New Results and Lessons Learned from the MOVE-II and MOVE-IIb CubeSats

This paper covers the operations and lessons learned for the MOVE-II and MOVE-IIb satellites. Both are 1U CubeSats, with their purpose being hands-on education for students of all technical fields related to aerospace. The hardware of the spacecraft consists of a commercial on-board computer and an electrical power system, while all other systems, including the software, were designed by the student team. The MOVE-II CubeSat was successfully launched on December 3rd, 2018 and remains active in orbit to this day with almost daily commanding. The operations were full of surprises that pre-launch simulations did not foresee. With on-orbit data, we were able to correlate thermal, electrical and attitude dynamics simulations, thus uncovering flaws in former assumptions. We present the evolution of key properties of the spacecraft over its lifetime, such as the internal battery resistance, temperature and hardware defects. Compared to the expected 23°C average temperature, the satellite is quite cold at 3°C average. Furthermore, it shows a tendency to spin up uncontrollably due to a current loop in the solar cell wiring. To replicate the real behavior with simulations, a thermal model and a solar cell wiring current loop were added to the model. We also corrected the internal resistance of the battery in the model from 0.42 Ω to 1.26 Ω and added a temperature dependency to the internal resistance. The tendency to spin up, combined with a tight power budget, has remained a problem since the beginning of on-orbit operations. Although the anomaly shows non-deterministic behavior, regular detumbling maneuvers keep the spacecraft at tumbling rates between 2.5°s−1 and 200°s−1. At low turn rates, we downloaded a significant amount of data from the attitude determination and control system, enabling us to calibrate the magnetometer on ground with data recorded and downlinked over a span of several months. Additionally, we were also able to conduct payload measurements. The MOVE-IIb CubeSat, which launched on July 5th 2019 from the Vostochny Cosmodrome, is a copy of MOVE-II with minor improvements to correct the flaws of its predecessor. Unfortunately, a signal strength of 15 dB less than MOVE-II hindered any practical operations but it has been confirmed as alive in space. As possible causes we analyzed our initial guesses of a faulty deployment of the solar panels and antennae but also a malfunction of the transmitter. With the lessons learned from the MOVE-II/IIb missions, critical mistakes can be avoided for future CubeSat missions. As part of these lessons learned, the most useful and most hindering features of the spacecraft and its ground infrastructure are discussed. Furthermore, the training routine for the Mission Control team and its changes over time are described. The impact of the COVID-19 pandemic on spacecraft operations is also discussed, including lessons learned for future missions. This paper takes a look at the evolution of this mission since 2018. It discusses new findings, degradation of the spacecraft, lessons-learned and operations of the CubeSats

Volatilomics-Based Microbiome Evaluation of Fermented Dairy by Prototypic Headspace-Gas Chromatography–High-Temperature Ion Mobility Spectrometry (HS-GC-HTIMS) and Non-Negative Matrix Factorization (NNMF)

Fermented foods, such as yogurt and kefir, contain a versatile spectrum of volatile organic compounds (VOCs), including ethanol, acetic acid, ethyl acetate, and diacetyl. To overcome the challenge of overlapping peaks regarding these key compounds, the drift tube temperature was raised in a prototypic high-temperature ion mobility spectrometer (HTIMS). This HS-GC-HTIMS was used for the volatilomic profiling of 33 traditional kefir, 13 commercial kefir, and 15 commercial yogurt samples. Pattern recognition techniques, including principal component analysis (PCA) and NNMF, in combination with non-targeted screening, revealed distinct differences between traditional and commercial kefir while showing strong similarities between commercial kefir and yogurt. Classification of fermented dairy samples into commercial yogurt, commercial kefir, traditional mild kefir, and traditional tangy kefir was also possible for both PCA- and NNMF-based models, obtaining cross-validation (CV) error rates of 0% for PCA-LDA, PCA-kNN (k = 5), and NNMF-kNN (k = 5) and 3.3% for PCA-SVM and NNMF-LDA. Through back projection of NNMF loadings, characteristic substances were identified, indicating a mild flavor composition of commercial samples, with high concentrations of buttery-flavored diacetyl. In contrast, traditional kefir showed a diverse VOC profile with high amounts of flavorful alcohols (including ethanol and methyl-1-butanol), esters (including ethyl acetate and 3-methylbutyl acetate), and aldehydes. For validation of the results and deeper understanding, qPCR sequencing was used to evaluate the microbial consortia, confirming the microbial associations between commercial kefir and commercial yogurt and reinforcing the differences between traditional and commercial kefir. The diverse flavor profile of traditional kefir primarily results from the yeast consortium, while commercial kefir and yogurt is primarily, but not exclusively, produced through bacterial fermentation. The flavor profile of fermented dairy products may be used to directly evaluate the microbial consortium using HS-GC-HTIMS analysis

Metabolic implication of tigecycline as an efficacious second-line treatment for sorafenib-resistant hepatocellular carcinoma

Sorafenib represents the current standard of care for patients with advanced-stage hepatocellular carcinoma (HCC). However, acquired drug resistance occurs frequently during therapy and is accompanied by rapid tumor regrowth after sorafenib therapy termination. To identify the mechanism of this therapy-limiting growth resumption, we established robust sorafenib resistance HCC cell models that exhibited mitochondrial dysfunction and chemotherapeutic crossresistance. We found a rapid relapse of tumor cell proliferation after sorafenib withdrawal, which was caused by renewal of mitochondrial structures alongside a metabolic switch toward high electron transport system (ETS) activity. The translation-inhibiting antibiotic tigecycline impaired the biogenesis of mitochondrial DNA-encoded ETS subunits and limited the electron acceptor turnover required for glutamine oxidation. Thereby, tigecycline prevented the tumor relapse in vitro and in murine xenografts in vivo. These results offer a promising second-line therapeutic approach for advanced-stage HCC patients with progressive disease undergoing sorafenib therapy or treatment interruption due to severe adverse events

Methanobactin and MmoD work in concert to act as the ‘copper‐switch’ in methanotrophs

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/100314/1/emi12150.pd

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Liver mitochondrial membrane crosslinking and destruction in a rat model of Wilson disease

Wilson disease (WD) is a rare hereditary condition that is caused by a genetic defect in the copper-transporting ATPase ATP7B that results in hepatic copper accumulation and lethal liver failure. The present study focuses on the structural mitochondrial alterations that precede clinical symptoms in the livers of rats lacking Atp7b, an animal model for WD. Liver mitochondria from these Atp7b–/– rats contained enlarged cristae and widened intermembrane spaces, which coincided with a massive mitochondrial accumulation of copper. These changes, however, preceded detectable deficits in oxidative phosphorylation and biochemical signs of oxidative damage, suggesting that the ultrastructural modifications were not the result of oxidative stress imposed by copper-dependent Fenton chemistry. In a cell-free system containing a reducing dithiol agent, isolated mitochondria exposed to copper underwent modifications that were closely related to those observed in vivo. In this cell-free system, copper induced thiol modifications of three abundant mitochondrial membrane proteins, and this correlated with reversible intramitochondrial membrane crosslinking, which was also observed in liver mitochondria from Atp7b–/– rats. In vivo, copper-chelating agents reversed mitochondrial accumulation of copper, as well as signs of intra-mitochondrial membrane crosslinking, thereby preserving the functional and structural integrity of mitochondria. Together, these findings suggest that the mitochondrion constitutes a pivotal target of copper in WD