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A novel PET perfusion radiotracer, ¹⁸ F-flurpiridaz, can diagnose coronary artery disease (CAD) in obese patients with a higher sensitivity and specificity compared to ^99m Tc-SPECT myocardial perfusion imaging (MPI), according to research presented at the 2023 Society of Nuclear Medicine and Molecular Imaging Annual Meeting. ¹⁸ F-flurpiridaz PET MPI obtained images at a lower radiation dose than ^99m Tc-SPECT MPI and performed similarly in both obese and non-obese patients.

Obese individuals frequently have medical conditions such as diabetes, high cholesterol, and high blood pressure that put them at higher risk of developing CAD. Due to these risk factors, imaging obese patients for CAD is very important.

“Due to their body shape, it’s often hard to image obese individuals,” said Krishna Patel, MD, assistant professor of medicine and cardiology at the Icahn School of Medicine at Mount Sinai in New York. “This can result in inferior image quality and diagnostic performance despite requiring a higher dose of radiation.”

“These findings suggest that primary care may be exerting a protective effect on postoperative morbidity and mortality,” wrote Sanford E. Roberts, MD, of the University of Pennsylvania in Philadelphia, and co-authors in JAMA Surgery.

Of note, Black patients with PCP exposure had similar adjusted odds of in-hospital mortality relative to patients with no PCP exposure (OR 1.09, 95% CI 0.75−1.57), while white patients with PCP exposure had a 21% decreased risk of in-hospital mortality compared with the same group (OR 0.79, 95% CI 0.70−0.90).

However, at 30, 60, 90, and 180 days post-surgery, both Black and white patients who had visited a PCP had significantly lower adjusted odds of mortality compared with those who had not seen a PCP, with no significant differences in the interactions between race and PCP exposure for mortality.

Using artificial intelligence (AI) to combine data from full-body x-ray images and associated genomic data from more than 30,000 UK Biobank participants, a study by researchers at The University of Texas at Austin and New York Genome Center has helped to illuminate the genetic basis of human skeletal proportions, from shoulder width to leg length.

The findings also provide new insights into the evolution of the human skeletal form and its role in musculoskeletal disease, providing a window into our evolutionary past, and potentially allowing doctors to one day better predict patients’ risks of developing conditions such as back pain or arthritis in later life. The study also demonstrates the utility of using population-scale imaging data from biobanks to understand both disease-related and normal physical variation among humans.

“Our research is a powerful demonstration of the impact of AI in medicine, particularly when it comes to analyzing and quantifying imaging data, as well as integrating this information with health records and genetics rapidly and at large scale,” said Vagheesh Narasimhan, PhD, an assistant professor of integrative biology as well as statistics and data science, who led the multidisciplinary team of researchers, to provide the genetic map of skeletal proportions.

Autophagy biology has emerged as a ray of hope in addressing age-related diseases such as neurodegenerative disorders. Substantial effort in academia has been directed at advancing our understanding of the field and paving the way for ground-breaking therapies. But with genuine challenges in harnessing the power of autophagy and in developing effective therapies in this disease area, how close are we to really finding the first autophagy boosting drugs…?

The devastating impact of neurodegenerative diseases such as Parkinson’s, Alzheimer’s and amyotrophic lateral sclerosis (ALS), the most common form of Motor Neurone Disease (MND), cannot be overstated. According to the WHO, neurological diseases affect over a billion people globally and are the leading cause of disability and the second leading cause of death worldwide [1, 2]. Incidence is increasing too, predominantly driven by population growth and aging. And, with no prospect of a cure, people who develop these conditions face a bleak future.

Justifiably, this disease area has been the subject of intensive research for many years and there have been some breakthroughs along the way, possibly offering hope for the development of new therapies. However, translating scientific breakthroughs into viable drugs for patients has been enormously challenging.

Acute respiratory infection is caused by a wide range of pathogens, and an etiologic diagnosis is established in only about one third of cases. As a result, broad-spectrum antibiotics are often unnecessarily prescribed and continued. The BioFire FilmArray^® Pneumonia Panel (BioFire PN) is a commercial multiplex polymerase chain reaction (PCR) assay directed against 33 targets, including viruses, bacteria, and antibiotic resistance genes. In critically ill patients, BioFire PN results have shown a high level of agreement with culture results when tracheal aspirates (TA) or bronchoalveolar lavage fluid were sampled.

Now, in a comparative study, 298 samples (286 expectorated sputum and 12 from TA) deemed of good or moderate quality were obtained from hospitalized adult patients with acute respiratory or cardiopulmonary illness. BioFire PN detected a total of 1.23 bacterial pathogens per sample. Hemophilus influenzae was detected most often (33.0%), followed by Streptococcus pneumoniae and Staphylococcus aureus (20.5% for both), gram-negative bacilli (18.5%), and Moraxella catarrhalis (12.4%). Standard bacterial culture detected only 0.48 organisms per sample (compared with BioFire PN; P90%. Viral pathogens were detected in 51% of samples. Based on adjudication, the specificity of BioFire PN was only 45.0%. This was attributed to the greater number of potential pathogens identified compared with standard culture.

The North Carolina plant produces drugs that are injected or go through an IV.

The plant makes drugs for anesthesia, medicines that treat infections, and drugs needed for surgeries. The latter are used in surgeries or intensive care units for patients who are placed on ventilators, said Mike Ganio, who studies drug shortages at the American Society of Health-System Pharmacists.

The Pfizer site does not make or store the company’s COVID-19 vaccine or treatments Comirnaty and Paxlovid.

Summary: Researchers reveal how a fertilized egg cell, or zygote, initiates its own genetic program, a process known as zygote genome activation.

The research identifies the OBOX gene family as master-regulators, crucial for this activation. These genes instruct the enzyme RNA polymerase II to transcribe the right genes at the right time, beginning the embryo’s development.

The team suggests that the genes’ functions are redundant to ensure this critical transition occurs successfully.

In a new study published in Nature Methods, researchers at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, describe improvements in the methods with which mutations can be introduced in human and other genomes—making these methods much more efficient and less error prone.

In the field of genome editing, scientists often need to change one letter—corresponding to one of the DNA bases Adenine, Guanine, Cytosine or Thymine—to another letter at one specific position in the genome. To do this, they use reagents that cut both strands of the DNA close to the position they want to change.

They then provide the cell with DNA molecules that contain the desired new letter in the hope that the cell’s repair systems will use these molecules to introduce the desired mutation when the DNA break is repaired. Since different repair systems in the cells compete with each other and only one of these systems is able to introduce the desired new mutation, applications of genome editing of single letters have so far been limited by low efficiency and unintended byproducts.

Neurologists at a memory clinic in China diagnosed a 19-year-old with what they believe to be Alzheimer’s disease, making him the youngest person to be diagnosed with the condition in the world.

The male teenager began experiencing memory decline around age 17, and the cognitive losses only worsened over the years.

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