EPFL scientists have recently developed awarded a research grant to the lab of Professor Bart Deplancke supporting the development of a web-based platform
Category: biotech/medical – Page 5
The clinical treatment of profound oxygen deprivation (hypoxemia) is time sensitive and requires skill and specialized equipment. When the airways or lungs become incapacitated (e.g., due to airway obstruction or lung injury), resuscitation is ineffective until oxygenation is restored. Many critically ill patients suffer organ dysfunction, cardiac arrest, or death within minutes. In this work, we describe a polymeric microparticle-based oxygen delivery technology capable of rapidly administering large volumes of oxygen gas through an intravenous line.
ABSTRACT: A continuous supply of oxygen to tissues is vital to life and interruptions in its delivery are poorly tolerated. The treatment of low-blood oxygen tensions requires restoration of functional airways and lungs. Unfortunately, severe oxygen deprivation carries a high mortality rate and can make otherwise-survivable illnesses unsurvivable. Thus, an effective and rapid treatment for hypoxemia would be revolutionary. The i.v. injection of oxygen bubbles has recently emerged as a potential strategy to rapidly raise arterial oxygen tensions. In this report, we describe the fabrication of a polymer-based intravascular oxygen delivery agent. Polymer hollow microparticles (PHMs) are thin-walled, hollow polymer microcapsules with tunable nanoporous shells. We show that PHMs are easily charged with oxygen gas and that they release their oxygen payload only when exposed to desaturated blood. We demonstrate that oxygen release from PHMs is diffusion-controlled, that they deliver approximately five times more oxygen gas than human red blood cells (per gram), and that they are safe and effective when injected in vivo. Finally, we show that PHMs can be stored at room temperature under dry ambient conditions for at least 2 mo without any effect on particle size distribution or gas carrying capacity.
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Gestational diabetes is a disorder characterized by abnormally high levels of blood glucose (also called blood sugar) during pregnancy.
Affected women do not have diabetes before they are pregnant, and most of these women go back to being nondiabetic soon after the baby is born. Gestational diabetes is often discovered during the second trimester of pregnancy.
The disease has a 30 to 70 percent chance of recurring in subsequent pregnancies.
Gestational diabetes mellitus (GDM) is influenced by both genetic and environmental factors. Polymorphisms in genes related to glucose metabolism and insulin signaling, such as TCF7L2, have been associated with increased risk. This gene influences insulin secretion and glucose production, affecting the body’s ability to regulate blood sugar during pregnancy. Other implicated genes include GCK, encoding glucokinase, and MTNR1B, involved in melatonin receptor signaling.
More information on genetic factors that contribute to the development of GDM is provided in the link below.
Sensory Processing Challenges in Children with Neurodevelopmental Disorders and Genetic Conditions: An Observational Study
Posted in biotech/medical, genetics, robotics/AI | Leave a Comment on Sensory Processing Challenges in Children with Neurodevelopmental Disorders and Genetic Conditions: An Observational Study
A variety of genetic conditions are known to affect brain development and, consequently, might potentially exhibit behaviours related to SIDs, as they impact areas involved in sensory processing and the perceptual integration of inputs. This is the case of Williams syndrome (WS), 22q11.2 deletion syndrome (22qDS) and pseudohypoparathyroidism (PHP). Although some previous research indicates sensory processing alterations in WS [20], this area remains largely unexplored in 22qDS and PHP.
The condition 22qDS, caused by a deletion in the q11.2 region of chromosome 22, is associated with significant brain abnormalities, along with cardiac anomalies, cleft palate, immune deficiencies, cognitive difficulties, and an increased risk of psychiatric disorders such as schizophrenia [21]. Common structural alterations include hypoplasia of the corpus callosum, which impacts interhemispheric communication, and anomalies in the thalamus, affecting the relay of sensory and motor information. Additionally, structural changes in the cortical brain regions, such as variations in cortical thickness, have been observed. These structural abnormalities are linked to disruptions in neural networks and can contribute to deficits in cognitive and emotional functions, impacting development and behaviour in individuals with the syndrome [22].
WS is caused by a microdeletion in the chromosomal region 7q11.23. It is characterised by a distinctive cognitive and behavioural profile, including strong social and verbal skills, accompanied by anxiety and attention problems. Additionally, individuals with WS may present with cardiovascular anomalies, hypercalcemia in infancy, and a distinctive facial phenotype [23]. MRI studies reveal reduced brain size and a more pronounced loss of white matter compared to grey matter in WS. The posterior brain regions are notably more affected, with reduced grey matter density observed in the superior parietal lobe and hypofunction near the intraparietal sulcus, areas associated with multisensory integration and perception [24].
A single dose of nitisinone (approximately 0.1 milligram per kilogram of body weight) could make someone’s blood deadly to mosquitoes for around five days, they found. However, no mosquito mortality was observed for “any single dose of ivermectin,” the team reported.
In a separate analysis, the researchers fed mosquitoes blood samples from three patients with alkaptonuria who regularly took 2 mg of nitisinone a day. All of the mosquitoes died within 12 hours of feeding. Blood from a patient with alkaptonuria who had not started the treatment was not toxic to mosquitoes.
Taken together, these findings suggest that nitisinone therapy could be a promising new malaria-control method. However, the researchers cautioned that there are still many hurdles to overcome before the drug could be used for this purpose.
CRISPR gene-editing removes SOX2 gene and eliminates 50% of head and neck tumors in mice, offering new hope for targeted cancer therapy.
The CL1 biological computer, manufactured by the Australian company Cortical Labs, is designed for biomedical research, but also promises to deliver a more fast-paced and energy-efficient computing system
ChREBP is a transcription factor that plays a crucial role in regulating glucose metabolism. It exists in two main isoforms: ChREBPα and ChREBPβ. This is the first study to identify and develop small molecules—termed “molecular glues”—that enhance the interaction between ChREBPα and 14−3−3 proteins in pancreatic beta cells.
The molecular glues in this case increase the binding between 14−3−3 proteins and ChREBPα, which is anchored in the cytoplasm of the beta cell by the 14−3−3 proteins. Under conditions of glucolipotoxicity, ChREBPα goes into the nucleus and starts making too much of ChREBPβ, which acts to disable and even kill the patient’s beta cells. By using a molecular glue designed to increase the binding of ChREBPα to 14−3−3 proteins, ChREBPα never leaves the cytoplasm, cannot enter the nucleus, and therefore does not make ChREBPβ
When tested in primary human beta cells, these molecular glues significantly reduced the toxic effects of glucolipotoxicity, thus preserving beta cell function and identity. This discovery represents a major shift in diabetes research, as transcription factors like ChREBP have long been considered “undruggable” targets. The study also highlights the broader potential of molecular glues for modulating similar interactions in other diseases.
The researchers have discovered a novel approach to protecting insulin-producing beta cells from the damaging effects of glucolipotoxicity—a harmful condition linked to the progression of type 2 diabetes (T2D). These findings, published in Nature Communications, could lead to promising treatments targeting beta cell dysfunction.
For patients, this research could lead to new treatments that protect the insulin-producing cells in the pancreas, potentially slowing or even preventing the progression of diabetes, thus reducing the need for insulin therapy and improving long-term blood sugar control. Unlike current therapies that primarily manage blood sugar levels, this approach would allow doctors to directly target beta cell loss, which could improve long-term disease outcomes for their patients.
“This is an exciting step forward in our understanding of beta cell protection and the prevention of diabetes deterioration,” said the lead author. “For the first time, we’ve shown that it’s possible to use small molecules to fine-tune carbohydrate response element binding protein (ChREBP) activity in a way that could have major therapeutic implications.”
Ketorolac in the perioperative management of acute type A aortic dissection: a randomized double-blind placebo-controlled trial
Posted in biotech/medical | Leave a Comment on Ketorolac in the perioperative management of acute type A aortic dissection: a randomized double-blind placebo-controlled trial
Acute Type A Aortic Dissection (aTAAD) is a severe and life-threatening condition. While animal studies have suggested that ketorolac could slow the progression of aortic aneurysms and dissections, clinical data on its efficacy in aTAAD patients remain limited. This study seeks to evaluate the safety and effectiveness of ketorolac in this patient group.
Patients were randomly assigned to receive either ketorolac or a placebo (0.9% saline). Treatment began at least 2 h prior to surgery (60 mg ketorolac or 2 ml saline administered once intramuscularly) and continued for 48 h post-surgery (30 mg ketorolac or 1 ml saline administered intramuscularly twice daily). The primary endpoints included assessing the safety and efficacy of ketorolac in improving the prognosis of aTAAD, focusing on mortality and organ malperfusion syndrome. Secondary endpoints included drug-related adverse events, blood test results, and other postoperative outcomes.
Of 179 patients who underwent aTAAD repair, 110 met the inclusion criteria and were randomized into two groups of 55. One patient discontinued the intervention due to erythroderma on the first postoperative day, leaving 54 patients in the ketorolac group and 55 in the placebo group for analysis. No significant differences were found in the primary endpoints. However, the ketorolac group showed lower intraoperative bleeding (median: 1.8 L vs. 2.0 L, P = 0.03), shorter intensive care unit (ICU) stays (median: 6.5 days vs. 8 days, P = 0.04), and lower total hospital costs (median: ¥170,430 vs. ¥187,730, P = 0.03).