Podcast appearances and mentions of brian byrd

KIDS AND TRAUMA Jeffrey Griffith - TPS | Lead Counselor | StudentSupports Marya Singleton - TPS | School CounselorAnna - TPS | School Facility DogFollowing the death and discovery of 13-year old Kei'ManiLatiigue, TPS Lead Counselor Jeff Griffiths told WTOL 11, “it has been rough for certain students. This has acted like a trigger for some of the trauma that they've had in the past.” It wasn't long after the loss of Kei'Mani that we discoveredthat Joaquin Simmons had also tragically been killed in a senseless act of violence. But how are parents and counselors supposed to help themthrough it - especially if these kids are either scared to ask for help, or too unaware of what they need?  BRIAN BYRD'S CANCER FIGHTBrian Byrd - Fmr. Toledo Fire Chief/Fmr. Toledo SafetyDirector He's been a pillar of strength and leadership in thecommunity. In his spare time, this former Toledo Fire Chief and Toledo Safety Director teaches CCW classes. He maintains that he exercised and ate well. So how is it, that this guy who seemed to have the world bythe tail at some points in his life, is in his biggest challenge yet. Brian Byrd has cancer - and is not backing down - though he might be weakened - he's ready for his next test.

Brandi Waller-Pace, the organizer and visionary behind Fort Worth's African American Roots Festival, joins us in the studio. She shares her motive for bringing such a curated experience to the city and how Fort Worth can be a destination for art and music that uplifts marginalized voices. As usual, we go through our short stories, wins, and losses!SHORT STORY #1: Measles Outbreak: Where is our Health Director Brian Byrd?- Tarrant County is preparing for measles: " Moderate to high likelihood of a case here- Nate Schatzline Tempertantrum Attacking Bud Kennedy- Nate Schatzline dangerous propaganda celebrating anti-vaxxers during a Measles outbreak in Texas- Brian Byrd weak response to MeaslesSHORT STORY #2:  Fort Worth proposes urban rail system emanating from downtownSHORT STORY #3: Tarrant County Sheriff's son arrested in Arlington, accused of soliciting a minorBIG STORY: Brandi Waller-Pace and the Fort Worth African American Roots Music Festival: March 15th- Spotify list to get ready!WINS AND LOSSESAnn:

Ann and EJ record early and update you on TAD, the Election Integrity Committee, and an overview of what was shared at the Democratic National Convention in El Paso. The big story is Cooks Children fighting for their Medicaid program and Dr. Brian Byrd becoming the Tarrant County Public Health Director.SHORT STORY #1: Chair of Tarrant Appraisal District review board resigns just days before hearing casesSHORT STORY #2: Tarrant County Election Integrity Task Force reports 82 voter fraud complaints, no cases filedHere's how many illegal voters Tarrant County's election integrity unit has investigatedSHORT STORY #3: Texas Democratic Convention Brief OverviewUnlike Republicans, Texas Democrats are not interested in closed primariesBIG STORY: Health News in Fort Worth, Tarrant County, and TexasState rejects health insurers' pleas to halt plan that will shake up coverage for 1.8 million TexansTexas stands by its decision not to award major Medicaid contract to Cook Children'sFort Worth cancer support center to close as Tarrant health care challenges escalateFormer Fort Worth council member Dr. Brian Byrd to serve as Tarrant public health directorWINS AND LOSSESAnn:

Ann and EJ are joined by Tarrant County Democratic Chair Chrystal Gayden. She gives updates on the future of the party and how we can come together to support talented options in our local elections. As usual, we start with three short stories and end with wins and losses.  Make sure to follow the Tarrant County Democratic Party and support where you can!

Mableton woman accused of intent to murderSerina Renee Alexander, a 44-year-old woman from Mableton, has been charged with aggravated assault and intent to murder. She is accused of using a knife to cut the neck of Brian Byrd on July 30 at a residence on Charlotte Drive in Mableton. A responding officer found a blood trail leading to the front door and, after getting no response, entered the home and detained Alexander. Byrd had sustained a bleeding neck laceration and head wound. Alexander is facing charges of aggravated assault with intent to murder and obstruction of law enforcement. She was arrested on site and is currently held without bond in the Cobb County Adult Detention Center.**Hiram man charged with shooting at police officersJoahan Aragon, a 21-year-old Hiram man, has been charged with firing five 9mm rounds at police officers during their investigation of another incident. Armed with a Glock 17 pistol, Aragon allegedly fired at officers while also being in possession of 24 grams of marijuana with the intent to distribute. The incident took place on July 30 at 2750 S. Cobb Industrial Boulevard SE in Smyrna. Aragon struck a wall four times, and one shot was aimed at officers but missed the building. He had a black bag in his vehicle containing marijuana, a digital scale, plastic bags, and $965 in cash. Aragon faces charges including intent to distribute, possession of a firearm during a crime, and aggravated assault on a public safety officer. He was arrested on July 30, booked into the Cobb County Adult Detention Center, and released on a $30,000 bond.**University System of Georgia contributes more than $20 billion to economyIn fiscal year 2022, the University System of Georgia (USG) reported a total economic impact of $20.1 billion, marking an increase of $800 million or 4.14% from the previous year. This impact comprised $14.2 billion from direct spending by students, colleges, and universities, while the remaining $5.9 billion represented the multiplier effect benefiting local communities. The USG's 26 public colleges and universities significantly contribute to Georgia's economy by creating both on-campus (32%) and off-campus (68%) jobs, totaling 159,034 positions. The economic study, conducted by the University of Georgia's Terry College of Business, also revealed that USG institutions collectively generate an employment impact equivalent to the state's top five employers combined. Additionally, graduates of USG programs are projected to earn over $1.1 million more over their lifetimes for bachelor's degree holders and $1.4 million more for those with master's degrees, according to a companion study by Terry College's Selig Center for Economic Growth.Report: Cobb growing slower than metro AtlantaCobb County experienced a population increase of 6,100 residents from April of the previous year to April of the current year, according to a report by the Atlanta Regional Commission. The county's population reached 785,349 on April 1, with a growth rate of 0.78%. This growth was slower than the broader 11-county metro Atlanta region, which grew by 1.3%. Over the past year, the fastest population growth was observed in Atlanta and the region's exurban counties, particularly Cherokee (2.5%), Forsyth (2.1%), and Henry (2.1%). The report suggests that metro Atlanta's population growth is attributed to strong employment opportunities, with a 5.4% increase in the employment base since the pandemic began.Roller-coaster ‘hoteling' of Georgia foster children at record lowGeorgia's foster care system currently has only seven children "hoteling," according to the Commissioner of the Georgia Department of Human Services (DHS), Candice Broce. "Hoteling" refers to temporarily housing foster children in state offices or hotels. This number has fluctuated, with a recent high of 95 children and a record low of seven as of Tuesday night. The state legislature allocated $10 million to address this issue in the fiscal 2024 budget. A bill was also passed to establish a uniform process for placing children in the custody of the Georgia Division of Family and Children Services (DFCS). The DHS is launching a pilot program to aid families in accessing treatment and services. The reunification of children with their parents remains a primary goal for DFCS. The study committee plans to continue meetings to make recommendations for the upcoming legislative session.KSU's economic impact exceeded $2 billion last yearKennesaw State University (KSU) had a significant economic impact on Georgia, totaling over $2.03 billion in fiscal year 2022, which was a 10.3% increase from the previous year's $1.84 billion. The university, with 40,162 enrolled undergraduate and graduate students, is the third-largest in Georgia after Georgia State University and UGA. The University System of Georgia's report stated that KSU's economic contribution stemmed from various sources, including personnel and operating expenses, student spending, and community purchases driven by the institution, its employees, and students. KSU's employment of 15,917 individuals led to the creation of 2.8 additional jobs in the local community for each job on campus. KSU's president, Kathy Schwaig, highlighted the university's positive impact on the state's economy through academic programs, research, enrollment, and partnerships.Kell's Brown commits to South FloridaCJ Brown, the 6-foot-2 point guard from Kell High School, has committed to playing college basketball at the University of South Florida. Brown, a three-star recruit, announced his commitment on social media, expressing gratitude for the offers he received from various college coaches. He will join South Florida's basketball program, which is now part of the American Athletic Conference. Brown was a key player in leading Kell High School to a 28-2 record and their first state championship. He will play under the coaching of Amir Abdur-Rahim, the former Kennesaw State coach who recently took over the South Florida program. Brown's commitment comes after receiving offers from several other schools, including Georgia, Georgia Tech, and Mississippi State.Girls Cross Country Preview: Marietta in position to repeat as state champion The Marietta girls cross country team is in a strong position, having secured their third consecutive state title with five titles in six years. Their success is attributed to a close-knit and hardworking team culture. The team's dominance was evident in their recent state championship win, scoring only 33 points with top placements. The majority of their runners remain young, with only one graduate out of the seven who competed in the state championship. Marietta's youth shone through last season, with notable performances from freshmen and sophomores. Their success has made them a consistent threat in the state, despite competition from rivals like Harrison and Walton. Overall, Cobb County has a strong presence in girls cross country, with several schools making significant impacts in state championships. **Georgia ranked No. 1 in preseason coaches pollThe University of Georgia's football team, the two-time defending national champion, has secured the top spot in the 2023 preseason coaches poll. In the USA TODAY Sports AFCA Coaches Poll, Georgia received 61 out of 66 first-place votes. The Bulldogs, led by Coach Kirby Smart, will begin their season against Tennessee-Martin on September 2nd. Michigan holds the No. 2 position, its highest preseason ranking since the poll's inception in 1991. Alabama is ranked third, receiving four first-place votes, while Ohio State claimed the remaining one for fourth place. LSU stands at fifth, contributing to the SEC's strong presence in the top five.www.cuofga.org  www.henssler.com  www.ingles-markets.com  www.drakerealty.com  www.powerselectricga.com  www.esogrepair.com www.elonsalon.com  www.jrmmanagement.com  www.daycosystems.com  See omnystudio.com/listener for privacy information.

Radio show host, Gary Calligas will have Brian Byrd and Dr. Ravi Gupta from Centerwell Primary Care Center in Bossier City on his Saturday, March 5th “The Best of Times Radio Hour” at 9:05 AM on News Radio 710 KEEL to discuss the benefits of senior primary care services. This radio show is part of a senior health fair until 12 noon at 2900 East Texas Street in Bossier City. Also, the debut of the 2022 Silver Pages - senior resource direcoty. You can also listen to this radio talk show streaming LIVE on the internet at www.710KEEL.com. and streaming LIVE on 101.7 FM or via the RadioPUP or KEEL app on apple and android devices. For more information, please visit these websites at www.thebestoftimesnews.com and www.hebertstandc.com. This radio show is proudly presented by AARP Louisiana and Hebert's Town and Country of Shreveport featuring – Dodge, Chrysler, Ram, and Jeep vehicles and service.

The guys discuss the big NBA free agent moves, trade rumors and the implementation of the new "Harden Rules" with Special Guest Society Standard Founder & CEO Brian Byrd. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app Support this podcast: https://anchor.fm/backpage-sports/support

The results are here! The people of Fort Worth have voted. Now, what?!? Jimmy and EJ have been looking forward to this episode after months of breaking down the mayoral and city council races. They sit down with a friend of the pod and political science professor at TCU, Emily Farris, to share her analysis and give some potential next steps for the people of Fort Worth.

Jimmy and EJ react to the election results that came on Saturday night. They go through each district council seat and let you know which ones are going to a runoff. Lastly, they go through their wins and losses and why they are still hopeful for the city.Reference Links:Doyle Fine: https://www.facebook.com/watch/?v=1821475568002375Fort Worth Memories Museum: https://fortworthreport.org/2021/04/28/meet-fort-worths-biggest-history-buff-holding-mayoral-candidates-accountable/

Jimmy is back!  We start the podcasts catching up and getting one another's take on when North Texas will hit herd immunity.  We then discuss surprise comments by Tarrant County Judge Glen Whitely and American Airlines about Senate Bill 7.  The big story is that mayoral finance reports were due, so we go through them to learn who supports who and why that matters. Deborah Peopleshttps://www.fortworthtexas.gov/files/assets/public/city-secretary/documents/elections/deborah-peoples-30-day-cfr.pdfAnn Zadehhttps://www.fortworthtexas.gov/files/assets/public/city-secretary/documents/elections/ann-zadeh-30-day-cfr.pdfBrian Byrdhttps://www.fortworthtexas.gov/files/assets/public/city-secretary/documents/elections/brian-byrd-30-day-cfr.pdfMattie Parkerhttps://www.fortworthtexas.gov/files/assets/public/city-secretary/documents/elections/mattie-parker-30-day-cfr.pdf

This is a jampacked episode as we talk about the opening of vaccines for all Texas adults 16 and older and what it means for getting out of our houses. The big story is Senate Bill 7 and Republicans looking to suppress Texans' ability to vote. We also interview Dr. Jared Williams, City Council candidate for District 6. We then dive into wins and losses, including why Steve Penate is a good thing for the local mayoral race.Data: How the latest spike in migrants at U.S.-Mexico border compares to past years https://www.ksat.com/news/local/2021/03/26/data-how-the-latest-spike-in-migrants-at-us-mexico-border-compares-to-past-years/Schedule your vaccine:https://tcph.quickbase.com/db/bq98sxk7f

This week the hosts for the 817 podcast sit down with mayoral candidate Mattie Parker CEO of Cradle to Career and the T3 Partnership to discuss her goals for the city. Tony and EJ share their perspective on the stimulus package and as well opinions on the Arts Council of Fort Worth 2021 Mayoral Candidate Forum.Watch the Arts Council of Fort Worth 2021 Mayoral Candidate Forum: Learn about Mattie Parker

First, this is a BIG comprehensive episode with a lot of updates for the month of March as we prepare for the mayoral election! Early voting is April 19th.Second, we have a guest co-host who will be our podcaster in resident for the month as Jimmy is on the open road.Today we interview Tara Wilson who is running for city council in District 4 against incumbent Cary Moon. She is a medical professional and frontline worker who shares her experience about COVID and opinions on Governor Abbott's removal of the mask mandate in the state of Texas.

My next guest is Dr. Brian Byrd a true entrepreneur who has decided to run for Mayor! He comes from a long line of entrepreneurs and earned a degree at UT in Marketing and International Business. His life changed forever because of a knee injury in college. He was introduced to the medical field through having surgery. The lightbulb went off and he immediately started shadowing physicians while he was still in college.He followed through and opened Texas Family Medicine right out of medical school. Then he launched Texas Hospice in 2007 and sold it in 2013. What Next??He successfully ran for City Council and served for 4 years and is now running for Mayor of Cowtown!Useful Links and Book Mentions:Brian Byrd"Surprised by Oxford" by Carolyn Weber

#009.  Shawn Waugh has guest Brian Byrd from the 'Red Pill and Chill' Podcast 'On The Level' as they discuss post election results and the current fallout.  What are President Trump's chances moving forward and where are we as a country when the voting system cannot be trusted?  They discuss this plus what America will look like with a 78 year old Joe Biden in office and what to expect the next 4 years.The pre-election Podcast where Shawn & Brian discussed the early voting numbers is HERE.

Brian joins Shawn Waugh on "On the Level" to discuss early voting data. Shawn and Brian discuss the trends showing up in early voting data and what we can learn about the outcome of the 2020 Presidential race at this point. Check out more episodes of "On the Level" at OntheLevel.online For more insights and news from the Freedom First Press go to freedomfirstpress.com

#002 Host Shawn Waugh dives into the early voting numbers with Red Pill and Chill Podcast host, Brian Byrd.  They discuss what the numbers are looking like and what the chances are for both Democrats and Republicans with only 5 days until official election day.  From swing states to the different ethnic vote they cover it all.  If you are worried about the state of the race then feel free to take a listen and MAYBE feel more at ease.

The guys discuss the Nuggets shocking the Clippers, the Bucs losing to the Saints, the Lakers ending the Rockets, Celtics Heat Picks and Recap the NFL weekend with Special Guest Brian Byrd. --- Support this podcast: https://anchor.fm/backpage-sports/support

The Crew is joined by UA Rich Mountain head soccer coach Brian Byrd, along with assistants Chloe Crook and Bruno Guarda. Will there be high school sports this fall, and who will fulfill the quarterback role for Arkansas this season?

The Filtrate:Joel TopfSwapnil HiremathSamira FaroukMatt SparksJordy CohenAnd special guests:Brian Byrd, a cardiologist investigating aldosteronism at the University of MichiganandSusan Steigerwalt, a nephrologist and hypertension specialist who unfortunately due to technical problems largely was cut out of this episode

Husband and Wife Brian & Hidi talk about a cancer diagnosis, Cancer Video Diary and the importance of a caregiver.

Dr. J. Brian Byrd is an assistant professor of internal medicine at the University of Michigan Medical School. Stephen Morrissey, the interviewer, is the Executive Managing Editor of the Journal. J.B. Byrd, G.M. Chertow, and V. Bhalla. Hypertension Hot Potato — Anatomy of the Angiotensin-Receptor Blocker Recalls. N Engl J Med 2019;380:1589-1591.

On this episode of Paint ED, Brian Byrd, a fitness professional at Train For Life Studios, specializing in injury rehab, talks about ways anyone in the painting industry can keep their body fit and energy efficient. It only takes a few minutes each day to stretch and hydrate, and the long-term results are very worth the time. If you're a manager at any level, you might want to think about encouraging your employees to remember to stretch and hydrate more often. It's good for short-term health, for long-term health, and it's good for production because safe and healthy people are more efficient. Learn more about Brian Byrd at Train For Life on Instagram, Facebook, and Twitter.

Jane Ferguson: Hi everyone. Welcome to episode 20 of Getting Personal Omics of the Heart, the podcast brought to you by the Circulation: Genomic and Precision Medicine Journal and the American Heart Association Council on Genomic and Precision Medicine. I'm Jane Ferguson from Vanderbilt University. It's September 2018 and let's dive straight into the papers from this month's issue of Circulation: Genomic and Precision Medicine.                                 We're starting off with some pharmacogenomics. Bruce Peyser, Deepak Voora and colleagues from Duke University published an article entitled, "Effects of Delivering SLCO1B1 Pharmacogenetic Information in Randomized Trial and Observational Settings."                                 Although statins are generally well tolerated, 5-15% of patients taking statins for LDL lowering and cardiovascular protection end up developing statin associated muscular symptoms. Because onset of muscular symptoms associated with discontinuing statin use, as well as increased cardiovascular morbidity, there is a clear need to identify ways to prevent or reduce symptoms in these people. Variants affecting statin related myopathy have previously been discovered through GWAS, including a variant in the SLCO1B1 gene, which also has been shown to relate to statin myalgia and discontinuation of statin use. The risks appear to be greatest with simvastatin, indicating the people at risk of muscle complications may do better on either low-dose Simvastatin or another statin. However, there's still some uncertainty surrounding the risks and benefits of various statins as they pertain to risk of muscular symptoms.                                 The authors have previously shown that pharmacogenetics testing led to increased number of people reporting statin use, but effects of pharmacogenetic testing on adherence, prescribing, and LDL cholesterol had never been tested in a randomized control trial. In this study, they randomized 159 participants to either genotype informed statin therapy or usual care, and then followed them for months to eight months.                                 25% of participants were carriers of the SLCO1B1 star five genotype. The authors found that statin adherence was similar in both groups, but gene type guided therapy resulted in more new statin prescriptions and significantly lower LDL cholesterol at three months, and levels that were lower but no longer significantly different at eight months.                                 In individual's randomized to usual care who then crossed over to genotype informed therapy after the trial period ended, there was an additional decrease in LDL cholesterol. Overall, genotype informed statin therapy led to an increase in re-initiation of statins and decreases in LDL cholesterol, but did not appear to affect adherence.                                 The authors also examined the effects of commercial genetic testing for SLCO1B1 variants in an observational setting by looking at over 92000 individuals with data available in the EHR. They found the people who receive genetic testing results had a larger drop in LDL cholesterol compared to untested controls. Overall, the study indicates that carriers of the SLCO1B1 risk variant may benefit from genotype informed statin therapy, while for non-carriers receiving their results may has limited effects.                                 If you want to read more on this, Sony Tuteja and Dan Rader from UPenn wrote an editorial to accompany this article, which was published in the same issue.                                 We're staying on the topic of statins and LDL for our next paper. This article comes from Akinyemi Oni-Orisan, and Neil Risch and colleagues from the University of California and is entitled, "Characterization of Statin Low-Density Lipoprotein Cholesterol Dose-Response Utilizing Electronic Health Records in a Large Population-Based Cohort."                                 They were interested in understanding what determines variation in statin induced LDL reduction, particularly the genetic component, and they used a large EHR derived data set, the Kaiser Permanente Genetic Epidemiology research on adult health and aging cohort to address this important question. An EHR dataset does have intrinsic limitations, but also has some clear strengths, not only as a readily available and cost-effective data source for large sample sizes, but also because it reflects real world clinical care in diverse individuals, which is not always well represented within the selective constraints of a randomized trial.                                 There were over 33000 individuals who met their inclusion criteria. To account for differences in potency between different statins and doses, the authors generated a defined daily dose value, with one defined daily dose equal to 40 milligrams per day of Lovastatin. The slope of the dose response was similar across statin types and across different sex and race or ethnicity groups. But there were differences by statin type in the response independent of dose, as well as differences in absolute responses by sex, age, race, smoking, and diabetes.                                 Based on these differences, the authors revised the defined daily doses and they highlight how previously defined equivalencies between different statins may not be accurate. They found that individuals with East Asian ancestry had an enhanced response to therapy compared with individuals of European ancestry.                                 The authors identified related individuals within the data set and the estimated heritability of statin response using parent-offspring and sibling pairs. They found only modest heritability, indicating that non-genetic factors may be more important in determining variability in statin response. Overall, this large single cohort study adds to our knowledge on determinants of statin response and raises further questions on the relative effects of different statins and doses within patient subgroups.                                 Okay, so now let's talk about GWAS and Athero. Sander van der Lann, Paul de Bakker, Gerard Pasterkamp and coauthors from University Medical Center Utrecht published a paper entitled, "Genetic Susceptibility Loci for Cardiovascular Disease and Their Impact on Atherosclerotic Plaques."                                 Over the past decade, genome-wide association studies in large cohorts have been very successful in identifying cardiovascular risk loci. However, relating these to subclinical disease or two mechanisms has been more challenging. The authors were interested in understanding whether established GWAS loci for stroke and coronary disease are associated with characteristics of atherosclerotic plaque, the idea being that some of the risk loci may alter disease risk by determining the development and stability of plaque. They identified seven plaque characteristics to study and histological samples, including intraplaque fat, collagen content, smooth muscle cell percentage, macrophage percentage, calcification, intraplaque hemorrhage, and intraplaque vessel density.                                 They selected 61 known loci and examined association of those SNiPA with black phenotypes in over 1400 specimens from the athero express biobank study. Out of the 61 loci, 21 were associated with some black phenotype compared with zero of five negative control loci, which were chosen as established GWAS loci for bipolar disorder, which, presumably, should share limited mechanistic etiology with plaque. They used the software package VEGAS to run gene-based analyses. They also assessed SNiPA relationships with gene expression and methylation in multiple tissues derived from two independence Swedish biobanks, which included atherosclerotic arterial wall, internal mammary artery, liver, subcutaneous fat, skeletal muscle, visceral fat, and fasting whole blood.                                 One CAD locus on chromosome 7q22 that survived correction for multiple testing was associated with intraplaque fat, and was also an EQTL for expression of several genes across multiple tissues. In addition, it was also a methylation QTL.                                 The authors focused on this locus and looked at correlation of expression within the LDL receptor and noted associations with HDL and LDL cholesterol in the global lipids genetics contortion data, which suggests that this locus may have a role in the metabolism. At this locus, the HBP1 gene expressed foam cells may be an interesting candidate as a causal gene in determining plaque-lipid accumulation and cardiovascular risk.                                 So next up, we have a paper that is also about athero and is coauthored by many of the same group as did that previous study. So yeah, this group's productivity is kind of making the rest of us look bad this month. So Martin Siemelink, Sander van de Lann, and Gerard Pasterkamp and their colleagues published, "Smoking is Associated to DNA Methylation in Atherosclerotic Carotid Lesions."                                 Okay. So I think one of the few things we can all definitely agree on is that smoking is bad. But, does smoking exert any of its cardiovascular damage by altering within atherosclerotic plaques? That's the question this group set out to answer.                                 They carried out a two-stage epigenome-wide association study, or EWAS, with discovery and replication of differentially methylated loci with tobacco smoking within carotid arteriosclerotic plaques of a total of 664 patients undergoing carotid endarterectomy and enrolled in the arthero-expressed biobanks study. In discovery, they found 10 CpG loci within six genes that associated with smoking. Four of the CpG loci replicated. These four loci mapping within six genes showed reduced methylation in current smokers compared with former or never smokers.                                 However, there was no difference in specific plaque characteristics based on methylation at any of the four loci. There was also no significant difference in plaque gene expression at these loci based on smoking status. However, a SNiPA at a nearby locus located in the 3' UTR of the PLEKHGB4 Gene was associated with methylation at AHRR, and was a [inaudible 00:09:58] QTL for PLEKHGB4 of expression but not a AHRR expression. The authors speculate that PLEKHGB4 may co-regulate AHRR expression. The authors also examined blood methylation in a subset of the same subjects, and they were able to replicate previously identified CPG sites associated with smoking.                                 This is a really complex area, and it's hard to identify mechanisms and causality from these multiple layers of data, but the authors demonstrate the importance of using disease relevant tissues to start to understand how environmental factors interact with genetics and other underlying physiology to modify methylation and function within the vasculature.                                 Our final full-length research paper this issue from Brian Byrd and colleagues Michigan, is actually the subject of our interview today. So I won't go into too much detail on it right now, but keep listening for an interview with Brian about their paper, "Human Urinary mRNA as a Biomarker of Cardiovascular Disease: A Proof-of-Principle Study of Sodium-Loading in Prehypertension."                                 Our review article this month is about the "Dawn of Epitranscriptomic Medicine" from Konstantinos Stellos from Newcastle University and Aikaterini Gatsiou from Goethe-Universität Frankfurt. In this paper, they're taking us to the next level beyond just RNA, but towards RNA epigenetics. Given the large number of possible modifications that can and are made to RNA during RNA name metabolism, there's huge potential to gain a new biological and mechanistic understanding by studying the RNA epitranscriptome. I think we'll ignore this at our peril. So if you need to catch up on this new field, this comprehensive review will get you right up to speed.                                 Moving on, our research letters are short format papers that allow authors to present focused results. These are also a great avenue to submit findings from replication studies that might not necessitate a full-length paper. So if you have some data from a replication study that you've been procrastinating writing up, a short research letter is a great format to consider.                                 This month, Bertrand Favre, Luca Borradori and coauthors from Bern University Hospital published a letter entitled, "Desmoplakin Gene Variants and Risk for Arrhythmogenic Cardiomyopathy: Usefulness of a Functional Biochemical Assay." The desmoplakin is essential for the cell-cell adhesion complex's desmosomes. Mutations in this gene have been associated with a wide range of phenotypes, including some in skin and hair, but also in heart, which can manifest arrhythmogenic or dilated cardiomyopathy. This protein anchors intermediate filaments, so mutations that alter binding to intermediate filaments may pathogenicity.                                 The author selected seven reported amino acid altering mutations in desmoplakin, and they screened for effects on binding using a novel fluorescence binding assay. They found that three of the seven mutations had a clear impact on binding. This assay is a novel way to assess functional impact of desmoplakin variants, and may be useful to inform the severity of future phenotypes in individuals carrying a desmoplakin mutation.                                 Finally, if you want to stay up-to-date on the genetics of aortic disease and Marfan syndrome, you can find a letter from Christian Groth and colleagues and an author response from Norifumi Takeda and colleagues regarding their previously published paper on impact of pathogenic FBN1 variant types on the progression of aortic disease in patients with Marfan syndrome.                                 I am joined today by Dr. Brian Byrd from the University of Michigan, who is the senior author on a Manuscript published in this month's issue, entitled, "Human Urinary mRNA as a Biomarker of Cardiovascular Disease: A Proof-of-Principle Study of Sodium-Loading in Prehypertension."                                 So welcome Brian. Thanks so much for coming on the podcast. Brian Byrd:          Thank you for having me. Jane Ferguson: So before we get started, could you give a brief introduction of yourself to the listeners and maybe tell us a little bit about how you got into the field? Brian Byrd:          Absolutely. So I am a cardiologist and a physician scientist. I'm an assistant professor at the University of Michigan, where I have a laboratory engaged in clinical investigation. My background is that I did my Internal Medicine Residency at Vanderbilt University. And after I finished residency, I entered Nancy Brown's lab. She's the Chair of Medicine at Vanderbilt, as I know you're aware. And she had a laboratory focused, and still does have a laboratory focused, on the investigation of high blood pressure, with a lot of focus on understanding high blood pressure as it occurs in humans. And I got a Master of Science degree in clinical investigation while I was in her lab, and we did some work on a number of topics related to the renin-angiotensin-aldosterone system, which has been a long-standing interest of mine ever since then.                                 So, at the same time, I was learning how to take care of patients with very complex blood pressure problems, who required three, or four, or five, or six blood pressure medications, in some cases, to control. And it's with that background that I became very interested in the science that underlies treatment-resistant high blood pressure in people and what we might be able to do about that. Jane Ferguson: Wow. Nice. Yeah and I think that background of sort of the combination of clinical and experimental is really nice and really important. I think your paper actually exemplifies that really nicely, so using humans but also some basic science techniques and combining them to really have a very patient focused instead of mechanistic interrogation.                                 So as I mentioned, you just published this really nice manuscript using urine as a source of mRNA biomarkers, which has relevance to hypertension and potentially also to other diseases. But before we get sort of too much into the weeds on the specific details, for any of our listeners who didn't get a chance to read your paper yet, maybe you could briefly summarize what you did? Brian Byrd:          Okay, so the general overview of what we were interested in was that the patients who have treatment resistant high blood pressure tend to have a lot of activation of a receptor in the kidney called the mineralocorticoid receptor. And this receptor helps control salt in bladder in the body. Obviously the amount of salt in the blood stays very, very homeostatic, but we if eat more salt one day then the next and there needs to be a system to help regulate the homeostasis. And so, you waste more or less salt in the urine depending upon how much sodium you're taking in.                                 And one of the functions of the mineralocorticoid receptor is to control this salt and bladder regulation or to fine tune it anyway. And the reason we know that that's an important receptor in patients with treatment-resistant high blood pressure is because of a series of studies done by David Calhoun and Brian Williams and others, showing that mineralocorticoid receptor blockers, or antagonists, are very effective in the treatment of tough to control high blood pressure.                                 And so, we had some insight that there would be something interesting to study there, and one of the things that we knew was that the mineralocorticoid receptor is a ligand activated transcription factor. So when it gets activated by it's ligan which canonically is a steroid hormone from the adrenal gland aldosterone, the receptor, which is in the cytoplasm, ordinarily dimerizes and translocates to the nucleus, where it controls the regulation of a number of genes. We also were aware that cells secrete RNA, and others had the idea that it might be inside vesicles because there's a lot of ribonuclease and biofluids. And you would think it might be difficult to pass the RNA if it were sort of naked as it were.                                 And it turns out that that's right. If you, for example, introduced synthetic RNAs into biofluids, the RNAs will be gone very quickly in a matter of seconds. So, we had this idea that we might be able to look at RNA that was being secreted by cells probably in vesicles, and assay the activity of the receptor potentially. We weren't sure if that was going to be possible or not.                                 One of the things we did was we used part of the available data to look at the transcriptome of vesicles in the urine that had been isolated from 3300 milliliters of urine by ultracentrifugation [inaudible 00:18:57]. Jane Ferguson: So it's a big centrifusion. Brian Byrd:          Exactly. Jane Ferguson: Like you [inaudible 00:19:00] Brian Byrd:          It must have been some project. So that was the work of Kevin Miranda and colleagues, and we were able to compare that transcriptome to the transcriptome of human kidney cortex samples from the GTEx project, which a large consortium focused on human transcriptomics.                                 And that was sort of the first part of what we presented in this paper, and the second thing that we did was we looked within a crossover study in a collaboration with Scott Hummel, one of my close collaborators here at the University of Michigan. We looked at individuals who had been put on a low salt diet activating renin-angiotensin-aldosterone system and causing more activation of the mineralocorticoid receptor. And then, those same individuals underwent saline infusion, so salt loading, and we knew that that would suppress the renin-angiotensin-aldosterone system. And we measured the [inaudible 00:20:02] measures of the renin-angiotensin-aldosterone system, but we also took the urine samples that had been recently banked from that experiment and we centrifuged them to try to palette the cells. We took the supernatant and we extracted RNA after trying to enrich for extracellular vesicles.                                 And with that approach, we measure targets that we thought would be regulated my the mineralocorticoid receptor, as well as some things that we did not think would be regulated by mineralocorticoid receptor. So that's the general overview of what we undertook. Jane Ferguson: Great. Right. So it's very cool. I guess we can break it down into sort of the two different parts, because I think it was a really nice examples of using public data to sort of start addressing your question and then actually doing a human experiment. But so for the GTEx data and the urinary data, you looked at few different tissues, right? And was kidney the one that you were thinking upfront would sort of most likely to correlate, or were you also looking at bladder and other sort of tissues that could potentially be of relevance to urine? But what sort of the ... I guess sort of tell me more about those different tissues that you looked at and what you found and what surprised you or not. Brian Byrd:          Great question. So, the kidney was on our minds from the outset. We knew that Mark Knepper at the National Institute of Health had published in the [inaudible 00:21:25] National Academy of Sciences back in 2004 that there are urinary extracellular vesicles. And he had found proteins that are very characteristic of the aldosterone sensitive distal nephron, that part of the kidney that we're interested in, embedded in the vesicles.                                 So we became quite interested in the idea that it seemed that there was likely a population of vesicles in the urine that is of kidney origin. And that's not to say that there weren't also plenty of vesicles from other origins as well, and there could very well be RNA that is not vesicle enclosed, but is rather ribonucleic protein bound or even bound to other carriers potentially. That could be there as well, and it's possible that the origin of those things could be any number of tissues. I don't really think that we know yet where the possible tissue origins are.                                 But we were curious to know ... I guess the direct answer to your question is we thought from the outset that we probably would find some sort of signal related to the kidney. But we wanted to also consider the possibility that our findings were not very specific to the kidney. And so we thought that the brain would be an interesting negative control. If we say very high correlation with the brain, it would suggest that maybe what we're looking for is a signal that's not really coming from the kidney.                                 And we also wanted to look at the bladder just to try to understand whether or not the signals that we're detecting could be coming from the bladder. It's certainly true that some aspects of the system that we're interested in are present in the bladder, so I wondered whether that might even serve as a signal amplifier for what we were looking for since there's, presumably, quite a bit of bladder tissue right around the urine. It might be contributing vesicles.                                 So that's sort of the rationale for why we looked at those things. Jane Ferguson: And you found mostly enrichment for kidneys. So sort of I guess what you were hoping to find came true? That actually there was sort of evidence that even though there may be contribution from other tissues, that really kidney seem to be the predominant contributor to the expression of the genes in the urine. Brian Byrd:          I think there's a lot of truth to that. One of the things I would say is we found high correlation looking across all genes. But it occurred to us ... As soon as we thought that, we realized, wait a second, that could be driven by ubiquitously expressed genes. Housekeeping genes.                                 So we really wanted to stratify our analysis by things we thought would be expressed in the kidney as well as things that we thought would be ubiquitously expressed to make sure that we could see signals that correlate ... That the transcriptome of the kidney, per se, had a good correlation with those same in terms of the abundance of the gene counts or recounts. They said it was similar to what was in the vesicles.                                 And so, we looked in the literature, and we found that a group had already established a number, 55 genes actually, that were highly kidney enriched as well as over 8000 genes that were ubiquitously expressed. And so we started the analysis from this perspective of the stratification. We thought that was a very important aspect of the analysis. And it's definitely true that if you look at our findings with respect to the kidney enriched genes, as you might expect, they correlate quite well with what is in the urinary extracellular vesicles compared to the kidney cortex.                                 You look at the brain as you might expect the expression of those kidney enriched genes is not well correlated with what's happening in the urine. And then, with respect to the bladder, it's sort of somewhere in between. Jane Ferguson: Okay. Interesting. So I know that some people look at small non-coding RNAs in urine, but you were mostly focused on mRNAs. Is that right? Brian Byrd:          That's right. I thought of this as sort of frontier, something that I knew from some early publications was probably measurable. But I didn't know what it would signify, if anything, with respect to physiology. And I knew that there were quite a few papers about micro RNAs and I wanted to do something a little bit innovated, partly.                                 But the main reason that I was interested in the RNAs was because I could relatively easily tie those to the existing literature from animal models. Preclinical animal models and cell culture studies showing what happens when the mineralocorticoid receptor's activated. That was really the driving reason that I was interested in the RNA. Because if you think about what is the approximate event that might be a readout for activation of a new growth hormone receptor like the mineralocorticoid receptor, it's really the transcriptional events that happen when the receptors translocates to the nucleus and serves its ligan activated transcription factor role. Jane Ferguson: Right. So, [inaudible 00:26:43] sort of the first part of analysis, you saw these really nice correlations between expression and kidney and in urine. And then, a lot of the times when you tried to publish that kind of thing, people are like, "Okay, so what? So you didn't do any intervention. We don't really know what that means."                                 But I like that you took it to the next step and you did sort of a human intervention experimental model. So tell me more about that model and how that worked. Brian Byrd:          Right. Well, I'll just mention also that the work that was done in terms of RNA [inaudible 00:27:14] was done in collaboration with Mark Bertini in Italy as well as Dr. [inaudible 00:27:19]. They were fundamental to getting that work done.                                 With respect to the collaboration with Scott Hummel, one of my colleagues here at the University of Michigan, what we did in that setting was to look at whether or not we could identify within these urinary mRNA signals that are in the supernatant in the urine, whether we could identify changes in physiology. That was the question that was of greatest interest scientifically.                                 And for a very practical or blind perspective, the question was could we detect the activation of the receptor that might determine whether or not people should get a certain medication. Of course, we're not saying that that's an established fact yet, but this is sort of concept, that there's something here to explore further.                                 And so, what we found was that a number of genes that are regulated by the mineralocorticoid receptor, including genes encoding the subunits of the amiloride-sensitive epithelial sodium channel that regulates the salt that I was talking about earlier. We found that those genes changed with sodium loading in terms of their abundance in the expected direction.                                 We also found that several of the assays that we made changed ... I'm sorry. That they correlated with the serum aldosterone concentration. So the concentration of the ligan for the receptor whose readout we were looking for. And we also noticed an inverse correlation with urinary sodium excretion, which is what we would expect if we really identified a readout of the mineralocorticoid receptor's activity.                                 So this study supported the idea that we have identified a way to measure this nuclear hormone receptors activity in living humans. Jane Ferguson: Right. Which is really nice. So there's probably a huge amount of extra things you could do with this, some sort of different ways you could look at it. So how did you pick the time point? So, I suppose when you think about it, I mean the genes, they're transcribed and then that takes a little bit of time, and then it takes a little bit of time for that to sort of make its way into the urine and to be excreted.                                 So how did you decide on sort of what time points to use, and do you think you would see the same things or different things [inaudible 00:29:39] if you did repeated sampling or if you looked at different time points? Brian Byrd:          That's a fantastic question. So this was a study that had already been completed, and I had mentioned to Scott what we were working on. And he said, "You know, we have these samples from this study and it might be possible for us to collaborate."                                 So, we didn't get to pick the timeframes. Jane Ferguson: Right. Brian Byrd:          So, that's a great point. And what I would say is that, as you can imagine, we're very focused on exactly the questions you're asking now. What about sort of signal refinement? What about the chrono-biology of these signals, and how do we understand when we see what in the urine?                                 So, I'm actively pursuing those questions. Jane Ferguson: Right. So, I know as well, there was quite a lot of sort of technical challenges I think to doing this work. Sort of getting to be even able to amplify and get a signal from these RNAs that are really present, sort of pretty low abundance in urine compared to tissues or biofluids that we're used to working with.                                 So tell me maybe a little bit about that process and sort of how much optimization was required to get these essays to work? Brian Byrd:          Great question. So, I had known [inaudible 00:30:58] since 2014 when I took a course on isolation of extracellular vesicles in Heidelberg, Germany. And I had talked to him at a meeting in Washington DC, and I had mentioned what we were trying to do. And he said, "You know, if you were trying to do that, you might want to consider preamplification." You know, using something like 15 cycles of preamplification. And he was willing to share that protocol that he had with me, because they were interested in similar issues. So, I was able to use that protocol to evaluate these gene targets in the urine. And so that was immensely helpful.                                 And the other thing that we did was we used locked nucleic acid probes to try to increase the sensitivity and specificity of our assays. Finally, we just tried to use good logic in the design of the assays. So we were concerned that the RNA might be fragmented, so where it was possible to do so within the design constraints that I'll mention in a second, we made multiple assays per gene target just in case this was fragmented. Which makes the analysis a little more complicated, but I think it was probably the right thing to do, given the state of knowledge that we had then.                                 And one of the other things we did was we made sure that the primers either ... Within a primer, there was an intron or between the primers there was an intron, so that if we actually did try to amplify DNA, abundant amounts of DNA, with those primers just to make sure that our theorizing about the inability to amplify things was actually factual. And that turned out that we couldn't amplify anything at 40 cycles with those.                                 So, we spent a lot of time thinking about how not to get fooled, but also to have adequate signal detection. And have included in the supplement quite a bit of information about the technical merits of the assays and showing how close the technical replicates were. They tended to be very, very similar to one another. We didn't see a signal in every urine sample for every participant at both time points, and I think that was interesting to me about that there tended to be a very binary result, so that you'd either see three technical replicants for the QPCR assays, our QPCR assays that were extremely similar to each other, or you would see no CT value detected.                                 [inaudible 00:33:47] That these were valid assessments of very low copy numbers. Jane Ferguson: Right. And that's probably related to up front of what happens to urine right after it's collected and stored, or during that RNA extraction. But it seems like once you've got RNA, then downstream assays were sort of ... They held through, but I guess ... I mean, and you obviously didn't have necessarily a huge amount of control over how these urine samples were collected. So it's kind of nice that you were able to see something even though these were collected possibly in a way that was not optimized for preserving RNAs.                                 But do you think those ... Are there ways that you could make this even sort of more streamlined and better as far from the get go of how you collect the urine, whether you could be extracting stuff right away? Is that anything you sort of looked into of how this could be improved? Brian Byrd:          That's really been the focus of the labs work since we completed that project, is sort of understanding how would we do this in a prospective study in the best possible way so that the results are highly repeatable, that we get a CT value in everybody so that we're really ... I mean, as you can imagine, that actually has something to do with the input volume of urine that you use. So if you have too little input volume, then you won't be able to detect the targets that you might be interested in every person.                                 However, if you have more, then you can do more with that. But then you have to think about how you're going to deal with the larger volumes of urine. There are lots of questions that we've been interested in related to extract the RNA and the stability of the RNA. And so we have done some experiments of that type, and we continue to work in that area. And I do think that those questions you're asking are the right questions with respect to next steps. Jane Ferguson: All right. So you looked at sort of specific targets, which I think made a lot of sense. Sort of this proof of principle. But do you think this would work on a transcriptome wide level? I mean, could you look at all the genes, or do you think that's just sort beyond the possibility right now given sort of the RNA fragmentation and how you have to sort of amplify it before being able to detect anything? Brian Byrd:          I think it's possible. So the group that had preceded our work with 3300 mils of urine, isolating the vesicles from there, eight have showed that that's something that can be done. The question that's of interest to me is does it actually require such large volumes of urine? And I think the answer to that question is going to be no from what we're overseeing so far.                                 And so, we're thinking along exactly the lines that you are. And certainly some of the feedback we've gotten as we've discussed this project with people is, "Hey, could you look at everything rather than picking targets at [inaudible 00:36:41]."                                 I think there's advantages and disadvantages. I think we chose based on prior knowledge in a way that was rational. But at the same time, it may turn out that there are many things about activation of the mineralocorticoid receptor in humans, especially in the living in-tact human, that don't exactly mirror what's found in rabbits, rats, mice or cells, which are really the systems that have been evaluated the most thoroughly in the past.                                 So I'm very interested in exactly what you're proposing. Jane Ferguson: Yeah. I mean, I think it's exciting because it's obviously relevant for hypertension, but potentially a lot of other conditions, to be able to look at that sort of dynamic change. So I think it's really exciting. It's very cool. Brian Byrd:          And I appreciate your asking about this study. We were excited to do this work and very, very excited to see where we can in the future with this. And I agree with the point you were making, that here we've gone from a rather specific application driven question and we've, I think, made some insights that are probably useful outside the application that we had in mind. And it may turn out that the application where this is the most important is not even the one that we considered in the first place at all.                                 And so I'm pleased by that. I'm pleased by the fact that I think in a sense we're working in what Donald Stokes described as pasture's quadrant, which is a sense that the work is driven both by curiosity and by an intent to use the results. Jane Ferguson: Right. Brian Byrd:          And so that's really what gets me out of bed in the morning, is working that exact space. So that's what we were glad to have done and continue to do. Jane Ferguson: Yeah. No, I think it's grea.t and I feel like a lot of people will read this paper and be like, "Hey, I have urine stored in the freezer. What can I do with this now?" Brian Byrd:          Contact me. Let's talk. We'll see what we can do. But we certainly tried to describe the methods in such a way that people could easily follow in our footsteps if they want to apply these methods. Jane Ferguson: Yeah. Now having read through them, I think that ... Really thorough. I really liked the sort of attention to detail. It was definitely one of those ones where I was like, "Oh yeah. I can see exactly how I could do this if I wanted to. So I think that was great. Brian Byrd:          Thank you. Jane Ferguson: So yeah. Congratulations on the paper. Really nice work and thanks so much for talking to me. Brian Byrd:          Thank you. It was a delight. Jane Ferguson: That's it from me for September. If you haven't had enough yet, you can access all the papers online and you can choose to digest the papers in video format. Available on our website or the Circulation YouTube channel. Thank you for listening and subscribing. I look forward to bringing you more next month.  

Brian Byrd, the new Chief of Toledo Fire and Rescue

It’s hard to beat incumbents. Dr. Brian Byrd got the job done in Fort Worth and is here this week to share how he did it! Getting to help elect good men and women to office is what keeps me involved in politics and it’s my pleasure to count this week’s guest as a friend […] The post How to Beat Incumbents with Dr. Brian Byrd appeared first on My Campaign Coach.

Brian Byrd with the Midian Shrine Circus

In this episode I talk with a few different guest. First is Scott Holden, the host of ‘That Man on Fat Man' and co-host of ‘Bonecrushing Juggernaut', but also director of ‘What is a Podcast?' a documentary on podcasting. Which is on Indiegogo for crowd funding I also talk with Brian Byrd and Sarah Hollis, the writers of the indie comic ‘Bullets and Angels'. We talked about the Kickstarter going for B&A;, but also some of their upcoming work. What is a Podcast? Indiegogo – https://www.indiegogo.com/projects/what-s-a-podcast-a-documentary-film#/story Bullets and Angels' Kickstarter – https://www.kickstarter.com/projects/1028017026/bullets-and-angels-rosary

In this episode I talk with a few different guest. First is Scott Holden, the host of ‘That Man on Fat Man’ and co-host of ‘Bonecrushing Juggernaut’, but also director of ‘What is a Podcast?’ a documentary on podcasting. Which is on Indiegogo for crowd funding I also talk with Brian Byrd and Sarah Hollis, the writers of the indie comic ‘Bullets and Angels’. We talked about the Kickstarter going for B&A, but also some of their upcoming work. What is a Podcast? Indiegogo – https://www.indiegogo.com/projects/what-s-a-podcast-a-documentary-film#/story Bullets and Angels’ Kickstarter – https://www.kickstarter.com/projects/1028017026/bullets-and-angels-rosary ]]>

In this episode I talk with a few different guest. First is Scott Holden, the host of ‘That Man on Fat Man' and co-host of ‘Bonecrushing Juggernaut', but also director of ‘What is a Podcast?' a documentary on podcasting. Which is on Indiegogo for crowd funding I also talk with Brian Byrd and Sarah Hollis, the writers of the indie comic ‘Bullets and Angels'. We talked about the Kickstarter going for B&A;, but also some of their upcoming work. What is a Podcast? Indiegogo – https://www.indiegogo.com/projects/what-s-a-podcast-a-documentary-film#/story Bullets and Angels' Kickstarter – https://www.kickstarter.com/projects/1028017026/bullets-and-angels-rosary