LGC Clinical Diagnostics’ Post

New Blog Post! Infectious complications are a significant concern for patients after solid organ transplants. Molecular testing is a vital tool for the prevention of these complications. Read our latest blog "Managing Transplant Patient Health with Molecular Diagnostics" so you can ensure the accuracy of this critical information being placed in clinicians’ hands. https://hubs.ly/Q02_R3B-0 #moleculardiagnostics #infectiousdiseases #transplantorganhealth

Among the least concerning infections is HSV-1. An unsightly cold-sore. But what if Alzheimers was the ultimate price for that herpes infection that you got from your first kiss? There's good (but ambiguous) evidence: https://lnkd.in/eZ2QTNtR and it makes sense neurologically. Herpes viruses hang out in the central nervous system. You can't get rid of them (ask any porn star with HSV-2). This is why your childhood chickenpox returns as shingles in your 60s. It had been with you all along, waiting for your immunity to wane. There's a lot the same about shingles and Alzheimers in terms of onset and proportion of onset. Dr. Alzheimer himself was convinced that his namesake disease was due to an infectious agent. There's even evidence that a bout of shingles (a related virus) is protective against Alzheimers. Almost as though the immune system gets newly arisen to fight any Herpes Virus. https://lnkd.in/eWVVd348 Lecanemab and Aducanumab and Donanemab could even be exerting their (underwhelming but significant) positive effects just by drawing the immune system to where HSV-1 needs to be put down. This was, after all the premise behind injecting Pembrolizumab into President Carter's brain. What if a childhood vaccination against cold-sores would save hundreds of thousands of lives when those people hit their later years? Hmmmm. Problem is that the clinical trials would have to span a generation. And no one alive today would make a penny off it. #alzheimers #viruses #herpes #etiology #immunity #vaccines

#ARDS #COVID19 #IL4, #IL17, #IL16, #IL18, #IL10, #IP10, #SCGFbeta #Angiopoietin2? #TIE2Agonist? #PMC403 for sure! We observed differential cytokine expression between patients with persistent-mild disease and patients with mild-to-severe transformation. For instance, IL-4 and IL-17 levels significantly increased in patients with mild-to-severe transformation, indicating differences within the mild disease group. Subsequently, we analysed the changes in cytokine and chemokine expression in the plasma of patients undergoing two opposing processes: the transition from mild to severe illness and the transition from severe to mild illness. We identified several factors, such as reduced expression of IL-16 and IL-18 during the severe phase of the disease and up-regulated expression of IL-10, IP-10, and SCGF-β during the same period, indicative of the deterioration or improvement of patients’ conditions. These factors obtained from fine-tuned research cohorts could provide auxiliary indications for changes in the condition of COVID-19 patients. https://lnkd.in/gBG-BN2j

An accurate and early diagnosis is vital to reduce the high rates of mortality and morbidity that result from central nervous system infections, however this can be challenging. This article discusses the advantages of using metagenomic next-generation sequencing in this context, as well as exploring the issues that have to be worked through before this technology can become clinically impactful. #metagenomic #NGS #CNSInfection

A very interesting study by my friend, colleague and teacher Dr Paul Fleming, The study provides insights into immune pathways associated with early-life sepsis and identifies immune analytes as potential diagnostic adjuncts to standard tests to guide targeted antibiotic prescribing : https://lnkd.in/ggvkFMsu This is the future of neonatal sepsis treatment.

Finally our article on ‘Sarcoidosis in a young adult: A rare sequelae of COVID-19 infection’ is published on Wiley Online Library- Clinical case reports. Learning point from the article: This case illustrates sarcoidosis as a potential complication of COVID-19, highlighting the need for a comprehensive diagnostic approach, including histopathology and prolonged monitoring, to distinguish it from post-COVID fibrosis. Further research is crucial to elucidate these associations and understand their underlying mechanisms. Happy reading and reflecting. https://lnkd.in/dK9AZFkZ

Common Variable Immunodeficiency (CVID) is the second most common form of Primary Immunodeficiency Syndrome. A group of CVID patients (Blood 135:656–667) may not have obvious recurrent infections, but instead present with a prominent inflammatory phenotype featuring "autoimmune episodes", such as Evans syndrome or lesions in various organs, including the brain, which may sometimes be the only affected site. Check out our latest paper #cvid #inflammation #immunodeficiency #autoimmunity #raredisorders

Tackling the urgent issue of antibiotic-resistant bacteria Nate Stasko, Chief Executive Officer of Vast Therapeutics, states that patients deserve new treatment options like ALX1 in the fight against antibiotic-resistant bacteria. Chronic lung diseases lead to a harmful cycle of inflammation and infection. This can result in trouble breathing, frequent hospital stays, and, sadly, even death. Antibiotic-resistant bacteria have evolved defences against some of the medical field’s best drugs and have set up base camp in the lungs of patients with cystic fibrosis (CF), non-CF bronchiectasis (NCFB), and chronic obstructive pulmonary disease (COPD). Read the full Vast Therapeutics article here - #FREE https://lnkd.in/exfxf_hu #amr #antibioticresistance #health #publichealth #COPD #cysticfibrosis

June 19th marks #WorldSickleCellDay , a day dedicated to #raisingawareness about this inherited blood disorder. Here is what you need to know... 🩸Sickle cell disease causes red blood cells to become sickle-shaped, blocking blood flow and oxygen delivery throughout the body. It affects both red blood cells and hemoglobin, the protein that carries oxygen. This year's theme, "Hope Through Progress: Advancing Care Globally," highlights the ongoing fight for better #treatmentoptions. There are three main types of sickle cell disease: HbSS (Sickle Cell Anemia), Hbs beta-thalassemia (a combination of sickle cell and beta-thalassemia genes), and HbSc (carrying both sickle cell and another abnormal hemoglobin gene). 👩🔬Treatments for sickle cell disease currently focus on managing symptoms, including antibiotics for infection prevention, pain medication, fluids, blood transfusions, and in some cases, surgery. While there is currently no cure for sickle cell disease, research continues to offer hope for the future. This why, we have said it before, but we will say this again👇 👏 Supporting initiatives that promote and improve scientific research is vital. More effective #medical #research holds the key to unlocking better #treatment options and even preventative measures for this challenging disease. 👏 Let's stand strong together in the fight against #sicklecelldisease.

Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis Sepsis is responsible for nearly 20% of deaths worldwide. Current therapy for sepsis is restricted to antibiotics directed toward the initiating pathogen, combined with non-specific supportive care. There are no approved therapies aimed at the dysregulated host response which plays a critical role in the development of multiple organ dysfunction and mortality from sepsis. In this study, the authors found that small intestinal epithelial claudin-2 expression is selectively upregulated in septic patients. Mortality due to sepsis is markedly reduced in claudin-2 knockoot mice, which is, at least partly, due to claudin-2-dependent effects on sepsis-induced dysbiosis. Claudin-2 and its effects on the microbiome may be attractive therapeutic targets in sepsis. https://lnkd.in/d9YS5rkW