Podcasts about in this issue

#HOWCEE PRODUCTIONS GOSPEL  A SHOUT OUT TO THE FAMILY OF  Loretta Lynn, Feisty First Lady of Country Music, Dies at 90  http://www.cvmfeatures.christianvoicemagazine.com/2022/10/loretta-lynn-feisty-first-lady-of.html KEN AND JEAN GRADY GOSPEL MUSIC TODAY T V BROADCAST OCT 16 2022GMT610 10-15-22 AUDIO.mp3  @ kengrady@gospelmusictoday.comIN THIS ISSUE OCT 16 2022http://www.cvmfeatures.christianvoicemagazine.com/ IN THIS ISSUE...              October 2022 ON THE COVER 3 Heath Brothers are Diving into the Deep Features REMEMBERNG... Marie Henderson ​Artist Spotlight: Set Apart OCTOBER 11, 2022 The Harlem Gospel Travelers share new four-song radio sampler from their new LP "Look Up!" ​GODREPORT: The Testimony of Andrae Brooks ​Barbara Jean Smith When God Gives You a Gift, You Need to Use It ​Artist Spotlight: Aaron Green ​PLUS... Monthly Columns, Music News, Airplay Charts, Artist Appearances, and more CK OUT AIRPLAY DIRECT https://airplaydirect.com/  

What?! A new pod??! Yep! Join Process Party co-host Zack Soto for In This Issue… a podcast about formative comics reading experiences, with a focus on the single issue format. Every episode finds Zack and a special guest doing a close reading of a comic book (not a graphic novel!) and havin' a lively chat about it. This is a presentation of Episode 8 with cartoonist Adam DeSouza on Nausicaa of the Valley Of The Wind #1 by Hayao Miyazaki, Tom Orzechowski, Dana Lewis & Toren Smith, and published 1988 by Viz Comics. Fair warning: they both LOVE this comic, so Nausicaa haters beware!

THE ISSUE: Dirty Plotte #9 (aka Purty Plotte #9 aka New York Diary chapter 1) By Julie Doucet Published 1995 Drawn & Quarterly Jenn Woodall (Space Trash, Magical Beatdown) joins In This Issue... to discuss the ninth issue of Julie Doucet's seminal alt-comic comic series Dirty Plotte.  Lots of talk about art school, bad romances, skeezy dudes, illustration rates, zine aesthetics, collage, graffiti and more! Tune in next time for another close read with In This Issue...

Links to things we talked about:The Tripods series by John Christopher:The White Mountains, The City of Gold and Lead, The Pool of Fire, and Before the Tripods CameThe Amazing Adventures of Kavalier and Clay by Michael Chabon"The Amazing Adventures of Kavalier & Clay Limited Series Set At Showtime As Part Of Michael Chabon & Ayelet Waldman CBS TV Studios Overall Deal" —DeadlineChabon's (quite active!) InstagramHyperion by Dan Simmons "Why Bradley Cooper's Hyperion Movie Will Be Epic for Sci-FI Fans"  —MoviewebOur Plugs:François discussing Black Hole #1 with Zack Soto on his new podcast In This Issue...And François is interviewed on the Parker Edison ProjectNext Episode: The Fifth Season by N.K. Jemisin!Support the show by buying any of the books we spoke about from our Bookshop!Follow us:Instagram and TwitterJonas:Instagram and TwitterFrançois:Instagram

THE ISSUE: Nausicaa of the Valley of the Wind #1 By Hayao Miyazaki, Tom Orzechowski, Dana Lewis & Toren Smith Published 1989 by Viz Comics THE GUEST: Adam DeSouza Adam (Ish, A Gleaming) joins In This Issue... to discuss the first issue of animation legend Hayao Miyazaki's main contribution to comics, Nausicaa Of The Valley Of The Wind—specifically the 1988 first issue, which was released in what we might call "Prestige Format" (please excuse me while I tie an onion to my belt). Lots and lots of hot takes about Miyazaki in general and Nausicaa in particular in this extra-long episode, as we're both huge fans of this work and find it impossible not to wax rhapsodic over it. We do hope you'll excuse our enthusiasm! Tune in next time for another close read with In This Issue...

THE ISSUE: Hard Boiled #2 By Frank Miller, Geof Darrow, Claude Legris & John Workman  Published 1990 by Dark Horse Comics THE GUEST: Ian Densford Ian Densford (Trench Dogs, Soggy Landing) joins In This Issue... to discuss the second issue of the satirical maximalist epic Hard Boiled, which as a series arguably paved the way for a ton of vibes-and-ultraviolence-driven comics made since. Tune in next time for another close read with In This Issue...!

THE ISSUE: Marvel Comics Presents #100 By Howard Mackie, Sam Kieth, Glynis Oliver & Janice Chiang Published 1992 by Marvel Comics THE GUEST: Ian MacEwan Ian MacEwan (Roofstompers, MCMLXXV) joins In This Issue… to discuss the 100th issue of Marvel Comics Presents, which is essentially an early Sam Kieth showcase, as he draws the whole issue of what's normally an anthology title. Tune in next time for another close read with In This Issue…!

THE ISSUE: ACME Novelty Library #8 Written, illustrated, & lettered by Chris Ware Published 1997, Fantagraphics Books, Inc. THE GUEST: Austin English Domino Comics impresario Austin English joins In This Issue… to discuss our first experiences with the Chris Ware comic ACME Novelty Library #8. (We also briefly discuss the legacy of the Vertigo Comics release Dhampire: Stillborn (1997) by Nancy A. Collins & Paul Lee) _

THE ISSUE: SCUD: The Disposable Assassin #17 Written by Dan Harmon illustrated & lettered by Rob Schrab Published 1997, Fireman Press, Ltd. THE GUEST: Zac Gorman Zac Gorman (Magical Game Time, Costume Quest) joins In This Issue… to discuss the Rob Schrab/Dan Harmon comic SCUD: The Disposable Assassin #17. Tune in next time for another close read with In This Issue…!

Still having some issues with the new feed not showing everything so here's the third ep of Zack's new pod In This Issue... THE ISSUE: SCUD: The Disposable Assassin #17 Written by Dan Harmon illustrated & lettered by Rob Schrab Published 1997, Fireman Press, Ltd. THE GUEST: Zac Gorman Zac Gorman (Magical Game Time, Costume Quest) joins In This Issue... to discuss the Rob Schrab/Dan Harmon comic SCUD: The Disposable Assassin #17.

Still having some issues with the new feed not showing everything so here's the third ep of Zack's new pod In This Issue... THE ISSUE: SCUD: The Disposable Assassin #17 Written by Dan Harmon illustrated & lettered by Rob Schrab Published 1997, Fireman Press, Ltd. THE GUEST: Zac Gorman Zac Gorman (Magical Game Time, Costume Quest) joins In This Issue... to discuss the Rob Schrab/Dan Harmon comic SCUD: The Disposable Assassin #17.

another new episode of Zack's new pod In This Issue..., talkin' 'bout Heavy Metal Magazine vol.17 #4 and Druuna with David King! Go subscribe to ITI!

another new episode of Zack's new pod In This Issue..., talkin' 'bout that Druuna with David King! Go subscribe to ITI!

THE ISSUE: Heavy Metal Magazine V17 #4 By Paolo Eleuteri Serpieri and Various   Published 1992 by Metal Mammoth, Inc. THE GUEST: David King (website/insta/twitter) David King (Crime World, Loud House) joins In This Issue... to discuss the November 1992 issue of Heavy Metal Magazine in this double sized episode. We're focused on the central piece of the issue (Serpieri's Morbus Gravis: Creatura) but we talk a LOT about the other stories and the general publishing landscape of the time, as filtered through the masthead and included advertising. Tune in next time for another close read with In This Issue...!

Zack's new pod is over on it's own feed! Check out this second ep here and go subscribe! THE ISSUE: ACME Novelty Library #8 Written, illustrated, & lettered by Chris Ware Published 1997, Fantagraphics Books, Inc. THE GUEST: Austin English Domino Comics impresario Austin English joins In This Issue... to talk about our first experiences with the Chris Ware comic ACME Novelty Library #8. (We also briefly discuss the legacy of the Vertigo Comics release Dhampire: Stillborn (1997) by Nancy A. Collins & Paul Lee)

THE ISSUE: ACME Novelty Library #8 Written, illustrated, & lettered by Chris Ware Published 1997, Fantagraphics Books, Inc. THE GUEST: Austin English Domino Comics impresario Austin English joins In This Issue... to talk about our first experiences with the Chris Ware comic ACME Novelty Library #8. (We also briefly discuss the legacy of the Vertigo Comics release Dhampire: Stillborn (1997) by Nancy A. Collins & Paul Lee)

Hey y'all! Process Party is still on hiatus for a while but Zack has a new pod called IN THIS ISSUE... and it's all about "talkin' bout comics," one issue at a time. First up Francois Vigneault on Charles Burns' 1995 release, BLACK HOLE #1!

THE ISSUE: Black Hole #1 Written, illustrated, & lettered by Charles Burns Published 1995, Kitchen Sink Press THE GUEST: François Vigneault We kick things off on In This Issue... talking about our first experiences with Charles Burns' work, including a discussion of the short story where Burns first explored some of the ideas he'd later come back to in Black Hole—"Teen Plague," first published in Raw Vol.2 #1 (1989). From there, we dive into the plot/art/themes/symbolism/production design of Black Hole #1. A good time!

Mortgage Mom Radio airs weekly focusing on topics that will educate our listeners around mortgage lending. This week Debbie and Heidi discuss the new Experian Boost feature and explain everything you need to know if you are about to apply or are in the middle of applying for a mortgage. In This Issue "It is not in the stars to hold our destiny, but in ourselves." - William Shakespeare Sell in May and Go Away - When stocks go down, so do rates. 2021 Housing Market Predictions - After dealing with a year of uncertainty in 2020, the housing market looks to hit it big in 2021. Turn an Old Dresser Into a Unique Sink - This simple DIY project can turn an antique into a stunning sink for your bathroom. Q&A: Can You Qualify for a Mortgage Without Credit? - Is it possible to obtain a mortgage, even if you don't have any credit to your name? Knowing what options you have can help you purchase a home. Please feel free to forward this newsletter to friends, family or co-workers who may find it helpful. What To Watch Sell in May and Go Away - Explained Each spring, the same phrase pops up for stock investors: "Sell in May and go away." It's important to track, as generally stocks go down, and so do rates. That question is whether or not stock market investors will see “Sell in May and go away” this season. Yahoo Finance tells us that the full axiom was originally, "Sell in May and go away, and come on back on St. Leger's Day.” It has its roots in the city of London. Financial professionals would go on holiday in May for approximately four months to escape the summer heat and return for the St. Leger derby in mid-September. Traders and bankers in the U.S. appropriated the aphorism over the years and condensed it to its current form. The current form is based on the historical tendency for the stock market to produce its best gains between Halloween and May Day (the so-called “winter” months) and to produce well-below-average returns the other six months of the year (the “summer” months). We did not see “Sell in May” last year, as the stock markets were on a big surge higher after the huge losses seen in March due to the shutdowns. But with stocks at record high levels and high market volatility, there is a possibility of a move lower in stock prices after earnings season winds down at the end of the month. Despite never-ending stimulus, which stocks love, they cannot go straight up, and corrections big and small are always healthy and expected. If this were to occur, it could shift some investing dollars from stocks into bonds, which would help to further stabilize or cap the recent rise in mortgage rates that was seen from mid-January until the end of March. If "Sell in May" does not take place this year, do not get too worried. The Federal Reserve continues to try and hold rates at historically low levels and will do so until we see full employment and ideal inflation. Can mortgage rates increase marginally if the economy continues to grow? Yes, that would be normal in an an expanding economy. If the economy is strong, and if the job market continues to rebound, modestly higher rates should not be a deterrent to homeownership. Bottom line: Rates are still historically low, and now is still a great time to either refinance or consider purchasing a home. Source: Mortgage Market Guide   Housing News 2021 Housing Market Predictions The housing market is tricky to predict, especially since 2020 was a year full of unpredictability. Although no one can forecast what will happen with entire certainty, housing trends can give you an idea about what to expect when it comes to buying or selling a home. It should come as no surprise that 2020 saw huge fluctuations in the housing market as the country was hit with massive amounts of unemployment and extensive shelter-in-place orders. However, the housing market saw an uptick in pending home sales and rebounded much faster than other sectors of the eco...

Mortgage Mom Radio airs weekly focusing on topics that will educate our listeners around mortgage lending. Crista Hermance from Hermance Law joins us this week to educate us on wills vs trusts, power of attorney, community property vs joint tenants, taking property out of a trust for a refinance, and more. Plus we answer listener questions throughout the show. In This Issue "Never hope for it more than you work for it." -- Sonya Teclai Despite the pandemic hitting the country during the summer, low mortgage rates and evolving housing needs caused the housing market to thrive. We'll dive into these factors and more, including: What to Watch - 2020 is Coming to an End: Right now it's all about stimulus and vaccine hopes. Housing News - Summer 2020 Was a Selling Frenzy: Low mortgage rates and changing home needs fueled the summertime housing boom. Home Improvement - Painting Over Textured Materials: When wanting a change to your home's interior, what is the best way to paint over brick, stone, and wood? Q&A - Why Is the Market Thriving During a Pandemic? Learn why people are grabbing homes at record numbers. Please feel free to forward this newsletter to friends, family or co-workers who may find it helpful. 2020 is Coming to an End As 2020 comes to an end, with many saying bring on 2021, it's all about stimulus and vaccine hopes right now. The U.S. financial markets continue to await any headlines from D.C. and there is political pressure on both sides of Congress to get something done. Mortgage rates were unchanged last week at 2.92% and remain near record lows, but what could the near-term future hold as we head into the new year where rates are concerned? Even with the recent rise in the U.S.10-year yield, home loan rates have continued to improve thanks to the Federal Reserve's (the Fed) asset purchase program. There is some concern that upward pressure in rates exists, and in addition to the market looking forward at vaccines and more stimulus, there is real asset inflation everywhere: materials, commodities, Stocks, and housing. With the Fed and incoming president looking to add even more stimulus, there could be more asset inflation and potentially some upward pressure on mortgage rates. The good news is that should rates creep higher, the Fed will likely do even more to pin down long-term rates like measures such as QE and some sort of yield curve control. Source: Mortgage Market Guide Summer 2020 Was a Selling Frenzy Traditionally, September is a slow month for sales as families are already settled into the school year. However, the U.S. housing market saw a tremendous rally this September as low mortgage rates and buyers' demand for additional space during COVID-19 created the need for a change. The U.S. Census Bureau/HUD announced in October that new single-family home sales in September 2020 were at a seasonally adjusted annual rate of 959,000, which is 3.5% below the revised August rate of 994,000 but 32.1% higher than September 2019's estimate of 726,000. Of these new homes sold in September 2020, the median sales price was $326,800, while the average sale price was $405,400. Some of the shifts in the real state industry are due to low interest rates and changes in demographics. Demand for new housing in some parts of the country has overwhelmed home builders, making supplies an ongoing challenge. Analysts report that the high demand is due to the lack of existing home inventory available for purchase. Sources: Mansionglobal.com, Housing Wire, deseret.com Painting Over Textured Materials When you move into a new-to-you home, the previous homeowners might have had different decorating tastes than you. If you just plunked down a bunch of money for your new home, you might not have room in your budget for a complete remodel. Luckily, with a little elbow grease and a few tools, you can paint over certain materials yourself.

This bittersweet episode marks the end of an era. Lauren Prussky, AKA editor extraordinaire and Girly Mags loudmouth is on to greener pastures. But don’t fret - this episode is full of bangers, sing-a-longs, tears and tons of laughs, with a few freaky surprises along the way. We’re heading back to the time of holey jeans, 1-900 numbers and catty celebrity feuds of the ‘90s. Jump in the Girly Mags whip for another ride around the nostalgia block - this episode is one for the books! IN THIS ISSUE This Month in History - November 1994 Agony - Hotline Bling + Old Wrinkly Balls Hollywood Babble On - Celebrity Deathmatch The Surprising Things Men Find Sexy When Straight Women Marry Gay Men Quiz: Are You Ready for Romance? JOIN OUR PATREON + CHECK OUT OUR PLAYLISTS ON SPOTIFY! INSTAGRAM - GIRLY.MAGS TWITTER - GIRLY_MAGS

This month on the Discover CircRes podcast, host Cindy St. Hilaire highlights three featured articles from recent issues of Circulation Research and talks with Steve Lim and James M. Murphy about their article on nuclear FAK regulation of smooth muscle cell proliferation. Article highlights: Li et al: Histone Turnover in Adult Heart Kurosawa et al: Celastramycin Ameliorates Pulmonary Hypertension Urban et al: NOS3 Gene Polymorphism and Coronary Heart Disease   Transcript Cindy S.:                               Hi, welcome to Discover CircRes, the monthly podcast of the American Heart Association's journal, Circulation Research. I'm your host Cindy St. Hilaire, and I'm an assistant professor of medicine and bioengineering at the University of Pittsburgh. My goal as host of this podcast is to share with you highlights from recent articles published in the July 5th and July 19th issues of the Circulation Research Journal. We'll also have an in-depth conversation with Drs. Steve Limb and James Murphy, from the University of South Alabama College of Medicine, who are the lead authors in one of the exciting discoveries presented in the July 5th issue. Cindy S.:                               The first article I want to share with you is titled, Replication-Independent Histone Turnover Underlines the Epigenetic Homeostasis in the Adult Heart. The co-first authors are Yumei Li, Shanshan Ai, Xianhong Yu, and the corresponding author is Aibin He. This research was conducted at the Institute of Molecular Medicine Beijing Key Laboratory of Cardiometabolic Molecular Medicine and the Peking-Tsinghua Center for Life Sciences. Both of which are part of the Peking University in Beijing, China. Cindy S.:                               In the nucleus of cells, DNA is packaged into a structure called chromatin. Chromatin can reside in an open state that is permissive to gene transcription, or closed state where transcription is inhibited. The core units of chromatin are called nucleosomes. A nucleosome consists of DNA that is wrapped around proteins called histones. It's the position of these nucleosomes that determines whether the chromatin allows for DNA transcription or not. There is a large body of research that is focused on understanding the epigenetic processes that promote or repress transcription. Most of this research focuses on the processes that read, write, and erase covalent histone modifications. But, histones are proteins, and proteins, as we all know, have finite half-lives. Cindy S.:                               Far less research has been conducted to understand the dynamics of histone assembly and disassembly on specific regions of DNA. In this study, the authors took a novel approach of using a GFP-tagged histone H2B protein to track in vivo the rate at which nucleosomes are replaced in cardiac chromatin, and to what extent this rate varies across the genome of those cells. This is particularly interesting, and a particularly good cell type to study, as cardiomyocytes rarely divide or proliferate in the adult heart. What they found was intriguing. Nucleosome recycling is not even across the epigenome of cardiac cells. Instead, gene promoters, enhancer, and other regulatory regions that are known to promote gene transcription all exhibited a higher histone turnover rate than regions of the epigenome that are not occupied by these permissive remarks. Cindy S.:                               Further, they found greater histone turnover at loci for cardiac specific transcription factors as compared to loci for pluripotency transcription factors. This implies preferential access to these regions. Digging further into the mechanism, they discovered that the repressive chromatin regulator, EED, promoted this histone turnover. The epigenetic signature is what helps to define the identity and function of a fully differentiated cell. This study suggests that loss of histone turnover may promote loss of the proper epigenetic signature of a fully differentiated cell. These exciting findings suggest replication independent histone turnover is a requirement in maintaining both epigenetic and functional homeostasis in the adult heart. From this, one may hypothesize that perhaps aberrations in histone turnover contribute to age related diseases in the cardiac tissue, as well as possibly other tissues. Cindy S.:                               The next article I'd like to highlight is titled, Identification of Celastramycin as a Novel Therapeutic Agent for Pulmonary Arterial Hypertension-High-throughput Screening of 5,562 Compounds. The first author is Ryo Kurosawa, and the corresponding author is Hiroaki Shimokawa, both from the department of cardiovascular medicine at Tohoku University Graduate School of Medicine in Sendai, Japan. This article is focusing on the disease pulmonary arterial hypertension. Cindy S.:                               Pulmonary arterial hypertension, or PAH, is a disease that stems from the increased proliferation of arterial smooth muscle cells in the lungs. This proliferation leads to a progressive occlusion of the pulmonary arteries. This occlusion also causes increased pressure in the right heart ventricle. That can lead to heart failure, and ultimately death. Basal dilatory drugs are currently used as therapy in PAH, as they help to open the blood vessels, which can alleviate some of the symptoms. However, these drugs do not target the underlying cause of the symptoms, which is the hyperproliferation of the smooth muscle cell. Cindy S.:                               To identify novel compounds that inhibit smooth muscle cell proliferation, Kurosawa and colleagues used a high-throughput approach. They isolated cells from patients with pulmonary arterial hypertension and used these cells in a high-throughput approach to test 5,562 novel molecules on their ability to inhibit the proliferation of these cells. This unbiased approach yielded several potential compounds that potentially reduced smooth muscle cell proliferation from these patients, and also had very minimal deleterious effects on healthy control smooth muscle cells. From there, the team tinkered with the structure of the drug Celastramycin to try to increase its efficacy, and with that tinkering they found in vitro, that their new molecule could reduce both the inflammatory signal that helps to drive the proliferation of the smooth muscle cells, as well as reactive oxygen species, which helps to drive the inflammatory signaling. Cindy S.:                               Moving forward to in vivo studies, the team found that their new treatment also reduced right ventricle systolic pressure and hypertrophy in three different rodent models of pulmonary arterial hypertension. This treatment improved exercise capacity in one of the models. Together, these exciting results indicate that Celastramycin could be developed as a potential therapy for pulmonary arterial hypertension. Cindy S.:                               The last paper we're going to talk about before switching to our interview with Drs. Steve Limb and James Murphy, is a paper titled, 15-Deoxy-Δ12,14-Prostaglandin J2 Reinforces the Anti-Inflammatory Capacity of Endothelial Cells With a Genetically Determined Nitric Oxide Deficit. The co-first authors are Ivelina Urban, Martin Turinsky, Sviatlana Gehrmann, and the corresponding author is Marcus Hecker, all from the department of cardiovascular physiology at Heidelberg University in Heidelberg, Germany. Cindy S.:                               Nitric oxide is a vasodilatory and anti-inflammatory molecule, and thus, beneficial to cardiovascular health. Homozygosity of a single nucleotide polymorphism, or SNP, is a gene nitric oxide synthase results in reduced ability of endothelial cells to produce nitric oxide, specifically in response to fluid share stress. Decreased bioavailability of nitric oxide in the vessel wall helps to promote atherosclerosis. The SNP that we're referring to in this paper is called T-786C, where TT homozygosity is considered the control, or healthy genotype, and CC homozygosity is the disease associated. CC homozygosity of this SNP is predictive of atherosclerotic related diseases, and consequently, individuals with CC homozygosity have an increased risk for coronary heart disease. Cindy S.:                               Now, despite this detrimental evidence, homozygous patients do not develop atherosclerosis at an accelerated rate. This suggests that there's a compensatory mechanism at play. To identify how CC homozygous cells compensate for reduced nitric oxide synthase activity, the authors utilized human umbilical vein endothelial cells, that are also called huvecs, that harbored either the TT or the CC version of this SNP. They also used these in combination with a monocytic cell line. Cindy S.:                               Urban and colleagues found that under fluid share stress conditions, human endothelial cells homozygous with for the CC variant, had increased production of an anti-inflammatory prostaglandin called 15d-PGJ2. Signaling, via this prostaglandin, helps to compensate in part for the reduced endo production. This prostaglandin suppressed monocyte activation by reducing expression of pro-inflammatory genes such as aisle 1 beta, and decreased monocyte transmigration through endothelial cells. The team also found that patients with coronary heart disease were more likely to have the CC homozygous variant than age match controls. Thus, not only did they identify a partial compensatory mechanism, the authors suggest that 15d-PGJ2 could be a useful biomarker for the diagnosis of coronary heart disease. Cindy S.:                               So that's it for the highlights of the July issues of Circulation Research. Thank you very much to Ruth Williams, who writes the In This Issue copy for the journal, as well as the editorial team at the journal and at the podcast. Cindy S.:                               Okay, so now we're going to talk to our team of first author and last author. Today's paper that we're talking about is Nuclear Focal Adhesion Kinase Controls Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia Through GATA4-Mediated Cyclin D1 Transcription. The first authors of this papers are Kyuho Jeong, Jung-Hyun Kim, and James M. Murphy, and the corresponding author is Steve Lim. Today, we're going to be speaking with James and Steve about this paper. So thank you, both of you, for joining us today. Steve Lim:                           Thanks for having us today. Cindy S.:                               Great. Congratulations on your beautiful paper. I was wondering if maybe we could just start by both of you introducing yourselves, telling us your current position, and maybe about how you came into this field. Steve Lim:                           Hi, Cindy. We appreciate the opportunity to discuss our paper. I'm Steve Lim, an associate professor in the department of biochemistry and molecular biology and medicine at the University of South Alabama. I received my PhD from University of Alabama at Birmingham. I did my post-doctoral training studying the law of FAK in cancer biology at UC San Diego Moores Cancer Center. In 2012 I started my own lab here at South Alabama, where I decided to focus on vascular biology using some pharmacy data I generated at the end of my post-doctoral study. James Murphy:                 I'm James Murphy, I'm a post-doctoral fellow in Dr. Lim's lab at the University of South Alabama. My path to science was a little different than most. I got an undergraduate and graduate degree in mathematics before I joined the PhD program here at South Alabama. Due to a family history of cardiovascular related deaths, I decided to join Dr. Lim's lab due to his interest in studying vascular disease to find new therapeutic targets. Cindy S.:                               Interesting, a math major. James Murphy:                 Yeah. Cindy S.:                               Has that been able to help with any of your basic science studies? James Murphy:                 I'm pretty good at doing concentrations. Cindy S.:                               You're the expert in lab math. James Murphy:                 Yeah. I think the logic skills and critical thinking skills that I picked up in math really help out here in science. Cindy S.:                               Oh, I bet, that's wonderful. You're the dream PhD student who can hit the ground running with M1V1 equals M2V2. Great. Well, thank you so much. I really liked this paper because I love the mechanosensing and how does a cell read what's outside, and how does that message get brought to the inside. Really, that's what you're finding in this paper, specifically looking at how FAK is mediating transcriptional regulation. Maybe you can start by just telling us, what was your overarching question when you started this study? Steve Lim:                           Sure. It is very well-known fact that promotes cell proliferation and migration through interior receptors and gross factor receptor signaling. Both of which are key components in the smooth muscle cell hyperplasia. So naturally, we asked ourselves a simple question, "Is FAK activity important for smooth muscle cell proliferation, and leading into hyperplasia?" Cindy S.:                               So when you say FAK activity I think one thing that's interesting in your paper is, FAK really has kind of two different functions, and one is the kinase function. A kinase is when it can phosphorylate another protein, so it itself is an enzyme. But, then it has another function, so can you maybe tell us about those different functions of FAK? Steve Lim:                           Right. So FAK can function as a kinase, as well as a kind of independent scaffold, which can recruit different proteins. In the paper, we specifically described a kinase independent function as a nuclear function, nuclear FAK function. Cindy S.:                               Interesting. So what premise, or what gaps and knowledge were present before your study, that you were trying to address? Steve Lim:                           Actually, a study showed that the knocking off FAK in the smooth muscle cells prevented neointimal hyperplasia. As just you asked question, FAK has two different functions. Since FAK has both kind of dependent and independent [inaudible 00:14:48], this study lets the unanswered question, which of these two different functions of FAK plays a larger role in dealing with hyperplasia. We aimed to inhibit FAK activity to distinguish between FAK kind of dependent and independent roles in dealing with hyperplasia. Cindy S.:                               Interesting. How exactly were you able to do that? How could you take and dissect apart the two different functions of this protein? Steve Lim:                           We started off with a small pile of experiment to test if a small molecule FAK inhibitor could block neointimal hyperplasia, and we were very surprised at the degree to FAK inhibition actually prevented neointimal hyperplasia following vascular injury. Cindy S.:                               Yeah, and that's in figure one. I was looking at that, it's quite striking. Steve Lim:                           Actually, to distinguish these two different functions we generated new genetic FAK–Kinase-Dead mouse model in conjunction with a FAK inhibitor model, and that would allow us to study a lot of FAK activity in smooth muscle cells. Cindy S.:                               Great. James, could you tell us about the mouse model that you developed for this study, and the specific mutations that you created and what you were allowed to test with those models. James Murphy:                 So the FAK–Kinase-Dead knock-in model was actually generated during Dr. Lim's post-doctoral studies. Cindy S.:                               Is that the exciting data? James Murphy:                 The mutation is just a simple lysine to arginine mutation of amino acid 454. What they found was that, actually, homozygous kinase-dead embryos was lethal. So you need FAK activity to actually develop a full grown organism. We kind of had to cross a hetero wild-type kinase-dead mouse with a phlox FAK mouse, which eventually, if you cross with tissue-specific Cres, what you end up with is a phlox wild-type or a phlox kinase-dead mouse. Then, when you treat Tamoxifen in your Cre mouse, then you delete one copy of wild-type FAK and you're left with either a single copy of wild-type FAK, or a single copy of kinase-dead FAK. Cindy S.:                               Very nice. So for your study, you used, if I recall correctly, the myosin-11, Tamoxifen-inducible Cre model. Can you maybe talk about why you chose that model and why not the SM22 Cre or a non-inducible model? What was your strategy? James Murphy:                 As I mentioned, FAK activity is important for embryo genesis, so we thought we had to use an inducible model, so as to make sure we had an adult mouse at the time of the experiment. We originally actually had the SMA Cre model, however, some grant reviewers had told us that we should kind of shift to the more myosin-11 mouse to be more specific to the vascular. One downside to that, as we mentioned in the paper, is that that's actually only on the Y chromosome, so you can only use male mice. Cindy S.:                               Yes. But, at least it's in only the smooth muscle cells. Is that kind of the pros and cons of that model? James Murphy:                 Yes, and the MYH-11 Cre is kind of the most accepted model when you're doing smooth muscle studies. Cindy S.:                               Great. So can both of you go over some of the key findings of your paper? If we're going to say this in a tweet, what would we say? James Murphy:                 In a tweet. So I think, as we talked about, FAK can go to the nucleus. It's kind of constantly shuttling between the nucleus and the cytoplasm, at least what we've been able to observe in vitro. However, kind of a its localization in vivo still kind of was up in the air at the time. However, our immunostaining data actually rebuild that healthy uninjured arteries primarily showed FAK was in the nucleus. Suggesting that FAK was inactive, and maybe somehow suppressing smooth muscle cell proliferation by staying in the nucleus. But, after wire injury, FAK not only increased its activation, but also shifted to be primarily within the cytoplasm, and eventually we showed that that increase of GABA4 protein stability leading to proliferation. Cindy S.:                               Very interesting. That's great. So what was the hardest part of this whole study? James Murphy:                 Dr. Lim did the preliminary FAK inhibitor studies, but he had people when he started his own lab, he had to teach us how to do the wire injury. At first, learning gets kind of technical, you have to get used to using the microscope. Cindy S.:                               Could you describe the wire injury model for us? James Murphy:                 Yes. What you do is you anesthetize the mouse and you actually locate the femoral artery, and you want to kind of reveal the muscular branch. What you do is you add suture proximal and distal to the muscular branch of the femoral artery to stop blood flow. Then, you're going to cut a small incision in the muscular branch, and you insert a small wire through the branch up into the femoral artery towards the iliac branch. What this does is denude the endothelial layer and kind of causes an extension of the artery, damaging the smooth muscle layer. Once you remove it and suture off the muscular branch, then after a couple weeks you start to see hyperplasia. Cindy S.:                               Interesting. So what does this model clinically? James Murphy:                 This model kind of mimics angioplasty procedures that one may have if they have an occluded artery. There's multiple angioplasty procedures. There's a physical dislodging and opening of the artery. Then, there's some other methods such as using a stent to keep it open. Cindy S.:                               Great. Very interesting. What do you think would happen in maybe, I don't know, an LDLR knockout that was crossed with your FAK kinase deficient mutant? What do you think would happen in an athero model? James Murphy:                 We're actually- Cindy S.:                               Or is that the next paper? We don't have to talk about it if it's the next paper. James Murphy:                 We're actually currently testing that right now. Cindy S.:                               Oh, okay. James Murphy:                 So that's kind of our next step is to test this in atherosclerotic models to see what happens. Cindy S.:                               So, what might this mean for potential therapeutic target? How could we leverage this data to possibly translate it to the clinical setting, even if it's far off? What might we want to do moving forward? Steve Lim:                           Speaking of translational potential, currently most of the treatment options for narrow vessels rely on thrombolytic stents, that provides local delivery of anti-proliferative drugs. However, DES comes with several disadvantages, including location, work, size of these affected vessels. In fact, inhibitors are under cancer clinical development, have never been used in the vascular diseases. Our study, I think, at least to show the potential for using this type of FAK inhibitors in treating hyperplasia, which was not possible before. Cindy S.:                               That's interesting. So essentially, there's already potential, therapy's already available that would just have to be tested in this new ... in this new vascular realm, essentially. Steve Lim:                           Yeah. I was thinking about effication of these type of drugs. I think it could be, as you said, PAH could be one of the targets, because they're not really useful drugs available now. In the future, what we actually, we started already, but it's known, these moments of proliferation plays key role in the arthrosclerosis progression. Studies targeting neointimal hyperplasia and atherosclerosis, it's not existing. I think in the future probably, we would like to test whether in fact inhibition and the smooth muscle cells reduce its atherosclerity in animal models, and hopefully in humans. Cindy S.:                               Yeah, yeah, hopefully in humans, always. Yeah, and in those mouse models, there's always interesting studies where you can block things from the beginning. But, I think one of the beautiful things about the mouse model that you created, the fact that it's Tamoxifen inducible, you could essentially let that atherosclerotic plaque build up for a bit and then knock it out and see if it can reverse it. So the model you created is a really wonderful tool to use for a whole bunch of studies. So congratulations. Steve Lim:                           Thank you. Cindy S.:                               Yeah, I thought the most interesting aspect of this paper was really the fact that it could link this FAK protein, this integrin signal mediating protein to the transcription factor GABA4. So could you possibly tell us a little bit about that interaction, and exactly what GAB is doing in the smooth muscle cell? Steve Lim:                           I actually think that the identifying GABA4 factor actually was one of the difficulties, because normal cells do not express GABA4, that's what is known. I think it's because, based on our finding, the smooth muscle cells in vivo, you could package more predominantly localized in vivo, the nuclear FAK is predominant. So that nuclear FAK finds GABA4 and reduces ability through the process on degradation. But, actually, not changing ... Nuclear factor is not changed. GABA4 mRNA are the expression, so GABA4 is always expressed in smooth muscle cells. But, we never see in healthy, or very freshly isolated smooth muscle cells. We never see Gaba4. That was the most difficult part actually. Cindy S.:                               So the mRNA is always there, it's just never making it to a protein that accumulates in any measurable quantity. Steve Lim:                           So you become a protein, but FAK, nuclear FAK kills all GABA4 in the nucleus. Cindy S.:                               That's the proteasome mediated degradation? Steve Lim:                           Right. Then, GABA4 actually promotes cycling D1 transcription. So no GABA4, no cycling the new one, and smooth muscle cells do not cycle. Cindy S.:                               Interesting. So can you maybe close the loop and tell us essentially what's in figure nine, like this. Could you talk us through that? Steve Lim:                           It summarizes in figure nine, I think it would be best, we can put two different situations. In healthy R3, FAK is in the nucleus, and GABA4 is reduced, cycling D1 is not expressed, and smooth muscle cells become high acid. They don't proliferate. But, in injured, actually, FAK localization is it's the vaso injury promotes FAK localization, vaso injury shifts FAK nuclear localization to cytoplasm. Actually, FAK is activated. Now, GABA4, that increases cycling T1 expression. So that causes intimal hyperplasia. That could be a kind of summary. Cindy S.:                               No, that's perfect. Congratulations on a very nice paper. I thoroughly enjoyed reading it, and I enjoyed even more speaking with the two of you. So thank you very much. Steve Lim:                           Well, thank you so much. Cindy S.:                               Thank you for listening. I'm your host Cindy St. Hilaire, and this is Discover CircRes, your source for the most up to date and exciting discoveries in basic cardiovascular research.  

Cindy S.H.:                         Hi. Welcome to Discover CircRes, the monthly podcast of the American Heart Association's journal Circulation Research. I'm your host, Cindy St. Hilaire, and my goal is to bring you highlights of articles published in the Circ Research Journal as well as have in-depth conversations with senior scientists and the junior trainees who have led the most exciting discoveries in our current issues. Today is our premier episode, so I want to take some time to introduce myself, give you a little bit of background about the history of the journal, and then have a conversation with our new editor in chief, Dr. Jane Freedman, and my social media editor partner in crime, Dr. Milka Koupenova. Cindy S.H.:                         First, a little bit about me. I'm an assistant professor of medicine and bioengineering at the University of Pittsburgh. My lab is part of the division of cardiology and we're also a member of the Pittsburgh Heart, Lung and Blood Vascular Medicine Institute. I'm still a relatively new PI. I'm still learning as I go. One of the strengths of being a new PI in the current time is the amazing network we have through social media, whether it's through listening to podcasts or through Twitter or through select groups like one of my favorites, New PI Slack. Really one of my personal goals of starting this podcast for Circ Research is to have a career development angle. Because career development is so fresh in my mind and it's really something I want to incorporate into this podcast, we're hoping we can reach out to more junior trainees through these mediums. Really that's the impetus for Dr. Freedman wanting to have specific social media editors at the Circulation Research Journal. Cindy S.H.:                         I'm very honored to be the first host of this podcast and I'm very excited for this opportunity. As a team, Milka and I hope to expose the larger community to not only the most current and exciting discoveries in cardiovascular research but also a behind-the-scenes look of what it takes to get high-impact research done and published and planned and funded, and also talk about some of the maybe the non-bench aspects of this job, the networking, the behind-the-scenes look that really you learn on the fly as you go. Hopefully we can expose more people to these on-the-fly things in a slightly more rigorous manner. Cindy S.H.:                         Before I go into the articles summarized in this week's podcast, I want to give a very big thank you to Ruth Williams. Ruth is the person who writes the content of the In This Issue which is featured in every issue of the journal Circulation Research, and that content is extremely helpful in deciding which articles we're going to focus on in this podcast and also for helping me form the conversations and discussions. Thank you, Ruth, for all your hard work. Cindy S.H.:                         Now I'm going to highlight three articles that were featured in the June 21st issue of Circulation Research. The first is entitled Relationship Between Serum Alpha-Tocopherol and Overall and Cause-Specific Mortality: A 30-Year Prospective Cohort Analysis. The first author is Jiaqi Huang and the corresponding author is Demetrius Albanes , who are both at the Division of Cancer Epidemiology and Genetics at the National Cancer Institute, which is at the NIH in Bethesda, Maryland. Alpha-tocopherol is the more formal name for vitamin E, and vitamin E is an essential fat-soluble vitamin. By essential, that means that while your body absolutely needs it, it does not produce it itself. Therefore we need to consume products containing vitamin E. We do that by eating vegetable oils, nuts, seeds, whole grains and certain fruits and vegetables. Previously, population-based studies have shown inconsistent associations between circulating vitamin E and risk of overall death or death due to specific diseases such as cancer and cardiovascular disease. Cindy S.H.:                         To look more closely at cause-specific mortality, Huang and colleagues studied a cohort of close to 30,000 Finnish men, which is a huge study. Added to that, these men were in their 50s and 60s at the start of the study and then continued for the next 30 years of their life to be in this study. It's frankly an amazing achievement to keep that many individuals enrolled. From approximately 24,000 deaths, so about 80% of the original cohort, the authors adjusted for factors such as age and confounding things like smoking. They found that vitamin E levels were inversely associated with the risk of death from a variety of causes. What that means is that higher levels of vitamin E associated with lower risk of death. All of those causes of death that they found were cardiovascular disease, heart disease, stroke, cancer, and respiratory disease. This large prospective cohort analysis provides very strong evidence that higher vitamin E levels means greater protection. Cindy S.H.:                         It's really interesting to note though that this data did not seem to associate with a reduced risk of death by diabetes or, for that matter, injury and accidents, which I guess kind of makes sense. The authors say these results indicate that vitamin E may influence longevity, but they also highlight the need for further studies, specifically in more ethnically diverse populations and of course in women, because we all know a major limiting factor of a majority of cardiovascular studies is the fact that often there are just not enough women in these studies. But really that's a push now to include not only women but more ethnically and geographically diverse populations. Cindy S.H.:                         The second article I want to highlight is titled Mitochondria Are a subset of Extracellular Vesicles Released by Activated Monocytes and Induce Type I IFN and TNF Responses in Endothelial Cells . The first authors are Florian Puhm and Taras Afonyushkin , and the senior author is Christopher Binder. All three are in the Department of Laboratory Medicine, the Medical University of Vienna, in Vienna, Austria. This group is also part of the Research Center of Molecular Medicine of the Austrian Academy of Sciences. Cindy S.H.:                         I want to talk about this paper because I found that title extremely provocative. Extracellular vesicles or microvesicles are small particles that can be released from cells. These particles can act as cell-cell communicators. They can hold a variety of substances such as proteins and micro RNAs and minerals and all sorts of things that are derived from inside the cell. The matrix vesicle is then budded off. Matrix vesicles released from monocytes after bacterial LPS stimulation, so a stimulus that induces an inflammatory response, these matrix vesicles have been shown to contain mitochondrial proteins. Mitochondrial DNA-containing matrix vesicles have been reported in the mouse model of inflammation. From this premise, from these prior studies, Dr. Puhm and colleagues hypothesized that the mitochondrial content of matrix vesicles might actively contribute to pro-inflammatory effects. Cindy S.H.:                         What they then did was show that monocytic cells release free mitochondria and also matrix vesicles that contain mitochondria within them. These free and matrix vesicle-encapsulated mitochondria were shown to drive enothelial cells to induce inflammatory cytokines such as TNF-alpha and interferon. These circulating matrix vesicles were collected also in human volunteers that were injected with this same inflammatory substance, LPS. These circulating matrix vesicles isolated from humans also induced endothelial cell cytokine production. Very interestingly, inhibition of the mitochondrial activity drastically reduced the pro-inflammatory capacity of these matrix vesicles. Cindy S.H.:                         Together, this result suggests that the released mitochondria, whether it's free or whether it's encapsulated in a matrix vesicle, may be a key player in certain inflammatory diseases. This study shows that in addition to their central role in cellular metabolism, mitochondria, whether encapsulated or free, can actively participate in an inflammatory response in a cell other than the cell it was native in, which is just intriguing to think about. This work provides new insight to the contribution of mitochondria to the content and biological activity of extracellular vesicles. It also might suggest that perhaps targeting mitochondria and their release may represent a novel point for therapeutic intervention in inflammatory pathologies. Cindy S.H.:                         The last article I want to highlight is titled Macrophage Smad3 Protects the Infarcted Heart, Stimulating Phagocytosis and Regulating Inflammation . The first author is Bijun Chen and the senior author is Nikolaos Frangogiannis . When tissues are injured, there is localized increase in the cytokine TGF-beta. However, depending on conditions, this TGF-beta can function to stimulate macrophages to adopt either pro-inflammatory or anti-inflammatory phenotypes. To complicate matters more, the signaling pathway for both the pro- and anti-inflammatory phenotypes involves activation of the intracellular signaling protein Smad3. Inflammation, whether too much or too little, can influence the outcome of injuries, including injuries such as myocardial infarctions. An infarction, for those of you unfamiliar with the term, is a localized area of dead tissue and that results from a lack of blood supply. In this case, an infarction, a myocardial infarction, is essentially a heart attack that stops blood flow through the coronaries and causes death in the cardiac tissue and cells. Cindy S.H.:                         The authors hypothesized that in the infarcted myocardium, activation of TGF-beta and Smad signaling and macrophages may regulate repair and remodeling. They had a very specific question about a very specific cell type in the context of the whole heart. To address the role of Smad3, they utilized mice that were engineered to lack Smad3 in the myeloid lineage which produces macrophage cells. They found that these mice with myeloid cell-specific deletion of Smad3 had reduced survival compared to control mice. Additionally, the hearts from the animals with the myeloid cell-specific deletion of Smad3 exhibited increased adverse remodeling and greater impairment of function. That's a really interesting finding. The heart tissue itself was the same. All that was different were the cells of the myeloid lineage. Then to dig after what cells were mediating this effect, the investigators moved on to in vitro studies. They found that Smad3-lacking cells themselves showed reduced phagocytic activity, sustained expression of pro-inflammatory genes, and reduced production of anti-inflammatory mediators when compared with control macrophages. Cindy S.H.:                         In summary, these results suggest Smad3 is necessary for macrophages in the area of the infarction to transition to an anti-inflammatory phagocytic phenotype that protects against excess remodeling. However, we cannot go after global inhibition of Smad3 as a potential therapy post myocardial infarction, and that's because inhibition of Smad3 in cardiomyocytes is actually protective against the infarction. Inhibition in a macrophage is bad, but inhibition in a cardiomyocyte is good. Any potential Smad3-modifying therapies really needs to be designed to be cell type-specific and be able to be deployed to activate that cell type. Cindy S.H.:                         In addition to science, I love history. I thought I would take this opportunity of the first podcast to share with you a little bit of history about the Journal of Circulation Research. Circulation Research is now in its 66th year, but its origins can be traced to 1944. That was when the AHA established a council that was attempting to organize its research arm and its professional program arms. The AHA journal Circulation was already in existence, but in 1951 the executive committee decided to launch a basic research supplement, and it was called just that: Circulation Basic Research Supplement. But a few years later, Circulation Research was to be its own publication because of the interest and the excitement around the basic research supplements. The quote that I'm going to read is from that first executive committee meeting and there they wanted Circulation Research to be the authoritative new journal for investigators of basic sciences as they apply to the heart and circulation. Cindy S.H.:                         It's a fun little subgroup that they list after that. They list in anatomy, biology, biochemistry, morphology, which I just think is so neat to think about, pathology, physics, pharmacology, and others. It's interesting to think about what that would be today if we were now finding this journal. Biochemistry, genetics, molecular biology. It's fun to think about how much science has changed since they began this journal. Really the broader goal was to integrate and disseminate new knowledge. Leading that was Dr. Carl Wiggers, who was the first editor in chief of Circ Research. At the time, he was the head of physiology at Western Reserve University, and he's often referred to as the dean of physiology, as his research really provided much of the fundamental knowledge regarding the pressures in the heart and the vessels of the body and how they interact. Cindy S.H.:                         I actually went back and looked at some of the first titles in Volume One, Issue One, of Circ Research. It's really kind of neat. Some of them could be completely relevant today. I'm just going to read a few. Nucleotide Metabolism and Cardiac Activity, Fundamental Differences in the Reactivity of Blood Vessels in Skin Compared to Those in the Muscle. That was at the VRIC the other day. Haemodynamic Studies of Tricuspid Stenosis of Rheumatic Origin. Reading these for the first time I actually got chills because my two themes of my lab are both in that first Volume One, Issue One, of that journal. I study the extracellular nucleotide aCD73 and its impact on vascular homeostasis. I also study calcific aortic valve disease and are hugely curious about the role of inflammation and things like rheumatic heart disease in the progression of the disease. It's amazing how much science has changed, but yet how so much has stayed the same. Cindy S.H.:                         Dr. Wiggers wrote a few gems, a few quotes in his biography that I want to share with you. I find them inspiring and also humbling. The first is, "Research is a gamble in which the laws of chance favor the loser. The loser must remain a good sport," which I think is perfect to think about in science. I really wish I had read that after my first RO1 was triaged. The next two are more about the science writing and I think they're great not only for when we're thinking about papers but also grants. The first is, "Readers are greatly influenced in their judgment of a research project by literary style. A poor presentation can easily damage the best investigation," which is so true. No matter how good your science is, if you can't communicate it, it doesn't matter. And lastly, "A good paper, like a good glass of beer, should be neither largely foam nor flat. It should have just the right amount of head of foam to make it palatable." Cindy S.H.:                         With these nuggets of wisdom, we're now going to talk with Drs. Jane Freedman, who's now the editor in chief of Circ Research, and Dr. Milka Koupenova, who is the social media editor. Before I really introduce Jane, I want to recognize all of the former editors in chief of Circ Research, Dr. Carl Wiggers, Dr. Carl Schmidt, Dr. Eugene Landis, Dr. Julius Comroe, Dr. Robert Berne, Dr. Brian Hoffman, Dr. Francis Abboud, Dr. Harry Fozzard, Dr. Stephen Vatner, Dr. Eduardo Marbán, Dr. Roberto Bolli, and now Dr. Jane Freedman. Welcome, Jane. Thank you so much for this opportunity and congratulations on your new position. Dr. Freedman:                   Thank you very much. Cindy S.H.:                         I was wondering if you could just introduce yourself to the listeners and give us a little bit about your background. Dr. Freedman:                   Sure. I am the Budnitz Professor of Medicine at the University of Massachusetts, and I originally became interested in a scientific career while attending Yale University where I was both an architecture and geology major. Cindy S.H.:                         Interesting. Dr. Freedman:                   Yes, very interesting. Then, not exactly knowing what I wanted to do, I worked for a year as a research assistant for my later-to-be mentor Dr. Joe Loscalzo at Brigham and Women's Hospital. There one day he sent me up to the intensive care unit and said we need to get a tube of blood from someone who was in the throes of having a myocardial infarction. Really at that point I became hooked. Why was that person having a heart attack, and using their blood how could I figure out whether they would live, die, do well, not do well, or yield new things that might help us cure or diagnose people with heart attacks later on? After that. I went to Tufts Medical School. I did my residency and cardiology fellowship at Brigham and Women's Hospital and the Massachusetts General Hospital. After working at several different places, I have wound up at the University of Massachusetts where I am in the Division of Cardiology and where my laboratory currently resides. Cindy S.H.:                         Excellent. As the new editor in chief, what do you see as your vision for the journal? Dr. Freedman:                   I'm in a very fortunate position to be taking over a wonderful journal from an incredibly dedicated group of editors and associate editors and other supportive editors. Scientific pursuits and reporting and publications are really evolving at a rapid clip, so we hope to have several things happen over the next few years to survive and thrive. The first thing is we hope to define and expand Circulation Research's scientific identity. We want to extend its already outstanding portfolio of science that really demonstrates how elegant basic and translational mechanisms and pathways are part of a greater web of cardiovascular disease and stroke. This will include an increasingly diverse group of basic and translational sciences and they'll touch on both fundamental studies as well as how they translate to human disease. We also want to continue to pursue the excellence that Circulation Research already epitomizes and we want to extend its brand both to an increasingly diverse group of members, both nationally and internationally. Dr. Freedman:                   Circulation Research already has really wonderful publication metrics such as turnaround time, time to review, and we hope to maintain that so as to be a journal of choice for an increasingly growing number of investigators. We would also very much like to have greater interface with the American Heart Association. A lot of the research on our pages is funded by the American Heart Association, and the majority of science that the American Heart Association currently funds is basic cardiovascular science. We hope to have greater interface and help our users of the journal understand what the American Heart Association can do for them and for their scientific pursuits. Dr. Freedman:                   Last and very importantly, we really want to attract early and mid-career investigators to the journal. We already have some really nice programs that the previous editorship has started, such as Meet The First Author, but we would also like to be a site for education of how you can review papers, have a junior editor program and other types of programs that will help early and mid-career investigators in their future. One of the ways we're going to be doing that is to have enhanced social media programs. Cindy S.H.:                         Great. I really like that idea of having the junior editors because I think the best learning experience I had about how to write a grant did not happen until I actually served on a study section, because it was there you actually can understand all of those comments you got on your first grant that was triaged and why they were said. I think that is a key and really important aspect. Dr. Freedman:                   That's a perfect analogy because you want to remove the black box that people think is happening when they send their manuscripts in. There's so many reasons why manuscripts succeed and don't succeed, and we really do want to be as transparent as possible and we do want to educate investigators as much as possible about the process. Cindy S.H.:                         Actually, could you maybe tell us a little bit about that process? I made all my figures, I formatted my paper according to the instructions, I hit submit. Black box. What happens? What's the next step? Dr. Freedman:                   What's the next step? Cindy S.H.:                         What do you do? What does an editor in chief actually do? Dr. Freedman:                   I do have to say that none of this would happen, especially in the incredibly quick turnaround time, if we didn't have amazing support and help in our office that happens to be in Baltimore. The people there are just incredible. They make sure that papers move through. It's really 24/7. Our group has not been at it for very long, but I know Dr. Bolli's group as well as our group, people are handling manuscripts as fast as they really come in. We see the manuscript, they get quality checked. We try not to be too onerous with the first steps. Then typically they go to one of the associate or deputy editors who will handle them to send out for review. Cindy S.H.:                         Is that based on keywords or the title or how is that decided? Dr. Freedman:                   Sometimes it's based on keywords, so careful with your keywords. A lot of times, because each of the associate editors has an area of expertise that hopefully covers what your science is interested in, they will know experts in the field. We very heavily rely on our editorial board. We have an amazing editorial board at Circulation Research, and amazing contributions from the BCBS council. These individuals have over the years and currently provided just tireless and unsung, devoted help to making the journal run smoothly. It's a pretty quick turnaround time. Then the decision made based on the reviews of the article. Occasionally articles come in and they're not suitable for the journal because they're not what we perceive as what our readers would be interested in. Sometimes those articles don't go up for review. We don't want to keep them caught up, so we send them back right away. Dr. Freedman:                   When the articles come back in with the reviews, we're going to be discussing them at a weekly meeting. Other viewpoints will weigh in, and then we make a decision whether it's an accept, whether it's a revise, whether it needs a lot more science. That's called a de novo. Sometimes we think it's more suitable for one of the other 11 American Heart Journals and we might suggest that you consider sending it to that journal and we consult with that journal's editor. Cindy S.H.:                         Interesting. All that happens with about 14 days. Dr. Freedman:                   That's supposed to happen with 14 days. Cindy S.H.:                         It does pretty regularly based on the stats. That's amazing. One of the initiatives you mentioned was really the role of social media. Now I would like to introduce Dr Milka Koupenova, who is the co social media editor alongside me. Before I let Milka talk, I really have to be honest and say that my graduate school days were some of the best of my life. It was in part because Milka I were both in the same lab. We overlapped by a couple of years under the amazing mentorship of Dr. Katya Ravid. Every time we get together, all we'd talk about was how can we be like Katya? Maybe someday we'll actually have a podcast where we can get Katya in here and actually record all her nuggets of wisdom. Dr. Koupenova:                 I think the same thing about Katya. Cindy S.H.:                         How can it be more like Katya? But for now, Milka, welcome. Thank you. If you could just introduce yourself and give us a little bit about your background. Dr. Koupenova:                 Hi, everybody. My name is Milka Koupenova. I am an assistant professor at University of Massachusetts Medical School. Briefly about me, as Cindy mentioned, I did my PhD at Boston University and I studied at that time metabolism in atherosclerosis. Then I had this great opportunity to join this lab in thrombosis that studied these little cell fragments called platelets, which I knew something but not that much about. I joined Dr. Freedman lab as a postdoctoral fellow, and actually my interest evolved to be very much in platelet immunobiology and how platelets may contribute to thrombotic disease during viral infections. Luckily for me, I had two angels that I wanted to be. One of them was Katya Ravid, as you mentioned, and the other one was Dr. Freedman. Both set up a great example of scientists and how to do science in life. Cindy S.H.:                         Wonderful. Excellent. Thank you. I won't lie. I don't know if you feel this way. I definitely feel a little nervous about being a social media editor. I'm talking in a room to a box with a microphone on me and I don't know who's going to be listening. That's also exciting for me too. I get to disseminate all this cool knowledge and share our basic research with this huge audience. What are you most nervous about and excited about? Dr. Koupenova:                 You're doing the podcast, so I don't have to worry about that, that that particular part. I am quite excited actually about everything that's going to surround popularizing the science at Circulation Research. I think in the time that we live in and when social media is a huge part of our life, we definitely need to engage the community, scientific or lay, and communicate our ideas. I'm super excited about the creative part behind how we are going to achieve this via various social medias. Cindy S.H.:                         Can you talk about the platforms that you plan on using? Dr. Koupenova:                 We currently are using Twitter and Facebook. Please follow us on Twitter and Facebook. And we are going to launch Instagram. Find us, follow us, engage us. That will be great. You can always send us messages and like us, retweet whatever you decide. Cindy S.H.:                         Give podcast feedback on Twitter. Nice comments only. Dr. Koupenova:                 We'd like to hear your comments and we'd like to hear what you envision in certain cases when it comes to your Circulation Research, because this is your journal as much as it is ours. We're here for you. In addition to popularize and advertise the wonderful science that we're publishing in Circ Research, we want you to be engaged. We want you to be able to advertise in your own work and to think of it as something that you own and something you need to communicate to the rest of the world. That is one of the things that we want to do. Dr. Koupenova:                 Finally I'm going to echo on what Dr. Freedman said, is we want to attract truly early career and young investigators and help them be involved, help them own their science and help them communicate their ideas. That's pretty much what our social media platform is and we are going to evolve with you. That is perhaps one of the challenges. Cindy S.H.:                         I think one of the most interesting aspects, at least in academia as I see it, is really the role of self-promotion. It's something you're never taught and it's something that you don't really appreciate until you go to that conference. I remember my first conference as a new PI, I was standing there and I'm just like, "Okay, these are all other PIs. How are they all in groups? How does everybody know each other? Why are they all friends already?" It takes a lot of guts and you have to inject yourself. "Hi. I'm Cindy St. Hilaire and I'm new. Please be my friend," essentially, essentially. But it's important and I really liked the fact that when your journal is published you have that little button, share on Twitter, share on Facebook. I think that's really important. It helps you practice that self-promotion and can help really allow you to embrace your extrovert when you know how to. Dr. Koupenova:                 That's exactly what I was going to point out. Scientists or physician scientists, or physician scientists perhaps are a bit better. But as scientists we're very much introverted. But social media gives you a platform that it's not cheesy to popularize and communicate. Then you see those people on conferences and then you have your little group without- Cindy S.H.:                         It's amazing how many Twitter friends I have. "Oh, I met you on Twitter. It's so nice to meet you in real life." Dr. Koupenova:                 It's a new generation. We at Circ Research want to evolve with it. Is that correct, Dr. Freedman? Dr. Freedman:                   That is correct. Thank you very much. Cindy S.H.:                         It's exciting times. I guess maybe this is a question for all of us to talk about, but how do you think we can, number one, attract people to science, attract diverse people to science, and then really keep them in science and how do you think we can use Circ Research and also the social media aspects of Circ Research to do that? Dr. Freedman:                   I think, first of all, people have to see themselves in the journal. The journal, I think the first point I talked about, about being inclusive, inclusive types of people, way people consume science, types of science. We really want people to feel like Circ Research isn't just a journal that puts out scientific papers, but is a forum. It's a forum for them to exchange ideas and it's a forum for them to understand better about their scientific careers. Cindy S.H.:                         Great. Thank you. This has been an amazing first podcast. I'm so happy to share it with the two of you and I'm super excited for this opportunity. Again, Jane, I want to congratulate you on your new position as editor in chief and I can't help but mention as the first female editor in chief. That's a wonderful, wonderful thing. Cindy S.H.:                         You can find us on Twitter. The handle is @CircRes, at C-I-R-C-R-E-S. We're also on Instagram using the same name, C-I-R-C-R-E-S. We hope to hear from you there. Cindy S.H.:                         Thank you for listening. I'm your host, Cindy St. Hilaire, and this is Discover CircRes, your source for the most up-to-date and exciting discoveries in basic cardiovascular research.

Roll on that body glitter and let your thong hang out, all the way back to this February 2005 issue of Teen People. We’re giving you the 411 on forgotten couples, examining the bad gals of Hollywood and discussing the trials and tribulations of unofficial Whole Foods spokesperson Jessica Simpson. Also, James takes on the heroic task of Marilyn Mansplaining the entire plot of The Son of the Mask so that you never, ever have to watch it. You’re welcome. IN THIS ISSUE: 1.  This Month in History: February 2005 2.  Your Life, Busted: Oops! (There It Is) 3.  Hottest Celebrity Couples: Where Are They Now? 4.  Hollywood Bad Girls: Papa-Paparazzi 5.  The Goof-Proof Asking Them Out Guide: Is it Worth It, Let Me Work It 6.  Quiz: How Romantic is He?

This ep is gonna blow you out of the water, people. This week Girly Mags takes a lighthearted look at 2005, long after our futures became dim. Case in point: Paris Hilton was “so hot”, it was splitzville for Brad and Jen, and someone probably knew who Chad Michael Murray was. Sorry, Chad. This ep is full of laughs and some pretty craptastic stories. Definitely don’t eat during this one, y’all. We warned you.----more---- IN THIS ISSUE: 1.  This Month in History: January 2005 2.  Embarrassing Moments: Stick a Fork in ‘er, She’s Done! 3.  “Cool” Comebacks: The Itty Bitty Titty Committee 4.  Celebrity Scandals: First Take Hot Take 5.  Astro Guide: What’s the Tea (Leaves)? 6.  Quiz: Which Goddess Are You?

Drink from the Beverly Hills, 90210 fountain of eternal youth - all the way back to the era of post-grunge, rollerblades and the last days of Brenda Walsh. It was pretty much impossible for us to turn away from this issue. Tiffani-Amber is on the cover and she spells her hyphenated name with a friggin’ ‘I’ - could you GET any more ‘90s teen? In this episode we are joined by our ol’ pal Josh Lindley (remember him? Mr. Katie Holmes from Episode 19? Ya, we knew you would) and we flex our gag reflexes, learn about how to be true to ourselves, crown a new 90210 trivia champ, and, as per usual, laugh a hell of a lot. We promise you will too.IN THIS ISSUE:1.  This Month in History: December 19942.  Why Me? [Double Feature]: Brace Face / Baboobs3.  How 2 Say No 2 UR Friends: BANDRIES 1014.  Ask Jack: Feeling Guilty, Toledo, Ohio5.  Tiffani-Amber Thiessen: Shallow Val6.  Girly Mags Investigation: Mr. Jones and Me7.  Quiz: Jeo-party Hills, 90210

As we edge closer to the season of edging - Valentine’s Day - we invite you to join Girly Mags in this episode as we splash around in the waters of yesteryear. Do you remember 2002? It was the last time the Patriots played the Rams at Superbowl XXXIISII (who knows how to read Roman numerals anyway, NERDS!), and Crossroads starring Britney Spears won Best Screenplay at the Oscars. This ep is peppered with a bit of everything for everyone: public shame, stoney baloney, MURDER, Cheaters™, and the people who pronounce clique like “click.” (3/5 Girly Mags hosts agree - that just ain’t right).IN THIS ISSUE:1.  This Month in History: February 20022.  How Embarrassing! [Double Feature]: Readers’ Mail / Coitus Interruptus3.  Q&A Love: The Stoner Lunar Calendar4.  Life Like the Movies: My Dad’s a Murderer 5.  That’s Scandalous: Tricky Hickey6.  Twist Investigation: What Clique Are You In? 7.  Quiz: What’s Your Romance Style?

In this episode Heathendog goes solo: -Heathendog's Heathendogma: Marvel Super Heroes RPG (Advanced), TripleA, Avengers #681, Infinity Countdown Prime #1, and The Amazing Spider-Man #796 -------------------- Please Subscribe to our YouTube channel; like and share this video with your anime, comic book and gamer friends; and post your comments regarding the episode. Watch and chat with our hosts every Saturday evening at 8pm CST/CDT on Twitch. -------------------- HEATHENDOG'S HEATHENDOGMA: - 4:10 - Marvel Super Heroes RPG - 22:38 - Heathendog reviews TripleA (http://triplea-game.org/), Axis and Allies for the PC. - 34:32 - Avengers #681 - Who is Voyager? Valerie Vector, the forgotten founding Avenger, tells all! - 37:10 - Infinity Countdown Prime #1 - The Infinity Stones. Individually, they grant their wielder great power. Together, they grant the power of a god. - 40:50 - The Amazing Spiderman #796 - You’ve watched for months as Norman Osborn has scoured the globe for a cure to the genetic tampering that prevents him from becoming the Green Goblin. IN THIS ISSUE... HE FINDS IT! -------------------- WATCH & SUPPORT LEGION OF MYTH ON THE INTERNET - Twitch: https://twitch.tv/legionofmyth - YouTube: https://www.youtube.com/c/LegionofMyth_page - Support: https://www.patreon.com/legionofmyth - Donate: https://twitch.streamlabs.com/legionofmyth - Shop: https://shop.spreadshirt.com/legionofmyth INTERACT WITH LEGION OF MYTH ON SOCIAL MEDIA - Discord: https://discord.gg/xVgVB4W - Facebook Group: https://facebook.com/groups/legionofmyth - Facebook Message: http://m.me/legionofmyth - Reddit: https://www.reddit.com/r/LegionofMyth/ - Steam: http://steamcommunity.com/groups/legionofmyth - Twitter: https://twitter.com/legionofmyth WEEKLY LIVESTREAM PODCASTS - iTunes: https://itunes.apple.com/us/podcast/legion-of-myth-livestream/id1059235235 - SoundCloud: https://soundcloud.com/legionofmyth As always, thank you very much for your interest and support, we really appreciate it.

MSM 340:  History, Elections and Adolescents. Jokes You Can Use: Eileen Award: Twitter: Randy Ziegenfuss Advisory: The End of Adolescence https://aeon.co/essays/adolescence-is-no-longer-a-bridge-between-childhood-and-adult-life Middle School Science Minute by Dave Bydlowski (k12science or davidbydlowski@mac.com) GROUND PRONGS I WAS RECENTLY READING THE SUMMER, 2016 ISSUE OF "SCIENCE SCOPE," A MAGAZINE WRITTEN FOR MIDDLE SCHOOL SCIENCE TEACHERS, PUBLISHED BY THE NATIONAL SCIENCE TEACHERS ASSOCIATION. IN THIS ISSUE, I READ THE ARTICLE, "SCOPE ON SAFETY." IT WAS WRITTEN BY KEN ROY, DIRECTOR OF ENVIRONMENTAL HEALTH AND SAFETY FOR GLASTONBURY PUBLIC SCHOOLS IN GLASTONBURY, CT. THE ARTICLE FOCUSED IN ON THE SAFETY QUESTION OF THE MONTH, WHICH WAS: "WHY SHOULDN'T EXTENSION CORDS WITH BROKEN-OFF GROUND PRONGS BE USED?" From the Twitterverse: #mschat every Thursday at 8:00 pm Eastern Standard Time. And as Troy says, “The Twitter never stops!” Strategies: Letters to the Next President https://letters2president.org/ Resources: YouTube Copier Merge YouTube Playlists https://ctrlq.org/youtube/playlists/ How to search for publicly shared Google Documents, Presentations, and Spreadsheets. Great tips for searching Google. https://www.youtube.com/watch?v=rYDR4vaLBGE

The Newsletter for the City of Ann Arbor, Michigan                           August 2012, Volume 6, Number 8This is a reprinted version of the original, which was e-mailed to A2 City News subscribers on Aug. 1, 2012. Further information on featured topics and current news can be found at www.a2gov.org. IN THIS ISSUE  New police chief * Park millage update * A2NonMoto blog * FRA high-speed rail grant * Police golf outing * CTN podcasts * Vote Aug. 7 * Farmers Market turns 93 * Street resurfacing * Tree-care tips * A2 social media * “Around Ann Arbor” * Dates to rememberNew police chief appointedAnn Arbor City Council has appointed John Seto safety services administrator and police chief. Since April 1, 2012, Seto has served in this role on an interim basis. He was originally hired with the city as a patrol officer in 1990 and was appointed deputy chief of police, operations division, in 2008.  “The internal promotion of a candidate who meets the position's requirements of leadership, management experience, community involvement, judgment, and trustworthiness is healthy for the police department,” said Ann Arbor City Administrator Steve Powers. “I'm confident John has the experience necessary to serve our community well in this role.”Go online to read more. Park millage updateAt their June 19, 2012, meeting, the Ann Arbor Parks Advisory Commission unanimously passed a resolution to recommend placement of a renewal of the Park Maintenance and Capital Improvements Millage on the November 2012 election ballot. The resolution also recommends City Council reaffirm the administrative millage policies to inform voters of the manner in which it intends to oversee the administration of the millage if the proposed renewal is approved. This item has been placed on the (Thursday) Aug. 9, 2012, City Council agenda for review and approval. (The Council meeting is scheduled on a Thursday, instead of the usual Monday, due to Election Day.)The Aug. 9 City Council meeting will take place at 7 p.m. in the second floor Council chambers in Larcom City Hall (301 E. Huron St.). As with all other regular Council meetings, this meeting will be telecast live on CTN Channel 16 (Comcast Cable), or watch the meeting live online.  Parks improvements and maintenance activities status tables are available online, by fiscal year, and list park projects funded through your support of the 2008–2013 Park Maintenance and Capital Improvements Millage. Find your pathThe City of the Ann Arbor has launched a blog that celebrates the culture of nonmotorized transportation within the community: walking, cycling, etc. The “A2nonmoto”blog contains posts with a wide variety of features, such as bike helmet-cam videos, photos from bicycling commuters, pedestrian photos and news from the local and wider nonmotorized worlds. The blog serves as a platform for encouragement and education about the culture of nonmotorized transportation. For more information on the blog, or how to submit your own bicycling or pedestrian photos, please email the city's transportation office. City receives FRA high-speed rail grantAnn Arbor City Council recently voted to accept a planning grant from the Federal Railroad Administration (FRA) to support planning of a proposed new rail passenger station in Ann Arbor. The city, in cooperation with Michigan Department of Transportation (MDOT), applied to the FRA for funding under the FRA's High Speed and Intercity Passenger Rail program. The city was awarded a grant of $3.5 million to complete a comprehensive planning analysis, draft environmental documents and undertake preliminary engineering for the Ann Arbor station.   Originally identified as an element of the 2006 Ann Arbor Model for Mobility and included in the 2009 City Transportation Plan Update, this grant allows the city to continue planning for this essential component of our community's transportation system.City staff is coordinating closely with MDOT and Amtrak to assure thinking about this facility reflects the community's needs, state's investment in higher-speed intercity passenger rail along the Wolverine Line as well as the efforts to reintroduce commuter rail service from Ann Arbor to Detroit.  With MDOT investing to acquire and improve this corridor, increased rail service and demand for access to the rail system is expected. It is generally recognized that the current station needs to be improved. Long-term parking is inaccessible to many, as it requires a lengthy walk without provision for those with mobility limitations. The facility is located along Depot Street, a road heavily impacted by peak-hour traffic. Transit connections, limited today, are anticipated to be needed as the rail use and need for access to the rail service increases. Bus routing to the current station is impacted by the high volumes of traffic at the station site. With improved rail service, the shortcomings of the existing station will be exacerbated.The grant funds support preparation of a conceptual plan, environmental review and preliminary engineering. The conceptual planning process includes review of the current facility, identification of alternative sites and considerations of how to best proceed.  To date, the city has evaluated 15 sites, including the existing station site for accommodating the proposed future station. The concept planning process will occur simultaneously with the environmental review. Under this grant, the city will prepare a complete environmental assessment report seeking the FRA's approval of a project concept. Staff anticipates the project receiving a “Finding of No Significant Impact” (FONSI), a determination made by the FRA. Once the environmental review is completed, and FONSI is secured, the city will move forward and initiate preliminary engineering on the locally preferred alternative.Public participation is a fundamental part of this planning process. Recognizing there have been many public meetings as part of the Fuller Road Station project, this newly initiated work will provide additional opportunity for the project team to more fully evaluate and document the issues taken into consideration in this project. These materials will be subject to public review at project-related public meetings, as well as other city boards and commission meetings including the City Council, Planning Commission, Park Advisory Commission, among others. At this time, the next public meetings are anticipated to occur later this fall. For more information, please contact City Transportation Program Manager Eli Cooper. Police charity golf outingGet ready to golf for a good cause. Registration is going on now for the 21st annual Ann Arbor Police Charity Golf Outing Friday, Sept. 21 at Leslie Park Golf Course. This year's event is held in honor of two of the department's fallen officers, Jason Zogaib and Vada Murray, raising money for The Jason Zogaib Memorial Fund and The Vada Murray Fund for Cancer Research. The four-person scramble includes 18 holes of golf (and cart); a shotgun start at 9 a.m.; lunch; dinner; raffle, prizes and games; and more. Space is limited. Click here for details and the registration form(PDF). CTN helps you stay in the know, even on the goNew “On Air with CTN” podcasts provide an audio overview of everything happening on air and at the studios of Ann Arbor Community Television Network. Listen in and find out the line ups for CTN's four channels (16, 17, 18 and 19 on Comcast Cable), interviews with special guests, highlights of events new programs and a rundown of upcoming workshops for city residents and not-for-profit agencies.Follow us!Learn about upcoming meetings, facts, tips and more via the City of Ann Arbor's Facebook and Twitter pages. The city posts useful information — usually on a daily basis. In fact, a local realtor recently named the City of Ann Arbor's Twitter page as the No. 1 area “tweep” to follow. You can also subscribe to receive topic-specific bulletinsdirectly to your email. Find convenient links to each of these ways to stay connected on the homepage of the city website.Vote Aug. 7Polls will be open from 7 a.m. until 8 p.m. for the City Primary Election on Tuesday, Aug. 7. On Saturday, Aug. 4, the Ann Arbor City Clerk's office will be open 8 a.m.–2 p.m. for in-person absentee ballot requests.Go to the city election website, www.a2gov.org/elections, for ballot details and more information, or call 734.794.6140.Farmers Market turns 93Join the fun as the Ann Arbor Farmers Market turns 93 years old! On Saturday, Aug. 4 from 7 a.m.–3 p.m., the market, located at 315 Detroit St. in Kerrytown, will celebrate its birthday and its customers. At noon, free ice cream and toppings donated from market vendors will be served (while supplies last). Call for details, 734.794.6255, or go online. Paving the way to better streetsThe city's 2012 street resurfacing initiativebegan in the spring, and as of early August, 20 major and residential streets have been completed. Not only are streets' surfaces getting a makeover during this process, resurfacing also typically consists of removing/replacing sections of damaged or settled curb; repairing/replacing drainage inlets and utility structures (manholes); replacing corner ramps (to meet current Americans with Disability Act standards); and repaving the roadway. Among the roads undergoing work this month are:Geddes Avenue between Highland Road and Apple Way. Intermittent closures of Geddes to through traffic are in effect during construction, with detour routes posted. Local traffic will be maintained. Completion is expected in mid August.   Seventh Street between Pauline and Madison. Northbound traffic is being detoured. Completion is expected in the beginning of September.  When the initiative comes to a close this fall, 34 streets will have received upgrades. The 2012 street resurfacing project is funded by the Street Resurfacing Millage approved by voters in 2006.Visit the 2012 street resurfacing project Web page, and click on the red envelope to subscribe to receive regular street resurfacing project e-updates. You may also subscribe for e-updates to know which city streets have posted detours, on the city's road and lane closures Web page. http://www.a2gov.org/government/city_administration/City_Clerk/Elections/Pages/Elections.aspx Tree-care tipsThis spring and summer have been unusually dry, and — coupled with the recent very-high temperatures — both newly planted and established trees are showing signs of stress from lack of water. Wilting or curling leaves, leaf/needle drop and leaf scorch (caused by lack of water and high temperatures) are signs that your tree needs to be watered immediately.    In normal precipitation years, Mother Nature provides the water an established tree needs, and supplemental watering is typically not necessary. This season, however, calls for human intervention. A slow, deep watering is better than short, frequent watering, for both newly planted and established trees. For newly planted trees and small trees with a trunk diameter of up to 4 inches, a good watering is 10 gallons per inch of tree diameter applied in the mulched area around the tree, once per week. For established, medium trees (5–12 inches), a general guideline for watering during prolonged dry periods is 10 gallons of water for every 1-inch diameter, three times per month. Finally, for large trees, with a trunk diameter greater than 13 inches, 15 gallons of water is needed for every inch of diameter, twice monthly during prolonged dry periods. For established, trees do not water within 3 feet of the trunk, as this can lead to root rot.And how long should watering take place? In general, use this formula as a guideline: tree diameter inches x 5 minutes = total watering time.Find more information on tree watering, mulching, benefits and more on the city's forestry Web pages at www.a2gov.org/trees.Go "Around Ann Arbor" with CTNCommunity Television Network recently debuted “Around Ann Arbor,” a 10-minute weekly program featuring upcoming events in the city and surrounding communities. Following a news-style format, the show promotes events for the week ahead, making it convenient for viewers to plan their own calendars.“Around Ann Arbor” airs on A2TV Channel 17 on Comcast Cable on the following schedule.Sundays, noon and 9:05 p.m.Mondays, 10 a.m.Tuesdays, 3:50 p.m.Wednesdays, 7:30 p.m.Thursdays, 7:20 p.m.Fridays, 1 p.m.Saturdays, 1:35 p.m.And anytime on CTN Video On Demand.  “We've taken the electronic bulletin board and brought it to life, another great reason to tune into your community channels for local information,” said Melissa Cohn, assistant manager of the public and educational channels.To submit an event for consideration, free of charge, please email CTN.Dates to rememberAmong the many public meetings/events taking place in August, here are some of the highlights. Please go online for details and a complete list. Wednesday, Aug. 1, join the North Main Street-Huron River Corridor Task Force for a site tour. The Ann Arbor Farmers Market celebrates its 93rd birthday on Saturday, Aug. 4.  Also on Saturday, Aug. 4, the Ann Arbor City Clerk's office will be open 8 a.m.-2 p.m. to accept absentee ballot requests for the Aug. 7 State Primary Election, which takes place Tuesday, Aug. 7. A special Park Advisory Commission meeting is scheduled for Wednesday, Aug. 8.Because of the Tuesday, Aug. 7 State Primary Election, the City Council meeting will take place on Thursday, Aug. 9 rather than the usual Monday schedule.The first step to taking free production workshops at CTN is to attend the CTN Preview workshop, scheduled on Wednesday, Aug. 29. 

Why are you still getting this from here? The new name is "In This Issue" get it on iTunes or at www.uptoyouproductions.com