Podcast appearances and mentions of greg what

Cupcakes are back! In case you're unfamiliar, Cupcakes (Preston Graves, Greg Soran, Sol Snyder, Matt Walker) were the proverbial "next big thing" out of Chicago in 2000 when their eponymous album came out. The band imploded before they ever had a real shot, and most of the members moved on to higher-profile gigs (American Idol, Morrissey, Bryan Adams, B-52's). Singer Preston Graves joins me mere days before the band does their reunion show, headlining Metro on 2/29. So why are they getting back together after all this time, and what exactly happened back then? Fueling this week's chat is delicious food from north side staple (3400 N. Ashland). Thanks to the team there for providing the eats... go visit them and check it out for yourself! Discussed this week: Preston has zero working knowledge of Mexican cuisine. Thank goodness we had Cafe El Tapatio to help guide him. Preston's worked all over Chicago. The Chicago scene of the 90s. How and why Cupcakes are back together. The lack of rehearsals leading up to the 2/29 show. Greg's time performing with/on American Idol. All the juke and jiving that goes on. Sol Snyder: "I love me some Sol!" The band's expectations when they first got signed: "(be) on tour forever." "Woodshed" is a total Chicago term. How the band found out the label was done with them. Wait... HOW bad was it between Preston and Greg? What made Preston so impossible to deal with back in the day? The "incident" where Preston pissed me off live on stage at a radio event. Matt Walker has a cool LinkedIn profile. Also? He's a human metronome. We miss the Hothouse Flowers. GET TICKETS FOR THE METRO SHOW ASAP! This is a must-see event!   Thanks to our friends at C&H Financial Services for sponsoring this episode. We couldn't do it without them.

Cupcakes are back! In case you're unfamiliar, Cupcakes (Preston Graves, Greg Soran, Sol Snyder, Matt Walker) were the proverbial "next big thing" out of Chicago in 2000 when their eponymous album came out. The band imploded before they ever had a real shot, and most of the members moved on to higher-profile gigs (American Idol, Morrissey, Bryan Adams, B-52's). Singer Preston Graves joins me mere days before the band does their reunion show, headlining Metro on 2/29. So why are they getting back together after all this time, and what exactly happened back then? Fueling this week's chat is delicious food from north side staple Cafe El Tapatio (3400 N. Ashland). Thanks to the team there for providing the eats... go visit them and check it out for yourself! Discussed this week: Preston has zero working knowledge of Mexican cuisine. Thank goodness we had Cafe El Tapatio to help guide him. Preston's worked all over Chicago. The Chicago scene of the 90s. How and why Cupcakes are back together. The lack of rehearsals leading up to the 2/29 show. Greg's time performing with/on American Idol. All the juke and jiving that goes on. Sol Snyder: "I love me some Sol!" The band's expectations when they first got signed: "(be) on tour forever." "Woodshed" is a total Chicago term. How the band found out the label was done with them. Wait... HOW bad was it between Preston and Greg? What made Preston so impossible to deal with back in the day? The "incident" where Preston pissed me off live on stage at a radio event. Matt Walker has a cool LinkedIn profile. Also? He's a human metronome. We miss the Hothouse Flowers. GET TICKETS FOR THE METRO SHOW ASAP! This is a must-see event!   Thanks to our friends at C&H Financial Services for sponsoring this episode. We couldn't do it without them.

Picks for Wednesday, February 20, 2020 Johnny- Cryptoid HC & The Green Lantern: Season 2 #1 Greg- What’s Michael? Fatcat Collection v1 TPB Need suggestions for your LCS trip this week? Let Greg and this week’s guest host, Comic Syllabus’s Johnny Hall, point out the books hitting shelves on Wednesday they're most excited about in this four hundred twenty-first installment of their ongoing "Pull List" series! These episodes are the perfect way for anyone to kick off their comics: from the most curious newcomer to the most dedicated Wednesday Warrior! Robots From Tomorrow is a twice-weekly comics podcast recorded deep beneath the Earth’s surface. You can subscribe to it via iTunes or through the RSS feed at RobotsFromTomorrow.com. You can also follow Mike and Greg on Twitter. Enjoy your funny books.

On today's episode of Gritty Founder, Kreig Kent talks with Greg Mercer about how he built and grew Jungle Scout. Greg shares valuable advice on building a product, as well as tips for those interested in becoming Amazon sellers. Greg Mercer is the Founder and CEO of Jungle Scout, the leading software for Amazon sellers. Greg is a leader in the Amazon selling community, who built Jungle Scout from a Chrome extension into a robust suite of SaaS solutions. Greg is a graduate of Auburn University who loves big data, coffee, and traveling the world with his wife, Elizabeth. Some Questions Kreig asks Greg: - What does selling on Amazon mean, and how do people make money? (13:04) - How do you get started selling on Amazon, and where does Jungle Scout come in? (15:30) - What is the most success you’ve had selling on Amazon, and what was the product? (19:48) - If someone was gettings started today on Amazon, what do they need to learn or be good at? (21:54) - What do you think is the most important ingredient for a founder who is starting out today? (34:42) - What kind of company might disrupt Amazon? (46:04) In This Episode, You Will Learn: - About Greg’s background and how he became an entrepreneur (4:23) - How Greg got started selling on Amazon (13:16) - Why and how Greg started Jungle Scout (15:47) - Decrease the scope and increase the simplicity of your project (34:51) - Don’t take no for an answer (36:10) - How Greg initially promoted Jungle Scout (38:40) - Why Greg thinks social proof is becoming more important than brands (43:31) Connect with Greg Mercer: Twitter Personal Website Jungle Scout Also Mentioned on This Show... Greg’s favorite quote: “The reality is great highs, terrible lows and unrelenting stress. Don't think people want to hear about the last two.” ―Elon Musk Greg’s book recommendation: Radical Candor by Kim Scott More resources The Million Dollar Case Study

  Dr. Carolyn Lam: Welcome to Circulation On The Run, your weekly podcast summary and backstage pass to the Journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Greg Hundley, associate editor from the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, you know I'm vegetarian and any paper on plant-based diet will always interest me, and of course, we have one as a featured paper this week, very interestingly talking about changes in plant-based diet quality, meaning that there could be good plant-based diets and not so good plant-based diets. I mean we all know that potato chips, for example, are still plant-based. But, anyways, so this feature paper discusses the changes in these plant-based diet quality and association with total and cost-specific mortality. Neat, huh? Dr. Greg Hundley: Yeah. I can't wait to hear about that one. I know that's a favorite topic of yours. How about if we have a sip of coffee and jump into our other articles? Dr. Carolyn Lam: Sure. I'm sipping away, and have already picked my first paper. This talks about mutations in plakophilin 2, which are the most common cause of gene-positive familial arrhythmogenic right ventricular cardiomyopathy. Dr. Greg Hundley: No quizzes for me on plakophilin 2, please. Dr. Carolyn Lam: All right, well, let me tell you all about it. Plakophilin 2 is classically defined as a protein of the desmosome, which is an intracellular adhesion structure. Studies though have suggested that plakophilin 2 also translates information at the initiation. Recent studies have also shown that plakophilin 2 translates information initiated at the site of cell to cell contact into intracellular signals that maintain structural and electrical homeostasis. Now, the important thing is that mutations in plakophilin 2 associated with most cases of gene-positive arrhythmogenic right ventricular cardiomyopathy or ARVC. However, the molecular and cellular mechanisms responsible for arrhythmias in ARVC remain unclear. Dr. Carolyn Lam: In today's paper, Doctors Delmar and Cerrone from New York University School of Medicine and their colleagues studied the role of cardiomyocyte plakophilin-2 expression in cardiac function. To do that, they utilized a cardiomyocyte-specific, tamoxifen-activated, plakophilin-2 knockout murine line. They found that loss of plakophilin-2 expression caused, as an early event and predominantly in the right ventricle, a non-transcriptional and likely arrhythmogenic, connexin-43-dependent disruption of calcium homeostasis. Dr. Carolyn Lam: The phenotype included accumulation of calcium in three intracellular compartments, the junctional sarcoplasmic reticulum, the cytoplasm, and the mitochondria. Right ventricular myocytes also showed increased eagerness of ryanodine-receptor-2 channels to release calcium from the sarcoplasmic reticulum. Intrinsic ryanodine-receptor-2 properties were also modified further contributing to the pro-arrhythmogenic state. In summary, the authors postulated that disruption of calcium homeostasis in the right ventricle is a major arrhythmia trigger in patients with ARVC. The data identified both the ryanodine-receptor-2 channel and the connexin-43 hemichannel as targets for antiarrhythmic therapy in this population. Dr. Greg Hundley: Very interesting that ARVC is such a worrisome concern, and gathering this mechanistic information is just so helpful. Dr. Carolyn Lam: Exactly. Dr. Greg Hundley: I have a basic science paper, but it was actually interesting because of the conduct was in many, many human subjects. It emanates from the large Million Veteran Program. There are a whole list of coauthors that are recognized as equal contributors, but Scott Damrauer actually serves as the corresponding author from the VA Medical Center. What it's addressing, about 13% of African American individuals carry two copies of the APOL1 risk alleles, G1 or G2, that are associated with a one and a half to two and a half fold increase in the risk of chronic kidney disease. Dr. Greg Hundley: There've been conflicting reports as to whether an association exists between these APOL1 risk alleles and cardiovascular disease independent of the effects of the APOL1 on kidney disease. Here, the investigators thought to test the association of these G1 and G2 alleles with coronary artery disease, peripheral arterial disease, and stroke among African American individuals in the Million Veterans Program. Dr. Carolyn Lam: Seems like a great study population and designed to look at this. What did they find? Dr. Greg Hundley: Among 30,903 African American Million Veterans Program participants, 3,941 or about 13% carried the two APOL1 risk allele, high-risk genotype. Individuals with normal kidney function at baseline with the two risk alleles had a slightly higher risk of developing coronary artery disease compared to those with no risk alleles. Similarly, modest associations were identified with incident stroke and peripheral arterial disease. However, when modeling both cardiovascular and renal outcomes, APOL1 was strongly associated with incident renal disease while no significant association with the cardiovascular disease endpoints could be detected. In conclusion, what the authors are indicating is that the APOL1 risk variants display a modest association with cardiovascular disease, and this association is likely mediated by the already previously known association of APOL1 with chronic kidney disease. Dr. Carolyn Lam: Interesting. Dr. Carolyn Lam: My next paper also has to do with chronic kidney disease and this time looking at metformin use and clinical outcomes in patients with diabetes with or without heart failure or kidney dysfunction. We know that metformin is the first-line therapy for type 2 diabetes, although its effects on the cardiovascular system are actually, not fully proven. In this next paper, the authors examine metformin use in the SAVOR-TIMI 53 Trial. Dr. Greg Hundley: Tell us a little bit about that SAVOR-TIMI 53 Trial. How is that organized? Dr. Carolyn Lam: Just as a reminder, the SAVOR-TIMI 53 trial was a multinational, randomized, controlled cardiovascular outcomes trial that compared the dipeptidyl peptidase-4 or DPP4 inhibitor, Saxagliptin, with placebo, enrolling almost 16,500 patients with type 2 diabetes and cardiovascular disease or elevated cardiovascular risk. Dr. Carolyn Lam: Now, in the current paper led by Dr. Bergmark from TIMI study group in Brigham and Women's Hospital and Harvard Medical School, the authors performed the post hoc analysis and looked at patients in SAVOR-TIMI 53 with baseline biomarker samples of whom there were more than 12,000 patients and classified these patients as ever versus never taking metformin during the trial period. The associations between metformin exposure and outcomes were estimated using inverse probability of treatment weighting, Cox modeling. Dr. Carolyn Lam: They found that among patients with type 2 diabetes and high cardiovascular risk in the SAVOR-TIMI 53 trial, metformin use was associated with lower rates of all-cause mortality including after adjustment for clinical variables and biomarkers, however not lower rates of the composite endpoint of cardiovascular death, MI or stroke. This association was most apparent in patients without prior heart failure or moderate to severe chronic kidney disease. Dr. Greg Hundley: Excellent. Dr. Greg Hundley: I'm going to transition to another clinical trial and this one is looking at ezetimibe in elderly patients and looking at efficacy for preventing cardiovascular-related events. The paper comes from Yasuyoshi Ouchi from Toranomon Hospital in Japan. Evidence regarding the primary prevention of coronary artery disease events by LDL-C/lipid-lowering therapy in order individuals that are above the age of 75 years, is somewhat incomplete. This trial tested whether LDL-C lowering with ezetimibe is useful for the primary prevention of cardiovascular events in older patients. They implemented a multicenter, prospective, randomized but open-label, blinded, endpoint, however, evaluation design conducted among 363 medical institutions in Japan. Dr. Greg Hundley: In the study, there're 3,796 patients that are aged greater than 75 years with elevated LDLC without a history of coronary artery disease that already were receiving dietary counseling. They're randomly assigned one-to-one to receive as ezetimibe 10 milligrams once daily versus usual care with their randomization stratified in a block design on age, sex, and baseline LDL-C. The primary outcome is the composite of sudden cardiac death, myocardial infarction, coronary revascularization, and stroke. Dr. Carolyn Lam: Ooh, so tell us the results. Dr. Greg Hundley: There were several patients that had to be excluded, so what ended up happening, there's 1,716 and then 1,695 that are included in each of the two respective arms for the primary analysis. What they found is that as ezetimibe reduced the incidents of the primary outcome. Then, regarding some secondary outcomes, the incidents of composite cardiovascular events and coronary revascularization were lower in the ezetimibe group than in the control group. But, there was no difference in the incidents of stroke, all-cause mortality, or adverse events in the two different groups. Dr. Carolyn Lam: Can you sum it up for us, Greg? What should we take home regarding ezetimibe and what further do we need to do? Dr. Greg Hundley: Good point, Carolyn. I think what we can take away from this study is that LDL-C lowering therapy with ezetimibe prevented cardiovascular events, suggesting the importance of LDL-C lowering for primary prevention in individuals greater than 75 years of age with an elevated LDL-C. However, remember, it was open label, so I think a placebo, controlled, randomized clinical trial will be required to validate the data that were obtained in this study. I think another study is probably going to be needed. Dr. Carolyn Lam: Thanks, Greg. Well, let's move on to our feature discussion, shall we? Dr. Carolyn Lam: Today's feature paper is of personal interest to me and I'm sure of widespread interest to everybody. Why? It's on plant-based diet. We've heard a lot about it. I'm vegetarian and very, very loudly self-confessed, but does the quality of a plant-based diet actually matter? Such an important question. Dr. Carolyn Lam: I'm so pleased to have the authors of this very remarkable paper, Dr. Megu Baden as well as Dr. Shilpa Bhupathiraju, both from the Harvard T.H. Chan School of Public Health; and our associate editor, Dr. Mercedes Carnethon from Northwestern University Feinberg School of Medicine. Welcome, ladies. What a nice chat we're going to have on this very personal topic to me as well. Dr. Carolyn Lam: First of all, maybe, could I ask, Shilpa, do we need another study on plant-based diet? Could you tell us the rationale for what you did this time? Dr. Shilpa Bhupathiraju: Like you said, when we talk about plant-based diets and what people usually think is, well, it's vegetarian or not. But, I think there's much more to a vegetarian diet. It's the quality that matters. Previous studies really then differentiate the quality of a vegetarian diet. To this extent, we developed plant-based diet indices, which actually capture the quality of a plant-based diet, so we have an overall plant-based diet index which captures the amount of plant-based foods; a healthy plant-based diet index, which captures the quantity of healthy plant-based foods; and again, the unhealthy plant-based diet index, which captures the quantity of unhealthy, plant-based foods. Dr. Carolyn Lam: Thanks. Meg, if you don't mind, I know everybody is asking this as they're listening. Could you give us some examples of what an unhealthy plant-based diet index would consist of compared to healthy? Then, perhaps, tell us a little bit about your study and what you found. Dr. Megu Baden: First of all, let me explain again. In this study, we use three versions of plant-based diet indices that can assess the quality of plant foods in general population. The first index is an overall plant-based diet index, PDI for short. A second one is a healthful plant-based diet index, HPDI. The third one is an unhealthful plant-based diet index, UPDI. In order to create these indices, we divide all food groups into three larger categories. One is the healthy plant foods, which contains whole grains, fruits, vegetables, nuts, legumes, vegetable oils, tea, and coffee; less healthy plant foods such as fruits juice, refined grains, potatoes, sugar-sweetened beverages, and sweets or desserts; and animal foods, which is animal food, dairy, eggs, fish, meat, miscellaneous animals-based food. Dr. Megu Baden: We investigated the association between preceding trailblazing changes in these indices and subsequent total and cause basic mortality in two large US cohorts. We found that compared with participants whose diet remained stable, the hazard ratio for total mortality, among those risks, the greatest increase in PDI was 0.95; for the greatest increase in HPDI, the healthful versions of the PDI was 0.90; and the greatest increasing in unhealthful PDI was 1.12. In contrast, the hazard ratio among participants with the greatest difficulty is in PDI, was 1.09; the greatest decrease in healthful PDI was 1.10; and the greatest decreasing in unhealthful PDI was 0.93. For CVD mortality, the risk was 7% lower for our 10 point increase in PDI, and 9% lower for HPDI and 8% higher for UPDI. Dr. Megu Baden: In summary, we found that improving plant-based diet quality over a 12-year period was associated with a lower risk of total and CVD mortality, whereas increased consumption of unhealthful plant-based diet was associated with a higher risk of total and CVD mortality. Dr. Carolyn Lam: Could I ask, Shilpa, to maybe add a line of ... have you applied this information in any way yourself or with patients, or is there an overwhelming take-home message you'd like people to remember? Dr. Shilpa Bhupathiraju: Yeah, I'm not a clinician myself, but I'm a public health researcher. I'm in India currently and I'm giving a talk to South Asians and the emphasis on vegetarianism. But, again, the quality of the vegetarianism is important. Being a vegetarian is not enough, but what goes into it is really important. If it's a white rice and sugar-sweetened beverages, it's not good, so really the emphasis should be on whole grains, consuming more nuts and legumes. I think that's important. Dr. Carolyn Lam: Oh, that's great. Mercedes, we've discussed this paper as associate editors, so proud to be publishing this in circulation. Could you share some of your thoughts on the implications of these findings? Dr. Mercedes Carnethon: The authorship team has done an outstanding job of clarifying a very complicated issue. I think what we really like about this and the ways in which it really adds to the literature, what you point out, that every vegetarian diet isn't the same. I was very impressed with the thought that went into classifying vegetarian foods as healthy or unhealthy. I would be interested in hearing more from the authors, particularly, since I feel they did a good job of how they dealt with complicated foods or mixed foods. I think one example given was a pizza, which has tomato sauce, but it also has other things, so I would love to hear from the authors how they classified complicated foods. Dr. Shilpa Bhupathiraju: The decision to classify pizza as an animal food was somewhat, I would say, arbitrary. I do agree that there's lots of tomato sauce, but again, I think the decision that went to it, it does have a ton of cheese, processed cheese, I think that's why we classified that as an animal food. The other complicated foods are mixed dishes that we struggled with were cream soups. We thought about what the base was or what the general preparation of that would be. Given that heavy cream is a major ingredient, so those were again, classified as animal foods. Dr. Mercedes Carnethon: I think there's a lot of logic in that and I really like the thought and care that you put into that. The other questions I have, I feel that you did a really nice job of, are even portion sizes. Tell me how you handled portions. Dr. Megu Baden: We basically take the information from our food frequency questionnaire. All of them are per the serving sizes, so we considered how participants reported how often on average they had consumed each food of our standard portion size in the past year. I know it's difficult to indicate the portion size. Shilpa, would you add something for the portion size for that? Dr. Shilpa Bhupathiraju: Yes. Like Megu said, we use standardized portioning sizes, so a cup of fruit, a cup of vegetables, an eight-ounce, or a cup of tea or coffee, so that's how we use what people use in general. The portion sizes are all specified on the food frequency questionnaire, so the nurses or the health professionals, they understand exactly what they're reporting. Is it a glass of fruit juice or half a glass? Then, we can word those frequencies into standardized serving sizes onto servings per day. Dr. Carolyn Lam: Great. Shilpa, could I follow up from Mercedes very important question? How does the index account for portion size too, as an is too much of even a good thing become a bad thing? You know what I mean? Dr. Shilpa Bhupathiraju: The index itself is a score. The way we capture it, as you know, everything is converted from frequencies into servings per day for each participant. Then, what we did was we divided the participants based on the distribution of the data into quintiles. Those in the highest category of the healthy plant foods received the highest points. The scoring varied a little bit based on which index we were calculating. But, in general, what we did was we divided everybody into five groups or quintiles. Then, the scoring varied depending on what we were calculating. For the HPDI, which is the healthy plant-based diet index, those in the fifth group or the highest intake received the maximum number of points, which was five. For the unhealthy plant-based diet index, those people received the reverse scoring, so they received zero points. Essentially, the participants were divided into quintiles and the scoring was done accordingly. Dr. Carolyn Lam: Maybe I could ask you a question on a different track, and I'm not sure if you have some answers here, but I noticed that your study population was impressive, almost 49,500 women from the Nurses' Health Study, almost 26,000 men from the Health Professionals Follow-up Study. Did you find any sex differences? Dr. Shilpa Bhupathiraju: We didn't find any sex differences. We did some sensitivity analysis by cohort and we didn't find a statistically significant interaction, which is I think good to note because we would expect the effects to be similar in men and women. Dr. Carolyn Lam: I think both men and women need to hear that. None of us are excused from, I suppose, trying to gear towards a healthy plant-based diet. I think that's what I'm hearing. Mercedes, do you have more thoughts to add? Dr. Mercedes Carnethon: I do. One thing I really like about this particular paper is the way the you acknowledge some of the limitations that we face when interpreting findings from observational studies, particularly observational studies of a health behavior when we know that health behaviors often cluster or correlate with other health behaviors. Can you tell us a little bit about some of the cautions and interpretation that you certainly acknowledged and presented very well? Dr. Shilpa Bhupathiraju: Sure. Our primary analysis was looking at changes, so long-term changes. When people change a diet or their lifestyle, they change something else. As you can see from our paper, those who improve the plant-based diet quality, we're also, in general, tended to be healthier. This being an observational study, we tried to control for those as to the greatest extent possible, but again, they could be residual confounding. We maybe failed to measure for certain things that we were unaware of or that we did not measure. I think we really can't get at causality, but I think the consistency of the evidence from our previous papers and from this paper point to a suggestion that improving plant-based diet quality is definitely associated with better health outcomes and a lower risk of death. But, again, it is important to know that this is observational and there could be changes in other health behaviors that we did not measure that could explain this association. But, we did as well of a job as we could in trying to control for these changes and other behaviors, lifestyles or even health conditions. Dr. Mercedes Carnethon: Thank you. Dr. Carolyn Lam: Thank you so much, Meg and Shilpa. You've been listening to Circulation on the Run. Don't forget to tune in again next week. Dr. Carolyn Lam: This program is copyright American Heart Association 2019

In last week’s episode with Greg Hill we talked about the human side of digital transformations. Greg recently started his own consulting firm and is working with companies to help them realise the benefits and challenges that lie ahead transforming to cloud based platforms.Today I talk through what I believe are the drivers of digital transformation."Digital transformation is the integration of digital technology into all areas of a business, fundamentally changing how you operate and deliver value to customers. It's also a cultural change that requires organizations to continually challenge the status quo, experiment, and get comfortable with failure" – the Enterprisers Project – a community of CIOs discussing the future of business and IT.Digital transformations are a long-term investment, not just one project does it all.As I work with organisations, I understand the current top four (4) key drivers for change are:Replacing legacy systemsAutomating manual processesAnalysis and insights of dataProviding customers with self-service optionsIf you don't take the time to clarify the change drivers, organisations can experience these key problems:Jump to a solution without understanding the problem (or benefit)Think technology will solve performance issuesLack of funding for continuous improvementJC Three TipsMap strategy to operations, be clear with your blueprintBreak it down into achievable building blocks with strong foundationsInvest in your people, provide training for future skillsQuote from my conversation with Greg ‘"What is the effect on the people, roles change moving to cloud based platforms".

 Join the Resourcefully Speaking community by liking our Facebook Page and by going to pampippin.com! Pam Pippin wants to introduce you to Julie and Greg Gorman. In today's PAMCAST you will hear about how God used a difficult season in the Gorman's life to launch them into their purpose. Together they teach on having a purpose-filled marriage on stages across the world and have written 5 books. You will love their energy and their heart for people. Quick Episode Summary: Introductions When the Gorman's and Pam met Gorman's goals Obstacles that took place You are going through a process What would a day with Greg and Julie look like Showing unconditional love discovering that common ground What is next for Julie and Greg What the Gorman's would take on an island  SITES: facebook.com/marriedforapurpose www.instagram.com/marriedforapurpose/ twitter.com/marriedwpurpose www.linkedin.com/in/marriedforapurpose www.gormanleadership.com www.marriedforapurpose.com - for doable, efficient, resources that can be done in your home.  Designed for busy couples, to come together once a week where they can learn and then visit that principle every day. Published: Married For A Purpose Online Membership What I Wish My Mother Had Told Me About Marriage Two Are Better Than One Married for a Purpose

Dr Carolyn Lam:                Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm doctor Carolyn Lam, associate editor from the National Heart Center, and Duke National University of Singapore. Dr Greg Hundley:             And I'm Greg Hundley, associate editor from the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr Carolyn Lam:                Have you heard of long non-coding RNAs? Well, they are definitely the hot topic and our feature paper today discusses the first demonstration of the importance of a linked RNA in atherosclerotic lesions not just in mice but also in humans. You have to listen on, it's coming up right after our copy chat.                                                 Greg, what are your picks upon the journal this week? Dr Greg Hundley:             The first paper I wanted to discuss comes from France, and it's basically looking at ambulance density and outcomes after out of hospital cardiac arrest from Florence Dumas from Hôpital Cochin in Paris, France. This manuscript addresses the geographic disparities and survivorship of out of hospital cardiac arrest and the relevance of the patients characteristics versus whether ambulances are equipped with those trained in basic or advanced cardiac life support. So, what they did they had nineteen neighborhoods in Paris, and the number of BLS trained versus ALS ambulances was collected, and the authors assessed that respective associations of socio-economic characteristics of the patient population and the ambulance resources of these neighborhoods and compared those with successful return of spontaneous circulation or risk as the primary end point and then survival of out of hospital discharge as the second end-point.                                                 So, they had 80754 non-traumatic out of hospital cardiac arrests across the Paris area. 42% at ROSK 9% head survival at discharge, and after accounting for the patient's socio-economic status, greater than one and a half advanced cardiac life support ambulances per neighborhood and greater than 4 basic cardiac support basic life support units per neighborhood were associated with ROSK, but only the 1.5 ALS units per neighborhood were associated with survival. Dr Carolyn Lam:                Oh, interesting Greg. So does this we need more advanced life support units? Dr Greg Hundley:             So, Paul Dorian from St. Micheal's Hospital in Toronto, Canada wrote an excellent editorial, and one point he made related to these ALS units is that it was really a very small 1.3 adjusted odd ratio for survival to hospital discharge, and it's important to note that although the increase in survival was associated with more ALS units, there were many other variables that were likely important and not recorded in this study. For example, including the time to collapse, to calling for EMS, the time from the call to the deployment of that ALS unit to the scene, the time from collapse to the defibrillation, the total "no flow time" sort of in quotation, which is the total duration of collapse until CPR is started and so I think one of the points in this observational study is there could've been many differences that would've associated with the findings, interesting findings how about one of the papers that you liked? Dr Carolyn Lam:                So, the paper that I selected here is a first time that a targeted anti-inflammatory therapy has been shown to reduce hospitalization for heart failure and at-risk patients. So, you know that some clinical inflammation associates with an increased risk of heart failure and associates with the worst prognosis in patients with heart failure, and yet, so far, treatments specifically directed at reducing inflammation in patients with heart failure have not been shown to improve clinical outcomes. That's why today's paper is so special and it's from Dr Everett and colleagues from Brigham and Women's Hospital Harvard Medical School in Boston, and basically, the authors looked at CANTOS and tested the hypothesis that the interleukin -1β inhibitor can canakinumab would prevent heart failure hospitalizations and the composite of heart failure hospitalizations on heart failure related mortality in the CANTOS trial.                                                 Now, remember the CANTOS trial randomized more than 10 000 patients with a prior myocardial infarction and with high sensitivity C-reactive proteins at least two or greater, and they were randomized to canakinumab 50, 150, and 300 mg or placebos. Now, before randomization, these participated were asked if they had a history of heart failure and 22% said yes so the current paper actually looks at this stratification of patients who said they had heart failure, and during a meeting follow-up of 3.7 years, 385 patients had a new heart failure hospitalization event. Now, here's the key: the authors found a dose dependent reduction in the risk of hospitalization for heart failure as well as the composite of hospitalization for heart failure or heart failure related mortality among those allocated to Canakinumab. Dr Greg Hundley:             So, how does this differ from prior attempts targeting inflammation and heart failure? I mean is this ready for prime time thing? Dr Carolyn Lam:                So, we have to bear a few things in mind here you know. CANTOS was different from a previously published randomized controlled trials, which were basically neutral and that was like of infliximab and etanercept so the drug in CANTOS targets interleukin-1 beta whereas the prior ones targeted the TNF-alpha, and also very importantly, CANTOS did not specifically enroll patients with an established heart failure only. CANTOS patients had to have a history of myocardial infarction and there was no data on their ejection fraction or natriuretic peptides at the time of randomization nor at the time of heart failure hospitalization. So, by the way, we don't know whether there's a differentially effect on hep pef versus hep-ref. So, again difference from the heart failure focused trial previously that used an anti-inflammatory agents.                                                 The other thing: although there was a dose dependent reduction in the risk of hospitalization for heart failure no single dose of Canakinumab compared to the placebo had a statistically significant reduction in the risk of heart failure hospitalization. Only the trend was statistically significant so all in all, this was a pre-specified aim of CANTOS to look at heart failure, the data presented here should really be considered hypothesis generally, but really quite promising. And what about you Greg? What's your other paper? Dr Greg Hundley:             We're going to switch gears a little bit and shift over to the Jackson heart study. The large longitudinal cohort from Jackson, Mississippi that's recruited to follow for cardiovascular events, and it's an area of the United States where we have some of the highest cardiovascular disease event rates really across the nation so this study focuses on sleep apnea and is the Jackson's heart sleep study. It's a sub-study of this larger Jackson's heart study that involves 913 patients, and the investigators were looking at the association between sleep apnea and blood pressure control among those of a Black race. So, Dayna Johnson of Emerald University is the first author on the paper. What's nice about this sub-study, this sleep sub-study is that there are objective measures using an in-home type III sleep apnea study. They had clinical blood pressure measurements and then anthropometry as opposed to questionnaire derived data that may have been performed in the larger cohort.                                                 And the study determined these associations between moderate or severe obstructed sleep apnea with controlled, uncontrolled and resistant hypertension. So the analytic sample of the individuals with hypertension was 664, and they had an average age of about 64 years. They were predominately women 69%, obese 58%, College-educated at 51%. Among the sample, about a quarter had obstructive sleep apnea, which was untreated and unrecognized in 94% of the participants. That's an interesting point, just right there.                                                 Overall, 48% of the participants had uncontrolled hypertension and 14% had resistant hypertension. So, multiple medications, often four and still unable to control the blood pressure. So the findings participants with moderate or severe obstructive sleep apnea had 2 times higher odds' ratio of resistant hypertension. Dr Carolyn Lam:                Whoa Greg, that's a huge risk and very important finding. I mean if sleep apnea could be modifiable risk factor perhaps for very important issue among African Americans resistant hypertension. What do you think about clinical implication? Dr Greg Hundley:             One of the things to be considering now is what are we going to do about that cause as you know CPAP is really the preferred treatment for resistant hypertension, but it's efficacy hasn't been really that well studied in African Americans and CPAP tolerance is low so this study highlights for us potentially new mechanisms for resistant hypertension, but we still got to be thinking about what would be our next therapeutic intervention for this particular patient population. And what about your next study? Dr Carolyn Lam:                The next study is about Impella support for acute myocardial infarction complicated by cardiogenic shock. Now, we use it all the time, but did you know that to date, there is no large randomized study actually comparing the use of Impella to other contemporary cardiac support devices and medical treatment in stem related cardiogenic shock. So, Dirk Westermann and colleagues from University Heart Center in Hamburg tried to address this knowledge gap by using a multi-national database of patients with acute myocardial infarction complicated by cardiogenic shock and treated with the Impella device and compared in a matched fashion their outcomes to patients from the IABP Shock II trial, which you would recall is a randomized trial which demonstrated similar outcomes between IABP and medical treatment in myocardial infarction in cardiogenic shock.                                                 So, they looked at 237 matched-pairs so remember this was pairs from this registry of acute myocardial infarction with shock and using an Impella matched with IABP shock patients and what they found was that there was no significant difference in 30-day all-cause mortality. Instead, severe or life-threatening bleeding and peripheral vascular complications occurred significantly more often in the Impella group when they limited the analysis to the IABP treated group as controlled versus Impella that was still the same results. Dr Greg Hundley:             So, Carolyn, there are trying to match patient population from two different studies and they may have confounders in there that we can't account for so why we not able to produce large randomized trials of Impella devices in studies of patients with acute myocardial infarction? Dr Carolyn Lam:                The rate of acute myocardial infarction complicated by cardiogenic shock has really declined in the past decade. Furthermore, clinical signs of shock really appear in half to three quarter of cases several hours after hospital admission so making randomization before primary PCI of the AMI really very difficult. And finally, many interventional cardiologists believe that there's equipoise that has already been reached on the use of these cardiac assistive devices in patients with cardiogenic shock and this was from registry data, and so if interventionists believe this then they also believe its unethical to randomize these patients in trials. Still, I think that current study to date really causes us to pause and to acknowledge that we really need to evaluate this better and prospective randomize trials of Impella treatment are warranted.                                                 Let's now go to our featured discussion, shall we?                                                 For our featured paper discussion today, we are talking about a basic science paper, and we have none other than the best of the best Dr Charles Lowenstein, our associate editor from University of Rochester Medical Center joining us as well as the first author of a really fantastic paper on long non-coding RNA in a specific type involved in arthrosclerosis and plaque formation. This first author is Sebastian Creamer from Goethe University in Frankfurt.                                                 Charlie, could you start us off by telling us what is a long non-coding RNA? We've heard a lot about this in recent times. What's the big deal about them? Dr Charlie Lowenstein:  So in the last decade, scientists have learned that your genome, your DNA inside you, every cell codes about 20,000 genes and those 20000 genes encode proteins, but there are another 20000 genes that encode RNA only, RNA that never turns into protein that leaves RNA are an amazing diversity of different kinds of RNA really short micro RNA, longer RNA that defends the host from viruses and long non-coding RNA that have a huge variety of effects regulating genes, turning genes on and off in proliferation and cell growth and inflammation so long non-coding RNAs are increasingly appreciated as an important part of the genome. Dr Carolyn Lam:                What a perfect set up with that. Sebastian, could you tell us about your study please? Dr Sebastian Creamer:   Our laboratory was interested in non-coding RNAs for some time and previously, we've found that this specific non-coding RNA MALAT1 regulates endothelial cell functions and because we were interested in analyzing this particular RNA in the disease setting it shows at a risk growth so it's because also we saw that when it's regulated by flow and end of previous cells and so we cross MALAT1 deficient mice to Apoe mice and set them on a high fat diet and analyzed and subtracted in both groups. And while we only saw a modest increase in plaque size in MALAT1 deficient mice, we could appreciate a higher amount of inflammatory cells in plaque of aortic roots in those mice, which let us hypothesize that inflammatory responses was appreciated and is a very important contributor to arthrosclerosis in MALAT1 deficient mice. And to test this, we decided to transplant MALAT1 deficient bone marrow in Apoe knockout mice with MALAT1 and interestingly, we saw that now plaques were significantly larger than compared to mice who received controlled MALAT1 white cell bone marrow, and also inflammatory cells were more prominent in those mice. Dr Greg Hundley:             Sebastian, this is Greg Hundley. You also did some experiments in human subjects. Could you tell us a little bit about those too? Dr Sebastian Creamer:   So, because we saw this interesting phenotype, we were very much interested if this also translates into the human setting. Luckily, we got a really nice collaboration receding in Stockholm access to high impact material from patients with arthrosclerosis and what we could see here that MALAT1 expression was down regulated in patients with arthrosclerosis and it also correlated with disease progression. Moreover, in another collaboration, we consolidated those findings with experiments, which showed that human cells have less MALAT1 compared to normal vasculature. Dr Carolyn Lam:                It all sounds so sensible and logical and so on but let me just frame this for our audience. This is actually the first time that it's been demonstrated. The importance of long non-coding RNA in arthrosclerosis. Charlie, could you tell us a little bit about how significant these findings are? Dr Charlie Lowenstein:  Sure. So, I'm really interested in the final figure in this paper because there are lots of interesting human data, showing that MALAT1 expressed more in normal than atherosclerotic arteries and also that MALAT1 expression is correlated with fewer major adverse cardiac events so the whole story is a very nice story saying that the expression of this anti-inflammatory link RNA not only has an effect in mice but it can be extended into the human field of arthrosclerosis and inflammation. It's particularly important because there's a lot of attention in the last decade that inflammation drives atherosclerosis, and in light of CANTO trial showing that anti-inflammatory therapy can actually decrease atherosclerosis and decrease cardiovascular events in humans. This is important cause it shows another pathway, which regulates inflammation. Not only in mice, but also in humans, and in the human atherosclerotic setting. Dr Carolyn Lam:                Amazing. Sebastian, what are the next steps? How far are we away from clinical applications here? What are the next steps to get it in the clinic? Dr Sebastian Creamer:   So, the very difficult thing is that MALAT1 is down-regulated in atherosclerosis and also therapeutic approaches is very difficult in such a complicated disease like atherosclerosis to actually increase the expression of such a long non-coding RNA. What we are currently working on is to decipher more than the clinical malade-1 is actually influencing atherosclerosis so we have lots of hints or some evidence that adhesion of inflammatory substances altered and the bone marrow activity, which is very important in atherosclerosis and also in other cardiovascular diseases like myocardial infarction is altered so we think that malade-1 might actually influence the resolution of inflammation and when it's lacking, inflammation can be resolved. So, we are now putting somewhat mechanistic studies and finally, we hope that we can find another downstream target like micron AB, we talked about in our paper, which we can directly target in the future. Dr Charlie Lowenstein:  So, I agree with Sebastian. I think MALAT1 is going to turn out as one of those major link RNAs that controls inflammation possibly controlling the way in which the bone marrow reacts to systemic inflammation and produces cells and then have those cells home in on various inflammatory targets so I think this is an important observation that's going to have not only implications for atherosclerosis but also for other inflammatory diseases. Dr Carolyn Lam:                Excellent. If you don't mind, I would love to switch tracks a little bit. We find it that very special and we can discuss basic papers with people who can explain it so well because we understand that there's so much work that goes in to these papers and so on. Charlie, could you take behind the scenes a little bit with the editors and tell us what is it that circulation looks for in basic science papers that makes us published? Dr Charlie Lowenstein:  We get a lot of really good basic science papers, and it's a challenge for the associate editors, and the editors to figure out what's right for circulation and let me use this manuscript as a great example because this is a terrific paper. So, this paper is divided into four sections, and these sections are what we look for in any basic science paper that's going to reach an audience of clinicians who are interested in pathways and therapeutics so this paper has a section on mice. There's a gene in mice that's important then the paper delves into cells what's happening with cells and then a little bit of mechanisms and genes and proteins and then this paper takes the observation back into humans and shows that there's some human and clinical relevance so this is not only a great paper, but it is a classic example of what the associate editors are looking for in a basic science paper that's targeted towards clinicians. Dr Charlie Lowenstein:  There's some in vivo work with mice, there's some mechanistic work then they take it back to the humans. Plus, of course like anything that comes into circulation, it's going to be novel, interesting and has some important relevance to human cardiovascular disease. This paper that we're discussing is a great example of a paper that we love to publish in a circulation and it's a real tribute to Dr Dimmeler and her team and to Sebastian that they put this paper together and submitted it to us. Dr Carolyn Lam:                Thank you audience for joining Greg and I today. You've been listening to circulation on the run. Don't forget to tune in again next week.  

Welcome to Everything Trying to Kill You, the comedy podcast that talks about horror movies, and Happy Valentines/Horniest-Day-of-the-Year! In episode 34 about David Robert Mitchell’s 2014 film, It Follows, your hosts (Mary Kay, Mary, and Maegan) answer important questions like these:What beer should Maegan have immediately after delivering her first child? What’s the weirdest pickup that ever worked for you or on you? What’s the weirdest FAIL? What is the point of this movie? And what is the “it” that follows, which we are supposed to be afraid of? How does this movie invert the final girl trope? If we’re supposed to be afraid of sex to fill emotional voids, why is the best move to have sex with people who has a lot of sex, and would pass it on immediately? Can we talk about “also, probably the patriarchy?” Did you feel like this film was slut-shaming? Or that it was biased on gender? What exactly qualifies as “having sex?” Is it just vaginal penetration? Does the demon recognize same-sex intercourse as “passing it on?” How can I get rid of the demon? If I REALLY want to get rid of it, and I rape someone, does that count? Who is the most attractive baby man on Dawson’s Creek? How terrible is Jeff/Hugh? What about Greg? What did you think about the friend group as a whole? Is Florida better than prison? Did you like the costuming? How does Jay decide whom to fuck? What is the definition of consensual sex? How is important to Jay’s story that it’s not just buyer’s remorse? If you are initiating the sex, can it be consensual if your life is on the line? What do pools have to do with the set? What are the other homages to classic horror? Why is that lit professor teaching T.S. Eliot’s “The Love Song of J. Alfred Prufrock?” What does the intended audience have to do with these cultural allusions? In the end, does It follow them?It Follows (2014) – Directed and written by David Robert Mitchell. Performances by Maika Monroe, Keir Gilchrist, Olivia Luccardi Genre: Horror, Revenge, Thriller, Suspense, Supernatural Where to watch: AmazonSummary: For nineteen-year-old Jay, Autumn should be about school, boys and week-ends out at the lake. But after a seemingly innocent sexual encounter, she finds herself plagued by strange visions and the inescapable sense that someone, something, is following her. Faced with this burden, Jay and her friends must find a way to escape the horrors, that seem to be only a few steps behind. Written by Jose TamayoLinks: Thunder Snow Cone sideshow/kinkshowSims Fails

Greg Schreeuwer is a chiropractor, kinesiologist, human behavioural expert, innovator and visionary.He specialises in helping people just like you overcome the obstacles, limitations and challenges keeping them from accomplishing their goals and dreams in life.He works with a range of tools and techniques including NCR (NeuroCranial Restructuring), as well as Integrative Kinesiology and NET (Neuro Emotional Technique).These are kinesiology techniques for finding and removing imbalances related to unresolved stress in the body or mind.Join me as I ask Greg:What is Neuro Emotional Technique (NET)?What is chiropractic and Kinesiology?How often is emotional stress connected to physical ailments?How do we stay in balance?What is NeuroCranial Restructuring (NCR)?And Greg will share with us:The three levels of the brain.How he uses kinesiology to determine and resolve issues.How overcoming emotional blockages can help overcome obstacles to physical health.How NCR helps achieve balance.It was a pleasure to be able to share some of Greg’s wisdom in this podcast, such as:“The brain is a processor of emotion, it doesn't feel emotion like the physical body does.”“Nature doesn't like when things are out of balance.. ever.”“I believe the dealing with emotion can actually help you become even more empowered.”To find out more about Greg, visit http://www.gregschreeuwer.com or http://www.universalhealth.com.au/I’d love to know your thoughts and experiences - join the conversation on my Facebook page.For more episodes of Recipes For Life, find us on iTunes at https://apple.co/2NpsIba, Spotify at https://spoti.fi/2NpSiN0, Whooskhaa at https://www.whooshkaa.com/shows/recipes-for-life-with-pete-evans, click the link on https://peteevans.com, or just look up "Recipes For Life" in your favourite podcast app.I'd love to spread the knowledge in these podcasts far and wide. If you liked this episode, I'd love it if you could share it with your friends, and perhaps even leave a review on iTunes.This podcast is proudly presented by The Institute For Integrative Nutrition, or IIN for short.I've completed this amazing health training course through IIN, and I would thoroughly recommend it for anyone wanting to start a career in the health coaching and wellness space.This course is conducted over a year long period and it's constructed in a way that if you're a full time worker or a busy parent or wherever you are in your life you'll still be able to complete all the required curriculum and modules.Please see the link included in this post on my Facebook or Instagram page or on iTunes, to access the free sample class and first module of the program, to get a great taste of the format and structure as well as utilise my special discount that I can offer you if you decide to sign up.Just go to https://geti.in/2K2QcAw, email admissions@integrativenutrition.com or call +1 (212) 730-5433 outside the US, (844) 780-3300 within the US.Make sure you tell the admission team that you're part of the Pete Evans tuition savings to claim your very substantial discount. More info is at https://www.integrativenutrition.comTheme music by Mandharu. Audio production by Andy Maher. See acast.com/privacy for privacy and opt-out information.

Casey was again part of the faculty for TAPS, this time in Long Beach. He sat down with the other faculty: John Parks, Nick Mancini, Ted Atkatz, Shaun Tilburg, and Tim Jones, as well as students for this episode.Watch here. Listen below. If you cannot see the audio controls, your browser does not support the audio element 0:00 Intro and hello0:49 Comments on Don Greene’s class5:24 Bailey: What is the most important skill to have as a professional musician that’s not directly related to the actual act of playing or performing?15:46 Ted’s book “The Regimen” and self-publishing22:20 Milton: When did you realize you should be practicing for your own benefit to make yourself better so you can progress in the long-term and not so much just for school requirements?34:46 Greg: What are your personal stories about sponsorships?42:30 What’s your most embarrassing moment on stage during a performance and how did you recover from it?52:23 Emily: Here at TAPS we’ve been working on excerpts to prepare for a mock audition. What is your least favorite excerpt to see on an audition list?56:54 Wrap

In Episode 31 of GemTalk Podcast, our hosts investigate the last two episodes of January's Steven Bomb - The Zoo and That Will Be All! Will Steven and Co. manage to rescue Greg? What happened to Amethyst since she left the group? Will Blue Diamond get her own song? Find out as Shane and Ken discuss this and much more, including newly announced episode titles!