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Epigenetics in Learning and Memory.
Subcell Biochem
January 2025
Faculty of Medicine and Faculty of Life Sciences, Institute of Biomedical Sciences (ICB), Universidad Andres Bello, Santiago, Chile.
In animals, memory formation and recall are essential for their survival and for adaptations to a complex and often dynamically changing environment. During memory formation, experiences prompt the activation of a selected and sparse population of cells (engram cells) that undergo persistent physical and/or chemical changes allowing long-term memory formation, which can last for decades. Over the past few decades, important progress has been made on elucidating signaling mechanisms by which synaptic transmission leads to the induction of activity-dependent gene regulation programs during the different phases of learning (acquisition, consolidation, and recall).
View Article and Find Full Text PDFMitochondrial dysfunction is a major cause of thromboinflammation and inflammatory cell death in critical illnesses.
Inflamm Res
January 2025
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Background: Mitochondria generate the adenosine triphosphate (ATP) necessary for eukaryotic cells, serving as their primary energy suppliers, and contribute to host defense by producing reactive oxygen species. In many critical illnesses, including sepsis, major trauma, and heatstroke, the vicious cycle between activated coagulation and inflammation results in tissue hypoxia-induced mitochondrial dysfunction, and impaired mitochondrial function contributes to thromboinflammation and cell death.
Methods: A computer-based online search was performed using the PubMed and Web of Science databases for published articles concerning sepsis, trauma, critical illnesses, cell death, mitochondria, inflammation, coagulopathy, and organ dysfunction.
PPARα suppresses growth of hepatocellular carcinoma in a high-fat diet context by reducing neutrophil extracellular trap release.
JHEP Rep
January 2025
Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Background & Aims: The role of infiltrating neutrophils in hepatocellular carcinoma (HCC) is modulated by cellular metabolism, specifically lipid homeostasis. Throughout the progression of HCC, alterations in lipid metabolism are intricately linked with regulation of neutrophil function and the release of neutrophil extracellular traps (NETs). However, how much the protumor effect of a high-fat diet (HFD) depends on NETs and the potential interplay between NETs and other leukocytes in HCC remains uncertain.
View Article and Find Full Text PDFOptical tweezers in biomedical research - progress and techniques.
J Med Life
November 2024
Biophysics and Cellular Biotechnology Department, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
Optical tweezers, which leverage the forces exerted by radiation pressure, have emerged as a pivotal technique for precisely manipulating and analyzing microscopic particles. Since Arthur Ashkin's ground-breaking work in the 1970s and the subsequent development of the single-beam optical trap in 1986, the capabilities of optical tweezers have expanded significantly, enabling the intricate manipulation of biological specimens at the micro- and nanoscale. This review elucidates the foundational principles of optical trapping and their extensive applications in the biomedical sciences.
View Article and Find Full Text PDFClinical Application of PARP1 Inhibitors and Challenges in Cancer Therapy.
Curr Cancer Drug Targets
January 2025
Cancer Research Center, Shantou University Medical College, Shantou 515041, Guangdong, PR China.
Among the Poly(ADP-ribose) Polymerase (PARP) family in mammals, PARP1 is the first identified and well-studied member that plays a critical role in DNA damage repair and has been proven to be an effective target for cancer therapy. Here, we have reviewed not only the role of PARP1 in different DNA damage repair pathways, but also the working mechanisms of several PARP inhibitors (PARPi), inhibiting Poly-ADP-ribosylation (PARylation) processing and PAR chains production to trap PARP1 on impaired DNA and inducing Transcription- replication Conflicts (TRCs) by inhibiting the PARP1 activity. This review has systematically summarized the latest clinical application of six authorized PARPi, including olaparib, rucaparib, niraparib, talazoparib, fuzuloparib and pamiparib, in monotherapy and combination therapies with chemotherapy, radiotherapy, and immunotherapy, in different kinds of cancer.
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