Fiber‐optic oxygen microsensors, a new tool in aquatic biology

A new fiber-optic oxygen microsensor (microoptrode) based on dynamic fluorescence quenching has been developed to measure oxygen gradients in marine sediments and microbial mats. The microoptrodes are fabricated by immobilizing an oxygen-quenchable fluorophore at the tapered tip of an optical fiber. A special optoelectronic system has been designed to measure oxygen with these microoptrodes. It is based on small and cheap optical components and can easily be miniaturized for field applications. In contrast to oxygen microelectrodes, the new oxygen microoptrodes are easy to make, do not consume oxygen, and show no stirring dependence of the signal. In addition, they show excellent long-term stability and storage stability. Hydrogen sulfide, carbon dioxide, and other relevant chemical parameters do not interfere with the measurement. Oxygen profiles in marine sediments obtained from measurements with microoptrodes show good correlation to profiles measured with oxygen microelectrodes

A novel measuring system for oxygen microoptodes based on a phase modulation technique

New fiber optic oxygen microsensors (microoptrodes) for use in aquatic environments have recently been developed as an alternative to commonly used CLark-type oxygen microelectrodes. The microoptrodes have the advantage of no oxygen consumption and no stirring sensitivity combined with a simple manufacturing process of the sensors. To avoid problems inherent to luminescence intensity measurements like photobleaching, signal dependency on the optical properties of the surrounding medium and system drifts, a novel measuring system was developed. This system uses a phase modulation method to evaluate a signal phase shift that is caused by the oxygen dependent luminescence lifetime. The measuring system is based on simple solid state technology. High reliability and low costs of the system can therefore be combined with the ability of miniaturization and low power consumption. The system consists of three units: 1) the microoptrode with the optical setup [glass fiber coupler, optical filters, lenses, light source (light emitting diode) and light detection (photon multiplier tube)], 2) the analogue signal processing unit, including a special phase detection module, and 3) the digital signal processing unit, a personal computer or a microcontroller for control of the measuring system, display and data storage. First measurements of oxygen depth profiles in sediments and biofilms at high levels of ambient light demonstrated the advantages of phase shift based O2 measurements as compared to intensity based measurements with microoptrodes

Primary and albedo protons detected by the Lunar Lander Neutron and Dosimetry experiment on the lunar farside

The Lunar Lander Neutron and Dosimetry (LND) Experiment aboard the Chang’E-4 Lander on the lunar far-side measures energetic charged and neutral particles and monitors the corresponding radiation levels. During solar quiet times, galactic cosmic rays (GCRs) are the dominating component of charged particles on the lunar surface. Moreover, the interaction of GCRs with the lunar regolith also results in upward-directed albedo protons which are measured by the LND. In this work, we used calibrated LND data to study the GCR primary and albedo protons. We calculate the averaged GCR proton spectrum in the range of 9–368 MeV and the averaged albedo proton flux between 64.7 and 76.7 MeV from June 2019 (the seventh lunar day after Chang’E-4’s landing) to July 2020 (the 20th lunar day). We compare the primary proton measurements of LND with the Electron Proton Helium INstrument (EPHIN) on SOHO. The comparison shows a reasonable agreement of the GCR proton spectra among different instruments and illustrates the capability of LND. Likewise, the albedo proton measurements of LND are also comparable with measurements by the Cosmic Ray Telescope for the Effects of Radiation (CRaTER) during solar minimum. Our measurements confirm predictions from the Radiation Environment and Dose at the Moon (REDMoon) model. Finally, we provide the ratio of albedo protons to primary protons for measurements in the energy range of 64.7–76.7 MeV which confirm simulations over a broader energy range

Prostate cancer proliferation is affected by the subcellular localization of MCT2 and accompanied by significant peroxisomal alterations

Reprogramming of lipid metabolism directly contributes to malignant transformation and progression. The increased uptake of circulating lipids, the transfer of fatty acids from stromal adipocytes to cancer cells, the de novo fatty acid synthesis, and the fatty acid oxidation support the central role of lipids in many cancers, including prostate cancer (PCa). Fatty acid ß-oxidation is the dominant bioenergetic pathway in PCa and recent evidence suggests that PCa takes advantage of the peroxisome transport machinery to target monocarboxylate transporter 2 (MCT2) to peroxisomes in order to increase ß-oxidation rates and maintain the redox balance. Here we show evidence suggesting that PCa streamlines peroxisome metabolism by upregulating distinct pathways involved in lipid metabolism. Moreover, we show that MCT2 is required for PCa cell proliferation and, importantly, that its specific localization at the peroxisomal membranes is essential for this role. Our results highlight the importance of peroxisomes in PCa development and uncover different cellular mechanisms that may be further explored as possible targets for PCa therapy.This work was supported by the Portuguese Foundation for Science and Technology (FCT): PTDC/IMI-MIC/0828/2012, PTDC/BIA-CEL/31378/2017, CEECIND/03747/2017, SFRH/BPD/77619/2011, SFRH/BD/101942/2014, UIDB/04501/2020, under the scope of the Operational Program “Competitiveness and internationalization”, in its FEDER/FNR component. It was also funded by the Comissão da Região Centro CCDRC and FEDER through the integrated project pAGE-CENTRO-01-0145-FEDER-000003. This work was also supported by national funds (OE), through FCT, I.P., in the scope of the framework contract foreseen in the numbers 4, 5, and 6 of the article 23, of the Decree-Law 57/2016, of August 29, changed by Law 57/2017, of July 19

Progressive multifocal leukoencephalopathy in a multiple Sclerosis patient diagnosed after switching from natalizumab to fingolimod

Background: Natalizumab- (NTZ-) associated progressive multifocal leukoencephalopathy (PML) is a severe and often disabling infectious central nervous system disease that can become evident in multiple sclerosis (MS) patients after NTZ discontinuation. Recently, novel diagnostic biomarkers for the assessment of PML risk in NTZ treated MS patients such as the anti-JC virus antibody index have been reported, and the clinical relevance of milky-way lesions detectable by MRI has been discussed. Case Presentation and Conclusion: We report a MS patient in whom PML was highly suspected solely based on MRI findings after switching from NTZ to fingolimod despite repeatedly negative (ultrasensitive) polymerase chain reaction (PCR) testing for JC virus DNA in cerebrospinal fluid. The PML diagnosis was histopathologically confirmed by brain biopsy. The occurrence of an immune reconstitution inflammatory syndrome (IRIS) during fingolimod therapy, elevated measures of JCV antibody indices, and the relevance of milky-way-like lesions detectable by (7 T) MRI are discussed

Transition energy and lifetime for the ground state hyperfine splitting of high Z lithiumlike ions

The ground state hyperfine splitting values and the transition probabilities between the hyperfine structure components of high Z lithiumlike ions are calculated in the range $Z=49-83$. The relativistic, nuclear, QED and interelectronic interaction corrections are taken into account. It is found that the Bohr-Weisskopf effect can be eliminated in a combination of the hyperfine splitting values of the hydrogenlike and lithiumlike ions of an isotope. This gives a possibility for testing the QED effects in a combination of the strong electric and magnetic fields of the heavy nucleus. Using the experimental result for the $1s$ hyperfine splitting in ^{209}Bi^{82+}, the 2s hyperfine splitting in ^{209}Bi^{80+} is calculated to be \Delta E=0.7969(2) eV.Comment: The nuclear charge distribution correction \delta is corrected, 14 pages, Late

7T MRI in natalizumab-associated PML and ongoing MS disease activity: a case study

OBJECTIVE: To assess the ability of ultra-high-field MRI to distinguish early progressive multifocal leukoencephalopathy (PML) from multiple sclerosis (MS) lesions in a rare case of simultaneous presentation of natalizumab-associated PML and ongoing MS activity. METHODS: Advanced neuroimaging including 1.5T, 3T, and 7T MRI with a spatial resolution of up to 0.08 mm(3) was performed. RESULTS: 7T MRI differentiated between PML-related and MS-related brain damage in vivo. Ring-enhancing MS plaques displayed a central vein, whereas confluent PML lesions were preceded by punctate or milky way-like T2 lesions. CONCLUSIONS: Given the importance of early diagnosis of treatment-associated PML, future systematic studies are warranted to assess the value of highly resolving MRI in differentiating between early PML- and MS-induced brain parenchymal lesions

POLRMT regulates the switch between replication primer formation and gene expression of mammalian mtDNA

Mitochondria are vital in providing cellular energy via their oxidative phosphorylation system, which requires the coordinated expression of genes encoded by both the nuclear and mitochondrial genomes (mtDNA). Transcription of the circular mammalian mtDNA depends on a single mitochondrial RNA polymerase (POLRMT). Although the transcription initiation process is well understood, it is debated whether POLRMT also serves as the primase for the initiation of mtDNA replication. In the nucleus, the RNA polymerases needed for gene expression have no such role. Conditional knockout of Polrmt in the heart results in severe mitochondrial dysfunction causing dilated cardiomyopathy in young mice. We further studied the molecular consequences of different expression levels of POLRMT and found that POLRMT is essential for primer synthesis to initiate mtDNA replication in vivo. Furthermore, transcription initiation for primer formation has priority over gene expression. Surprisingly, mitochondrial transcription factor A (TFAM) exists in an mtDNA-free pool in the Polrmt knockout mice. TFAM levels remain unchanged despite strong mtDNA depletion, and TFAM is thus protected from degradation of the AAA(+) Lon protease in the absence of POLRMT. Last, we report that mitochondrial transcription elongation factor may compensate for a partial depletion of POLRMT in heterozygous Polrmt knockout mice, indicating a direct regulatory role of this factor in transcription. In conclusion, we present in vivo evidence that POLRMT has a key regulatory role in the replication of mammalian mtDNA and is part of a transcriptional mechanism that provides a switch between primer formation for mtDNA replication and mitochondrial gene expression