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The scale factor of thermal sensitivity serves as a crucial performance metric for micro-electromechanical system (MEMS) gyroscopes, and is commonly employed to assess the temperature stability of inertial sensors. To improve the temperature stability of the scale factor of MEMS gyroscopes, a self-compensation method is proposed. This is achieved by integrating the primary and secondary relevant parameters of the scale factor using the partial least squares regression (PLSR) algorithm. In this paper, a scale factor prediction model is presented. The model indicates that the resonant frequency and demodulation phase angle are the primary correlation terms of the scale factor, while the drive control voltage and quadrature feedback voltage are the secondary correlation terms of the scale factor. By employing a weighted fusion of correlated terms through PLSR, the scale factor for temperature sensitivity is markedly enhanced by leveraging the predicted results to compensate for the output. The results indicate that the maximum error of the predicted scale factor is 0.124% within the temperature range of −40 °C to 60 °C, and the temperature sensitivity of the scale factor decreases from 6180 ppm/°C to 9.39 ppm/°C.

MEMS gyroscopes are one of the core components of inertial navigation systems. The maintenance of high reliability is critical for ensuring the stable operation of the gyroscope. Considering the production cost of gyroscopes and the inconvenience of obtaining a fault dataset, in this study, a self-feedback development framework is proposed, in which a dualmass MEMS gyroscope fault diagnosis platform is designed based on MATLAB/Simulink simulation, data feature extraction, and classification prediction algorithm and real data feedback verification. The platform integrates the dualmass MEMS gyroscope Simulink structure model and the measurement and control system, and reserves various algorithm interfaces for users to independently program, which can effectively identify and classify seven kinds of signals of the gyroscope: normal, bias, blocking, drift, multiplicity, cycle and internal fault. After feature extraction, six algorithms, ELM, SVM, KNN, NB, NN, and DTA, were respectively used for classification prediction. The ELM and SVM algorithms had the best effect, and the accuracy of the test set was up to 92.86%. Finally, the ELM algorithm is used to verify the actual drift fault dataset, and all of them are successfully identified.

This paper presents a new type of three-axis gyroscope. The gyroscope comprises two independent parts, which are nested to further reduce the structure volume. The capacitive drive was adopted. The motion equation, capacitance design, and spring design of a three-axis gyroscope were introduced, and the corresponding formulas were derived. Furthermore, the X/Y driving frequency of the gyroscope was 5954.8 Hz, the Y-axis detection frequency was 5774.5 Hz, and the X-axis detection frequency was 6030.5 Hz, as determined by the finite element simulation method. The Z-axis driving frequency was 10,728 Hz, and the Z-axis sensing frequency was 10,725 Hz. The MEMS gyroscope’s Z-axis driving mode and the sensing mode’s frequency were slightly mismatched, so the gyroscope demonstrated a larger bandwidth and higher Z-axis mechanical sensitivity. In addition, the structure also has good Z-axis impact resistance. The transient impact simulation of the gyroscope structure showed that the maximum stress of the sensitive structure under the impact of 10,000 g@5 ms was 300.18 Mpa. The gyroscope was produced by etching silicon wafers in DRIE mode to obtain a high aspect ratio structure, tightly connected to the glass substrate by silicon/glass anode bonding technology.

Gene expression and growth rate are highly stochastic in Escherichia coli . Some of the growth rate variations result from the deterministic and asymmetric partitioning of damage by the mother to its daughters. One daughter, denoted the old daughter, receives more damage, grows more slowly and ages. To determine if expressed gene products are also allocated asymmetrically, we compared the levels of expressed green fluorescence protein in growing daughters descending from the same mother. Our results show that old daughters were less fluorescent than new daughters. Moreover, old mothers, which were born as old daughters, produced daughters that were more asymmetric when compared to new mothers. Thus, variation in gene products in a clonal E. coli population also has a deterministic component. Because fluorescence levels and growth rates were positively correlated, the aging of old daughters appears to result from both the presence of both more damage and fewer expressed gene products.

Cellular aging, a progressive functional decline driven by damage accumulation, often culminates in the mortality of a cell lineage. Certain lineages, however, are able to sustain long-lasting immortality, as prominently exemplified by stem cells. Here, we show that Escherichia coli cell lineages exhibit comparable patterns of mortality and immortality. Through single-cell microscopy and microfluidic techniques, we find that these patterns are explained by the dynamics of damage accumulation and asymmetric partitioning between daughter cells. At low damage accumulation rates, both aging and rejuvenating lineages retain immortality by reaching their respective states of physiological equilibrium. We show that both asymmetry and equilibrium are present in repair mutants lacking certain repair chaperones, suggesting that intact repair capacity is not essential for immortal proliferation. We show that this growth equilibrium, however, is displaced by extrinsic damage in a dosage-dependent response. Moreover, we demonstrate that aging lineages become mortal when damage accumulation rates surpass a threshold, whereas rejuvenating lineages within the same population remain immortal. Thus, the processes of damage accumulation and partitioning through asymmetric cell division are essential in the determination of proliferative mortality and immortality in bacterial populations. This study provides further evidence for the characterization of cellular aging as a general process, affecting prokaryotes and eukaryotes alike and according to similar evolutionary constraints., Competing Interests: The authors have declared that no competing interests exist.

Many bacteria produce small, spherical minicells that lack chromosomal DNA and therefore are unable to proliferate. Although minicells have been used extensively by researchers as a molecular tool, nothing is known about why bacteria produce them. Here, we show that minicells help Escherichia coli cells to rid themselves of damaged proteins induced by antibiotic stress. By comparing the survival and growth rates of wild-type strains with the E. coli ΔminC mutant, which produces excess minicells, we found that the mutant was more resistant to streptomycin. To determine the effects of producing minicells at the single-cell level, we also tracked the growth of ΔminC lineages by microscopy. We were able to show that the mutant increased the production of minicells in response to a higher level of the antibiotic. When we compared two sister cells, in which one produced minicells and the other did not, the daughters of the former had a shorter doubling time at this higher antibiotic level. Additionally, we found that minicells were more likely produced at the mother's old pole, which is known to accumulate more aggregates. More importantly, by using a fluorescent IbpA chaperone to tag damage aggregates, we found that polar aggregates were contained by and ejected with the minicells produced by the mother bacterium. These results demonstrate for the first time the benefit to bacteria for producing minicells. IMPORTANCE Bacteria have the ability to produce minicells, or small spherical versions of themselves that lack chromosomal DNA and are unable to replicate. A minicell can constitute as much as 20% of the cell's volume. Although molecular biology and biotechnology have used minicells as laboratory tools for several decades, it is still puzzling that bacteria should produce such costly but potentially nonfunctional structures. Here, we show that bacteria gain a benefit by producing minicells and using them as a mechanism to eliminate damaged or oxidated proteins. The elimination allows the bacteria to tolerate higher levels of stress, such as increasing levels of streptomycin. If this mechanism extends from streptomycin to other antibiotics, minicell production could be an overlooked pathway that bacteria are using to resist antimicrobials., (Copyright © 2018 Rang et al.)

The physiological asymmetry between daughters of a mother bacterium is produced by the inheritance of either old poles, carrying non-genetic damage, or newly synthesized poles. However, as bacteria display long-term growth stability leading to physiological immortality, there is controversy on whether asymmetry corresponds to aging. Here we show that deterministic age structure landscapes emerge from physiologically immortal bacterial lineages. Through single-cell microscopy and microfluidic techniques, we demonstrate that aging and rejuvenating bacterial lineages reach two distinct states of growth equilibria. These equilibria display stabilizing properties, which we quantified according to the compensatory trajectories of continuous lineages throughout generations. Finally, we show that the physiological asymmetry between aging and rejuvenating lineages produces complex age structure landscapes, resulting in a deterministic phenotypic heterogeneity that is neither an artifact of starvation nor a product of extrinsic damage. These findings indicate that physiological immortality and cellular aging can both be manifested in single celled organisms.

Non-genetic phenotypic variation is common in biological organisms. The variation is potentially beneficial if the environment is changing. If the benefit is large, selection can favor the evolution of genetic assimilation, the process by which the expression of a trait is transferred from environmental to genetic control. Genetic assimilation is an important evolutionary transition, but it is poorly understood because the fitness costs and benefits of variation are often unknown. Here we show that the partitioning of damage by a mother bacterium to its two daughters can evolve through genetic assimilation. Bacterial phenotypes are also highly variable. Because gene-regulating elements can have low copy numbers, the variation is attributed to stochastic sampling. Extant Escherichia coli partition asymmetrically and deterministically more damage to the old daughter, the one receiving the mother's old pole. By modeling in silico damage partitioning in a population, we show that deterministic asymmetry is advantageous because it increases fitness variance and hence the efficiency of natural selection. However, we find that symmetrical but stochastic partitioning can be similarly beneficial. To examine why bacteria evolved deterministic asymmetry, we modeled the effect of damage anchored to the mother's old pole. While anchored damage strengthens selection for asymmetry by creating additional fitness variance, it has the opposite effect on symmetry. The difference results because anchored damage reinforces the polarization of partitioning in asymmetric bacteria. In symmetric bacteria, it dilutes the polarization. Thus, stochasticity alone may have protected early bacteria from damage, but deterministic asymmetry has evolved to be equally important in extant bacteria. We estimate that 47% of damage partitioning is deterministic in E. coli. We suggest that the evolution of deterministic asymmetry from stochasticity offers an example of Waddington's genetic assimilation. Our model is able to quantify the evolution of the assimilation because it characterizes the fitness consequences of variation.

Evidence for ageing in symmetrically dividing bacteria such as Escherichia coli has historically been conflicting. Early work found weak or no evidence. More recent studies found convincing evidence, but negative results are still encountered. Because bacterial ageing is believed to result from non-genetic (e.g. oxidative) damage, we tested the possibility that the negative outcomes resulted from the lack of an extrinsic damage agent. We found that streptomycin, which produces mistranslated proteins that are more vulnerable to oxidation, was able to induce both damage and ageing in bacterial populations. A dosage effect relating the level of damage to the concentration of streptomycin was observed. Our results explain the previous inconsistencies, because all studies that failed to find evidence for bacterial ageing did not use a damage agent. However, all studies that succeeded in finding evidence utilized fluorescent proteins as a visual marker. We suggest that ageing in those studies was induced by the harmful effects of an extrinsic factor, such as the proteins themselves or the excitation light. Thus, all of the earlier studies can be reconciled and bacterial ageing is a real phenomenon. However, the study and observation of bacterial ageing require the addition of an extrinsic damage agent.

Single-celled organisms dividing by binary fission were thought not to age [1-4]. A 2005 study by Stewart et al. [5] reversed the dogma by demonstrating that Escherichia coli were susceptible to aging. A follow-up study by Wang et al. [6] countered those results by demonstrating that E. coli cells trapped in microfluidic devices are able to sustain robust growth without aging. The present study reanalyzed these conflicting data by applying a population genetic model for aging in bacteria [7]. Our reanalysis showed that in E. coli, as predicted by the model, (1) aging and rejuvenation occurred simultaneously in a population; (2) lineages receiving sequentially the maternal old pole converged to a stable attractor state; (3) lineages receiving sequentially the maternal new pole converged to an equivalent but separate attractor state; (4) cells at the old pole attractor had a longer doubling time than ones at the new pole attractor; and (5) the robust growth state identified by Wang et al. corresponds to our predicted attractor for lineages harboring the maternal old pole. Thus, the previous data, rather than opposing each other, together provide strong evidence for bacterial aging., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Bacteriophages are the most numerous entities in the biosphere. Despite this numerical dominance, the genetic structure of bacteriophage populations is poorly understood. Here, we present a biogeography study involving 25 previously undescribed bacteriophages from the Cystoviridae clade, a group characterized by a dsRNA genome divided into three segments. Previous laboratory manipulation has shown that, when multiple Cystoviruses infect a single host cell, they undergo (i) rare intrasegment recombination events and (ii) frequent genetic reassortment between segments. Analyzing linkage disequilibrium (LD) within segments, we find no significant evidence of intrasegment recombination in wild populations, consistent with (i). An extensive analysis of LD between segments supports frequent reassortment, on a time scale similar to the genomic mutation rate. The absence of LD within this group of phages is consistent with expectations for a completely sexual population, despite the fact that some segments have >50% nucleotide divergence at 4-fold degenerate sites. This extraordinary rate of genetic exchange between highly unrelated individuals is unprecedented in any taxa. We discuss our results in light of the biological species concept applied to viruses.

When a parent virus replicates inside its host, it must first use its own genome as the template for replication. However, once progeny genomes are produced, the progeny can in turn act as templates. Depending on whether the progeny genomes become templates, the distribution of mutants produced by an infection varies greatly. While information on the distribution is important for many population genetic models, it is also useful for inferring the replication mode of a virus. We have analyzed the distribution of mutants emerging from single bursts in the RNA bacteriophage phi6 and find that the distribution closely matches a Poisson distribution. The match suggests that replication in this bacteriophage is effectively by a stamping machine model in which the parental genome is the main template used for replication. However, because the distribution deviates slightly from a Poisson distribution, the stamping machine is not perfect and some progeny genomes must replicate. By fitting our data to a replication model in which the progeny genomes become replicative at a given rate or probability per round of replication, we estimated the rate to be very low and on the on the order of 10(-4). We discuss whether different replication modes may confer an adaptive advantage to viruses.

The growth physiology of Escherichia coli during colonization of the intestinal tract was studied with four animal models: the streptomycin-treated mouse carrying a reduced microflora, the monoassociated mouse with no other microflora than the introduced strain, the conventionalized streptomycin-treated mouse, and the conventionalized monoassociated mouse harboring a full microflora. A 23S rRNA fluorescent oligonucleotide probe was used for hybridization to whole E. coli cells fixed directly after being taken from the animals, and the respective growth rates of E. coli BJ4 in the four animal models were estimated by correlating the cellular concentrations of ribosomes with the growth rate of the strain. The growth rates thus estimated from the ribosomal content of E. coli BJ4 in vivo did not differ in the streptomycin-treated and the monoassociated mice. After conventionalization there was a slight decrease of the bacterial growth rates in both animal models.

It has been previously reported that for natural Escherichia coli isolates from the ECOR collection, there were differences in the ribosomal efficiencies and there was a direct correlation between growth rate and the ribosome efficiency (R-factor). The aim of this study was to determine whether strains freshly isolated (i.e. subcultured < 5 times) from the gastrointestinal tract ecosystem also exhibited this correlation. Eleven E. coli and two Enterobacter spp. isolates from either humans, pigs, rats or a mammoth were investigated. Considerable variability in the R-factor was noted using an in vitro translation assay, however no consistent correlation between the R-factor and growth rate was noted.