Results 61 to 70 of about 65,295 (252)

Bifunctional Artificial Enzymes‐Loaded Microgels With LOX‐ and CAT‐Like Activities for Metabolic Reprogramming and Scarless Wound Repair

Advanced Science, EarlyView.
A bifunctional lactate oxidase‐like and catalase‐like artificial enzyme (Metazyme) is integrated into a rod‐shaped microgel (MetaRgel) to enable cascade lactate oxidation and oxygen regeneration. By reprogramming the wound metabolic microenvironment, MetaRgel alleviates excessive lactate accumulation, oxidative stress, hypoxia, and inflammation ...
Yongyuan Kang, Pai Peng, Liang Song, Qiaoxuan Wang, Zilong Zhong, Dongchao Qiu, Yunfan Liu, Kefei Zhao, Xiaofei Dong, Changyou Gao   +9 more
wiley   +1 more source

Persistent Lactate Elevation in a Patient with Asthma Exacerbation and a Congenital Portosystemic Shunt: A Case Report and Literature Review

Reports
Background and Clinical Significance: When lactate production surpasses the body’s clearance capacity, hyperlactatemia (lactate ≥ 2 mmol/L) or lactic acidosis (lactate ≥ 4 mmol/L) can develop.
Wing Fai Li, Bailey Fink, Rehnuma Khan, Xinmiao Luo, Muhammad Fahimuddin   +4 more
doaj   +1 more source

Significant Lactic Acidosis from Albuterol

Clinical Practice and Cases in Emergency Medicine, 2018
Lactic acidosis is a clinical entity that demands rapid assessment and treatment to prevent significant morbidity and mortality. With increased lactate use across many clinical scenarios, lactate values themselves cannot be interpreted apart from their ...
Maxwell Hockstein, Deborah Diercks
doaj   +1 more source

Severe hepatopathy and neurological deterioration after start of valproate treatment in a 6-year-old child with mitochondrial tryptophanyl-tRNA synthetase deficiency [PDF]

, 2018
Background: The first subjects with deficiency of mitochondrial tryptophanyl-tRNA synthetase (WARS2) were reported in 2017. Their clinical characteristics can be subdivided into three phenotypes (neonatal phenotype, severe infantile onset phenotype ...
De Bruyne, Ruth, Menten, Björn, Roels, Frank, Roeyers, Herbert, Smet, Joél, Stepman, Hedwig, Van Coster, Rudy, Vanlander, Arnaud, Vantroys, Elise, Vergult, Sarah   +9 more
core   +1 more source

m.10010T>C Mitochondrial Disease: A Case Report With Hypoparathyroidism and Review of the Literature

American Journal of Medical Genetics Part A, EarlyView.
ABSTRACT Mitochondria are essential intracellular organelles that play a critical role in cellular metabolism, including the regulation of intracellular calcium signaling. Advances in genomic sequencing have facilitated the identification of rare pathogenic mitochondrial DNA (mtDNA) genetic variants in patients with unexplained endocrine disorders.
Jacob Mohr, Anja Lisbeth Frederiksen, Morten Duno, Anne Pernille Hermann, Trine Maxel Juul, Simone Rask Nielsen   +5 more
wiley   +1 more source

The synergism of cytosolic acidosis and reduced NAD+/NADH ratio is responsible for lactic acidosis-induced vascular smooth muscle cell impairment in sepsis

Journal of Biomedical Science
Background During sepsis, serve vascular dysfunctions lead to life-threatening multiple organ failure, due to vascular smooth muscle cells (VSMC) impairments, resulting in vasoplegia, hypotension and hypoperfusion.
Philipp Terpe, Stefanie Ruhs, Virginie Dubourg, Michael Bucher, Michael Gekle   +4 more
doaj   +1 more source

Interpreting the Consequences of Metformin Accumulation in an Emergency Context: Impact of the Time Frame on the Blood Metformin Levels

International Journal of Endocrinology, 2014
Objective. To clarify the link between metformin accumulation and its metabolic consequences by taking the time frame for metformin measurement into account. Research Design and Methods.
Jean-Daniel Lalau, Farshad Kajbaf
doaj   +1 more source

Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults. [PDF]

, 2019
Thiamine (vitamin B1) is an essential nutrient that serves as a cofactor for a number of enzymes, mostly with mitochondrial localization. Some thiamine-dependent enzymes are involved in energy metabolism and biosynthesis of nucleic acids whereas others ...
Adams, Alfadhel, Alfadhel, Alfadhel, Aljabri, Anwar, Aronson, Arts, Attwell, Baio, Banka, Barennes, Benton, Bettendorff, Bettendorff, Biesecker, Brown, Butterworth, Butterworth, Butterworth, Calhau, Carney, Chandrakumar, Chen, Cheung, Chornyy, Chugani, Colbert, Croft, Day, De Meirleir, Fattal-Valevski, Fattal-Valevski, Fleming, Forouhi, Foulon, Foulon, Fraccascia, Fraccascia, Fraser, Frustaci, Fujita, Galvin, Ganapathy, Gangolf, Ganie, Ghaleiha, Gibson, Giulivi, Gold, Greenwood, Gu, Harel, Hiffler, Hilker, Inaba, Ishaque, Israels, Jankowska-Kulawy, Junior, Kamasak, Karabatsiakis, Kelley, Kerns, Khaw, Kitamura, Kornreich, Kril, Laforenza, Leichter, Lindhurst, Liu, Lonsdale, Lonsdale, Lonsdale, Lorber, Lu, Lukienko, Luxemburger, Lương, Ma, Magos, Mahajan, Mahmood, Martel, Martin, Mayr, McLure, Mergenthaler, Mezzar, Mimouni-Bloch, Molina, Mulholland, Mulle, Muoio, Murata, Nabokina, Nabokina, Nardone, Navarro, Nikseresht, Obrenovich, Oishi, Opdenakker, Ortega Garcia, Ortigoza-Escobar, Pepersack, Perez-Duenas, Plaitakis, Prabakaran, Prohaska, Rabie, Randle, Renthal, Rindi, Rindi, Robinson, Roust, Rubio-Lopez, Said, Schaller, Scrimshaw, Sequeira Lopes da Silva, Shi, Singleton, Siu, Skjeldal, Smidt, Society, Song, Sperringer, Spiegel, Stargrove, Subramanian, Subramanian, Sweet, Tabarki, Talwar, Thomson, Thornalley, van den Brink, Vasconcelos, Vernau, Vernau, Vimokesant, Watkins, Wendel, Whitfield, Whitfield, Wierzbicki, Williams, Yang, Zhang, Zhao, Zuccoli   +154 more
core   +2 more sources

Expanding the Phenotype of TUFM‐Related Combined Oxidative Phosphorylation Deficiency 4

American Journal of Medical Genetics Part A, EarlyView.
ABSTRACT Combined oxidative phosphorylation deficiency 4 (COXPD4) is a rare mitochondrial condition caused by biallelic deleterious variants in the nuclear‐encoded gene TUFM. To date, most individuals with COXPD4 have presented with encephalopathy, hypotonia, and abnormal brain imaging. Many of the reported individuals died in infancy. We aim to expand
Noémie Villeneuve‐Cloutier, Jodi Warman‐Chardon, Danielle K. Bourque   +2 more
wiley   +1 more source

In-vitro activation of complement system by lactic acidosis in newborn and adults

Mediators of Inflammation, 2001
Introduction: Complement activation occurs secondary to a variety of external stimuli. Lactic acidosis has been previously shown to activate the complement factors C3a and C5a.
Friederike Hecke, Thomas Hoehn, Evelyn Strauss, Michael Obladen, Josef Sonntag   +4 more
doaj   +1 more source