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Bacterial strain breaks decades-old bottleneck in chemotherapy drug manufacturing

An international team of researchers has achieved a breakthrough in the production of doxorubicin, a vital chemotherapy agent. The study identifies and resolves molecular “bottlenecks” that have limited the natural production of this drug for over 50 years. The research is published in Nature Communications.

Doxorubicin is a chemotherapy drug that was first approved for medical use in the 1970s. It is a cornerstone in treating various cancers, including breast cancer, bladder cancer, lymphomas and carcinomas, with over one million patients receiving the treatment annually. However, bacteria naturally produce this important drug very inefficiently. Consequently, the pharmaceutical industry has relied on expensive, multi-step semi-synthetic processes.

“We have uncovered several independent factors that limit the formation of doxorubicin,” says researcher Keith Yamada, Ph.D., from the University of Turku in Finland, a lead scientist on the study.

Oligodendrocyte molecular perturbations associated with tau in Alzheimer’s

The findings suggest that in AD, part of what happens in the brain may involve changes in DNA tagging that affect the function of oligodendrocytes, particularly in relation to the buildup of the toxic protein tau.

Oligodendrocytes are the brain cells that make myelin, the insulation that helps nerve cells communicate. Scientists have theorized that disrupting neuron communication contributes to symptoms for people with AD. Researchers in this study found that nearly all significant methylation changes — small chemical tags added to DNA that help control when genes are turned on or off — were linked to the tau protein. This supports the idea that this protein plays a key role in brain cell changes tied to AD.

“Our team has previously shown that oligodendrocytes are affected in Alzheimer’s and another tau-related disease, progressive supranuclear palsy (PSP),” says the author. “These new results further highlight that problems in oligodendrocytes and myelin are central to AD. They also point to specific molecular pathways, particularly epigenetic changes, that could be targeted in future therapies.”

The study results identified new genes that may play a role in AD, including one called LDB3, and confirmed many findings across multiple independent datasets, showing its reliability. The identification of specific genes provides potential targets for future research — for example, scientists might investigate whether interventions that reverse methylation or support oligodendrocyte health can slow or modify disease progression for patients with AD. ScienceMission sciencenewshighlights.


In a study published in Nature Communications, the researchers have identified specific DNA-level changes in the brains of people with Alzheimer’s disease (AD). Using advanced biological analysis, the team mapped alterations in the brain’s regulatory landscape that may help explain why Alzheimer’s presents and progresses differently from person to person. The findings could also open new avenues for understanding other neurodegenerative diseases.

Alzheimer’s disease is the most common cause of dementia. Biologically, the disease begins with the formation of protein deposits, known as amyloid plaques, and neurofibrillary tangles in the brain. This causes brain cells to die over time and the brain to shrink. About 6.9 million people in the U.S. age 65 and older live with Alzheimer’s disease. There is no cure, and in advanced stages, complications can result in a significant decline in quality of life and death.

A gain-of-function Retsat variant from high-altitude adaptation promotes myelination via a neuronal dihydroretinoic acid-RXR-γ pathway

High-altitude survival gene in mammals may help reverse nerve damage from conditions like multiple sclerosis.

Neuron.


Li et al. report that a gain-of-function Retsat variant, associated with high-altitude adaptation, promotes myelination by boosting neuronal synthesis of the signaling metabolite ATDRA. This molecule activates RXR-γ in oligodendrocyte progenitors. Administration of the prodrug ATDR promotes remyelination in models of myelin disease.

Abstract: Tumor-intrinsic chromatin programs enforce immune evasion in glioblastoma:

Rongze Olivia Lu & colleagues provide a Commentary on Xinchun Zhang et al.: https://doi.org/10.1172/JCI195556


Address correspondence to: Rongze Olivia Lu, Helen Diller Comprehensive Cancer Center, University of California, San Francisco, 1,450 3rd St., Helen Diller Cancer Building, San Francisco, California 94,158, USA. Email: [email protected].

Cardiac Fibroblast Activation May Precede Myocardial Tissue Remodeling in Hypertrophic Cardiomyopathy

New HCM research: radionuclide-labeled fibroblast activation protein inhibitor (FAPI) imaging detects cardiac fibroblast activation before CMR-identified myocardial remodeling. Early detection may offer new insights into HCM.

Learn more in JACCIMG.


The Journal of the American College of Cardiology (JACC) stands as a leading global resource for impactful cardiovascular research, delivering essential peer-reviewed articles and crucial clinical practice guidelines. Gain access to authoritative medical content and vital CME resources designed to advance cardiovascular medicine and improve heart patient outcomes.

12 (Every) Plague That Wiped Out Humanity in Sci-Fi Movies — Explored

Humans think they can conquer everything in this world, like they have a solution for every problem, but this is where people get greedy, overambitious and most importantly, desperate. For example, in most of the science fiction and survival thrillers, people dig their own grave by creating deadly viruses in the labs, sometimes for political reasons and sometimes to create a medical miracle. These movies show how these man-made viruses wipe out humanity and make the world a living hell for a few immune survivors. Now, this has been a widely explored trope in every survival thriller, but deep beneath this layer, these films talk about something really ominous about our future.

#SciFi #ScienceFiction #SciFiMovies #SpeculativeFiction #scifiart

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