Researchers found persistent microclot and NET structures in Long COVID blood that may explain long-lasting symptoms.
Researchers examining Long COVID have identified a structural connection between circulating microclots and neutrophil extracellular traps (NETs). The discovery indicates that the two may interact in the body in ways that could lead to harmful effects when these processes become unregulated.
Understanding Microclots
A discovery from Australian researchers could lead to better treatment for children with neuroblastoma, a cancer that currently claims 9 out of 10 young patients who experience recurrence. The team at the Garvan Institute of Medical Research in Sydney, Australia, found a drug combination that can bypass the cellular defenses these tumors develop that lead to relapse.
In findings made in animal models and published today in Science Advances, Associate Professor David Croucher and his team have shown that a drug already approved for other cancers can trigger neuroblastoma cell death through alternative pathways when the usual routes become blocked. This discovery could lead to better treatment strategies for children whose cancers have stopped responding to standard chemotherapy.
Neuroblastoma is the most common solid tumor in children outside the brain, developing from nerve cells in the adrenal glands above the kidneys or along the spine, chest, abdomen or pelvis. It is typically diagnosed in children under 2 years old. While those with low-risk disease have excellent outcomes, around half of patients are diagnosed with high-risk neuroblastoma—an aggressive form where tumors have already spread. Of these high-risk patients, 15% don’t respond to initial treatment, and half of those who do respond will see their cancer return.
Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease; however, few biomarkers of its early identification are available. The aim of the study was to assess new biomarkers in the early stages of DKD in type 2 diabetes mellitus (DM) patients. This cross-sectional pilot study performed an integrated metabolomic profiling of blood and urine in 90 patients with type 2 DM, classified into three subgroups according to albuminuria stage from P1 to P3 (30 normo-, 30 micro-, and 30 macroalbuminuric) and 20 healthy controls using high-performance liquid chromatography and mass spectrometry (UPLC-QTOF-ESI MS). From a large cohort of separated and identified molecules, 33 and 39 amino acids and derivatives from serum and urine, respectively, were selected for statistical analysis using Metaboanalyst 5.0. online software.
Researchers around the world are studying how the human brain achieves its extraordinary complexity. A team at the Central Institute of Mental Health in Mannheim and the German Primate Center—Leibniz Institute for Primate Research in Göttingen has now used organoids to show that the ARHGAP11A gene plays a crucial role in brain development. If this gene is missing, key processes involved in cell division and structure become unbalanced.
The human brain distinguishes us from other living beings like no other organ. It enables language, abstract thinking, complex social behavior, and culture. But how can this extraordinarily powerful organ develop, and how is it ensured that nerve cells and supporting cells form in exactly the right places to create the complexity of the human brain?
A team led by Dr. Julia Ladewig at the Central Institute of Mental Health (CIMH) in Mannheim and Dr. Michael Heide at the German Primate Center (DPZ) in Göttingen has investigated this question at the molecular level.
Spermine, a small but powerful molecule in the body, helps neutralize harmful protein accumulations linked to Alzheimer’s and Parkinson’s. It encourages these misfolded proteins to gather into manageable clumps that cells can more efficiently dispose of through autophagy. Experiments in nematodes show that spermine also enhances longevity and cellular energy production. These insights open the door to targeted therapies powered by polyamines and advanced AI-driven molecular design.
As we get older, our brains start to change in ways that make them increasingly vulnerable to disease – and a detailed new study of these changes points to a way some of this wear and tear might be prevented or reversed.
Researchers from the Leibniz Institute on Aging – Fritz Lipmann Institute in Germany used mass spectrometry to analyze the balance of brain proteins in both young and old mice, finding differences in a process called ubiquitylation as the animals aged.
Ubiquitylation adds chemical tags to proteins, telling the brain which of these busy molecules are past their peak and should be recycled. In older mouse brains, the ubiquitylation tags really start to pile up on certain proteins.