A new point-of-care genetic test identifies CYP2C19*2 allele, a common variant associated with increased risk of major adverse events. The test enables personalized dual antiplatelet treatment, reducing complications and improving outcomes for patients after coronary interventions.
Researchers have discovered that Streptococcus gordonii can mimic human proteins to activate platelets and form unwanted blood clots. This triggers endocarditis, which can lead to growths on heart valves or inflammation of blood vessels.
A new class of platelet blockers has been shown to reduce the risk of recurrent cardiovascular events in patients with known atherosclerosis. Adding vorapaxar, an investigational platelet blocker, to standard antiplatelet therapy cuts the likelihood of another cardiac event by 13% compared to placebo.
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Scientists have determined the molecular 3D structure of a protein in blood platelets and a receptor that controls blood clot formation. This discovery helps understand the body's response to superbugs and potentially leads to new treatments.
Yale researchers found that megakaryocytes grow 10-15 times larger than other blood cells through endomitosis, but a malfunction in this process may lead to leukemia. The discovery reveals the formation of functional platelets and provides clues about what may go awry to transform normal megakaryocytes into malignant leukemia cells.
Researchers have identified five novel gene mutations associated with elevated blood platelet counts in African Americans, a group at higher risk of stroke and worse outcomes after a heart attack. The study's findings could lead to the development of new drugs to prevent coronary artery disease and clot formation.
Researchers have identified a gene responsible for Thrombocytopenia with Absent Radii (TAR), a rare inherited blood and skeletal disorder. The discovery enables the development of a medical test for prenatal diagnosis and genetic counseling in affected families.
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A team of chemists from Michigan State University has discovered a way to isolate and test the P2X1 receptor in blood platelets, unlocking its potential as a new drug target for diseases such as diabetes, hypertension, and cystic fibrosis. The research allows researchers to re-test existing medications by attaching to the receptor.
Researchers found that a new drug called cangrelor helped patients maintain platelet inhibition at higher rates than placebo before undergoing cardiac surgery. This was significant because premature discontinuation of antiplatelet therapy prior to surgery can lead to increased ischemic complications.
Researchers have discovered that administering aspirin after standard therapy for venous thromboembolism (VTE) may prevent the recurrence of potentially deadly blood clots. The WARFASA study found that low-dose aspirin reduced VTE recurrence by 6.6% compared to placebo, with a similar incidence of major and non-major bleeding.
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Researchers have identified 68 genetic variants involved in platelet formation, including a novel role for tropomyosin 1 in platelet production. The study found that genes associated with heart attacks and strokes overlap with those affecting platelets, offering potential new targets for treatments.
A study found that tripling the standard daily dosage of clopidogrel for patients with a genetic variation improving response to the medication significantly reduced platelet reactivity. Higher doses also improved platelet reactivity in those without the variant gene, guiding further clinical studies.
A study by MIT cancer biologists reveals that platelets release chemical signals inducing tumor cells to become more invasive and form new tumors. The findings suggest that direct physical contact between platelets and tumor cells is necessary for metastasis, highlighting potential targets for drug development.
The BRIDGE trial results demonstrate that cangrelor maintains target levels of platelet inhibition, supporting its use as a management strategy for patients requiring prolonged platelet P2Y12 inhibition after thienopyridine discontinuation. The study showed 99% of cangrelor-treated patients maintained target levels, compared to 19% of ...
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Researchers at St. Michael's Hospital have identified a potential new cause for unexplained miscarriages in mice, finding that massive clotting in the placenta can destroy the placenta and block blood flow to the fetus. The study suggests two possible treatments to prevent these miscarriages and has broader implications for heart attac...
A team of researchers has identified a non-classical form of Fetal and Neonatal Immune Thrombocytopenia (FNIT) that causes excessive platelet activation and blood clot formation in the placenta, leading to miscarriage. The condition can be prevented with intravenous IgG and anti-FcRn therapies.
Scientists at the Walter and Eliza Hall Institute have identified that pro-survival Bcl-2 family proteins are essential for keeping megakaryocytes alive to produce platelets. Chemotherapy kills megakaryocytes by activating 'pro-death' Bcl-2 proteins, leading to a drop in platelet numbers.
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A study examining platelet function testing before PCI procedures found that patients with high residual platelet reactivity had a higher risk of ischemic events, including cardiac death and heart attack. The study suggested that tailored therapy using new antithrombotic agents may be necessary for these patients.
Researchers found that the body's internal clock regulates human platelet function, causing a peak in platelet activation corresponding to the morning peak in adverse cardiovascular events. This discovery has potential to address the morning peak in cardiovascular risk and decrease related mortality.
A new analysis of the GRAVITAS trial found that achieving low platelet reactivity is associated with a reduced incidence of cardiovascular death, heart attack, and stent thrombosis. Patients who achieved this level of platelet reactivity had approximately half the risk of these events compared to those with high reactivity.
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Researchers launch pioneering study to create human platelet cells from stem cells to study inherited blood clotting abnormalities and genetic variations affecting platelet function. The goal is to develop a new approach to generating blood cells for patients in need of chronic infusions.
Researchers identified the NBEAL2 gene responsible for Gray Platelet Syndrome, a rare blood disorder characterized by gray platelets. The discovery enables early diagnosis with a DNA test, improving patient care and treatment options.
Researchers at the University of Pennsylvania have discovered that a single drug can induce bone marrow cells to quadruple platelet production. The study found that inhibiting myosin-II with the drug belebbistatin increases megakaryocyte growth, allowing them to produce more platelets in a soft environment.
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Researchers developed a new strategy to improve the outcome of genome-wide association studies by linking initial association signals to functional DNA changes. The framework streamlined discovery of functional DNA variants underlying GWA signals, benefiting scientists worldwide.
Scientists have identified a molecular sensor of temperature within immune cells, which primes the immune response to temperature shifts. This discovery could provide new insights into the mechanisms underlying fever and its effects on the immune system.
A new trial shows that standard-dose clopidogrel is as effective as double the dose for preventing cardiovascular events in patients with high on-treatment platelet reactivity. Researchers argue that a personalized approach to antiplatelet therapy may be more beneficial, warranting further investigation.
A preclinical study found VitaKine PCT to significantly enhance cardiac function, increasing ejection fraction by 23%, compared to controls. The therapy contains white blood cells in specific ratios and concentrations, offering a precise approach to treating heart attack patients.
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Researchers investigated the association between bleeding and mortality in patients on dual antiplatelet therapy (DAPT) versus aspirin alone. The study shows patients with moderate or severe bleeding had a higher incidence of all-cause, cardiovascular and cancer mortality.
A study of 2,214 patients found that high-dose clopidogrel did not reduce the risk of nonfatal heart attack, stent thrombosis, or cardiovascular death compared to standard-dose therapy. The treatment strategy for patients with high platelet reactivity remains undefined.
Researchers have developed mouse models of human MYH9 genetic disorders, which cause enlarged platelets and kidney disease. The models will aid in understanding the development of these diseases and identifying defects in the gene product.
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A Scripps Research scientist has identified a natural molecule that inhibits the activation of thrombin-activatable fibrinolysis inhibitor (TAFI), preventing stable clot formation. This discovery could lead to novel and cost-effective treatments for blood clotting diseases like Hemophilia A.
Researchers from Leicester and Cambridge discovered genetic markers that identify people at risk of developing potentially fatal blood clots. This breakthrough advances ways of detecting and treating coronary heart disease, a leading cause of premature death.
Researchers at Rockefeller University Press have successfully reprogrammed human skin cells to produce platelets that can be used in patients with thrombocytopenia. The breakthrough method involves culturing these cells in a cocktail of platelet-promoting factors, resulting in platelets that function like normal healthy platelets.
Dr. Benjamin Kile received the Science Minister's prize for his innovative research into cancer, stem cells and blood cell production. His discoveries have transformed our understanding of platelet biology and hold promise for developing new treatments for life-threatening conditions.
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A new study found that romiplostim, a drug mimicking the effects of thrombopoietin, is more effective than standard care in treating immune thrombocytopenia. The treatment significantly improved platelet levels and reduced the need for splenectomy in patients, enhancing their quality of life.
Researchers at UCI studied postmortem brain specimens from 33 individuals aged 71-105 and found cerebral microbleeds in 22 cases. The incidence rate is higher than previously reported MRI studies, suggesting age-related changes in blood vessel leakiness.
Scientists have identified a potential new method for replenishing platelet cells, which could treat individuals with low platelet counts. The approach involves infusing mature megakaryocytes into mice, producing functional platelets of normal size and function.
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Researchers found that maternal KIRs interacting with fetal HLA-C molecules determine trophoblast invasion, affecting recurrent miscarriage and preeclampsia. Meanwhile, a new approach to treating thrombocytopenia involves infusing mature megakaryocytes into mice to generate functional platelets.
CWRU researcher Erin Lavik is developing synthetic platelets using nanotechnology to treat traumatic injuries. Her lab aims to fine-tune the artificial platelets and integrate them with drug delivery systems.
Research reveals that oral bacteria can jailbreak from the mouth into the bloodstream and increase risk of heart disease. Poor dental hygiene allows bacteria like Streptococcus to cause tooth plaque and gum disease, leading to blood clots and cardiovascular problems.
A $3 million NIH grant will help scientists at Jefferson Medical College study variations in platelet function, specifically the genetics of platelet gene expression. The goal is to identify biomarkers for predicting cardiovascular disease risk and developing novel therapeutic strategies.
Researchers found that inhibiting platelet protein CLEC-2 may combat irregular blood clotting and cancer spread. The discovery paves the way for new research on platelets' role in both conditions.
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Researchers found a group of seven genes that significantly impact platelet clumping, offering new targets for developing diagnostic tests and treatments for arterial disease. The study used data from two large studies to identify the genetic factors behind blood clotting, providing insights into promoting healing and stalling disease ...
A team of bioengineers from the University of Pennsylvania Institute for Medicine and Engineering developed a simulator to predict how blood platelets respond to various conditions during a heart attack or stroke. The model accurately predicted intracellular calcium signaling responses, even distinguishing between different donors.
Scientists have discovered that platelets play a crucial role in cerebral malaria, a fatal form of the disease that ravages the brain. By targeting platelets, researchers hope to develop new treatment options for this devastating condition.
Scientists developed a modern intelligent drug that inhibits platelet activity at cool temperatures, preventing blood clots during therapeutic hypothermia. The new drug loses its function when the body is rewarmed, minimizing bleeding problems.
A recent commentary in the Canadian Medical Association Journal highlights inappropriate uses of frozen plasma, with 45% to 48% of audited transfusions found to be misuse. Experts recommend introducing measures to promote alternative use and screen orders against guidelines to improve practice.
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A new study found that lowering the platelet dosage in transfusions can help address frequent shortages in platelet supplies without increasing bleeding risks. The research involved 1,272 patients who received at least one transfusion and reported similar bleeding events regardless of the platelet dose used.
The discovery reveals QPD is caused by an extra copy of the PLAU gene, leading to overproduction of an enzyme that accelerates blood clot breakdown. This breakthrough genetic test will uncover many more cases and provide fundamental insights into how the uPA gene is controlled.
A study of six platelet function tests found that only three could predict atherothrombotic events, such as heart attack or death, with moderate accuracy. These tests were light transmittance aggregometry, VerifyNow, and Plateletworks, which were associated with high platelet reactivity at 1-year follow-up.
Researchers at Children's Hospital will engineer human cells into new tissues to treat blood diseases, cancer, and other disorders. Two NIH grants focus on developing embryonic stem cells for platelet supplies and induced pluripotent stem cells for custom-tissue production.
Researchers at the University of Utah discovered that platelets can reproduce themselves in the circulation, increasing their numbers. This finding has significant implications for treating low platelet counts and transfusion medicine.
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A team of researchers led by Erin Lavik developed synthetic platelets that show promise in halting internal and external bleeding. The synthetic platelets are designed to home in and link up with natural platelets at the site of an injury, resulting in clotting times about 25% faster than current treatments.
Researchers at Karolinska Institutet identify polyphosphate as a key player in the formation of blood clots and inflammation. The study suggests that phosphatases can break down polyphosphate, preventing both conditions.
Researchers at Virginia Tech have discovered novel molecular interactions at the surface of platelets that regulate blood clotting. The study found that sulfatides bind to Disabled-2 protein, preventing it from inhibiting clotting, while also recycling the protein for future use.
Researchers found that surfboard-shaped nanoparticles stay closest to blood vessel walls, offering a potential solution for targeted cancer therapy. The study suggests that current transfusion techniques may not be ideal, and alternative methods could establish proper blood arrangement faster.
Researchers found that green tea component EGCG can prolong the preservation of stored blood platelets by up to six days via anti-apoptosis properties. Additionally, EGCG was shown to preserve skin tissues by controlling cell division and preventing oxidation, allowing for the storage of skin grafts up to seven weeks.
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The PREDICT score identifies individual risk for poor responsiveness to clopidogrel through non-genetic factors. Studies show that response to clopidogrel is affected by genetic variants involving enzymes responsible for absorption and bio-activation of the medication.
A genetic variation, CYP2C19*2, affects platelet response to clopidogrel and is associated with an increased risk of cardiovascular events. The study found that carriers of the variant had a higher likelihood of experiencing a cardiovascular ischemic event or death compared to non-carriers after 1 year of follow-up.
Researchers at the University of Maryland School of Medicine have identified a common gene variant associated with reduced response to Plavix, a popular anti-clotting medication. The study confirms a previously reported link between the CYP2C19 gene and decreased response to clopidogrel.
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