Veronica Ferrer

📖 Welcome to read the latest publication from the Journal of #Molecular #Pathology: Exploring the Molecular Pathology of #Iatrogenic #Amyloidosis, by Dr. Bernardo Bonilauri from Stanford University. 🔗https://lnkd.in/eukKbZfu #JMP #pathologist

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We are happy to share a paper from our ELAINE members Dr. Mareike Fauser, Jan Philipp Payonk, Hanna Weber, Meike Statz, Dr. Revathi Appali, Prof. Ursula van Rienen, and Prof. Alexander Storch published in Frontiers in Cellular Neuroscience! The paper is entitled "Subthalamic nucleus but not entopeduncular nucleus deep brain stimulation enhances neurogenesis in the SVZ-olfactory bulb system of Parkinsonian rats". It investigated the effects of deep brain stimulation (DBS) in the subthalamic nucleus (STN) and the entopeduncular nucleus (EPN) on neurogenesis in 6-hydroxydopamine (6-OHDA)-lesioned hemiparkinsonian rats. If you are curious about the details, you can find the article under the following link: https://lnkd.in/eHYGvttg.   We want to thank all authors for their hard work and dedication, and a special mention to Deutsche Forschungsgemeinschaft (DFG) - German Research Foundation for their funding support.   Please feel free to check out the paper and share your thoughts.

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Chemotherapy kills cancer cells. But the way these cells die appears to be different than previously understood. Researchers from the Netherlands Cancer Institute, led by Thijn Brummelkamp, have uncovered a completely new way in which cancer cells die: due to the Schlafen11 gene. "This is a very unexpected finding. Cancer patients have been treated with chemotherapy for almost a century, but this route to cell death has never been observed before. Where and when this occurs in patients will need to be further investigated. This discovery could ultimately have implications for the treatment of cancer patients." They publish their findings in Science. Many cancer treatments damage cell DNA. After too much irreparable damage, cells can initiate their own death. High school biology teaches us that the protein p53 takes charge of this process. p53 ensures repair of damaged DNA, but initiates cell suicide when the damage becomes too severe. This prevents uncontrolled cell division and cancer formation. That sounds like a foolproof system, but reality is more complex. "In more than half of tumors, p53 no longer functions," says Thijn Brummelkamp. "The key player p53 plays no role there. So why do cancer cells without p53 still die when you damage their DNA with chemotherapy or radiation? To my surprise, that turned out to be an unanswered question." His research group then discovered, together with the group of colleague Reuven Agami (both research groups are part of Oncode Institute), a previously unknown way in which cells die after DNA damage. In the lab, they administered chemotherapy to cells in which they carefully modified the DNA. Thijn: "We were looking for a genetic change that would allow cells to survive chemotherapy. Our group has a lot of experience in selectively disabling genes, which we could perfectly apply here." Read more ➡️ https://bit.ly/3WJSCwA #NKI #science #chemotherapy

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Rita Almeida Calado, Joao Conde and collaborators developed a preclinical antibiotic-free cationic surfactant-based cellulose hydrogel for treating sexually transmitted infections. The N-dodecylpyridinium bromide (C12PB)-hydrogels provided sustained surfactant release, enhancing their biocompatibility and antibacterial activity without inflammation or epithelial disruption of the vaginal tract. In a preclinical model of Neisseria gonorrhoeae infection, a single application of the C12PB-hydrogel showed a 2- to 3-fold reduction in infection. This lays the foundation for the future development of C12PB-hydrogels for sexually transmitted infections, demonstrating potent antibacterial activity and minimal risk of antimicrobial resistance or inflammation. #Matter https://lnkd.in/ezae8dWe

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#Sleep2024 is less than a month away, and like last year, Onera Health is warming up to the scientific discourse by sharing a series of interesting developments in our field! The start marks an exciting research breakthrough in narcolepsy type 1 diagnosis! A recent study by Marco Vilela et al. used machine learning techniques on polysomnography (PSG) data to identify key sleep features that help distinguish narcolepsy type 1 from other hypersomnolence disorders. The researchers analyzed quarter-night periods of sleep and found nuanced sleep patterns, emphasizing the importance of temporal dynamics in sleep assessment. Notably, they found that rapid eye movement sleep onset is a significant marker. These findings highlight the need for thorough sleep evaluations in diagnostic protocols and treatment effectiveness assessments, underscoring the essential role of innovative PSG systems like the Onera STS in advancing sleep medicine. Learn more about the study here: https://lnkd.in/eHrH7Dny For more information about the Onera STS, visit https://lnkd.in/efN_Mixf #MedicalDevices #SleepDiagnostics #SleepMonitoring #Polysomnography #ClinicalStudies

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When Dr. Alexander Hoischen, Professor of Genomic Technologies for Immune-Mediated and Infectious Diseases at Radboud University Medical Centre Nijmegen, the Netherlands discovered optical genome mapping (#OGM), the workflow reignited his excitement about the potential of structural variant detection to impact rare genetic disease research. OGM's intrinsic simplicity makes it a powerful tool in Dr. Hoischen's rare immune disorder research. Learn more about Dr. Hoischen's work and why he believes that the greatest expansion of use cases for new techniques like OGM will come from users working together to solve challenging rare diseases and move the field forward. Watch here 👉 https://bit.ly/45B7kZb #raredisease #rarediseaseresearch #geneticdisorders #geneticdiseaseresearch #Bionano #MoveForward

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New research from the Frontiers in Congenital Disorders of Glycosylation Consortium (FCDGC): ✅ Exploring #Proteomics and N-#Glycoproteomics in ALG1-#CongenitalDisorderOfGlycosylation (CDG) ✅ Exploring the #Neurological Characteristics of PMM2-CDG Using Human In Vitro Neural Models Listen and read more: https://lnkd.in/d9tgrVZF

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In a groundbreaking study published in Springer Nature Group's Nature Cell Biology, researchers from the Mass General Cancer Center have identified a gene that plays a pivotal role in the spread of cancer cells throughout the body. This gene, known as Gstt1, is crucial for metastatic cancer cells to modify their environment and thrive in new locations. 🧬 The study reveals that Gstt1 encodes an enzyme part of a superfamily that protects cells from toxins. More importantly, it allows cancer cells to alter and secrete fibronectin, a protein essential for cell attachment to the extracellular matrix. 🎯 Silencing the Gstt1 gene in lab models prevented metastatic growth, offering a beacon of hope for new treatment strategies, particularly for pancreatic cancer patients who often face a diagnosis at the metastatic stage. 💡 This discovery is not just a scientific triumph but a potential lifesaver. It underscores the importance of persistent research and innovation in the battle against cancer. 🤝 Join us in applauding the Mass General Cancer Center team for their dedication and breakthrough that may pave the way for novel therapeutic avenues targeting metastatic cancer, which is responsible for 90% of cancer-related deaths. cc: Dr. Jessica Lin, Dr. Justin Gainor #CancerResearch #Metastasis #Genetics #Innovation #Healthcare #ScienceNews https://lnkd.in/dH5yBKrM

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𝗟𝗮𝗯-𝗠𝗮𝗱𝗲 𝗦𝘂𝗴𝗮𝗿𝘀 𝗮𝗻𝗱 𝗡𝗮𝗻𝗼𝗯𝗼𝗱𝗶𝗲𝘀 𝗳𝗿𝗼𝗺 #𝗔𝗹𝗽𝗮𝗰𝗮𝘀 𝗔𝗴𝗮𝗶𝗻𝘀𝘁 #𝗖𝗮𝗻𝗰𝗲𝗿: 𝗢𝗿𝗲𝗻 𝗠𝗼𝘀𝗰𝗼𝘃𝗶𝘁𝘇 𝗪𝗶𝗻𝘀 𝗣𝗿𝗲𝘀𝘁𝗶𝗴𝗶𝗼𝘂𝘀 𝗛𝗲𝗿𝗺𝗮𝗻𝗻 𝗡𝗲𝘂𝗵𝗮𝘂𝘀 𝗣𝗿𝗶𝘇𝗲: Dr. Oren Moscovitz has been awarded €25,000 by the Max Planck Society for his promising research toward treatments and non-invasive diagnostics for cancer, which could potentially reduce overall cancer-related deaths. Moscovitz and his team exploit unique sugar patterns found on cancer cells and develop ultra-small antibodies from alpacas (known as nanobodies) that bind to these sugars. Two start-ups are already working to bring these findings closer to public fruition. Dr. Oren Moscovitz started as a group leader at the Max Planck Institute of Colloids and Interfaces in 2018, focusing his efforts on cancer. "I firmly believe that the sugar layer that surrounds all our cells holds the solution to drastically reduce the nearly 10 million cancer-related deaths worldwide each year," he explains, "We just need the right keys to unlock it.” Moscovitz is committed to an ambitious goal: expanding the toolbox available for fighting cancer, from early non-invasive diagnosis to tailored therapy. The Max Planck Society recognized the potential impact of his research and the start-ups he launched with the Hermann Neuhaus Prize (€25,000). 𝗧𝘄𝗼 𝘀𝘁𝗮𝗿𝘁-𝘂𝗽𝘀 𝗮𝗿𝗲 𝗮𝗹𝗿𝗲𝗮𝗱𝘆 𝘄𝗼𝗿𝗸𝗶𝗻𝗴 𝘁𝗼 𝗯𝗿𝗶𝗻𝗴 𝘁𝗵𝗲𝘀𝗲 𝗳𝗶𝗻𝗱𝗶𝗻𝗴𝘀 𝗰𝗹𝗼𝘀𝗲𝗿 𝘁𝗼 𝗽𝘂𝗯𝗹𝗶𝗰 𝗳𝗿𝘂𝗶𝘁𝗶𝗼𝗻: https://lnkd.in/ecM9W-jy

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A team from ZHAW Zurich has showcased the transferability of CHO-cell-based mAb production processes from geometrically dissimilar stirred bioreactors for fed-batch and perfusion processes, the team has opened up new possibilities for cost savings and increased yields. Their study found that the high volumetric productivity in the perfusion processes can lead to cost savings, smaller bioreactor sizes, and maintained manufacturing capacity in production plants. Alternatively, yields could be increased by a factor of 2.8 to 3.2 while still using the same bioreactor size. We look forward to seeing how it will impact the future of antibody production. #biotech #antibodyproduction #research https://lnkd.in/eA9992FV

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Our #NFDITalk next Monday is about FAIR Data in #Immunology. 📅 1 July 4 PM – Online    🎤 Speaker: Dr. Christian Busse (Speaker of NFDI4Immuno)   ℹ About the talk: Immunologists observe the immune system on various levels of detail, ranging from molecular measurements to clinical trials, and utilize a diverse set of experimental methods. In this talk we will have a look at the recent progress, but also on the remaining challenges, in managing the heterogeneous data types that are produced in the course of such studies.   ➡ Join the Zoom Meeting: http://www.nfdi.de/talks   ➡ YouTube stream: https://lnkd.in/eQekvAYU #rdm #fdm #researchdata

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Glycosylation, a process activated in asthma and other lung disorders, can be used to develop novel biomarkers and treatments. In this review we discuss key glycoproteins whose functions control lung disease development.  CHIT1 by modulating the process of glycosylation is an attractive therapeutic target affecting multiple molecular pathways. OATD-01 is the only clinical stage CHIT1 inhibitor, currently in Phase II with lung sarcoidosis patients. #lungs #drugdevelopment #sarcoidosis #asthma #glycobiology #macrophages #clinicaltrails

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Morphogens ensure that we develop two arms and ten fingers. Check out this interesting article in the Swiss research magazine "Horizons" about the Affolter lab's research on unraveling the role of these molecules in embryonic development using nanoparticles. #Biozentrum #UniBasel #Basel #Switzerland #research #lifesciences #development #biology #nanotechnology https://lnkd.in/dGPVXEY6

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Our recommendation for today is the recently published paper "Back to the Basics of SARS-CoV-2 Biochemistry: Microvascular Occlusive Glycan Bindings Govern Its Morbidities and Inform Therapeutic Responses", by Scheim et al. Check out the full article here: https://lnkd.in/gF_tjrsT

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The structure of the DNA double-helix was published in 1953, but it took another 13 years to actually crack the genetic code. The two key questions after the structure of DNA was figured out were: 1) How is it copied? 2) How does it code for proteins? The first question was answered by Meselson and Stahl in 1958. DNA is copied ‘semi-conservatively’ - the old strands serve as a template for creating the new complementary strands. The second question wasn’t fully resolved until 1966. There, of course, were theories about how this occurred and Francis Crick gave a seminal lecture in 1957 (published as a paper in 1958), ‘On Protein Synthesis,’ which laid out the basic formula for how he believed this all worked. He got it mostly right. He proposed that there must be an 'adaptor' which carries the amino acids (we now call this transfer RNA, tRNA) to the template RNA (this became messenger RNA, mRNA) to synthesize the protein chain. But Crick also hypothesized in this lecture that the genetic code is read 3 nucleotides at a time. It was known that there were 20 amino acids and so Crick reasoned that since there are only 4 nucleotides in DNA and RNA, the ‘code’ for each amino acid couldn’t be 2 nucleotides (4x4) because that’s only 16 combinations, so optimally, it was a 3 nucleotide code (4x4x4) because that combination gave 64 possibilities - ~3 combinations for each of the 20 amino acids. The first indication that Crick’s hypothesis was true came in 1961 when Nirenberg and Matthaei showed that an RNA sequence containing only U’s coded for poly-phenylalanine. Inspired by this result, Crick showed that insertion or deletion of 1 or 2 bases causes proteins to become non-functional, but 3 base mutants still produce functional protein. The code must be a triplet! Nirenberg and Leder followed up in 1964 with triplet codes for a handful of amino acids but they frustratingly couldn't determine all of them. That problem was solved by Har Gobind Khorana, an Indian American scientist, whose work is the subject of this #FigureFriday. While Nirenberg and team were using binding assays to try to capture the RNA-amino acid associations, Khorana approached it differently by synthesizing repeating dinucleotide and trinucleotide RNA polymers and seeing which amino acids ended up linked together in the resulting protein chain. The outcome of this work can be seen below (underlines), and this is the first presentation of a nearly complete codon table. The only missing assignment is UGA, the third and final stop codon. Unsurprisingly, Khorana, Nirenberg and Holley (he determined the structure of tRNA) shared the Nobel Prize in 1968 for deciphering how nucleic acids code for proteins. ### Khorana HG, et al. 1966. Polynucleotide Synthesis and the Genetic Code. CSHL Symposia on Quantitative Biology. DOI:10.1101/sqb.1966․031.01․010 --- Want this in your inbox? Visit my website ⬆️

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Recent Long COVID Research: Potential Role of Antibodies A post in Science last week featured two recent studies shedding light on the potential mechanisms behind Long COVID symptoms, focusing on the role of antibodies. Research teams from Yale University and Amsterdam UMC / UMC Utrecht conducted separate studies involving antibodies from Long COVID patients. Both teams observed that mice injected with these antibodies developed symptoms similar to those reported by the human donors, particularly increased pain sensitivity, suggesting that certain antibodies might play a role in driving some Long COVID symptoms. Link to original papers: https://lnkd.in/ev7EByva https://lnkd.in/esDCue6i These findings propose that #LongCOVID might have an immune-mediated component, potentially opening new avenues for treatment approaches, possibly targeting specific antibodies. #COVID19 #Immunology #Research Illustration EMxDE3

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How do mitochondrial Damage-Associated Molecular Patterns (mtDAMPs) within extracellular vesicles initiate neuroinflammation in neurodegenerative disorders? Carla Lopes, from Universidade de Coimbra, will elucidate this mechanism during her presentation at Targeting EVs 2024 in Malta on October 17-18. 🔗 Read more: https://lnkd.in/dPGU9gFg Stay tuned to explore groundbreaking EVs advancements that could reshape our understanding and treatment of neurodegenerative diseases. 🌐 Conference website: https://lnkd.in/dMm8jZjd #Neuroinflammation #EVs #Mitochondria #TargetingEVs

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