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must help other doctors in this situation wherever possible.” Dr Roman Cregg on sending medical kits, drugs and equipment to aid the humanitarian crisis in Ukraine


Powerful antiviral for Ebola virus


New research suggests the combination of two potent antibodies could make an antiviral therapy to treat prominent ebolaviruses. The study, by scientists from La Jolla Institute for Immunology (LJI) and the National Institute for Allergy and Infectious Diseases, discovered that two human antibodies can target two prevalent ebolavirus species at once: Ebola virus and Sudan virus.


“Finding antibodies with this breadth is important because we don’t know which virus in the genus of ebolaviruses is going to break out next,” said LJI president and CEO Erica Ollmann Saphire. To learn more about these antibodies, LJI postdoctoral fellows Xiaoying Yu and Jake Milligan spearheaded the use of cryo-electron microscopy.


This technique revealed how the two antibodies, called 1C3 and 1C11, bind to vulnerable sites on a key ebolavirus protein, called the glycoprotein. The team


was surprised that instead of sticking to one site on the glycoprotein, the 1C3 lodged itself in an asymmetrical configuration, blocking three glycoprotein sites at once. Meanwhile, the paired antibody 1C11 binded to the fusion machinery the virus normally uses to enter and infect host cells. As Saphire explains, because the fusion machinery is critical, it looks very similar in both strains. “This is a site of very broad recognition and resistance to any antibody escape,” she said. “That’s how this antibody gets its breadth.” While there are antibody therapies against Ebola virus, some antibodies in these therapies do not neutralise it. Instead, they home in on a decoy protein, called soluble glycoprotein, that the virus makes. Fortunately, 1C3 and 1C11 ignore the decoy and go straight for the virus’s actual surface glycoprotein structure. This means the researchers could use fewer antibodies to target Ebola virus and Sudan virus.


Shortness of breath linked to heart attack mortality


Just 76% of heart attack patients with dyspnoea or fatigue as their main symptom are alive at one year, compared with 94% of those with chest pain as the predominant feature. That is the finding of research presented at a scientific congress of the European Society of Cardiology. Chest pain is the hallmark presentation of a heart attack, but patients can suffer from other complaints, such as shortness of breath, upper abdominal and neck pain or transient loss of consciousness (blackouts). “Patients presenting with shortness of breath or fatigue had a worse prognosis than those with chest pain,” said study author Dr Paulo Medeiros of Braga Hospital, Portugal. “They were less likely to be alive one year after their heart attack and also less likely to stay out of hospital for heart problems during that 12-month period.”


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Despite the correlation established by the study, Medeiros pointed out that patients with dyspnoea and fatigue were significantly older (and mostly female) than those in the other two groups, with an average age of 75 compared with 68 years in the chest pain group and 74 years in the group that had syncope as their main symptom. Patients with dyspnoea and fatigue as their main symptom were also more likely to have high blood pressure, diabetes, chronic kidney disease and chronic obstructive pulmonary disease. “This study highlights the need to consider a diagnosis of myocardial infarction even when the primary complaint is not chest pain. This may be particularly important for women and older patients where diagnosis could be delayed and result in worse outcomes.


A new biomarker for


Alzheimer’s disease An international group of researchers led by the Universitat Autonoma de Barcelona (UAB) analysed the genes that are expressed in neurons and brain cells called astrocytes, based on data from nearly 800 individuals and compared what happens in Alzheimer’s patients with people that do not have diagnosed dementia. The results suggest changes in astrocytes could be a potential biomarker of Alzheimer’s disease. The study, published in Neurobiology of Disease, revealed that as the disease progresses, astrocytes decrease the expression of genes that code for mitochondrial proteins, which prevents the mitochondria of these cells from functioning well. The international team of researchers believe this could be an adaptation of the astrocytes to compensate for the toxicity of the amyloid protein, which would impair communication between astrocytes and neurons. “We believe that this adaptation by astrocytes contributes to the worsening of the disease and could therefore be a key point in preventing its progression,” said Elena Galea, researcher at the institut de neurociències at UAB and first author of the article.


In order to gather data, the researchers looked at certain RNA molecules, or cellular transcriptome, in 766 post- mortem brain samples to determine which of all the genes are being expressed and to what extent. “By studying the transcriptome, we can see if there are silenced or overexpressed genes, and we can understand what is happening inside neurons and astrocytes”, explains Galea. The samples came from the alzheimer’s disease knowledge portal and were generated by three American clinics: Mount Sinai Hospital, the Mayo Clinic and the religious order Study/ Memory and Aging Project. It is one of the most thorough transcriptomic studies of human astrocytes in Alzheimer’s disease ever conducted.


Every 36 seconds


The frequency with which one person dies in the US as a result of heart disease. CDC, Underlying Cause of Death Data


Practical Patient Care / www.practical-patient-care.com


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