Wojciech Marlicz’s Post

#CGPR signaling directly via the #pain itself (regardless of the cause) or via a specific #spicy diet or microbiota CGPR production may improve the thickness of mucus and health of the Gut Barrier !!! NOTES: - Mice that lacked these Pain-mediating neurons > mucus thickness was significantly decreased compared with that of the control group > nociceptor neurons might be involved in mucus production > activate the nociceptor neurons, which induced dramatically increased mucus thickness. - Pain signaling > neurons used a signal called #CGRP to communicate with goblet cells > produce mucus. - Gut microbes can cause neurons to produce CGRP and induce goblet cells to produce mucus. - mice that lacked either nociceptor neurons or CGRP were more susceptible to colitis. - #Capsaicin, the ingredient in #Chili peppers found in spicy foods, also induced neurons to produce CGRP and induce mucus production by the gut. - Headaches and migraines > taking drugs to block CGRP or its receptor RAMP1 > blocking this pathway could lead to gut barrier problems, including mucus production and potentially also microbiome problems. - It is already known that blocking CGRP can lead to #Constipation in the gut. - Generally blocking Pain signaling with opioids or other drugs could have unforeseen consequences on gut barrier function or mucus production that we should be cautious about. MyNote: - May #chili and Co. be used for colitis-related illnesses (very interesting controversy)?

Our new publication in the American Journal of Gastroenterology of the American College of Gastroenterology is now online! 🎉 Check it out ahead of print here: https://lnkd.in/e3jkqHwn Yes, it is my first last authorship. "Where are immune cells?", you wonder. I also wonder, dear reader. 🤨 I'll summarize it for you, though. Essentially, we wanted to check whether specific #microbiota parameters could be linked to abdominal #pain in patients with #IBS. It turns out that: - IBS patients have more Staph aureus that have superantigen genes in their stool 💩; - Patients with superantigen-encoding bugs have higher pain scores! 📈 But also: - IBS patients with higher proteolytic activity in the stool also have higher pain scores! 👾 (couldn't find a Pac-man, so it'll have to be a space invader) - P. clara and A. putredinis, which can degrade proteases, are decreased in IBS - On the other hand, B. obeum is increased, which is associated with increased proteolytic activity. This bacterium was predicted by AI to contribute to proteolytic activity, but this remains to be shown - F. prausnitzii (which has nothing to do with proteolytic activity) is decreased in IBS, particularly in patients with severe pain! Bugs bugs bugs 🐛 . Anyway, I'll be getting back to immune cells now 👋

Abdominal aortic aneurysms (AAAs) are a serious condition often linked to aging, with rupture leading to high mortality rates. Currently, there is no effective medical therapy to prevent AAA rupture. The C–C chemokine receptor type 2 (CCR2) pathway plays a critical role in inflammation and extracellular matrix degradation, both of which contribute to AAA formation and rupture. Researchers hypothesized that ketosis could modulate CCR2 and prevent the progression of AAA. In this study, male rats underwent AAA formation and were assigned to one of three interventions: a standard diet, a ketogenic diet (KD), or exogenous ketones (EKB). Rats receiving KD and EKB achieved a state of ketosis and demonstrated a significant reduction in AAA expansion and rupture rates. Rats that received a KD demonstrated the most notable effects. Key findings: 🔷 Reduced AAA expansion: Rats on the ketogenic diet showed a 42% decrease in AAA diameter after 2 weeks compared to controls. 🔷 Lower rupture rates: Rats on the ketogenic diet showed a 67% reduction in rupture rate. 🔷 CCR2 downregulation: Ketosis reduced the expression of CCR2 in the aortic wall, leading to lower inflammation and extracellular matrix degradation. CCR2-knockout mice showed a similar protective effect. 🔷 Improved matrix metalloproteinase (MMP) balance: Active MMP9, which promotes AAA formation, was reduced, while the stabilizing MMP9/TIMP1 complex increased, preserving the aortic wall structure. These results suggest that ketosis could serve as a potential therapeutic approach for stabilizing AAAs and reducing the risk of rupture. Further clinical studies are needed to evaluate its efficacy in humans — Sastriques-Dunlop et al. Ketosis prevents abdominal aortic aneurysm rupture through C–C chemokine receptor type 2 downregulation and enhanced extracellular matrix balance. Sci Rep. 2024;14(1):1438. doi: 10.1038/s41598-024-51996-7. 📌 Link to study: https://lnkd.in/gN8UPmem 📌 Find more research summaries on our website: https://lnkd.in/gKeXEcEN #Keto #KetoDiet #Research

🎉 Just Published! 📚🔬 📝 Paper Title: "Cross-sectional and longitudinal associations of Iron biomarkers and cardiovascular risk factors in pre- and postmenopausal women: leveraging repeated measurements to address natural variability" 🌟I'm thrilled to share that the third paper from my PhD thesis has been published in Cardiovascular Diabetology! 📊 Key Findings: By leveraging both cross-sectional and longitudinal analyses, we uncovered intriguing insights into how these associations evolve over time, highlighting the importance of repeated measurements to capture natural variability. This research delves into the complex relationship between iron biomarkers and cardiovascular disease risk factors among women, with a particular focus on how these dynamics shift in the context of menopause. 🔗 Full Paper: Feel free to check out the full paper here: https://lnkd.in/e5mUWWFx #Research 🧪 #PhD 🎓 #CardiovascularHealth ❤️ #IronBiomarkers 💉 #WomenHealth 👩⚕️ #CardiovascularDiabetology

Researchers at the School of Postgraduate Studies and Research, including Dr Manjula Nandakumar, Dr PRIYA DAS, Professor Alexandra Butler and Professor Stephen Atkin in collaboration with faculty from Hull York Medical School, conducted a cross-sectional study entitled: "Cardiovascular Risk Biomarkers in Non-Obese Women with and without Polycystic Ovary Syndrome: The Role of Vitamin D". The study aims to understand the connection between vitamin D levels and the risk of cardiovascular disease in lean women with and without polycystic ovary syndrome (PCOS), as Vitamin D is believed to help protect against heart and cardiovascular disease, though the mechanism is not clearly understood. Study findings suggested that even though the non-obese women with PCOS did not have high levels of overall inflammation, 9 out of the 54 cardiovascular health proteins that were studied, were elevated compared to the women without PCOS. All 9 of these proteins were related to inflammation, 5 of which correlated with the levels of Vitamin D in the PCOS group, suggesting that even in PCOS patients who do not have obesity or insulin resistance, there may be an ongoing, underlying inflammatory process that is influenced by Vitamin D levels. To read the full research article, visit the link below: https://bit.ly/3yUThSc #RCSIBahrain #Research #PCOSResearch

𝐁𝐞𝐧𝐞𝐟𝐢𝐭 𝐨𝐟 𝐀𝐥𝐛𝐮𝐦𝐢𝐧 𝐈𝐧𝐟𝐮𝐬𝐢𝐨𝐧 𝐢𝐧 𝐚𝐧 𝐄𝐥𝐝𝐞𝐫𝐥𝐲 𝐂𝐢𝐫𝐫𝐡𝐨𝐭𝐢𝐜 𝐏𝐚𝐭𝐢𝐞𝐧𝐭 𝐨𝐧 𝐃𝐎𝐀𝐂 Author: AIT OUALI LAMIA Hypoalbuminemia is frequently observed in decompensated cirrhotic patients, exacerbated by nutritional status, renal insufficiency common that are in elderly patient leading to infectious, hemodynamic, hydroelectrolytic complications and increased bioavailability of certain drugs like DOACs. Albumin perfusion, alone or in combination with other medications, has been suggested for treating various cirrhosis complications [1]. We invite you to look into the case of our patient cirrhotic Child- Pugh A on DOAC that was infused with albumin. 𝐂𝐚𝐬𝐞 𝐏𝐫𝐞𝐬𝐞𝐧𝐭𝐚𝐭𝐢𝐨𝐧 The patient is an 89-year-old female with a history of type II diabetes on diet control, left partial nephrectomy with moderate chronic renal insufficiency, metabolic cirrhosis (NASH) CHILD-PUGH A on DOAC for atrial fibrillation. Admitted to geriatric FRC (Follow-up and Rehabilitation Care) unit for rehabilitation following Oedema-as- cites decompensation due to urinary sepsis. Clinical presentation on arrival and during hospital stay: 𝐂𝐚𝐫𝐝𝐢𝐚𝐜 𝐚𝐬𝐬𝐞𝐬𝐬𝐦𝐞𝐧𝐭: Atrial fibrillation arrhythmia with CHADS VASC score of 5. Dabigatran anticoagulation switched to Eliquis due to worsening renal function with creatinine clearance at 21.5 ml/min. Calcified aortic stenosis (TAVI). Global cardiac decompensation in the context of SARS-CoV-2 infection. 𝐏𝐮𝐥𝐦𝐨𝐧𝐚𝐫𝐲 𝐚𝐬𝐬𝐞𝐬𝐬𝐦𝐞𝐧𝐭: Non-oxygen-requiring SARSCoV2 pneumonia with signs of pulmonary arterial hypertension (PAH). 𝐈𝐧𝐟𝐞𝐜𝐭𝐢𝐨𝐮𝐬: Severe sepsis originating from urinary source with ESBL Klebsiel- la pneumoniae Hepatic side : Edematoascitic decompensation cirrhosis, Elastometry at 46.5 kPA. Renal side : Hepatorenal syndrome. To read full article: https://lnkd.in/gYFXKFss Thanks for Reading, Herald Scholarly Open Access #casereport #gastroenterology #hepatology This post is public so feel free to share it.

𝐑𝐞𝐬𝐞𝐚𝐫𝐜𝐡 𝐭𝐞𝐚𝐦 𝐢𝐧𝐯𝐞𝐬𝐭𝐢𝐠𝐚𝐭𝐞𝐬 𝐝𝐢𝐟𝐟𝐞𝐫𝐞𝐧𝐜𝐞 𝐛𝐞𝐭𝐰𝐞𝐞𝐧 𝐛𝐚𝐛𝐲 𝐟𝐨𝐫𝐦𝐮𝐥𝐚 𝐚𝐧𝐝 𝐡𝐮𝐦𝐚𝐧 𝐦𝐢𝐥𝐤'𝐬 𝐞𝐟𝐟𝐞𝐜𝐭 𝐨𝐧 𝐢𝐧𝐭𝐞𝐬𝐭𝐢𝐧𝐚𝐥 𝐠𝐫𝐨𝐰𝐭𝐡 An article published in Gastro Hep Advances by a team of Yale researchers and led by Lauren Smith, MD, hospital resident, finds parental milk and donor human milk support intestinal health and epithelial growth and differentiation, while formula specifically inhibits certain growth factors and prevents differentiation. Researchers also discovered that growth and improvement for certain cell types, like enteroendocrine cells that support proper digestion and peristalsis, were improved specifically with parental milk. https://lnkd.in/duSJGZcn

It's terrifying and concerning. High levels of triglycerides in the blood raise the risk of heart disease and stroke. When we have higher circulating triglycerides, it is NOT good. Researchers at Mayo Clinic showed that higher triglycerides could lead to hypertriglyceridemic acute pancreatitis (1) (1) https://mayocl.in/48PkVOd ADDReB Lab of Stanford Cardiovascular Institute collaborated with Chun's lab at Yale on this critical issue of what causes fatty acid deposition to the organs #2. Chun's lab showed that increasing apelin signaling prevents organ fatty acid deposits. Apelin signaling decreased endothelial FABP4 and prevented excess tissue FA accumulation. The bottom line is that EXERCISE or improving apelin signaling is curative to many complications. #2 https://lnkd.in/gT3aFDaA Euan Ashley, Joseph C. Wu, Michael Snyder, Hyung Chun

Check our latest publication "Glycolytic Lactate in Diabetic Kidney Disease" at the JCI insight! This elegant work was led by Dr. Kumar Sharma, in collaboration with Dr. David Z.I. Cherney (University Health Network , Toronto, Canada), the Kidney Precision Medicine Project, and Chronic Renal Insufficiency Cohort Study (CRIC) study investigators. Congratulations to Dr. Manjula Darshi and all co-authors! Link to publication: https://lnkd.in/gSM-nzmC Key highlights: ✔ This study explores lactate as a biomarker for mitochondrial dysfunction in Diabetic Kidney Disease (DKD). ✔ Elevated urine lactate in DKD patients in HUNT3, SMART2D, and CRIC cohorts. ✔High urine lactate/creatinine levels linked to faster kidney function decline. ✔ Lactate production in T1D patients connected to glucose levels, with SGLT2 inhibition reducing lactate production.

In this week’s Research Review, we delve into the critical relationship between periodontal disease, oral health, and systemic health. Emerging research underscores that the health of our gums and teeth significantly influences overall well-being, with periodontal disease serving as a key indicator of age-related decline and its potential impact on systemic conditions such as cardiovascular disease and diabetes. Periodontal disease encapsulates several hallmarks of aging, illustrating how chronic inflammation can lead to substantial tissue damage and systemic health complications. One promising therapeutic approach gaining attention is low-dose rapamycin, which has shown potential in addressing these challenges. By effectively reducing systemic inflammation and enhancing autophagy, rapamycin helps to mitigate the destructive cycle of inflammation and tissue degeneration associated with periodontal disease. This dual action not only protects gum health but also contributes to a rejuvenation of oral tissues, restoring them to more youthful levels. In this Research Review, authored by Shreshtha Jolly from the Johns Hopkins Department of Molecular Biology, we will explore the mechanisms through which rapamycin exerts its effects on periodontal health. We will examine how its modulation of inflammatory pathways and promotion of autophagy can improve tissue repair and regeneration, thereby offering a novel therapeutic strategy for enhancing oral health. Through this lens, we gain valuable insights into the interconnectedness of oral health and systemic well-being, emphasizing the importance of managing periodontal disease as part of a holistic approach to healthspan. https://lnkd.in/gg79ZZJH