The Influence of Temporal Disturbances in EKF Calculations on the Achieved Parameters of Flight Control and Stabilization of UAVs.

This article investigates the causes of occasional flight instability observed in Unmanned Aerial Vehicles (UAVs). The issue manifests as unexpected oscillations that can lead to emergency landings. The analysis focuses on delays in the Extended Kalman Filter (EKF) algorithm used to estimate the drone's attitude, position, and velocity. These delays disrupt the flight stabilization process. The research identifies two potential causes for the delays. First cause is magnetic field distrurbances created by UAV motors and external magnetic fields (e.g., power lines) that can interfere with magnetometer readings, leading to extended EKF calculations. Second cause is EKF fusion step implementation of the PX4-ECL library combining magnetometer data with other sensor measurements, which can become computionally expensive, especially when dealing with inconsistent magnetic field readings. This can significantly increase EKF processing time. The authors propose a solution of moving the magnetic field estimation calculations to a separate, lower-priority thread. This would prevent them from blocking the main EKF loop and causing delays. The implemented monitoring techniques allow for continuous observation of the real-time operating system's behavior. Since addressing the identified issues, no significant problems have been encountered during flights. However, ongoing monitoring is crucial due to the infrequent and unpredictable nature of the disturbances.

Yeast model analysis of novel polymerase gamma variants found in patients with autosomal recessive mitochondrial disease.

Replication of the mitochondrial genome depends on the single DNA polymerase (pol gamma). Mutations in the POLG gene, encoding the catalytic subunit of the human polymerase gamma, have been linked to a wide variety of mitochondrial disorders that show remarkable heterogeneity, with more than 200 sequence variants, often very rare, found in patients. The pathogenicity and dominance status of many such mutations remain, however, unclear. Remarkable structural and functional conservation of human POLG and its S. cerevisiae ortholog (Mip1p) led to the development of many successful yeast models, enabling to study the phenotype of putative pathogenic mutations. In a group of patients with suspicion of mitochondrial pathology, we identified five novel POLG sequence variants, four of which (p.Arg869Ter, p.Gln968Glu, p.Thr1053Argfs*6, and p.Val1106Ala), together with one previously known but uncharacterised variant (p.Arg309Cys), were amenable to modelling in yeast. Familial analysis indicated causal relationship of these variants with disease, consistent with autosomal recessive inheritance. To investigate the effect of these sequence changes on mtDNA replication, we obtained the corresponding yeast mip1 alleles (Arg265Cys, Arg672Ter, Arg770Glu, Thr809Ter, and Val863Ala, respectively) and tested their effect on mitochondrial genome stability and replication fidelity. For three of them (Arg265Cys, Arg672Ter, and Thr809Ter), we observed a strong, partially dominant phenotype of a complete loss of functional mtDNA, whereas the remaining two led to partial mtDNA depletion and significant increase in point mutation frequencies. These results show good correlation with the severity of symptoms observed in patients and allow to establish these variants as pathogenic mutations.

Deletion of one nucleotide within the homonucleotide tract present in the hsdS gene alters the DNA sequence specificity of type I restriction-modification system NgoAV.

As a result of a frameshift mutation, the hsdS locus of the NgoAV type IC restriction and modification (RM) system comprises two genes, hsdS(NgoAV1) and hsdS(NgoAV2). The specificity subunit, HsdS(NgoAV), the product of the hsdS(NgoAV1) gene, is a naturally truncated form of an archetypal specificity subunit (208 N-terminal amino acids instead of 410). The presence of a homonucleotide tract of seven guanines (poly[G]) at the 3' end of the hsdS(NgoAV1) gene makes the NgoAV system a strong candidate for phase variation, i.e., stochastic addition or reduction in the guanine number. We have constructed mutants with 6 guanines instead of 7 and demonstrated that the deletion of a single nucleotide within the 3' end of the hsdS(NgoAV1) gene restored the fusion between the hsdS(NgoAV1) and hsdS(NgoAV2) genes. We have demonstrated that such a contraction of the homonucleotide tract may occur in vivo: in a Neisseria gonorrhoeae population, a minor subpopulation of cells appeared to have only 6 guanines at the 3' end of the hsdS(NgoAV1) gene. Escherichia coli cells carrying the fused gene and expressing the NgoAVΔ RM system were able to restrict λ phage at a level comparable to that for the wild-type NgoAV system. NgoAV recognizes the quasipalindromic interrupted sequence 5'-GCA(N(8))TGC-3' and methylates both strands. NgoAVΔ recognizes DNA sequences 5'-GCA(N(7))GTCA-3' and 5'-GCA(N(7))CTCA-3', although the latter sequence is methylated only on the complementary strand within the 5'-CTCA-3' region of the second recognition target sequence.

Characterization of the NgoAXP: phase-variable type III restriction-modification system in Neisseria gonorrhoeae.

Methyltransferases associated with type III restriction-modification (RM) systems are phase-variably expressed in a variety of pathogenic bacteria. NgoAXP, the type III RM system encoded by Neisseria gonorrhoeae, was characterized in this study. The cloned resngoAXP and ngoAXPmod genes were expressed in Escherichia coli strains. The restriction and modification activities of NgoAXP were confirmed in vivo by the lambda phage restriction and modification test and in vitro by the methylation of DNA substrates in the presence of [methyl-(3)H]AdoMet. As in all known type III systems, the restriction activity needed the presence of both genes, while the presence of the ngoAXPmod gene was sufficient for DNA methylation. Following its overexpression, the DNA methyltransferase M.NgoAXP was purified to apparent homogeneity using metal affinity chromatography. The specific sequence recognized by this enzyme was determined as a nonpalindromic sequence: 5'-CCACC-3', in which the adenine residue is methylated. We observed that in E. coli cells, the expression of the restriction phenotype associated with NgoAXP switched randomly. This phase variation was associated with the change in the number of pentanucleotide repeats (5'-CCAAC/G-3') present at the 5'-end of the coding region of the ngoAXPmod gene.