About Howard Lake Howard Lake is a digital fundraising entrepreneur. Publisher of UK Fundraising, the world’s first web resource for professional fundraisers, since 1994. Trainer and consultant in digital fundraising. Founder of Fundraising Camp and co-founder of GoodJobs.org.uk. Researching massive growth in giving. 35 total views, 1 views today AddThis Sharing ButtonsShare to TwitterTwitterShare to FacebookFacebookShare to LinkedInLinkedInShare to EmailEmailShare to WhatsAppWhatsAppShare to MessengerMessengerShare to MoreAddThis Howard Lake | 31 January 2009 | News Personal Telephone Fundraising is a leading provider of outbound telephone-based fundraising, serving the UK’s not-for-profit sector.There is a simple philosophy at Personal Telephone Fundraising:To provide the finest quality in telephone fundraising, perfectly in tune with our clients, their campaigns and their supporters.Whatever the rationale for calling, our uniquely skilled, professional and committed fundraisers will make the calls successfully, sensitively, and with the best possible return on fundraising investment.– Donor Acquisition– Donor Retention– Donor Development– Specialist Fundraising Services– Consultancy & Training Tagged with: Consulting & Agencies Donor acquisition Telephone fundraising Personal Telephone Fundraising AddThis Sharing ButtonsShare to TwitterTwitterShare to FacebookFacebookShare to LinkedInLinkedInShare to EmailEmailShare to WhatsAppWhatsAppShare to MessengerMessengerShare to MoreAddThis Advertisement
Sean Pavone/iStockBy IVAN PEREIRA, ABC News(ASHEVILLE, N.C.) — Leaders in Asheville, North Carolina, have taken a historic step to repair centuries of racial prejudice by unanimously voting to provide reparations.The Asheville City Council voted 7-0 on a resolution Tuesday night that formally apologized to its Black residents for the city’s role in slavery, discriminatory housing practices, and other racist policies throughout its history.The measure also calls for a plan to provide reparations to its Black residents in the form of investments in their community such as “increasing minority home ownership,” “increasing minority business ownership and career opportunities,” and “strategies to grow equity and generational wealth,” according to the resolution.Councilman Keith Young, who spearheaded the resolution, told ABC News in a statement that the council was looking “to embed systemic solutions.”“This process begins and is perpetual, repeating this process over and over again,” Young, who is Black, said in the statement. “There is no completion box to check off.”The resolution, which was signed by Mayor Esther Manheimer, calls for the creation of a Community Reparations Commission that will be made up of businesses, local groups and elected officials. The commission will issue detailed recommendations, with plans to implement the reparations in the short and long term.“As far as the timeline goes, we will have some steps to report on within six months and every six months after that,” Young said in a statement. “This work does not end and will be adaptive, no matter what governing body holds office or who runs our city.”Asheville has a population of 92,870, 83% of which is white, according to the U.S. Census. Minorities own roughly 9.7% of the town’s 12,785 businesses, according to Census data.The council’s resolution also calls on the state and federal governments to come up with their own reparation policies.“It’s clear to me that federal reparations legislation would be the most impactful,” Mayor Manheimer said in a statement. “However, this is a conversation that is happening among diverse groups of people in cities and towns throughout the United States and through our resolution the City of Asheville has joined in this conversation.”On Wednesday evening, Providence, Rhode Island, Mayor Jorge Elorza signed an executive order that would explore reparations for his city’s Black and Indigenous residents.The order will examine the history of slavery and genocide of Native Americans and go through a “reconciliation” process with its Black and Indifenous residents. The order will then explore a process for reparations that would “reverse the injuries resulting from the truth findings and advise what appropriate policies, programs, and projects.”“A lot of folks are going to jump straight to the reparations question,” Elorza said. “How much? What form? For how long? Whose eligible? Those are all legitimate questions, but they’re questions for another day.” Copyright © 2020, ABC Audio. All rights reserved.
<a href=”https://www.youtube.com/watch?v=WMI-msIAI84″ rel=”nofollow” target=”_blank”> <img src=”https://img.youtube.com/vi/WMI-msIAI84/0.jpg” alt=”0″ title=”How To Choose The Correct Channel Type For Your Video Content ” /> </a> Researchers from the Broad Institute of MIT and Harvard, Harvard Medical School, the Harvard Stem Cell Institute (HSCI), and Harvard-affiliated hospitals have uncovered an easily detectable, “premalignant” state in the blood that significantly increases the likelihood that an individual will go on to develop blood cancers such as leukemia, lymphoma, or myelodysplastic syndrome.The discovery, which was made independently by two research teams affiliated with the Broad and partner institutions, opens new avenues for research aimed at early detection and prevention of blood cancer. Findings from both teams appear this week in the New England Journal of Medicine.Most genetic research on cancer to date has focused on studying the genomes of advanced cancers, to identify the genes that are mutated in various cancer types. These two new studies instead looked at somatic mutations — mutations that cells acquire over time as they replicate and regenerate within the body — in DNA samples collected from the blood of individuals not known to have cancer or blood disorders.Taking two very different approaches, the teams found that a surprising percentage of those sampled had acquired a subset — some but not all — of the somatic mutations that are present in blood cancers. These individuals were more than 10 times likelier to go on to develop blood cancer in subsequent years than those in whom such mutations had not been detected.The “premalignant” state identified by the studies becomes more common with age; it is rare in those under the age of 40, but appears with increasing frequency with each decade of life that passes, ultimately appearing in more than 10 percent of those over the age of 70. Carriers of the mutations are at an overall 5 percent risk of developing some form of blood cancer within five years. This “premalignant” stage can be detected simply by sequencing DNA from blood.“People often think about disease in black and white — that there’s ‘healthy’ and there’s ‘disease’ — but in reality most disease develops gradually over months or years. These findings give us a window on these early stages in the development of blood cancer,” said Steven McCarroll, senior author of one of the papers. McCarroll is an assistant professor of genetics at Harvard Medical School and director of genetics at the Broad’s Stanley Center for Psychiatric Research.Benjamin Ebert, co-director of the HSCI Cancer Program, associate member of the Broad, and associate professor at Harvard Medical School and Brigham and Women’s Hospital, is the senior author of the other paper.The mutations identified by both studies are thought to originate in blood stem cells, and confer a growth-promoting advantage to the mutated cell and all of its “clones” — cells that derive from that original stem cell during the normal course of cell division. These cells then reproduce at an accelerated rate until they account for a large fraction of the cells in a person’s blood. The researchers believe these early mutations lie in wait for follow-on, “cooperating” mutations that, when they occur in the same cells as the earlier mutations, drive the cells toward cancer. The majority of mutations occurred in just three genes; DNMT3A, TET2, and ASXL1.“Cancer is the end stage of the process,” said Siddhartha Jaiswal, a Broad-associated scientist and clinical fellow from Massachusetts General Hospital who was first author of Ebert’s paper. “By the time a cancer has become clinically detectable it has accumulated several mutations that have evolved over many years. What we are primarily detecting here is an early, premalignant stage in which the cells have acquired just one initiating mutation.”The teams converged on these findings through very different approaches. Ebert’s team had hypothesized that, since blood cancers increase with age, it might be possible to detect early somatic mutations that could be initiating the disease process, and that these mutations also might increase with age. They looked specifically at 160 genes known to be recurrently mutated in blood malignancies, using genetic data derived from approximately 17,000 blood samples originally obtained for studies on the genetics of type 2 diabetes.They found that somatic mutations in these genes did indeed increase the likelihood of developing cancer, and they saw a clear association between age and the frequency of these mutations. They also found that men were slightly more likely to have mutations than women, and Hispanics were slightly less likely to have mutations than other groups.Ebert’s team also found an association between the presence of this “premalignant” state and risk of overall mortality independent of cancer. Individuals with these mutations had a higher risk of type 2 diabetes, coronary heart disease, and ischemic stroke as well. However, additional research will be needed to determine the nature of these associations.In the related paper, McCarroll’s team discovered the phenomenon while studying a different disease. They, too, were looking at somatic mutations, but they were initially interested in determining whether such mutations contributed to risk for schizophrenia. The team studied roughly 12,000 DNA samples drawn from the blood of patients with schizophrenia and bipolar disorder, as well as healthy controls, searching across the whole genome at all of the protein-coding genes for patterns in somatic mutations.They found that the somatic mutations were concentrated in a handful of genes; the scientists quickly realized that they were cancer genes. The team then used electronic medical records to follow the patients’ subsequent medical histories, finding that the subjects with these acquired mutations had a 13-times elevated risk of blood cancer.McCarroll’s team conducted follow-up analyses on tumor samples from two patients who had progressed from this premalignant state to cancer. These genomic analyses revealed that the cancer had indeed developed from the same cells that had harbored the “initiating” mutations years earlier.“The fact that both teams converged on strikingly similar findings, using very different approaches and looking at DNA from very different sets of patients, has given us great confidence in the results,” said Giulio Genovese, a computational biologist at the Broad and first author of McCarroll’s paper. “It has been gratifying to have this corroboration of each other’s findings.Jaiswal will present the findings on Dec. 9 at the American Society of Hematology annual meeting in San Francisco.All of the researchers involved emphasized that there is no clinical benefit today for testing for this premalignant state; there are no treatments currently available that would address this condition in otherwise healthy people. However, they say the results open the door to entirely new directions for blood cancer research, toward early detection and even prevention.“The results demonstrate a way to identify high-risk cohorts — people who are at much higher than average risk of progressing to cancer — which could be a population for clinical trials of future prevention strategies,” McCarroll said. “The abundance of these mutated cells could also serve as a biomarker — like LDL cholesterol is for cardiovascular disease — to test the effects of potential prevention therapies in clinical trials.”Ebert agreed: “A new focus of investigation will now be to develop interventions that might decrease the likelihood that individuals with these mutations will go on to develop overt malignancies, or therapeutic strategies to decrease mortality from other conditions that may be instigated by these mutations,” he said.The researchers also say that the findings show just how important it is to collect and share large data sets of genetic information: Both studies relied on DNA samples collected for studies completely unrelated to cancer.“These two papers are a great example of how unexpected and important discoveries can be made when creative scientists work together and with access to genomic and clinical data,” said Broad Deputy Director David Altshuler, one of Ebert’s co-authors. “For example, Steve’s team found stronger genetic relationships to cancer than they have yet found for the schizophrenia end point that motivated their original study. The pace of discovery can only accelerate if researchers have the ability to apply innovative methods to large data sets.”
There are 168 hours in a week, 730 hours in a month, and 8,760 hours in a year. It doesn’t matter whether you’re Jeff Bezos or the CEO of a credit union; everyone has the same amount of time. The difference between successful and unsuccessful leaders lies in how they choose to use that time.According to Cassie Holmes, an associate professor at UCLA’s Anderson School of Management, most people tend to look at time from a ground-level perspective, which means that instead of looking at a broad overview of time, they only think about things in light of yesterday, today, and tomorrow. That’s a problem. When making decisions with this limited view, every activity incurs a short-sighted opportunity cost.For example, performance reviews are coming up, and you have to work on those right now. This means having to set aside that project that would allow you to expand your membership opportunities or delay working on the new loan product that would result in a huge opportunity for your credit union and your members. Or in another instance, spending an evening or weekend catching up on email equals the inability to spend intentional time with your family and friends. There’s always a trade-off.As part of every strategic planning session I’ve lead over the last few years, we help clients build a game plan for successfully executing their strategy by asking “What can hold you back from accomplishing these goals?” Can you guess the number one answer for almost every project? “Task saturation.” Today’s credit union leaders are stretched thin. Overseeing numerous compliance issues while managing day-to-day operations leaves them feeling overwhelmed, ineffective, drowning in busyness. continue reading » ShareShareSharePrintMailGooglePinterestDiggRedditStumbleuponDeliciousBufferTumblr
Golf is about to return to the U.S. after a pandemic-caused break with a red-hot feud between Brady Schnell and Vijay Singh.Singh, a PGA Tour veteran, is set to enter the Korn Ferry Challenge at TPC Sawgrass, which is generally meant for lower-tier players scrapping for cash and a chance at a bigger stage. The 35-year-old Schnell, who has bounced between pro levels, took exception to Singh’s imminent presence in the competition. Schnell felt Singh was unfairly taking the spotlight and potential earnings from others. He made his voice heard Thursday via social media.”Hey @VijaySinghGolf you are a true piece of trash if you except money playing in a Korn Ferry Tour event and I’ll say it right to your face,” wrote Schnell on Twitter.Hey @VijaySinghGolf you are a true piece of trash if you except money playing in a Korn Ferry Tour event and I’ll say it right to your face— Brady Schnell (@brady_schnell) May 7, 2020MORE: Must-watch NFL games for 2020Schnell continued to take issue with Singh in back-and-forths with people in his replies. “He’s a complete turd for playing,” Schnell wrote. “He’s got his money and he’s got his career. Just wait another month and roll with your senior friends (on the Champions Tour).”Its one spot?! Do you know how much those points and money could do for a young kid? He’s a complete turd for playing. He’s got his money and he’s got his career. Just wait another month and roll with your senior friends— Brady Schnell (@brady_schnell) May 7, 2020Schnell eventually apologized for the tone of his messages but maintained he was frustrated at Singh, 57, who has earned more than $70 million in his golf career.Singh has not responded to Schnell’s comments.