S. typhimurium mutants with altered sensitivity to fusidic acid (more resistant or more sensitive than the original culture) were selected. The mutants studied changed some of their properties (morphology, antigenic structure, and biochemical activity). They were characterized by a lower growth rate and probably by some alterations in the envelope cell structures- Some mutants acquired cross resistance or sensitivity to other antibiotics. As the mutants were selected by increased resistance or sensitivity to fusidic acid which affected the translocation factor G of the ribosome cycle, such pleiotropic changes of their properties could be due to some alterations in the G-factor itself.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Sensitive dependence of pairing symmetry on Ni-e crystal field splitting in the nickelate superconductor LaNiO.
Nat Commun
January 2025
NYU-ECNU Institute of Physics, NYU Shanghai, Shanghai, China.
The discovery of high-temperature superconductivity in LaNiO under pressure has drawn great attention. However, consensus has not been reached on its pairing symmetry in theory. By combining density-functional-theory (DFT), maximally-localized-Wannier-function, and linearized gap equation with random-phase-approximation, we find that the pairing symmetry of LaNiO is d, if its DFT band structure is accurately reproduced by a downfolded bilayer two-orbital model.
View Article and Find Full Text PDFSensitivity of coronary hemodynamics to vascular structure variations in health and disease.
Sci Rep
January 2025
Mechanical Engineering, Carnegie Mellon University, Pittsburgh, 15213, USA.
Local hemodynamics play an essential role in the initiation and progression of coronary artery disease. While vascular geometry alters local hemodynamics, the relationship between vascular structure and hemodynamics is poorly understood. Previous computational fluid dynamics (CFD) studies have explored how anatomy influences plaque-promoting hemodynamics.
View Article and Find Full Text PDFAdvanced sleep phase syndrome: Role of genetics and aging.
Handb Clin Neurol
January 2025
Sleep Medicine Center, Department of Neurology, Villa Serena Hospital, Città S. Angelo, Pescara, Italy; Villaserena Research Foundation, Città S. Angelo, Pescara, Italy.
Advanced sleep phase (ASP) is seldom brought to medical attention because many individuals easily adapt to their early chronotype, especially if it emerges before the age of 30 and is present in a first-degree relative. In this case, the disorder is considered familial (FASP) and is mostly discovered coincidentally in the presence of other sleep disorders, mainly obstructive sleep apnea syndrome (OSAS). The prevalence of FASP is currently estimated to be between 0.
View Article and Find Full Text PDFModelling the human Coenzyme Q deficiency in Drosophila melanogaster.
Free Radic Biol Med
January 2025
Centro Andaluz de Biología del Desarrollo, Universidad Pablo de Olavide-CSIC-JA, Sevilla, Spain; CIBERER, U729, Instituto de Salud Carlos III, Madrid, Spain. Electronic address:
The interference of the expression of each of the genes involved in the synthesis of coenzyme Q (CoQ) in Drosophila melanogaster can help to understand the pathophysiology of CoQ-dependent mitochondrial diseases in humans. We have knocked-down all genes involved in the CoQ biosynthesis pathway at different temperatures to induce depletion of CoQ at different levels throughout the body and in a tissue-specific manner. The efficiency of the knockdowns was quantified by Q-RTPCR and determination of CoQ levels by HPLC-UV+ECD.
View Article and Find Full Text PDFLight chain Split Luciferase assay implicates pathological NOTCH3 thiol reactivity in inherited cerebral small vessel disease.
J Biol Chem
January 2025
Departments of Neurology, University of Michigan, Ann Arbor, MI 48109; Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109; Neurology Service, VA Ann Arbor Healthcare System, Department of Veterans Affairs, Ann Arbor, MI 48105. Electronic address:
Stereotyped mutations in NOTCH3 drive CADASIL, the leading inherited cause of stroke and vascular dementia. The vast majority of these mutations result in alterations in the number of cysteines in the gene product. However, non-cysteine altering pathogenic mutations have also been identified, making it challenging to discriminate pathogenic from benign NOTCH3 sequence variants.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!