Chirality—often described as “handedness”—is a fundamental property of nature, underlying the behavior of molecules ranging from DNA to pharmaceuticals. While chemists have long known how to separate left- and right-handed forms of organic compounds, achieving the same control in inorganic crystals has remained a major scientific challenge.
A team led by UT Southwestern Medical Center researchers has uncovered a molecular pathway that links obesity to widespread inflammation, providing long-sought insight into why obesity increases the risk of type 2 diabetes, cardiovascular disease, fatty liver disease, and certain cancers.
The findings, published in Science, identify a molecular “switch” that triggers this inflammation and point to potential new therapeutic targets.
“It’s been known for a long time that obesity causes uncontrolled inflammation, but no one knew the mechanism behind it. Our study provides novel insights about why this inflammation occurs and how we might be able to stop it,” said Zhenyu Zhong, Ph.D., Assistant Professor of Immunology and member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. Dr. Zhong co-led the study with Danhui Liu, Ph.D., a former postdoctoral researcher in the Zhong Lab.
The mitochondria are membrane-bound intracellular organelles present in almost all eukaryotic cells (Kasahara & Kato, 2018). They generate energy through oxidative phosphorylation, and are responsible for 90% of cellular ATP (Greenfield et al., 2017). In mammals, the mitochondria are present in all cells, except the enucleated red blood cells, being more present in tissues that need energy metabolism, with several units of the organelle. They have a round or oval shape and are about 0.5 to 1 µm in diameter, and up to 7 µm in length (Laureano, 2015). Together with the cell nucleus, they are the only cell organelle having their own genome, an extremely compact molecule, with 16.500 base pairs and 37 genes: 13 messenger RNAs, 22 RNAs, and 2 ribosomal RNAs. The D-loop is the only non-coding region in mtDNA, since introns and intergenic regions are non-existent or restricted to a few nucleotides (Chiaratti et al., 2018).
In addition to the production of reactive oxygen species due to the release of free electrons generated from the respiratory chain, mitochondria have few repair systems and therefore are subject to genetic mutations, causing diseases that affect approximately 1 in 5,000 people (Laureano, 2015). Mitochondrial diseases can affect organs that depend on energy metabolism, such as skeletal muscle, cardiac, central nervous system, endocrine, retina and liver (Nogueira et al., 2015; Laureano, 2015), giving rise to several incurable diseases, such as: deafness, diabetes mellitus, myopathies, glaucoma and others (Costa et al., 2016). These metabolic disorders, lead to inefficient oxidative phosphorylation, impairing cell energy production (Craven et al., 2017). They are difficult to diagnose and most of the time untreated, affecting adults and children (Nogueira et al., 2015).
Mitochondria are inherited only from the female gamete; therefore, the mitochondrial DNA is of exclusive maternal inheritance (Volobueva et al., 2018). The genetic mutations present in this material can be avoided using mitochondrial substitution techniques (Adashi & Cohen, 2018), where the nuclear genome is withdrawn from an oocyte, which carries mitochondrial mutations, and is implanted in a normal enucleated donor (Greenfield et al., 2017).
Each year, more than two million people die from advanced chronic liver disease (ACLD). Previous research has linked gut microbiome disruptions to this condition and suggested that bacteria typically found in the mouth may colonize the gut.
A new study published in Nature Microbiology now shows that identical bacterial strains occur in both the mouth and gut of patients with advanced chronic liver disease and also reveals a mechanism by which oral bacteria affect gut health. The researchers also found that this process coincides with worsening liver health.
Monoclonal antibodies (mAbs) aid the body against autoimmune diseases and cancer, among other things. Patients have to pick up the medicine every few weeks. It would be easier for them to be able to inject the medicine themselves at home, but this would only be possible if the medications were highly concentrated but not too viscous.
A team at Ruhr University Bochum, Germany, led by Professor Lars Schäfer from the Center for Theoretical Chemistry and the company Boehringer Ingelheim Pharma have developed a quick and realistic simulation method to make this possible. This method can predict how formulations will behave.
The team reports its findings in the Journal of Physical Chemistry.
Researchers at the Francis Crick Institute and AlveoliX have developed the first human lung-on-chip model using stem cells taken from only one person. These chips simulate breathing motions and lung disease in an individual, holding promise for testing treatments for infections like tuberculosis (TB) and delivering personalized medicine.
The research is published in the journal Science Advances.
Air sacs in the lungs called alveoli are the essential site of gas exchange and also an important barrier against inhaled viruses and bacteria that cause respiratory diseases like flu or TB.
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Penn-led researchers have turned a deadly fungus into a potent cancer-fighting compound. After isolating a new class of molecules from Aspergillus flavus, a toxic crop fungus linked to deaths in the excavations of ancient tombs, the researchers modified the chemicals and tested them against leukemia cells. The result? A promising cancer-killing compound that rivals FDA-approved drugs and opens up new frontiers in the discovery of more fungal medicines.
“Fungi gave us penicillin,” says Sherry Gao, Presidential Penn Compact Associate Professor in Chemical and Biomolecular Engineering (CBE) and in Bioengineering (BE) and senior author of a new paper in Nature Chemical Biology on the findings. “These results show that many more medicines derived from natural products remain to be found.”
Too much fat can raise blood pressure, but the type matters more than the amount.
Researchers at Rockefeller University uncovered how thermogenic fat keeps blood vessels flexible by shutting down a vessel-stiffening enzyme.
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Promoting brown fat activity could counteract hypertension by reshaping the molecular signals that govern vascular stiffness.
The barrel-shaped structures found by the thousands in most animal cells are one of biology’s biggest mysteries. But although researchers haven’t figured out the function of these “vaults,” they now report a new use for the puzzling particles.
Enigmatic ‘vaults’ can be engineered to eavesdrop on RNA, aiding cancer studies and more.
Breakthrough in DNA sequencing offers clues to why most smokers do not develop lung cancer.
“Our data suggest that these individuals may have survived for so long in spite of their heavy smoking because they managed to suppress further mutation accumulation,” says pulmonologist and genetics researcher Simon Spivack, a co-author on the study. “This leveling off of mutations could stem from these people having very proficient systems for repairing DNA damage or detoxifying cigarette smoke.”
Researchers who study the health effects of cigarette smoke have used all kinds of methods — from giving lab animals high doses of chemicals found in tobacco to combing through archives to determine which diseases smokers get more often — to figure out how the habit affects the body. Those studies have made it clear that cigarettes contain hundreds of harmful chemicals, including dozens of carcinogens.
For decades, researchers didn’t have any way to measure the mutations in lung cells that actually cause lung cancer. Five years ago, researchers at Albert Einstein College of Medicine in New York found a way to overcome technical limitations that had made it impossible to sequence the genome. That is, they figured out how to determine the exact order of the A, T, C, and G molecules of the DNA within a single cell without introducing too many errors in the process.