gaps or clumps in alignment are observed (Figure 1G, M). As in the mutant, the level of Slit was reduced (Table 1), and strikingly, Slit was detected between ipsilateral cells, a membrane domain from which it is normally excluded (arrowheads, Figure 1G, M) [19, 29]. We further assessed the distribution of βPS1 Integrin (Figure 1H, N) and Pericardin (Figure 1I, O) and encountered phenotypes intermediate between wildtype and scb 2 . Lower levels of βPS1 were observed subsequent to scb RNAi expression, possibly because of some perdurant αPS3 protein. Very low levels of βPS1 labeling subsequent to mysRNAi (Figure 1N) suggests that quantities of maternally contributed βPS1 are limited. Nevertheless, for both Integrin knockdown genotypes, Slit and Pericardin distribution was abnormal (Figure 1G, I, M, O).
Considered together with the data from the zygotic mutants, we conclude that Integrin function is required for orderly alignment of the CBs, is essential for establishing an apical or luminal domain for CBs, and polarises Pericardin on the pericardial cells. The reduction in the level and apical deposition of Slit in mutants indicates that Integrins are required to target or stabilise this morphogen apically.
Previous studies have established that apicalisation of Slit is required to establish a lumen in the Drosophila heart [23, 25]. Given the mislocalisation and reduced levels of Slit subsequent to reduced Integrin function, we sought to determine if lumen formation was similarly affected. A well developed lumen was visualised in cross-sections of stage 17 hearts, and no lumen was detected between contralaterally apposed CBs in the heart region of scb 2 mutants (Figure 2A, B). However, expression of a αPS3 transgene in the CB of scb 2 mutants partially restored lumen formation (Figure 2C). These data are consistent with a model wherein Integrin acts to apicalise Slit binding and signaling, which is a pre-requisite for lumen formation. We addressed this model directly by determining whether restoring αPS3 expression to the CBs in a scb mutant would restore apicalisation of the Slit receptor, Robo. In contrast to wildtype (Figure 3A), Robo levels are reduced and incompletely apicalised in scb mutants (Figure 3B and inset). As expected, mesodermal expression of αPS3 in scb mutants did not restore normal dorsal closure. However, Robo, was concentrated apically (Figure 3C), and no longer laterally as seen in scb 2 mutants. Truncation of the short cytoplasmic domain of αPS2 locks the Integrin into an "excessively active" high affinity receptor, forming ectopic adhesions . Rescue of scb mutants with a similarly truncated transgene was sufficient to restore apicalisation of Robo, also expanding the apical area of Robo expression (Figure 3D).
During their medial migration, the CBs are in an intermediate state of polarisation. The CBs adhere to their ipsilateral neighbours, which is likely Cadherin based , and the advancing and trailing edges interact with the ECM, which is likely Integrin based. However, when the CBs meet their contralateral partners, the leading edge of the cells will develop a luminal domain that concentrates Slit and Robo. Given that a luminal domain fails to develop in scb mutants, and that luminal markers require scb function to apicalise, we speculated that Integrins may be instructive in establishing the location of the luminal domain. We therefore sought to determine how the distribution of Integrins reflected the transition from a migratory phenotype to epithelial differentiation. In stage 15 embryos, before the leading processes of the CBs make contact across the midline, the βPS1 Integrin was localised primarily on the leading edge of the migrating CBs (Figure 4A, arrow) while much less label was detected on the trailing edge (Figure 4A, arrowhead). The preponderantly apical distribution was not significantly altered once the lumen was formed (Figure 4D). In contrast, Robo protein was located on apical, lateral and basal surfaces of the CB during migration (Figure 4B), and is entirely luminal by stage 17 (Figure 4E). Dystroglycan, another apical membrane protein required for lumen formation, was also excluded from lateral membrane domains at both stages, although more basal labeling was evident during migration that was reduced after lumen formation (Figure 4C, F, arrowheads).
Previous studies demonstrate that the apical surface of mature CBs are subdivided into a junctional (J) domain and a luminal (L) domain . We sought to determine whether formation of these domains required Integrin function, and whether early Integrin apicalisation reflected early establishment of the luminal domain. We therefore examined migrating CBs in cross-sectional view to determine whether Integrin was spatially restricted to a subdomain of the leading edge membrane before midline fusion. The dorsal limit of a wildtype CB at stage 16 extended Dystroglycan labeled membrane towards the midline (Figure 5A, arrowhead), yet this extension was missing in scb mutants (Figure 5D, arrowhead). βPS1 Integrin accumulated immediately ventral to the dorsal extension during migration, and this domain contributed to the Integrin rich luminal membrane at stage 17 (Figure 5A, B, arrowheads). The accumulation of Integrin was reduced in scb mutants, but a presumptive luminal domain was still apparent (Figure 5D, E, arrowheads). At stage 17, Dystroglycan labeling outlined the heart lumen (L domain; Figure 5B, C, arrowhead), and Discs-large accumulated at the adhesive junction between contralateral CBs (J domain; Figure 5C, arrow). When Integrin function was reduced, the Discs-large domain is uninterrupted, and a small domain expressing both Discs-large and Dystroglycan was observed (Figure 5F).
These data suggest that early Integrin aggregation presages the formation of the luminal domain during CB migration, and Integrin may therefore be instructive in localizing factors like Robo, also required to establish the lumen. These data do not exclude the possibility that other apical signals work in concert with Integrin. We also explored the possibility that Robo signaling augments apical signaling. In embryos lacking function of both Robo1 and Robo2 (robo 1 lea 54-14 ), βPS1 and Dystroglycan distribution were remarkably less polarised at both stages 15 and 17 (Figure 4G, H, I), even though Robo was not normally apically concentrated until stage 17 (Figure 4E). At stage 15 it is unlikely that CBs can detect contralateral Slit. Therefore, autocrine Slit signaling may contribute to CB polarisation during migration.
Cell migration requires polarised membrane and cytoskeletal trafficking, and instructive polarising signals may require outside-in signals from Integrins [8, 34]. Of the apical markers examined, only Integrin is concentrated at the apical leading edge before stage 16. Embryos mutant for scb 2 appear to lack a leading membrane process (Figure 5D). We therefore sought to determine whether the exploratory activity of the leading edge requires normal Integrin function. Leading edge activity is effectively assessed with fluorescently tagged moesin, which binds to submembrane actin, outlining lamellipodia and filopodia . We compared the density and length of membrane processes of wildtype CBs (Figure 6A) with those of zygotic mys (Figure 6B) and scb mutants (Table 1). Although leading edge activity was clearly present in mys, only 12% of the leading edge was active, while in contrast, membrane activity was more vigorous in wildtype, incorporating 41% of the leading edge of CBs (Table 1). A phenocopy of this effect subsequent to dsRNA interference of mys or scb could not be generated, possibly due to the presence of an additional UAS target (UAS-mCherry). The low level of leading edge activity in Integrin mutants may reflect maternally contributed Integrin function, or compensation by other apicalising signals. It remains to be resolved whether Integrin signaling from the pre-luminal domain affects leading edge activity, or whether Integrins function in the leading processes, but are not detectable after histochemical processing.
A contribution by Integrin function to CB migration or polarisation can be revealed through genetic interactions between scb and mutations in genes that act in the same, or a converging pathway. We have surveyed possible interactions with genes coding components of the ECM, and with genes that act to mediate adhesive or morphogenetic signals. Similar phenotypes were observed in embryos heterozygous for scb 2 , and also heterozygous for mutations in βPS1 or known Integrin ligands Collagen IV (vkg) Laminin chains α3,5 and α1,2 (lanA, wb) and Tiggrin (tig, not shown) (Figure 7B, C, D, E respectively). Phenotypic interactions were characterised by interruptions in the continuity of each CB leading edge, evidenced by either small gaps (Figure 7, asterisks) or spans or clumps of CBs, three or more cells across (Figure 7 arrows). We also screened for interactions between scb and genes for intracellular factors that mediate cytoskeletal responses to signals from the membrane. Interestingly, embryos doubly heterozygous for scb and Talin (rhea) had a phenotype similar to that seen for the ECM gene interactions, suggesting that Talin, which links Integrins to the actin cytoskeleton, mediates the effects of adhesion to the ECM (Figure 7F). In contrast, perturbations in heart morphology were less stereotyped for genes believed to affect actin remodeling, and acting downstream of Robo (dab, dock, and abl; Figure 7H, and data not shown) or Integrin (ilk, Figure 7G). These data suggest that Integrin function in CB alignment is more sensitive to factors affecting adhesion than to changes in cytoskeletal signaling.
Morphogenesis of the Drosophila heart provides an accessible genetic model to dissect the signals that orient migrating mesenchymal cells, and enable the cells to transform to a differentiated, stable epithelial structure with luminal and basal identity. A diversity of genes has been identified that are required for lumen formation in the heart. They include genes encoding ECM proteins, such as Laminin A, homophilic adhesion, such as Cadherin, and genes associated with mediating cell guidance, such as Slit or NetrinB [19, 26–28]. This work establishes that Integrins are also required for CB polarisation- during cell migration, for apical leading edge motility, and during lumen formation. A lumen fails to develop in the hearts of embryos lacking scb function, but the luminal domain can be restored by expression of αPS3 in the CBs of a scb mutant.
Although Robo is believed to be key to the establishment of the luminal domain, the mechanisms that localise Robo function are unclear [27, 29]. Our previous studies establish a close functional relationship between Robo function and Integrins, in both axon guidance, and in heart morphogenesis [23, 36]. Apical accumulation of βPS1 Integrin precedes apicalisation of the proposed lumen determinants, Slit and its receptor, Robo. Furthermore, in scb 2 mutants, Robo and Slit do not accumulate apically, and in fact, are found on lateral cell surfaces, associated with Cadherin based adhesion. Restoring scb function with either normal or high affinity αPS3 restores Robo apicalisation- suggesting that regulating Integrin affinity for the ECM is not critical for its apical signal.
Robo signaling prevents local accumulation of Cadherin in both neurons and CBs - and in the heart, it has been proposed that this is the basis of generating an non-adherent luminal domain [29, 37]. Our data suggests that Robo signaling must act in concert with Integrin to restrict Cadherin from the apical domain. In the salivary gland model of lumen development, Cadherin is removed from the luminal domain by endocytosis, employing Rho family GTPases and Pak1 , which in turn, are downstream of Integrin and Robo signals [39, 40].
Given that mutation of any one of 7 cell surface receptors (Cadherin, Integrin, Robo, Neurexin, Syndecan, Dystroglycan and Unc5) is sufficient to block lumen formation, it is likely that cooperative signaling defines the luminal domain and luminal differentiation [19, 24, 26–28]. Of the 7 required receptors, Robo, Syndecan, Dystroglycan, Integrin and Unc5 locate to the luminal domain. Integrin, its ligand Laminin , and Unc5  concentrate in the presumptive luminal domain before the others, and likely are instructive. Our data also suggests that the presumptive luminal domain is defined by Integrin accumulation during migration, and before contact with contralateral CBs.
At stages 15 and 16, βPS1 Integrin localises apically when Robo is still expressed on all membrane domains. Nevertheless, at this stage, polarised Integrin distribution requires Robo function. It is possible that Integrins suppress Robo turnover at the apical surface only, and Robo signaling stabilises the Integrins, culminating in the apical aggregation of Robo seen by late stage 16. Leading edge membrane motility becomes most pronounced during stage 16. Loss of Integrin function reduces the fraction of the Leading Edge that is active. In contrast, loss of robo function reduces Leading Edge activity uniformly, and filopodia are rare ([27, 29] and unpublished observations), suggesting that Integrin dependent accumulation of Robo augments membrane activity.
The sensitivity of scb function to ECM genes Collagen IV and Laminin suggest that Integrin effects on apicalisation are adhesion dependent. The genetic interaction of scb with rhea (Talin) further suggests that assembly of a complex of ligand-bound Integrin, linked to the actin cytoskeleton through Talin, both stabilises the apical membrane domain, and enables Robo accumulation. An understanding of how the luminal domain differentiates requires future study on signaling by this multi-receptor complex.
We have characterised the contribution of Integrin function to cell migration and lumen formation in a mesodermal organ, the Drosophila heart. Integrins are required to maintain the alignment of the migrating CB leading edge cells, and are also required for normal levels of leading edge motile membrane activity. A pre-luminal domain, first revealed by early Integrin accumulation, is defined before the CBs meet their contralateral partners. Integrin accumulation is required to stabilise the morphogen Slit, and its receptor Robo, to the pre-luminal domain. This is consistent with Robo signaling contributing to leading edge membrane activity. Even through Robo does not aggregate apically in migratory CBs, its expression is required to stabilise Integrins in the pre-luminal domain.
We confirm an earlier report that αPS3 Integrin is required for heart lumen formation . Integrin function is also required to localise a uniform ECM around the heart, as visualised with Pericardin. Genetically, this function is most sensitive to genes required for adhesion, such as for Talin, and ECM ligands. Slit signaling during axon guidance and salivary gland migration is also sensitive to Integrin function [14, 36]. Integrins may have a conserved function in establishing membrane domains rich in Robo to enable localised morphogen signaling.
The mutant strains scb 2 , scb 01288 , mys 1 , mew M6 , lea 2 , robo 1 lea 54-14 , sli 2 , wb SF11 , wb 09437 , dock 04723 , vkg 177-2 , ilk ZCL3111 , ilk 2 , dab M54-R and rhea 1 were obtained from the Bloomington Stock Center. The laminin allele lan A9-32 was provided by C. Goodman (Berkeley), ras 5703 by D. Montell (Johns Hopkins University), lea 5418 by C. Klämbt (Münster), vkg p1003-83 by N. McGinnis (University of Massachusetts) and tig X was provided by T. Bunch (University of Arizona). Multiple alleles of each gene were tested when possible. All stocks were maintained over β-galactosidase marked balancers. The following GAL4 and UAS lines were used for ectopic expression and knockdown experiments: dMef-GAL4, P[TRiP HMS00043](mys), and P[TRiPJF02696](scb) from the Bloomington Stock Center, UAS-scb RNAi (KK106326) and UAS-mys RNAi (KK100518) from the Vienna Stock Center. UAS-scab was constructed using 5'-TGG CGT AGA ATT CAT CTG TTG-3' (EcoRI site) and 5'-TCA CGA TCT AGA GGA CAT TC-3' (XbaI site) as primers for a PCR reaction to amplify the full length protein ScabA from the original EST clone (RE41844, Berkeley Drosophila Genome Project). The lacZ enhancer trap line B2-3-20 used to visualize the cardial cell nuclei was provided by E. Bier . tup-F4-GFP was provided by R. Schulz  and UAS-moe-mCherry was provided by T. Millard .
Embryonic development proceeded at 25°C for all experiments, except the RNAi experiments, performed at 29°C. Immunohistochemistry techniques were adapted from . Embryos were collected, dechorionated, fixed and incubated in primary antibody diluted in phosphate buffered saline (PBS) containing 0.1% Triton X and 10% normal goat serum. β-galactosidase was detected with a chicken antibody (1:150) . The following monoclonal antibodies were obtained from the Developmental Studies Hybridoma Bank, under the auspices of the NICHD: anti-Robo (1:30), anti-Slit (1:30), anti-Discs Large (1:30), anti-Pericardin (1:30), anti-βPS1 (1:30). Dystroglycan antiserum (1:600) was kindly provided by W. Deng . To visualize muscle cell nuclei, polyclonal anti-MEF2 antibodies were generated by injecting a His tagged MEF2 fusion protein (amino acids 1-168, construct provided by H. Nuygen)  into New Zealand white rabbits by use of standard conditions. Embryos were incubated in fluorescent secondary (1:150 dilution, Alexa 488, 594, 647 and 546; Molecular Probes). β-Gal was detected using biotinylated secondary antibody (1:150; Vector Laboratories) followed by incubation with Vector Laboratories Elite ABC and 3,3-Diaminobenzidine Tetra hydrochloride (DAB, Gibco-BRL). Embryos were visualized by confocal microscopy using a Leica SP5 microscope. All images shown are projections of 3 to 5 optical sections, processed using OpenLab, ImageJ and Adobe Photoshop.
Timelapse microscopy was performed from a tup-F4-GFP, dMEF-GAL4, UAS-moe-mCherry background to visualise cardioblast nuclei and the cardioblast leading edge, employing the hanging drop protocol , on a Leica SP5 microscope.
Dechorionated embryos were fixed in heptane equilibrated with 25% glutaraldehyde (Fluka) in 0.1 M Sodium Cacodylate. Embryos were manually devitellinated in 4% paraformaldehyde and 2.5% glutaraldehyde in cacodylate buffer, post-fixed in 1% osmium tetroxide, and stained in uranyl acetate before embedding in Epon-Araldite . Lead stained 0.1 μm sections were examined on a JEOL 1200EXII microscope. We examined over 120 sections from specimens of each genotype.
We thank Mihaela Georgescu and Christine Elder for technical assistance. Drosophila stocks were provided by the Bloomington Stock Centre, the Vienna Drosophila RNAi Centre, G. Tear, D. Montell, N. McGinnis and T. Bunch. Antibodies were obtained from the Developmental Studies Hybridoma Bank developed under the auspices of the NICHD. LVP was supported by CONACyT scholarship and JV was supported by NSERC CGS-D. This work was supported by Canadian Institutes for Health Research Grant MOP81365, and infrastructure supported by the Leaders Opportunity Fund of the Canada Foundation for Innovation.
JV and LVP carried out all the genetic and phenotypic studies. AM generated the αPS3 transgenes and transgenics, and some of the data in Figure 7. JRJ generated the data in Figure 2 and drafted the manuscript. All authors read and approved the final manuscript.


Seattle, Washington always has been a city with a rich sports tradition whether at the high school, college, or professional level. In a town best known as The Kid's playground after Ken Griffey Jr. during his stint in Seattle from 1989 to 1999, where he captured an MVP award in 1997.
Other athletes that can be credited with that same honor are individuals such as Jamal Crawford, Nate Robinson, Russell Wilson, Richard Sherman, Earl Thomas, Kam Chancellor, Doug Baldwin, Walter Jones, Brandon Roy, Norris Fredrick, Sue Bird, Lauren Jackson, Kenny Easley, Doug Christie, Jason Terry, and many more.
Seattle and its surrounding areas have sent several natives to the NBA such as Aaron Brooks, Doug Christie, Nate Robinson, Jason Terry, Brandon Roy, Allonzo Trier, Terrence Williams, Tony Wroten Jr to name a few.
Earlier this season, I spoke with Nuggets guard Isaiah Thomas about where he had Jamal Crawford ranked amongst basketball players to come out of the Emerald City.
"He is number one. 1A & 1B him and Jason Terry," said Thomas.
The Sacramento Kings were in town recently to take on the Dallas Mavericks. Before the game, I asked Doug Christie to name his top five players from the Seattle area.
" Jamal Crawford, myself, Brandon Roy, IT [Isaiah Thomas], JT [Jason Terry] and I'm sure I am leaving someone out," said Christie.
During his career, Doug Christie adverage 11.2 points, 4.2 rebounds, 3.6 assists per game, and made the All-Defensive team four times. He was also a part of the All-Time Sacramento Kings during the early 2000s, which gave the Los Angeles Lakers, and Spurs difficulty on the court with their passing ability and versatility.


Villa Cecilia is an exceptional property on the island of Corfu in Greece. With a traditional and stylish ambience, Villa Cecilia and its garden, is a unique and charming location for your relaxing holiday, destination wedding, special celebration, creative workshop and any other occasion or gathering.
Villa Cecilia is a truly unique and exceptional property in Corfu. Located in the mountains on the West coast above the long and sandy beaches. The villa has no neighbours in a distance of 500m. Privacy is guaranteed. Villa Cecilia has been designed, built and crafted to an exceptionally high standard by the owner. The property has been used as a family home, and as a smart private venue for weddings & events, film and photo shoots. The attention to detail and style sets it apart from any other villa in the area.
We organise your wedding or private dinner party in a romantic, luxurious setting. We provide chefs, serving staff, creative decorations and tents as required. Our mission is to provide a memorable and exciting experience. Villa Cecilia is open for marriages and dinner parties up to 80 - 100 persons, other locations are also possible where we aim to provide the same excellent service. We would love to assist you and your friends & family to write the most beautiful love story location for your wedding festivities.


U.G.(REGULAR) COURSES FOR ARTS/ COMMERCE & SCIENCE .
The college offers P.G. teaching in English, Odia, Geography, Computer Science, Zoology, Commerce, Economics, Education & Chemistry subjects.
The admission into the above PG subjects is made strictly on the basis of merits. Candidates who have passed the final degree examination fron any recognized university with 45% marks in the concerned Honours subject can apply manually to the college for admission as per the scheduled fixed by the college.
College offers 3 years BBA as one of the self financing course having 60 seats to the students in which merit basis manual system of admission is continuing under the system the applicant has to purchase the application form and submit in the college counter/department as per the scheduled fixed by the college.
College offers 2 years MBA as one of the self financing course having 60 seats to the students in which the admission is made as per the merit ranks issued by ODISHA JEE.
A student shall offer one Honours subject and two elective subjects(Elective-A & Elective-B) Apart from the compulsory subjects. Honors subjects shall be allotted to the applicants for admission by taking in to consideration the option of the applicants in the application form. Further a student has to choose one elective –A for 1st year and another Elective-B for 2nd year classes at the time of admission. However a student cannot offer an elective subject directly to his Honours subjects .a student offering a language subject as Honours/elective subject cannot offer another language as elective subject.
CBCS (CHOICE BASED CREDIT SYSTEM) PATTERN - 2015 FOR U.G.
The college offers 2 years B.A. B.Ed./B.Sc. B.Ed., 4 years Integrated B.A. B.Ed./B.Sc. B.Ed & 3 Years BBA Courses.
The college offers 2 years Post Graduate Degree Courses in MASTER IN BUSINESS ADMINISTRATION.


BRUSSELS (Reuters) - Monsanto said it would abide by Latvia's and Greece's requests under a new EU opt-out law to be excluded from its application to grow a genetically modified (GM) crop across the European Union, but accused them of ignoring science.
Under a law signed in March individual countries can seek exclusion from any approval request for GM cultivation across the EU. While the European Commission is responsible for approvals, requests to be excluded also have to be submitted to the company making the application.
GM crops are widely-grown in the Americas and Asia, but Monsanto's pest-resistant MON810 is the only variety grown in Europe, where opposition is fierce.
France and Germany have said they are opposed to GM cultivation, and while Britain is in favor, the Scottish government is against.
The EU law has riled the GM industry and the United States, which wants Europe to open its doors fully to U.S. GM crops as part of a planned EU-U.S. free trade deal.
In a statement on Thursday, the European Commission confirmed that so far only Latvia and Greece had asked for opt-outs from Monsanto's request to continue to grow MON810.
In its formal response to Latvia, seen by Reuters, Monsanto says Latvia's request "contradicts and undermines the scientific consensus on the safety of MON810".
GM in Europe is a small fraction of Monsanto's activity and Monsanto said in an emailed statement that these opt-outs would have no impact on its business.
"Nevertheless, we regret that some countries are deviating from a science-based approach to innovation in agriculture and have elected to prohibit the cultivation of a successful GM product on arbitrary political grounds," the statement said.
In a statement on Thursday, the Commission said its zero-tolerance policy against non-authorized GM products remains in place and it was simply seeking advice on "a scientific question" unrelated to trade negotiations with the United States.


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Romeo Santos, Enrique Iglesias win big at 2015 Billboard Latin Music Awards
Romeo Santos, Enrique Iglesias and Carlos Santana were all big winners at the 2015 Billboard Latin Music Awards in Miami, Florida.
MIAMI, FL -- It was a big night for two artists at last night's 2015 Billboard Latin Music Awards in Miami, Florida.
Romeo Santos was the night's biggest winner, going home with 10 awards in all. He awards included artist of the year, songwriter of the year, producer of the year, Hot Latin Songs artist of the year and Top Latin album.
Enrique Iglesias took home nine awards. The majority were for his song "Bailando" which won Latin pop song of the year, digital song of the year, streaming song of the year, hot Latin song of the year and airplay song of the year. Iglesias also won Latin pop songs artist of the year and Latin pop album of the year.
Newcomer J Balvin and Banda Sinaloense MS de Sergio Lizrraga each picked up three awards. Carlos Santana and Wisin each went home with two awards.
You can see a full list of winners here.
HIGHLIGHTS: Jennifer Lopez pays tribute to Selena
Jennifer Lopez pays tribute to Selena
Jennifer Lopez paid tribute to Selena at the 2015 Billboard Latin Music Awards
arts & entertainmentbillboard music awards
PHOTOS: Jennifer Lopez pays tribute to Selena


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How Liam Payne is interacting with fans in Quarantine
By Fareya Noor	 Last updated May 20, 2020
Liam of One Direction is one fun guy. He has a knack for being socially active and groovy. We love his music and work from when the band was together and now. One of his latest hits, 'Midnight' in collaboration with Alesso shows how dedicated he is to his fans and work. The entire song was created being 2000 miles away from Alesso and they even shot a video. He sure showed that COVID-19 Coronavirus (SARS-CoV2) is not stopping him. To top it all, Liam Payne has been keeping his beloved fans engaged in Quarantine in many different ways at the same time. And we, are all for it!
How Liam Payne is staying in touch with fans in Quarantine
Alright so, the first thing would be how Liam Payne is doing many interviews to keep fans engaged and updated with the One Direction Reunion. Now it may not seem as much but, Liam is giving his fans constant updates and news to go about. This keeps them involved and also helps them stay up to date with their favorite musician.
Next, Liam Payne has set 2 teams on Twitter for his fans. The Purple House and the Blue house. These are two teams that are competing by creating games, stream parties, and threads to interact with one another and have some fun during Quarantine. There are giveaways that await at the end of Quarantine for the team that wins.
https://twitter.com/LJPayneItalia/status/1259491708250853377
Lastly, Liam Payne has started his own YouTube series. as part of his #HomewithLiam initiative where he uploads weekly to keep fans updated on his life and everything that happened in the week. It is honestly too unreal that a celebrity would be going out of their way to keep fans entertained.
However, we have to say that one of the things fans most look forward to are updates from Liam Payne about the One Direction Reunion!
Related: Liam Payne does online concert for HUGO
Liam PayneLiam Payne fansOne DirectionOne Direction ReunionQuarantine
Fareya Noor 473 posts
Fareya Noor is currently an undergraduate student who takes up writing as her passion. She writes theatre scripts and works as a content writer to exert her creative side. To her, there is no simpler yet complex way to express perspectives other than words.
Following this, she has started writing content that might just be the daily scoop of entertainment you need!
Tamar Braxton doesn't have drama with Traci Braxton
Jimmy Kimmel response to Donald Trump's feud with him
Here's Why Blake Shelton's song 'Minimum Wage' Got a Lot of Backlash
Ringo Starr talks about performing with Paul McCartney


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Centre for Research on Families and Relationships
Edinburgh, Glasgow, Aberdeen and Stirling
CRFR produces and stimulates high quality research and commentary on families and relationships and disseminates such work widely. It is a consortium research centre, whose main office is at the University of Edinburgh, with partners at Glasgow Caledonian University, the University of Aberdeen, University of Glasgow, and University of Stirling.
CRFR takes a broad approach to research on families and relationships across the lifecourse and generations. The research programme is collaborative and inclusive and produces high-quality cutting-edge research relevant to Scotland today. CRFR research is both qualitative and quantitative.
The centre's aims are to:
enhance infrastructure to conduct research on families and relationships;
act as a focal point in Scotland for all those with an interest in research on families and relationships including researchers, policy makers and practitioners;
consolidate and strengthen links and networks across the academic research and the policy and practitioner communities, and between researchers and higher education institutions throughout Scotland;
produce high quality collaborative inclusive research relevant to key issues in families and relationships;
make research more accessible for use by academics, policy makers and practitioners.


Lurssen has its supporters and detractors around here, but this looks kind of interesting for anyone looking to master on his or her own. I imagine the demonstration will showcase the desktop version, but it's pretty much the same as the iOS version. It airs today, August 7, at 10:30 am PST and 1:30 pm EST.
It's a good song and watching and hearing him do his thing is quite inspiring.
Of course, the parts are wonderfully recorded and played, which is also a pleasure. He's got a few nuggets of wisdom about reverb and EQ.
@supanorton Thanks for the link!
Yeah thanks for posting this @supanorton will watch it later when I get a chance.
Have always liked the sound of this app with the demo version I used to play with but was put off by a combination of price and your trouble's getting it fixed last(?) year.
@ikmultimedia is this app still supported?
Absolutely. It is still an important supported product.


Liking any particular piece of jewelry enough to spend a handful on it over others is more on the challenging side of things. Such high-priced purchases are often delayed by moments of two-mindedness. One such tough choice is to decide between an infinity band and a solitaire. Solitaires pull out an easy yes, but not since the jewelers refreshed the section of infinity bands. The privilege of both is reserved for those who are going to get married. But for others, it has to be one or the other. So how do you make a pick between the two without feeling like missing out on the other?
Let's take a look at both styles from close quarters. That perspective is integral to finding out which one you want.
One thing that can be said right off the top of the head is that solitaires are more gorgeous than infinity rings. But, are they really? In reality, the difference stands not in the degree of gorgeousness, but in the styles. Solitaire rings use one central stone, and more often than not it's an achromatic diamond. There is never much work at the back of the bands. In solitaires, all of the details is placed around the stone. Everything about the design of a solitaire is aimed at aggrandizing and highlighting the stone. Hardly ever does a solitaire ring have works all over the band. So, if you are a design person, then solitaires might not be the best choice for you. Solitaires appeal directly to the diamond lovers and you may not be one among them. If you are not, then let's move over to your section which is infinity bands.
Lately, these bands have been designed in great many styles to reignite the common interest. Designers have been largely successful in pulling away customers from the solitaire section. To be fair, this is a good change after what seemed like the longest era of solitaire rings. Infinity rings make potential choices for diamond lovers too, because gemstones are now generously used in the items of these section. Infinity rings inlaid with cluster diamonds is a new favorite among women. Styles like split bands, interlaced bands, multi-row gemstone settings, have changed the plain band trend of infinity rings.
It is advisable to spend all that money only on the one you fully like.


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2018 Big Machine Records Pro Late Model Series Champion Michael House practicing at Five Flags Speedway during the 51st Snowball Derby Weekend. (Daniel Vining/PixelatedSPEED)
NASHVILLE, Tennessee (January 16, 2019) -- The Fairgrounds Speedway in Nashville, Tennessee is home to some racing's legendary drivers and hosts one of the crown jewels of late model racing. In 2019, fans will be treated to a double dose of All American action, get dirty with some Outlaws, and enjoy the return of super late models and plus the track's home pro late model series.
Nashville made headlines in the racing world in December after Formosa Productions, Marcus and Bruton Smith in conjunction with Bristol Motor Speedway announced a partnership with the goal of bringing a NASCAR nationally sanctioned event back to the Fairgrounds for the first time in almost two decades. The NASCAR Busch Series and Craftsman Truck Series last visited the venue in 2000. While plans on the exact details of how this return is set to occur are unclear at present time, the notion of NASCAR returning to Nashville has brought a much needed dose of positive attention to the speedway following the postponement of the 34th All American 400 due to inclement weather.
Speaking of the All American 400, fans will be treated to the first of a double dose of crown-jewel super late model racing in 2019 as the aforementioned 34th Annual All American 400 will be contested on the weekend of April 13-14th. After being rained out in November, participating teams will re-qualify and be given a free set of tires, plus a waived entry fee. There are a couple of options that were made available for ticket holding fans; contact the speedway for details.
Super late models return on May 4th with the return of the Southern Super Series. The Southern Super Series will be making it's third stop of the 2019 season as the Fairgrounds plays host to the Nashville 100.
Following the supers, the 2019 season will roll on and begin a six week program that will span from the middle of May through to November and focus on the core local divisions of the speedway, headlined by the Big Machine Pro Late Models and also including Legends, Trucks, Pure Stocks and more.
Things get dirty on the weekend of May 30th - June 1st when the World of Outlaws visit for the Music City Outlaw Nationals. The quarter-mile track will be covered with dirt for the event, which will feature the WoO Sprint Cars for the first time at Nashville in a race that will be $25,000 to win.
The 2019 season comes to a close with the running of the 35th Annual All American 400 on the weekend of November 2-3. The traditionally scheduled time frame for this historic race will once again feature the stars of the super late model world, which will include pro late models and local divisions.
Log on to http://fairgroundsspeedwaynashville.com or follow the speedway on Facebook for complete details on events being held in 2019.
2019 Fairgrounds Speedway Nashville Schedule:
April 14 -- 34th Annual All American 400 Makeup Race
May 4 -- Nashville 100 - Southern Super Series
May 30 -- Music City Outlaw Nationals - WoO Sprint Cars Night 1
June 1 -- Music City Outlaw Nationals - WoO Sprint Cars Night 2
June 22 -- Weekly Racing Action
July 13 -- Weekly Racing Action
August 10 -- Weekly Racing Action
September 7 -- Weekly Racing Action
October 5 -- Weekly Racing Action
November 3 -- 35th Annual All American 400
PixelatedSPEED would like to wish the entire Wood family good speed and hope to see Glen recover quickly.
PixelatedSPEED is a motorsports news and views website covering all things racing and has been "Bringing Pixels 2 Pavement Since 2018". If you've made it this far into the post, thank you. Please consider sharing this content on the interwebs and following PixelatedSPEED on Facebook and Twitter and joining in on the conversation. http://facebook.com/PixelatedSPEED & http://twitter.com/PixelatedSPEED
PixelatedSPEED is a part of the Gravel Network. Copyright - 2018, 2019
Labels: Fairgrounds Speedway Nashville, NASCAR, Schedule, Short Track Racing
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