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Category: biotech/medical – Page 87

Researchers at the University of Houston, in collaboration with Baylor College of Medicine, are developing new devices for treating children with hyperleukocytosis, a condition that develops when the body has an extremely high number of white blood cells, often due to leukemia.

Leukemia is the most common type of cancer in , with an annual incidence of about 5 per 100,000 children in the United States. Up to 20–30% of patients with acute leukemia develop hyperleukocytosis, placing them at risk for life-threatening complications.

Although definitive treatment for acute leukemia involves chemotherapy, leukapheresis—to urgently reduce dangerously elevated white blood cell counts—is a potentially life-saving therapeutic option. During leukapheresis, a large machine uses centrifugation to separate white blood cells, or leukocytes, from the rest of the blood, which is then returned to the patient.

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In the search for solutions to diseases like cancer, scientists are pursuing a new frontier in biology—the spatial and temporal places where our cells live.

Where first generation drugs targeted , over time evolving their own resistance, and techniques are needed to keep ahead of resistant diseases by targeting the surrounding cellular space.

Much of this exploration is taking place at the surface of our cells—the protein-packed semi-permeable membranes that act as protectors and as signaling posts to other cells in the surrounding area.

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University of Florida researchers have led a multicenter study demonstrating that Automated Imaging Differentiation for Parkinsonism (AIDP), a machine-learning method using magnetic resonance imaging (MRI), accurately distinguishes Parkinson’s disease (PD) from atypical parkinsonian disorders. Findings suggest this approach could significantly improve diagnostic precision and clinical care.

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For the first time, scientists have witnessed the very moment DNA begins to unravel, revealing a necessary molecular event for DNA to be the molecule that codes all life. A new study from King Abdullah University of Science and Technology (KAUST), published in Nature, captures the moment DNA begins to unwind, allowing for all the events that follow in DNA replication.

As an initial step, we selected ARDs associated with hallmarks of aging. These included a total of 83 diseases linked to one or more hallmarks of aging, based on the taxonomy put forward in ref. 4 (Supplementary Table 2). Support for this taxonomy comes from multiple sources. Analyses of electronic health records from general practice and hospitalizations identified more than 200 diseases with incidence rates increasing with chronological age6,22. Researchers linked a subset of these ARDs to specific hallmarks of aging using several approaches: mining 1.85 million PubMed abstracts on human aging, identifying shared genes in the genome-wide association study catalog, conducting gene set enrichment analysis and analyzing disease co-occurrence networks within each hallmark4.

We confirmed the co-occurrence of ARDs within each hallmark in 492,257 participants from the UK Biobank study23. The presence of one ARD increased the risk of developing another ARD related to the same hallmark, with clustering coefficients ranging from 0.76 for LOP-specific ARDs to 0.92 for SCE-specific ARDs. These findings corroborated the hallmark-specific clustering of ARDs (Extended Data Figs. 3 and 4)23.

In time-to-event analyses of UK Biobank and FPS participants without these ARDs at baseline (n ranging from 477,325 to 492,294 in the UK Biobank and from 278,272 to 286,471 in the FPS, depending on the social disadvantage indicator and ARD), social disadvantage—indicated by education and adult SES (neighborhood deprivation)—was associated with a higher risk of developing ARDs. In the UK Biobank, the age-, sex-and ethnicity-adjusted hazard ratio for developing any ARD was 1.31 (95% confidence interval (CI) 1.29–1.33) for individuals with low compared with high education. For individuals with high versus low adult SES, the hazard ratio was 1.21 (95% CI 1.20–1.23). In the FPS, the corresponding hazard ratios were 1.28 (95% CI 1.25–1.31) and 1.23 (95% CI 1.20–1.27), respectively.

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A research team led by Rice University’s Yang Gao has uncovered new insights into the molecular mechanisms of ADAR1, a protein that regulates ribonucleic acid (RNA) induced immune responses. Their findings, published in Molecular Cell March 17, could open new pathways for treating autoimmune diseases and enhancing cancer immunotherapy.

ADAR1 converts adenosine to inosine in double-stranded RNA, a process essential for preventing unwarranted immune responses, yet the molecular basis of this editing had remained unclear. Through detailed biochemical profiling and structural analysis, researchers found that ADAR1’s editing activity depends on RNA sequence, duplex length and mismatches near the editing site. High-resolution structures of ADAR1 bound to RNA reveal its mechanisms for RNA binding, substrate selection and dimerization.

“Our study provides a comprehensive understanding of how ADAR1 recognizes and processes RNA,” said Gao, assistant professor of biosciences and a Cancer Prevention and Research Institute of Texas (CPRIT) Scholar. “These insights pave the way for novel therapeutic strategies targeting ADAR1-related diseases.”

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Researchers have corrected a disease-causing gene mutation with a single infusion carrying a treatment that precisely targeted the errant gene.

This was the first time a mutated gene has been restored to normal.

The small study of nine patients announced Monday by the company Beam Therapeutics of Cambridge, Mass., involved fixing a spelling error involving the four base sequences — G, A, C and T — in DNA. The effect was to change an incorrect DNA letter to the right one. The result was a normal gene that functioned as it should, potentially halting liver and lung damage of patients with a rare disorder.

The small study in patients with a rare disorder that causes liver and lung damage showed the potential for precisely targeted infusions.

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