Podcasts about pmns

The retail media juggernaut is showing no signs of slowing down as retailers seize the opportunity to monetize first-party consumer data. Payments media networks (PMNs) are emerging as the next frontier, extending the reach of CPG advertising while revolutionizing the loyalty landscape.From empowering CPG brands to connect with millions of banking customers to providing loyalty benefits for shoppers and top-of-wallet status for banks, PMNs are reshaping the retail advertising ecosystem in profound ways. As president of SnippMedia, Tom Burgess is leveraging his years of digital advertising and loyalty experience to ignite exciting new opportunities in the payments media space.Carol and Tom discuss the multi-stakeholder benefits of payments media networks along with best practices, pitfalls, and future possibilities as retail media and payments media networks converge.Highlights from the interview:·       How PMNs complement and amplify the benefits of retail media networks. ·       Why flexible redemption models enhance shopper participation and loyalty.·       How SKU-level offers are changing the PMN game.·       Why offsetting interchange fees is no longer an elusive goal for retailers. Guest contact information:SnippMediaTom Burgess on LinkedInWant to be a guest on Spieckerman Speaks Retail? Contact team@spieckermanretail.comCheck out more of Carol's retail insights and updates Follow Carol on LinkedInFollow Carol on Twitter

This week we're myth-busting! The Inner Critic is a popular name for that inner voice who is known to tear us down when we're 'PMNS-ing', but Melanie Swan, womb medicine woman at @the_sacred_womb wants to realise this isn't normal, its not something we should learn to work with, but is in fact one way trauma shows up in our menstrual cycle. Melanie and I are talking about this myth of the inner critic: why it happens, how to heal it, and Melanie shares an easy, practical, beautiful exercise that you can do straight away towards the end of this episode to connect in with your womb and this voice. Melanie goes deep on: How this inner critic has evolved into being, and why we relate to this voice as an inner critic, How it's related to trauma that's held in the body, and How we can work through patterns that are coming up in this lifetime and past lifetimes as well to understand the origin of this inner critic,As well as how to release it's hold from our lives and cycles. So if you experience what you call an inner critic voice, particularly in the pre-menstrual phase of your cycle - or at any other phase as well - then this is going to be a really great one to listen to.Come find me on Instagram and leave a comment! How does your inner critic show up? Can you connect with it as trauma? Has it felt like something you just have to accept and live with? Are you curious about past life healing through the womb? Let me introduce Mel. Besides being a Midland gal from the UK like me, Melanie is a Womb Medicine Woman and Multi-dimensional trauma healer who helps women to come home to their true nature by embodying the multi-faceted menstrual cycle, healing multi-dimensional trauma & co-creating with the divine through the portal of the Womb. Ooh how amazing does that sound.Connect with Mel at https://www.thesacredwomb.com, and tune into her podcast here.Happy listening! Don't forget to subscribe and please share with a cycle sister, leave a rating, or even better yet, a review. Thank you! Charlotte xxxThanks so much as ever for supporting me to host Wild Flow Podcast! It means such a lot to receive your ratings, reviews, and to be tagged in your IG stories @charlotte.pointeaux.coach! Please share with your soul sisters who are learning to honour their cycles and live as an embodied cyclical woman too, so they can receive the wisdom they're searching for. Find the full show notes at https://charlottepointeaux.com/podcast/ Charlotte xxx PS: Would you love to belong to a soul-nourishing sisterhood of women who are deeply connected to their inner seasons, cycles and body's wisdom? If so, I'd love to invite you to become a treasured member of our Wild Flow Coven membership and Subscribe for your free cycle magick rituals guides. Want to dive deeper and be held in your own private container for inner healing? Find my coaching and programs here at https://charlottepointeaux.com/coaching/

This week I sat down with Dr. Richard E. Engler, B&C's and The Acta Group's (our consulting affiliate) Director of Chemistry, to discuss the new chemical bias. Our listeners know that Rich Engler has worked for decades reviewing Premanufacture Notifications submitted under the Toxic Substances Control Act (TSCA). PMNs are applications to manufacture or import chemical substances that are not listed on the TSCA Inventory and thus are considered “new.” Much has changed in terms of the new chemical review process since Congress revised TSCA six years ago. As we discuss in our podcast, however, one thing has not changed: the new chemical bias is as potent today as it was before Lautenberg was enacted in 2016. Rich and I discuss the new chemical bias, explain why it continues to confound chemical innovators, and what is being done to eliminate the bias and level the playing field. ALL MATERIALS IN THIS PODCAST ARE PROVIDED SOLELY FOR INFORMATIONAL  AND ENTERTAINMENT PURPOSES. THE MATERIALS ARE NOT INTENDED TO CONSTITUTE LEGAL ADVICE OR THE PROVISION OF LEGAL SERVICES. ALL LEGAL QUESTIONS SHOULD BE ANSWERED DIRECTLY BY A LICENSED ATTORNEY PRACTICING IN THE APPLICABLE AREA OF LAW. ©2022 Bergeson & Campbell, P.C.  All Rights Reserved

In our final stop in our Cytopenias series, we discuss the ins and outs of neutropenia. This is another very commonly seen issue in the clinic and in the hospital so most definitely high yield!Why is neutropenia dangerous?Prone to infections, especially gut translocation of bacteriaDefinition of neutropenia:NORMAL: WBC 4400-11000 cells/microL; neutrophils make up 40-70% of thatNeutropenia defined by ANC: WBC (cells/microL) x percent (PMNs + bands) ÷ 100 Breakdown:Neutropenia: ANC

  Contributor: Sam Killian, MD Educational Pearls: Spontaneous bacterial peritonitis (SBP) is an infection of peritoneal fluid that typically occurs in cirrhotic patients Symptoms may include abdominal pain, fever, and/or altered mental status Paracentesis is diagnostic test of choice. Diagnostic criteria includes > 250 polymorphonuclear cells (PMNs) or a positive gram stain/culture Treatment is typically a 3rd generation cephalosporin ·30-40% of SBP patients will go into renal failure and SBP associated with sepsis has an ~80% mortality References Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis--bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther. 2015 Jun;41(11):1116-31. doi: 10.1111/apt.13172. Epub 2015 Mar 26. PMID: 25819304. MacIntosh T. Emergency Management of Spontaneous Bacterial Peritonitis - A Clinical Review. Cureus. 2018 Mar 1;10(3):e2253. doi: 10.7759/cureus.2253. PMID: 29721399; PMCID: PMC5929973.   Summarized by Jackson Roos, MS4 | Edited by Erik Verzemnieks, MD   The Emergency Medical Minute is excited to announce that we are now offering AMA PRA Category 1 credits™ via online course modules. To access these and for more information, visit our website at www.emergencymedicalminute.com/cme-courses/ and create an account. 

Session 22 Today, we tackle a pathophysiology question related to pancreatitis. Once again, we're joined by Dr. Karen Shackelford from BoardVitals. Check out their QBanks containing 1,700+ questions for Step1/Level 1. Use the promo code BOARDROUNDS to save 15% off. [01:50] Question of the Week A 45-year-old male presents to the hospital with abdominal pain and vomiting. He began to experience a dull pain in the epigastrium two days prior to admission that has progressively worsened. The pain radiates to his back. He's had several episodes of bilious non-bloody vomiting. He has no prior medical conditions. And he takes no medications. He has a 20-pack per history of tobacco and drinks 6-10 beers daily. The vital signs vary, has a temperature of 100 degrees Fahrenheit, and a heart rate of 102 beats per minute. He appears uncomfortable. On exam, his abdomen is soft and mildly distended, with marked right upper quadrant in epigastric tenderness to palpation. There is no rebound or guarding. He has hypoactive bowel sounds and no palpable masses or hepatosplenomegaly are appreciated. Laboratory studies through the hemoglobin of 12.8 g/dL, leukocytes 14,500 cells per mm3, with 81% PMNs and 16% lymphocytes. Platelet count is 178,000 and total bilirubin is 1gm/dL with the direct bilirubin of 0.4 g/dL. Alkaline phosphatase is 90 IU/L and aspartate aminotransferase (AST) is 88, alanine aminotransferase is 78, and serum amylase is 1,447 IU/L. What is one of the pathophysiological mechanisms of this patient's condition? (A) Pancreatic duct obstruction due to a stone (B) Activation of pancreatic stellate cells (C) Viral infection (D) Intraductal stone formation (E) Toxic fatty acids in pancreatic microcirculation [04:00] Thought Process Behind the Correct Answer Hemoglobin is normally low. White blood cells are minimally elevated. Platelets are normal. Bilirubin is a little bit elevated. Alkaline phosphatase is slightly elevated as well as the aspartate aminotransferase (AST), alanine aminotransferase and amylase. The condition of the patient is actually pancreatitis. The lipase is also slightly elevated which is more specific for pancreatitis and amylase which can be released by other cells as well. The most common cause of pancreatitis is gallstone pancreatitis but this guy has a history of pretty heavy drinking. The second most common cause of pancreatitis is related to alcohol. It's not clear though exactly how they're related but most chronic alcoholics do not end up with chronic alcoholic pancreatitis. But there may also be other risk factors to be considered here. One of the mechanisms is the hyperactivation of the pancreatic stellate cells. These cells that get activated by alcohol as well as by acetaldehyde. They regulate the deposition and the degradation of the pancreatic extracellular matrix protein. They secrete the matrix proteins and metalloproteinases that degrade the matrix proteins. So they regulate all the extracellular matrix proteins in the pancreas. Whenever they're overactivated by phenol and acetaldehyde, the metabolite of ethanol, the matrix becomes fibrotic. That's one of the mechanisms of chronic pancreatitis. Another interesting thing is that the stellate cells also express ADH and whenever overactivated, it seems to perpetuate a cycle of autocrine reactivation. So it's self-perpetuated. Another mechanism of alcoholic pancreatitis is that the alcohol is metabolized by both oxidative and non-oxidative mechanisms. There are changes in acinar cells that increase the activation of intracellular digestive enzymes. Hence, there's an autodigestive component. There is a transient decrease in pancreatic blood flow that results from the action of ethanol. 10:17 There's also an increase in ductal permeability related to alcohol use. It then makes it possible for these improperly activated enzymes to leak out of the duct into the surrounding tissue which just adds to the inflammation and fibrosis. Any of those mechanisms could be asked on the USMLE. [11:00] Understanding the Other Answer Choices It's not completely known what causes pancreatitis. After an obstruction, there's an increase in pancreatic pressure. Studies showed that the flow of biliary salts itself does not cause pancreatitis. This patient doesn't have a previous history given the biliary colic. Bilirubin is relatively normal and patients with a stone obstruction usually have a direct hyperbilirubinemia. The viral infection mumps and Kawasaki virus have been implicated in some sporadic cases of pancreatitis. But this is unusual and this patient doesn't have a history of it. Intraductal stone formation is what causes pancreatitis in patients who have hypercalcemia due to hyperparathyroidism or some other conditions. They usually have additional features mentioned in the history that are associated with hypercalcemia. These may include constipation or kidney "stones, bones, groans, and moans." Finally, fatty acid deposition with ensuing inflammation is the mechanism of pancreatitis in patients who have familial hyperlipidemia. They have those really high triglycerides. They would usually have other features mentioned like xanthelasma or early atherosclerosis or family history. Links: BoardVitals (Use the promo code BOARDROUNDS to save 15% off.)

Anaplasma phagocytophilum (Ap) is a gram-negative, obligate intracellular bacterium that is able to infect different animal species and humans worldwide. Based on DNA sequencing, Ap has newly been reallocated from the genus Ehrlichia to the genus Anaplasma in the family Anaplasmataceae (DUMLER et al. 2001). In humans and animals, the clinical signs of Ap infection vary from mild symptoms to severe clinical outcomes, including death. However, the disease generally presents as undifferentiated fever accompanied by leucopenia, thrombocytopenia and increased serum transaminase activities (DUMLER et al. 2005; DUMLER et al. 2007; RIKIHISA 2011). Hard-bodied ticks of the genus Ixodes (family Ixodidae) are the main vectors for Ap dissemination. Compared to other pathogens such as Neorickettsia and Wolbachia spp., which can be transmitted from adult ticks to their offspring, Anaplasma and Ehrlichia spp. are the only Rickettsiales that are not transmitted transovarially (RIKIHISA 2011). Thus, ticks need to acquire Ap through blood feeding from infected hosts to complete the life cycle of Ap. During attachment of the tick, the bacterium is released by salivary secretion and is transmitted to the host. It is known that Ap multiplies within membrane-bound vacuoles (or called ‘morulae’) in the cytoplasm of peripheral granulocytes. The binding and infection of bacteria depends on the tetrasaccharide sialyl Lewisx (sLex or CD15s) of P-selectin glycoprotein ligand 1 (PSGL-1) on the surface of host cells, a factor expressed on peripheral granulocytes and HL-60 cells (GOODMAN et al. 1999; HERRON et al. 2000; RENEER et al. 2006; RENEER et al. 2008). Only little information is known about the transmission pathway of Ap after tick bite in the very early stage of infection. It is described that Ap is able to evade and replicate within microvascular endothelial cells in vitro (MUNDERLOH et al. 2004), while endothelial cells lining the inner lumen of blood vessels allow them to easily interact with any circulating blood cells. Since granulocytes do not return back to the blood stream after extravasation, it is reasonable to postulate that Ap evades and replicates within microvascular endothelial cells in the initial transmission, and subsequently transmits into peripheral granulocytes for ongoing dissemination. Therefore, the objective of the study was to establish a flow culture model that mimics the physiological environment in the blood vessel to study the possible transmission pathway of Ap between endothelial cells and polymorphonuclear leukocytes (PMNs). For this purpose, a novel ex vivo flow culture system was established. For experimental setup, human microvascular endothelial cell line (HMEC-1) and primary human dermal microvascular endothelial cells (HDMEC) were used. Under static conditions, Ap evades endothelial cells within 24 h, supporting the hypotheses that endothelial cells might be the first infection site of the pathogen in the host. Thereby a high level of interleukin-8, a chemokine that is known to recruit PMNs, secreted by Ap-infected endothelial cells was detected. Using the investigated flow culture model, it was shown for the first time, that Ap is able to translocate from endothelial cells to PMNs under dynamic flow conditions. Furthermore, under defined shear stress, an increased binding of PMNs to Ap-infected endothelial cells monolayer was observed, resulting from the elevated expression of adhesion molecules associated with PMNs recruitment on endothelial cells. The flow culture model investigated in this study can be used to study the interaction between Ap-infected endothelial cells and PMNs under physiological flow conditions, and is therefore helpful to study the infection mechanism in the early stage of Ap dissemination in the host.

Chronische Extremitätenischämien stellen eine sowohl subjektiv belastende als auch volkswirtschaftlich bedeutende Krankheitsentität dar. Dabei können etliche Patienten mit den zur Verfügung stehenden konventionellen Verfahren nicht befriedigend therapiert werden. Neuere Konzepte zur Zelltherapie der chronischen Therapie führten in der klinischen Erprobung dabei zu eher ausbaufähigen Resultaten. Unsere Gruppe konnte in Vorarbeiten zeigen, dass die exogene Applikation embryonaler Endothelprogenitorzellen (eEPCs) im Tiermodell zu einem deutlichen Effet auf die chronische Ischämie führt. Um diesen Effekt weiter zu steigern, wurde ein künstliches Fusionsmolekül aus dem Chemokin SDF-1 als Kopf, der Mucindomäne des Fractalkine als Rückgrat und einem GPI-Teil zur Verankerung im Endothel (SDF-Fractalkine-GPI oder S1FG) kloniert. Wir konnten ebenfalls in Vorarbeiten zeigen, dass dieses S1FG eEPCs in vitro und in vivo rekrutiert, und dass eine Vortransfektion des Endothels des Ischämiegebietes vor Applikation der eEPCs zu einer Steigerung des funktionellen Effekts führt. Wir stellten die Hypothese auf, dass ein Ersatz der exogenen Applikation der eEPCs durch eine Mobilisierung endogener vaskulärer Progenitorzellen ebenfalls zu einem guten funktionellen Effekt führt. Weiterhin sollte der genaue Rekrutierungsmechanismus des S1FG untersucht werden. Zur Untersuchung des funktionellen Effekts wurde wie in den Vorarbeiten ein Kaninchenmodell der chronischen Hinterlaufischämie gewählt, bei dem an Tag 0 die rechte Femoralarterie entfernt wurde. Nach Entwicklung eines chronischen Zustandes wurde am Tag 7 eine Angiographie beider Femoralisstromgebiete durchgeführt und entweder S1FG oder eGFP liposomal per Retroinfusion transfiziert. An den Tagen 9, 10 und 11 wurde jeweils 1 mg des kurzwirksamen CXCR4-Antagonisten AMD3100 oder 1 ml NaCl intraperitoneal injiziert. An Tag 35 wurde eine erneute Angiographie durchgeführt, das Tier getötet und die Hinterlaufmuskulatur entnommen. Die Angiogenese wurde über die mittels PECAM-1-Färbung bestimmte Kapillardichte gemessen, die Arteriogenese über die Mengenzunahme der in der Angiografie sichtbaren Kollateralen. Zur Messung der Perfusion wurden die Flussgeschwindigkeit in der Angiographie sowie fluoreszierende Mikrosphären verwendet. Um das Rekrutierungsprofil des S1FG in vitro zu eruieren, wurden statische Adhäsionsversuche mit PMNs auf transfizierten HMECs sowie Adhäsionsversuche in Flusskammern von THP-1-Zellen auf transfizierten HUVECs verwendet. Es zeigte sich, dass signifikant weniger PMNs auf S1FG-transfiziertem Endothel adhärieren, als auf Fractalkine-transfizierten HMECs, während die eEPC-Adhäsion signifikant besser war. Bei den Versuchen unter Schubspannung ergab sich durch S1FG-Transfektion keine signifikante Änderung der Anzahl rollender Zellen, während die Anzahl fest haftender Zellen signifikant höher war. Durch Zugabe eines L-Selektin-Antikörpers zu den THP-1-Zellen vor Superfusion konnte die Anzahl fest haftender Zellen wieder auf Kontrollniveau reduziert werden, während die Anzahl rollender Zellen leicht reduziert wurde. Zugabe von AMD3100 führte dort nicht zu einer signifikanten Änderung der Anzahl adhärierender Zellen, jedoch wurde durch AMD3100 die Stärke der Interaktion, gemessen als Anzahl nach Applikation hoher Flüsse noch adhärierender Zellen, wieder auf Kontrollniveau reduziert. Ein über andere Adhäsionsmoleüle vermitteltes Zellrollen ist also vermutlich eine Voraussetzung für eine adäquate S1FG-Funktion. Dabei würde es über SDF-1-CXCR4-Interaktion zu einer Erhöhung der Festigkeit der Bindung kommen. In Bezug auf den funktionellen Effekt im Tiermodell führte Verwendung von S1FG und AMD3100 zu einer signifikanten Steigerung von Kapillardichte, Kollateralenwachstum und Perfusion gegenüber der Kontrolle. Die Werte lagen dabei im selben Bereich wie durch Verwendung von S1FG und eEPCs erzielte Ergebnisse. Transfektion von S1FG ohne weitere Behandlung führte nicht zu einer signifikanten Änderung eines Parameters zur Kontrolle, während die Verwendung von AMD3100 zu moderaten Steigerungen bei Kapillardichte, und Kollateralenwachstum führte. Die Werte waren jedoch immer noch signifikant geringer als die nach Kombination von S1FG und AMD3100 erreichten Werte. Verwendung einer proteaseresistenten, funktionell jedoch aktiven Mutante für das SDF-1 im S1FG-Molekül führte nicht zu signifikanten Änderungen bei funktionellen Parametern, bis auf eine zwar signifikante, quantitativ jedoch geringe Verringerung des Kollateralwachstums. Zusammenfassend kann man sagen, dass die lokale Applikation eines künstlichen Adhäsionsmoleküls gemeinsam mit einer Mobilisierung knochenmarksständiger endothelialer oder vaskulärer Progenitorzellen zu einem deutlichen funktionellen Effekt führt, der den der Zellmobilisierung ohne Adhäsionssteigerung übertrifft. Dennoch birgt der Ansatz einige Risiken, wie die versehentliche Förderung von Tumorangiogenese oder die Beschleunigung des Wachstums atherosklerotischer Plaques. Zusätzlich bleibt unklar, welche Zellen genau durch das Adhäsionsmolekül rekrutiert werden, und ob es sich überhaupt um eine homogene Zellpopulation handelt. Weiterhin bleibt zu überprüfen, in welcher Weise die Wirksamkeit der Therapie durch chronische Defekte der Progenitorzellmobilisierung und -funktion, wie sie beispielsweise bei Diabetes oder Nikotinabusus auftreten, beeinträchtigt wird, und ob gegebenenfalls Optimierungsmöglichkeiten in Bezug auf das Mobilisierungsregime, den Aufbau des Adhäsionsmoleküls oder die Applikationsart bestehen. Nichtsdestotrotz stellt diese Methode einen vielversprechenden neuen Ansatz zur Verbesserung der bisher eher zwiespältigen Ergebnisse der Zelltherapie dar.

1. Bei Patienten mit FL kommt es in der Akutphase der Erkrankung zu einer neutrophilen Alveolitis. In der Lavageflüssigkeit dieser Patienten fanden sich im Vergleich zu gesunden Normalpersonen erhöhte Spiegel an IL-8. Die Lavageflüssigkeit hatte eine verstärkte chemotaktische Aktivität gegenüber PMNs im Vergleich zur Lavageflüssigkeit von gesunden Kontrollpersonen. Nach Neutralisation von IL-8 durch Zugabe von Anti- IL-8-Antikörpern konnte ein signifikanter Rückgang der Chemoattraktion von PMNs durch die Lavageflüssigkeit festgestellt werden. 2. Es fand sich eine signifikante Korrelation zwischen der chemotaktischen Aktivität der Lavageflüssigkeit auf PMNs sowohl mit den in der Lavageflüssigkeit enthaltenen Endotoxinspiegeln als auch den in der Lavageflüssigkeit enthaltenen Spiegeln an IL-8. 3. Nach Stimulation mit Heustaub reagierten Alveolarmakrophagen mit der Sekretion von TNF-alpha, IL-6 und IL-8. Aus diesen Ergebnissen lässt sich folgendes Modell für die Pathogenese des akuten Schubs der FL ableiten: Im Heustaub enthaltenes Endotoxin stimuliert nach Inhalation Alveolarmakrophagen zur Sekretion von proinflammatorischen Zytokinen. Diese führen zu einer systemischen und lokalen Entzündungsreaktion. Sezerniertes IL-8 bewirkt eine neutrophile Alveolitis. Die von aktivierten PMNs ausgeschütteten Proteasen greifen das Strukturgerüst der Lunge an und stören die strukturelle Integrität der Lunge. Durch den in der Folge einsetzenden Regenerationsprozess mit Proliferation von Fibroblasten kommt es zur Ausbildung einer Lungenfibrose.

Wed, 1 Jan 1992 12:00:00 +0100 https://epub.ub.uni-muenchen.de/10293/1/10293.pdf Schönharting, M.; Dammer, U.; Arbogast, Helmut; Stiegler, H.; Strohmenger, R.; Meier-Ewert, H.; Dendorfer, A.; Nees, S.