Results 41 to 50 of about 213,023 (309)

Beta-Blocker Type Effect on Substrate Oxidation during HIIE in Heart Failure Patients: Pilot Data

Arquivos Brasileiros de Cardiologia
The effect of third and second-generation type of beta-blocker on substrate oxidation especially during high-intensity exercises are scarce. The objective of the study is to explore differences of beta-blocker regimens (vasodilating vs.
Paula Aver Bretanha Ribeiro, Eve Normandin, Philippe Meyer, Martin Juneau, Michel White, Anil Nigam, Mathieu Gayda   +6 more
doaj   +1 more source

Specificity in the action of hypolipidemic drugs: increase of peroxisomal beta-oxidation largely dissociated from hepatomegaly and peroxisome proliferation in the rat.

Journal of Lipid Research, 1982
Hypolipidemic drugs increased 3- to 4-fold the activity of the peroxisomal beta-oxidation system in rat liver, with modest or no effects on catalase activity, liver weight, or peroxisome abundance.
P B Lazarow, H Shio, M A Leroy-Houyet
doaj   +1 more source

Mechanisms of parasite‐mediated disruption of brain vessels

FEBS Letters, EarlyView.
Parasites can affect the blood vessels of the brain, often causing serious neurological problems. This review explains how different parasites interact with and disrupt these vessels, what this means for brain health, and why these processes matter. Understanding these mechanisms may help us develop better ways to prevent or treat brain infections in ...
Leonor Loira, Sílvia Arroz‐Madeira, Cláudio A. Franco, Sara Silva Pereira   +3 more
wiley   +1 more source

Metabolic interplay between peroxisomes and other subcellular organelles including mitochondria and the endoplasmic reticulum

Frontiers in Cell and Developmental Biology, 2016
Peroxisomes are unique subcellular organelles which play an indispensable role in several key metabolic pathways which include: (1.) etherphospholipid biosynthesis; (2.) fatty acid beta-oxidation; (3.) bile acid synthesis; (4.) docosahexaenoic acid (DHA)
Ronald J.A. Wanders, Hans R. Waterham, Sacha eFerdinandusse   +2 more
doaj   +1 more source

An upstream open reading frame regulates expression of the mitochondrial protein Slm35 and mitophagy flux

FEBS Letters, EarlyView.
This study reveals how the mitochondrial protein Slm35 is regulated in Saccharomyces cerevisiae. The authors identify stress‐responsive DNA elements and two upstream open reading frames (uORFs) in the 5′ untranslated region of SLM35. One uORF restricts translation, and its mutation increases Slm35 protein levels and mitophagy.
Hernán Romo‐Casanueva, Ariann E. Mendoza‐Martínez, P. Abril Medina‐Flores, Carlos Campero‐Basaldua, Alexander DeLuna, Soledad Funes   +5 more
wiley   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 more
wiley   +1 more source

Multiple lipid oxidation products in low density lipoproteins induce interleukin-1 beta release from human blood mononuclear cells.

Journal of Lipid Research, 1994
Oxidized low density lipoproteins (LDL) induce the release of interleukin-1 beta (IL-1 beta) from human peripheral blood mononuclear cells, a process that may contribute to atherogenesis.
C.E. Thomas, R.L. Jackson, D.F. Ohlweiler, G. Ku   +3 more
doaj   +1 more source

Inhibition of CDK9 enhances AML cell death induced by combined venetoclax and azacitidine

Molecular Oncology, EarlyView.
The CDK9 inhibitor AZD4573 downregulates c‐MYC and MCL‐1 to induce death of cytarabine (AraC)‐resistant AML cells. This enhances VEN + AZA‐induced cell death significantly more than any combination of two of the three drugs in AraC‐resistant AML cells.
Shuangshuang Wu, Jianlei Zhao, Aaban Asfar Azmi, Avanti Gupte, Jenna Thibodeau, Shuang Liu, Jinli Yang, Guan Wang, Holly Edwards, Lisa A. Polin, Juiwanna Kushner, Sijana H. Dzinic, Kathryn White, Julie Boerner, Maik Hüttemann, Jay Yang, Yue Wang, Jeffrey W. Taub, Yubin Ge   +18 more
wiley   +1 more source

Polysaccharide monooxygenase-catalyzed oxidation of cellulose to glucuronic acid-containing cello-oligosaccharides

Biotechnology for Biofuels, 2019
Background Polysaccharide monooxygenases (PMOs) play an important role in the enzymatic degradation of cellulose. They have been demonstrated to able to C6-oxidize cellulose to produce C6-hexodialdoses. However, the biological function of C6 oxidation of
Jinyin Chen, Xiuna Guo, Min Zhu, Chen Chen, Duochuan Li   +4 more
doaj   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

Molecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source