Researchers found high levels of sticky NETs were associated with the most severe cases of COVID-19 and led to acute respiratory distress syndrome. The study also identified potential therapeutic strategies for dismantling or preventing NET formation.
The study found that female neutrophils have enhanced proinflammatory genes and responses to inflammatory stimuli compared to male neutrophils. Sex hormones may drive these differences, with males exhibiting increased mitochondrial metabolism in their neutrophils.
Neutrophils, a key player in the immune system, have been found to preferentially phagocytose (eat) rod-shaped particles. This preference may lead to targeting neutrophils and leaving other white blood cells to do their jobs, potentially preventing acute respiratory distress syndrome caused by COVID-19.
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A new study finds that disrupted sleep increases the risk of atherosclerosis and stroke by promoting inflammatory pathways. Sleep fragmentation was associated with higher neutrophil counts and coronary artery calcium, two markers of atherosclerosis pathology.
Researchers have developed a more effective neutrophil depletion model that outperforms existing methods. This improvement enables scientists to study the role of neutrophils in various diseases, including COVID-19, with greater accuracy and precision.
Researchers have discovered a novel drug that selectively controls excessive inflammation, a key driver of conditions like osteoarthritis and COVID-19. APPA demonstrates anti-inflammatory potential without compromising the body's ability to fight off infections.
Researchers identified a novel strategy to address underlying causes of LAD1 patients' symptoms by mimicking the efferocytosis process, which was absent in these individuals. The study found that small-molecule compounds that stimulate this process alleviated signs of inflammation and promoted bone regeneration in animal models.
Researchers found a link between higher blood levels of NETs and a more severe disease course in patients with COVID-19. NETs, a product of neutrophil cell death, may be relevant to understanding the inflammatory storm triggered by SARS-CoV-2 infection.
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Researchers at Cincinnati Children's Hospital Medical Center create a new platform to study the single-cell genomics of various diseases, potentially making genetic-based diagnoses more precise and effective. The study focuses on linking gene mutations to disease-causing processes in blood diseases like severe congenital neutropenia.
Researchers at Monash University have discovered a key mechanism that enables hookworms to evade the human immune system. By understanding how these parasites destroy neutrophil extracellular traps, scientists may be able to develop vaccines to boost immunity and prevent reinfection.
Researchers found that tumor-derived ANGPTL2 stimulates lung epithelial cells, promoting primary tumor-induced neutrophil recruitment and pre-metastatic niche formation. Targeting ANGPTL2 signaling reduced metastatic load in lungs.
Scientists at Karolinska Institutet have discovered two proteins, IL-4 and IL-13, that prevent immune cells from attacking joints and causing inflammation. These proteins regulate neutrophil behaviour, a type of immune cell commonly found in inflamed joints.
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Researchers at CNIC discovered a 'disarmament' mechanism in neutrophils that reduces their toxic capacity to prevent damage to healthy tissues. This innate system, driven by CXCR2 and circadian rhythms, helps regulate the immune response and could have implications for treating conditions like myocardial infarction and stroke.
Researchers have found that a balance between neutrophils and T cells can accurately predict which patients will respond to immunotherapy. A clinical trial is underway to test a drug that reduces neutrophil levels in tumors, boosting the efficacy of checkpoint inhibitors.
The NeutroCure project focuses on harnessing the potential of reactive oxygen species (ROS) produced by neutrophils to treat inflammatory diseases. By developing safe ROS amplifiers, the consortium aims to selectively target pathogenic inflammation and cancer cells while minimizing damage to healthy tissues.
Researchers created an artificial intelligence tool to identify neutrophils primed for NETosis, a process where white blood cells expel inflammatory DNA into circulation. The new technology allows scientists to measure NETosis in different diseases and test drugs that may inhibit or promote the process.
A combined test of Renal Angina Index (RAI) and urinary Neutrophil Gelatinase Associated Lipocalin (NGAL) can predict severe acute kidney injury risk in critically ill children, according to a recent study. This early identification allows for targeted interventions to reduce morbidity and hospital stay duration.
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A new treatment approach for inflammatory diseases, including sepsis, stroke, rheumatoid arthritis, acute lung injury, and atherosclerosis, has been discovered using nanoparticles. The technology selectively kills 'rogue' white blood cells that drive exaggerated immune responses, while leaving beneficial cells unharmed.
Researchers discovered a mechanism behind malaria's severe complications: an immune reaction that damages the patient's own tissue. The parasite triggers an escalation of neutrophil activity, leading to organ failure and death in severe cases.
A team of researchers at FAU has discovered the mechanism behind gallstone formation, finding that neutrophil granulocytes cover crystals with their genetic material to form stones. The discovery opens up new treatment options, including the use of beta blockers and PAD inhibitors.
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A study published in Nature Immunology identified neutrophils as a key player in the development of allergic asthma, particularly in pro-allergic environments such as excessive hygiene and air pollution. Compounds like pulmozyme may prevent disease development by destroying DNA released by neutrophils.
Researchers found large diversity in neutrophil and macrophage frequencies, with some tumors attracting one type while others attract the other. The study highlights heterogeneity of tumor cells and immune microenvironment as important considerations for therapy.
Researchers discover that sticky meshworks of DNA and proteins extruded by neutrophils act as the glue that binds together calcium and cholesterol crystals during gallstone formation. Inhibiting NETs reduces gallstone growth in mice, offering new strategies for treating gallstone disease.
A WSU researcher has created a new technology that harnesses the immune system to target diseased tissues, improving drug delivery and reducing side effects. The technology uses neutrophils to deliver drugs directly to inflammatory sites, showing promise in treating acute lung injury and potentially other diseases.
Researchers from Kumamoto University found that nsPEFs can stimulate immune cells to respond as if they were being stimulated by bacteria. This was achieved through the release of chromosomal DNA and histone citrullination in neutrophils, similar to the process occurring when neutrophils are exposed to bacteria.
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A recent study has discovered that IgG antibodies can contribute to drug-induced anaphylactic shock by activating neutrophils, leading to high doses of vasodilating mediators. This finding explains up to 10-20% of previously unexplained cases and may help improve diagnosis and treatment for patients with this condition.
A study of 86 patients reveals how anesthesia drugs can induce life-threatening allergic reactions through alternative immune pathways. Hyperactive immune cells, including neutrophils and macrophages, play a key role in this process, which could lead to the development of new diagnostics for anaphylaxis during anesthesia.
Researchers have identified a new pathological mechanism responsible for 10-20% of unexplained anaphylactic cases involving IgG antibodies that activate neutrophils, releasing harmful vasodilating mediators. This discovery may help improve diagnosis and treatment for patients with anaphylactic shock.
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Researchers found a protein called FATP2 that causes neutrophils to weaken the body's reaction against tumors and decrease cancer treatment efficiency. Suppressing its activity delays cancer development.
Researchers at the University of Toronto have discovered two distinct neutrophil states in blood, which vary depending on patient health and infection status. These findings may lead to new models for disease detection and monitoring, such as tracking primed neutrophils to predict inflammatory diseases.
In a mouse model of atypical EAE, researchers found that dysregulated neutrophils cause damage and exhibit hyper-activated phenotypes, producing excessive reactive oxygen species. Neutralizing treatments reduced disease severity, highlighting the detrimental role of neutrophils in autoimmune neuroinflammation.
Patients with severe asthma have reduced microbiome diversity, highlighting a potential relationship between neutrophils and the microbiome. This finding may lead to new targeted asthma therapies by better understanding the link between these two factors.
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A KAIST research team visualized pulmonary microcirculation in vivo using a custom-built 3D intravital microscope imaging system. They found that neutrophils aggregate inside capillaries during sepsis-induced acute lung injury, leading to tissue hypoxia and damage.
Researchers discovered that neutrophils can induce a previously unrecognized type of cell death in tissues, leading to the destabilization of atherosclerotic plaques. This process causes inflammation, which increases the likelihood of plaque rupture and subsequent cardiovascular events.
Researchers discover that inhibiting neutrophils, a type of white blood cell, can prevent blood clots in patients with antiphospholipid syndrome. The study found that two drugs, CGS21680 and dipyridamole, reduced the formation of sticky structures called NETs that trigger blood clots.
A new study found that HIV-infected individuals have a longer lifespan of white blood cells called neutrophils, which may contribute to intestinal inflammation. Lactobacillus bacteria, commonly used in probiotics, could be an effective therapeutic strategy to reduce neutrophil-driven inflammation.
The microbiota controls neutrophil activity by producing Serum Amyloid A (Saa), a host protein that restricts aberrant activation while enhancing migration to wounds. Saa reduces bactericidal activity and expression of pro-inflammatory genes in neutrophils.
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Researchers at Cardiff University found that genetic neutropenia is a benign condition in people of African descent that can lead to lower neutrophil levels. This allows more individuals with treatment-resistant schizophrenia to receive the medication clozapine without risk of rare side effects.
A study published in Scientific Reports identifies changes to neutrophils that increase vulnerability of obese and diabetic individuals to infection. Alterations to neutrophils, a type of white blood cell, lead to impaired activation of toll-like receptors (TLRs), weakening the immune system's ability to combat pathogens.
Researchers identified ELMO1 as a surprising contributor to rheumatoid arthritis, which may lead to a new treatment and blood test for early detection. The discovery also challenges the understanding of genes' roles in the body.
Researchers use a novel database on the neutrophil proteome to make genetic diagnoses for two children with severe congenital neutropenia whom typical sequencing had failed. The technique combines proteomic and genomic screening, which shows huge potential for personalized medicine at low cost.
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Researchers at the University of Basel found that neutrophils help tumor cells form metastases by escorting circulating tumor cells. This alliance enhances their ability to seed metastasis, and blocking it could lead to new anti-metastatic drugs.
Researchers successfully recreated microscopic networks of fibers made of DNA, called NETs, in the laboratory. The study found that these microwebs can capture and kill bacteria, potentially leading to more effective antibiotics and a new approach to treating infections.
Researchers at CNIC discovered a daily cycle that regulates neutrophil activation, protecting against infection but potentially causing damage to the cardiovascular system. The study suggests that manipulating this clock could lead to new treatments for patients at risk of cardiovascular events or infections.
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Researchers have identified midkine as a key driver of inflammation in the heart muscle that can lead to heart failure in patients with myocarditis. The study found that inhibiting midkine reduced neutrophil infiltration and improved heart function.
A new study reveals that the protein Del-1 plays a vital role in clearing inflammation by connecting dying neutrophils to macrophages. The 'location principle' suggests that homeostatic molecules perform different regulatory functions depending on their location.
Researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) have discovered a new mechanism that controls tissue infiltration by neutrophils, which are tasked with eliminating the source of infection or inflammation. This regulation prevents excessive tissue injury and is essential to understanding immune system balance.
Researchers at Huntsman Cancer Institute discovered that different types of lung tumors recruit distinct immune cells, which can help or hinder tumor growth. The study found that high levels of neutrophils are associated with a bad response to immunotherapy, suggesting them as a potential target for new treatments.
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Neutrophils isolated from bone marrow of mouse models and patients with early stage tumors exhibit increased spontaneous migration to tissues and promote tumor cell seeding. These neutrophils lack immunosuppressive characteristics, but display potent ability to spontaneously migrate and facilitate metastasis.
Researchers found that carprofen pretreatment before experimental heart attack in mice impairs the resolution of acute inflammation after cardiac injury. This leads to a non-resolving inflammation characterized by an amplified CD47 marker on neutrophils, which resists clearance and triggers more inflammatory responses.
Researchers at the University of California San Diego have developed nanosponges that can safely absorb and neutralize a variety of proteins involved in rheumatoid arthritis progression. These nanosponges effectively treated severe rheumatoid arthritis in two mouse models, reducing swelling and minimizing cartilage damage.
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A team of researchers at La Jolla Institute for Immunology has identified a previously unknown progenitor population with neutrophil characteristics, which promotes tumor growth. The discovery could serve as an early warning sign for cancer and drive new therapeutic approaches for treating neutropenia, chronic inflammation, and cancer.
Researchers from Massachusetts General Hospital found that immune cells responding to a stroke or brain injury in an animal model are more likely to come from the skull's bone marrow. Microscopic channels were discovered in the skull's inner layer, allowing inflammatory cells to migrate directly to the brain surface.
Researchers discovered tiny tunnels in the skull that connect bone marrow to the lining of the brain, enabling immune cells to quickly reach injured tissue. The study found that these channels play a crucial role in inflammation and may be important in various brain disorders.
Researchers found that myeloperoxidase can degrade both single-layer and few-layer graphene, opening up new avenues for developing biodegradable graphene-based materials. This discovery is crucial for ensuring the safe use of graphene in biomedical applications.
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A new study by Brigham and Women's Hospital researchers models allergic lung inflammation in mice, revealing the role of neutrophil extracellular traps (NETs) in triggering and amplifying an allergen-initiated immune response. The findings have implications for designing more precise clinical trials for severe asthma treatment.
Researchers found that immune cells called neutrophils may be disrupting the moisturizing glands of the eyelid, causing dry eye. The study suggests that inflammation is a common cause of Meibomian gland dysfunction (MGD) and could lead to new treatment strategies.
Researchers create FluVision technology to visualize influenza infection in real-time, observing differences between highly-pathogenic H5N1 and milder H1N1 strains. The tool reveals increased damage caused by H5N1, including pulmonary leakage and immune cell activation.
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Researchers discovered how bronchiectasis impairs immune cells, leading to repeated lung infections. Treatments targeting these cells could reduce chest infections and improve quality of life.
Researchers have found evidence that dissolving NETs can reduce swelling and improve blood flow after traumatic brain injuries. A drug called DNase, which is currently used to thin out lung mucus in cystic fibrosis, appears to dissolve NETs and has shown promise in reducing swelling and improving recovery.