Статті в журналах: "Strain mechanisms"

1

Martcheva, Maia, Benjamin M. Bolker, and Robert D. Holt. "Vaccine-induced pathogen strain replacement: what are the mechanisms?" Journal of The Royal Society Interface 5, no. 18 (April 25, 2007): 3–13. http://dx.doi.org/10.1098/rsif.2007.0236.

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Host immune systems impose natural selection on pathogen populations, which respond by evolving different antigenic signatures. Like many evolutionary processes, pathogen evolution reflects an interaction between different levels of selection; pathogens can win in between-strain competition by taking over individual hosts (within-host level) or by infecting more hosts (population level). Vaccination, which intensifies and modifies selection by protecting hosts against one or more pathogen strains, can drive the emergence of new dominant pathogen strains—a phenomenon called vaccine-induced pathogen strain replacement . Here, we review reports of increased incidence of subdominant variants after vaccination campaigns and extend the current model for pathogen strain replacement, which assumes that pathogen strain replacement occurs only through the differential effectiveness of vaccines against different pathogen strains. Based on a recent theoretical study, we suggest a broader range of possible mechanisms, some of which allow pathogen strain replacement even when vaccines are perfect —that is, they protect all vaccinated individuals completely against all pathogen strains. We draw an analogy with ecological and evolutionary explanations for competitive dominance and coexistence that allow for tradeoffs between different competitive and life-history traits.

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2

Xiong, Hao, and Xiumin Diao. "Stiffness analysis of cable-driven parallel mechanisms with cables having large sustainable strains." Proceedings of the Institution of Mechanical Engineers, Part C: Journal of Mechanical Engineering Science 234, no. 10 (January 24, 2020): 1959–68. http://dx.doi.org/10.1177/0954406220902165.

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A cable-driven parallel mechanism is driven by a group of cables. Cable-driven parallel mechanisms can use various cables (e.g. steel cables, nylon cables, isoprene rubber cables, and extension springs) with different sustainable strains. This paper studies the stiffness of cable-driven parallel mechanisms with cables having large sustainable strains, aiming to achieve significantly adjustable overall stiffness. The overall stiffness of a cable-driven parallel mechanism can be decomposed into the constant base stiffness and the adjustable strain stiffness. This paper proposes and mathematically proves a theorem that guarantees that the overall stiffness of a cable-driven parallel mechanism at an arbitrary stable pose can be dominated by the adjustable strain stiffness when cable strains are larger than 100%. The theorem employs the minimum eigenvalues of stiffness matrices to characterize the stiffness of cable-driven parallel mechanism. The theorem provides a sufficient condition that guarantees that the overall stiffness of a cable-driven parallel mechanism at an arbitrary stable pose can be significantly adjusted (i.e. the adjustable strain stiffness contributes more than the constant base stiffness in determining the overall stiffness). The theorem is verified through the simulation of a cable-driven parallel mechanism with six degrees of freedom and seven cables.

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3

Cheng, Yi-Hsiang, Tzu-Wen Huang, Chih-Han Juan, Sheng-Hua Chou, Yao-Yi Tseng, Ting-Wen Chen, Tsuey-Ching Yang, and Yi-Tsung Lin. "Tigecycline-non-susceptible hypervirulent Klebsiella pneumoniae strains in Taiwan." Journal of Antimicrobial Chemotherapy 75, no. 2 (November 8, 2019): 309–17. http://dx.doi.org/10.1093/jac/dkz450.

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Abstract Objectives Emergent antimicrobial-resistant hypervirulent Klebsiella pneumoniae (hvKp) is an important public health issue. We aimed to investigate resistance mechanisms and hypervirulent traits among tigecycline-non-susceptible (TNS) K. pneumoniae clinical strains, focusing on one hvKp strain with in vivo evolution of tigecycline resistance. Methods TNS K. pneumoniae strains causing invasive diseases in a medical centre in Taiwan between July 2015 and April 2018 were collected. Resistance mechanisms were determined and hvKp strains were defined as rmpA/rmpA2-carrying strains. Isogenic strains with and without tigecycline resistance were subjected to WGS and in vivo virulence testing. Further, site-directed mutagenesis was used to confirm the resistance mechanism. Results In total, 31 TNS K. pneumoniae strains were isolated, including six hypervirulent strains. Tigecycline resistance mechanisms were mostly caused by overexpression of AcrAB and OqxAB together with up-regulation of RamA or RarA, respectively. One TNS hypervirulent strain (KP1692; MIC=6 mg/L) derived from its tigecycline-susceptible counterpart (KP1677; MIC=0.75 mg/L) showed acrAB overexpression. WGS revealed four genetic variations between KP1677 and KP1692. In addition, using site-directed mutagenesis, we confirmed that a 1 bp insertion in the ramA upstream region (RamR-binding site), leading to ramA and acrAB overexpression in KP1692, was responsible for tigecycline resistance. The in vivo virulence experiment showed that the TNS hvKp strain KP1692 still retained its high virulence compared with KP1677. Conclusions hvKp strains accounted for 19.4% among TNS strains. We identified alterations in the ramA upstream region as a mechanism of in vivo tigecycline resistance development in an hvKp strain.

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4

Sakai, Taku, and Hiromi Miura. "Mechanisms of Ultrafine Grain Formation in Severe Plastic Deformation." Materials Science Forum 638-642 (January 2010): 98–103. http://dx.doi.org/10.4028/www.scientific.net/msf.638-642.98.

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The evolution mechanisms of ultrafine grains processed by severe plastic deformation are studied in ferritic steel, copper and aluminum alloys. The structural changes are characterized by the evolution of deformation bands such as microshear bands (MSBs) at moderate strains. The process of strain-induced grain formation can be subdivided in the following three stages irrespective of deformation temperature: i.e. an incubation period for new grain evolution in low strain; grain fragmentation by frequent development of MSBs in medium strain, and a full development of new grains in large strain. A mechanism of new grain formation during SPD, i.e. the MSB-based model, is proposed and discussed comparing with the subgrain-based model.

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5

Hong, P., G. B. Olson, and A. L. Roytburd. "Nucleation mechanisms for strain transformations." Acta Crystallographica Section A Foundations of Crystallography 49, s1 (August 21, 1993): c434. http://dx.doi.org/10.1107/s010876737808770x.

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6

THOMASEY, DOUGLAS H., and MAIA MARTCHEVA. "SEROTYPE REPLACEMENT OF VERTICALLY TRANSMITTED DISEASES THROUGH PERFECT VACCINATION." Journal of Biological Systems 16, no. 02 (June 2008): 255–77. http://dx.doi.org/10.1142/s0218339008002484.

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Strain replacement occurs when after a vaccination campaign one (or more) strains decline in prevalence while another strain (or strains) rise in prevalence. Differential effectiveness of the vaccine is the widely accepted and the most important mechanism which leads to this replacement effect. Recent theoretical studies have suggested that strain replacement may occur even if the vaccine is perfect, that is, the vaccine is completely effective with respect to all strains present. It has already been shown that perfect vaccination, along with a trade-off mechanism, such as co-infection or super-infection, lead to strain replacement. In this paper, we examine the hypothesis that strain replacement with perfect vaccination occurs only with trade-off mechanisms which allow a strain with a lower reproduction number to eliminate a strain with a higher reproduction number in the absence of vaccination. We test this hypothesis on a two-strain model with vertical transmission. We first show that vertical transmission as a trade-off mechanism can lead to dominance of a strain with suboptimal reproduction number. Based on the hypothesis we expect, and we show, that strain replacement occurs with vertical transmission.

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7

van Niel, Ed W. J., Johan Palmfeldt, Rani Martin, Marco Paese, and BÃ¯Â¿Â½rbel Hahn-HÃ¯Â¿Â½gerdal. "Reappraisal of the Regulation of Lactococcal l-Lactate Dehydrogenase." Applied and Environmental Microbiology 70, no. 3 (March 2004): 1843–46. http://dx.doi.org/10.1128/aem.70.3.1843-1846.2004.

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ABSTRACT Lactococcal lactate dehydrogenases (LDHs) are coregulated at the substrate level by at least two mechanisms: the fructose-1,6-biphosphate/phosphate ratio and the NADH/NAD ratio. Among the Lactococcus lactis species, there are strains that are predominantly regulated by the first mechanism (e.g., strain 65.1) or by the second mechanism (e.g., strain NCDO 2118). A more complete model of the kinetics of the regulation of lactococcal LDH is discussed.

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8

Kaatz, G. W., and S. M. Seo. "Mechanisms of fluoroquinolone resistance in genetically related strains of Staphylococcus aureus." Antimicrobial Agents and Chemotherapy 41, no. 12 (December 1997): 2733–37. http://dx.doi.org/10.1128/aac.41.12.2733.

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Fluoroquinolone resistance in Staphylococcus aureus results from amino acid substitutions at particular locations in the DNA gyrase A and B subunits as well as in the topoisomerase IV A subunit and from NorA-mediated efflux. More than one resistance mechanism may be present in a single strain. Fluoroquinolone-resistant derivatives of SA-1199, a methicillin-susceptible S. aureus strain, were selected in vivo or in vitro, and their mechanisms of fluoroquinolone resistance were identified. We found that many of the resistance mechanisms described above can develop in derivatives of a single parent strain, either singly or in combination, and can arise in a single step. Variances in MICs for strains with the same apparent resistance mechanisms likely are due to the presence of new or undetected but established means of fluoroquinolone resistance. NorA-mediated resistance can occur in the apparent absence of topoisomerase mutations and in some strains may be the result of a promoter region mutation causing increased expression of norA. However, increased expression of norA can occur independently of this mutation, suggesting that a regulatory locus for this gene exists elsewhere on the chromosome.

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9

Rocque, Michael. "Strain, coping mechanisms, and slavery: a general strain theory application." Crime, Law and Social Change 49, no. 4 (March 18, 2008): 245–69. http://dx.doi.org/10.1007/s10611-008-9106-8.

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10

Zhang, Xu-Sheng, and Ke-Fei Cao. "The Impact of Coinfections and Their Simultaneous Transmission on Antigenic Diversity and Epidemic Cycling of Infectious Diseases." BioMed Research International 2014 (2014): 1–23. http://dx.doi.org/10.1155/2014/375862.

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Epidemic cycling in human infectious diseases is common; however, its underlying mechanisms have been poorly understood. Much effort has been made to search for external mechanisms. Multiple strains of an infectious agent were usually observed and coinfections were frequent; further, empirical evidence indicates the simultaneous transmission of coinfections. To explore intrinsic mechanisms for epidemic cycling, in this study we consider a multistrain Susceptible-Infected-Recovered-Susceptible epidemic model by including coinfections and simultaneous transmission. We show that coinfections and their simultaneous transmission widen the parameter range for coexistence and coinfections become popular when strains enhance each other and the immunity wanes quickly. However, the total prevalence is nearly independent of these characteristics and approximated by that of one-strain model. With sufficient simultaneous transmission and antigenic diversity, cyclical epidemics can be generated even when strains interfere with each other by reducing infectivity. This indicates that strain interactions within coinfections and cross-immunity during subsequent infection provide a possible intrinsic mechanism for epidemic cycling.

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11

Chand, Hitendra S., Melissa Drysdale, Julie Lovchik, Theresa M. Koehler, Mary F. Lipscomb, and C. Rick Lyons. "Discriminating Virulence Mechanisms among Bacillus anthracis Strains by Using a Murine Subcutaneous Infection Model." Infection and Immunity 77, no. 1 (November 3, 2008): 429–35. http://dx.doi.org/10.1128/iai.00647-08.

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ABSTRACT Bacillus anthracis strains harboring virulence plasmid pXO1 that encodes the toxin protein protective antigen (PA), lethal factor, and edema factor and virulence plasmid pXO2 that encodes capsule biosynthetic enzymes exhibit different levels of virulence in certain animal models. In the murine model of pulmonary infection, B. anthracis virulence was capsule dependent but toxin independent. We examined the role of toxins in subcutaneous (s.c.) infections using two different genetically complete (pXO1+ pXO2+) strains of B. anthracis, strains Ames and UT500. Similar to findings for the pulmonary model, toxin was not required for infection by the Ames strain, because the 50% lethal dose (LD50) of a PA-deficient (PA−) Ames mutant was identical to that of the parent Ames strain. However, PA was required for efficient s.c. infection by the UT500 strain, because the s.c. LD50 of a UT500 PA− mutant was 10,000-fold higher than the LD50 of the parent UT500 strain. This difference between the Ames strain and the UT500 strain could not be attributed to differences in spore coat properties or the rate of germination, because s.c. inoculation with the capsulated bacillus forms also required toxin synthesis by the UT500 strain to cause lethal infection. The toxin-dependent phenotype of the UT500 strain was host phagocyte dependent, because eliminating Gr-1+ phagocytes restored virulence to the UT500 PA− mutant. These experiments demonstrate that the dominant virulence factors used to establish infection by B. anthracis depend on the route of inoculation and the bacterial strain.

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12

King, Geoffrey C. P., and Charles G. Sammis. "The mechanisms of finite brittle strain." Pure and Applied Geophysics PAGEOPH 138, no. 4 (1992): 611–40. http://dx.doi.org/10.1007/bf00876341.

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13

Walker, Daniel J., Jessica L. Pitsch, Michael M. Peng, Brian L. Robinson, Wallace Peters, Jamaree Bhisutthibhan, and Steven R. Meshnick. "Mechanisms of Artemisinin Resistance in the Rodent Malaria Pathogen Plasmodium yoelii." Antimicrobial Agents and Chemotherapy 44, no. 2 (February 1, 2000): 344–47. http://dx.doi.org/10.1128/aac.44.2.344-347.2000.

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ABSTRACT Artemisinin and its derivatives are important new antimalarials which are now used widely in Southeast Asia. Clinically relevant artemisinin resistance has not yet been reported but is likely to occur. In order to understand how the malaria parasite might become resistant to this drug, we studied artemisinin resistance in the murine malaria parasite Plasmodium yoelii. The artemisinin-resistant strain (ART), which is approximately fourfold less sensitive to artemisinin than the sensitive NS strain, accumulated 43% less radiolabeled drug in vitro (P < 0.01). Within the parasite, the drug appeared to react with the same parasite proteins in both strains. The translationally controlled tumor protein, one of the artemisinin target proteins, did not differ between the strains. No DNA sequence difference was found, but the resistant strain was found to express 2.5-fold-more protein than the sensitive strain (P < 0.01). Thus, the phenotype of artemisinin resistance in P. yoelii appears to be multifactorial.

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14

Asahara, Takashi, Masatoshi Takahashi, Koji Nomoto, Hiroo Takayama, Masaharu Onoue, Masami Morotomi, Ryuichiro Tanaka, Teruo Yokokura, and Naoya Yamashita. "Assessment of Safety of Lactobacillus Strains Based on Resistance to Host Innate Defense Mechanisms." Clinical Diagnostic Laboratory Immunology 10, no. 1 (January 2003): 169–73. http://dx.doi.org/10.1128/cdli.10.1.169-173.2003.

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ABSTRACT Seven Lactobacillus strains belonging to four species were evaluated for pathogenicity as well as for in vitro sensitivity to the bactericidal mechanisms of macrophages in a rabbit infective endocarditis (IE) model. Two bacteremia-associated strains, L. rhamnosus PHLS A103/70 and L. casei PHLS A357/84, as well as the L. rhamnosus type strain and the probiotic L. rhamnosus strain ATCC 53103, showed moderate infectivity, and the virulence of the probiotic L. casei strain Shirota and type strains such as L. acidophilus ATCC 4356T and L. gasseri DSM 20243T in the model was negligible. The strains that showed pathogenic potential in the rabbit IE model (PHLS A357/84, PHLS A103/70, and ATCC 53103) were more resistant than strain Shirota to intracellular killing activity by mouse macrophages in vitro and also to bactericidal nitrogen intermediates, such as nitric oxide and NO2 − ions. These results suggest that resistance to host innate defense systems, which would function at inflammatory lesions, should be considered in the safety assessment of Lactobacillus strains.

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15

Markushin, S. G., O. A. Svitich, A. R. Kinkulkina, I. B. Koptyaeva, and K. V. Lisovskaya. "MECHANISMS OF ATTENUATION OF COLD-ADAPTED STRAIN A/KRASNODAR/101/35/59 (H2N2)." Journal of microbiology, epidemiology and immunobiology, no. 2 (April 28, 2016): 49–56. http://dx.doi.org/10.36233/0372-9311-2016-2-49-56.

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Aim. Study of mechanisms of attenuation of cold-adapted (ca) influenza virus strain A/ Krasnodar/101/35/59 (H2N2), associated with disruption of NS1 protein functions. Materials and methods. Study of interferonogenic activity of ca strain A/Krasnodar/101/35/59 (H2N2), its parent variant A/Krasnodar/101/59 (H2N2), virulent strain A/WSN/33 (H1N1) and a number of single gene and multiple gene reassortants between these strains, obtained using reverse genetics, was carried out. Study of dynamics of IFNp gene expression was carried out by using a methodical approach of RT-PCR in real time mode. Results. Inclusion of PB-1 gene of ca strain A/ Krasnodar/101/35/59 (H2N2) with reversion to wild type into genome composition of virulent strain А/WSN/33 (H1N1) does not result in a sharp change of interferonogenic activity of the reassortant. At the same time, similar inclusion of PB-1 gene of ca strain resulted in an incredible growth of interferonogenic activity of the reassortant. On the other hand, inclusion of NP-gene of wild type strain A/Krasnodar/101/59 (H2N2) into genome composition of the wild type strain А/WSN/33 did not differ by effect on interferonogenicity of the reassortant from inclusion of NP-gene of ca strain. Conclusion. Both constellations of genes of parent variants and mutations localized in these genes could affect formation of attenuation phenotype of reassortants. The data obtained allow to assume possible mechanisms of attenuation of ca strains, associated with disruption of NS gene function.

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16

PIRGAZI, HADI, and ABBAS AKBARZADEH. "CHARACTERIZATION OF NANOSTRUCTURED ALUMINUM SHEETS PROCESSED BY ACCUMULATIVE ROLL BONDING." International Journal of Modern Physics B 22, no. 18n19 (July 30, 2008): 2840–47. http://dx.doi.org/10.1142/s0217979208047663.

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An ultrafine grained (UFG) aluminum sheet was produced using severe plastic deformation (SPD) by a process known as accumulative roll bonding (ARB). Electron Back Scattered Diffraction (EBSD) method and Transmission Electron Microscopy (TEM) were utilized for characterization of the subgrain and grain structures of the processed sheets. The results indicate that different mechanisms at different levels of strain lead to the gradual evolution of ultrafine or nanocrystalline grains. Grain fragmentation as well as the development of subgrains are the major mechanisms at the early stages of ARB. Strain induced transformation of low angle to high angle grain boundaries and formation of a thin lamellar structure occur at the medium level of strain. Finally, the progressive fragmentation of these thin lamellar structures into more equi-axed grains is the dominant mechanism at relatively high strains which results in grain size reduction to submicron scale.

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17

Gonzalez-Jimenez, Irene, Jose Lucio, Jorge Amich, Isabel Cuesta, Rafael Sanchez Arroyo, Laura Alcazar-Fuoli, and Emilia Mellado. "A Cyp51B Mutation Contributes to Azole Resistance in Aspergillus fumigatus." Journal of Fungi 6, no. 4 (November 26, 2020): 315. http://dx.doi.org/10.3390/jof6040315.

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The emergence and spread of Aspergillus fumigatus azole resistance has been acknowledged worldwide. The main problem of azole resistance is the limited therapeutic options for patients suffering aspergillosis. Azole resistance mechanisms have been mostly linked to the enzyme Cyp51A, a target of azole drugs, with a wide variety of modifications responsible for the different resistance mechanisms described to date. However, there are increasing reports of A. fumigatus strains showing azole resistance without Cyp51A modifications, and thus, novel resistance mechanisms are being explored. Here, we characterized two isogenic A. fumigatus clinical strains isolated two years apart from the same patient. Both strains were resistant to clinical azoles but showed different azole resistance mechanisms. One strain (CM8940) harbored a previously described G54A mutation in Cyp51A while the other strain (CM9640) had a novel G457S mutation in Cyp51B, the other target of azoles. In addition, this second strain had a F390L mutation in Hmg1. CM9640 showed higher levels of gene expression of cyp51A, cyp51B and hmg1 than the CM8940 strain. The role of the novel mutation found in Cyp51B together with the contribution of a mutation in Hmg1 in azole resistance is discussed.

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18

Lin, Quan, Yasuko Rikihisa, Norio Ohashi, and Ning Zhi. "Mechanisms of Variable p44 Expression by Anaplasma phagocytophilum." Infection and Immunity 71, no. 10 (October 2003): 5650–61. http://dx.doi.org/10.1128/iai.71.10.5650-5661.2003.

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ABSTRACT The human intragranulocytic bacterium Anaplasma phagocytophilum promotes variation of P44s, which are surface-exposed proteins encoded by a p44 multigene family. In the present study, the specific p44 gene expression loci in four strains of A. phagocytophilum were identified and it was determined that each consisted of four tandem genes, tr1, omp-1X, omp-1N, and p44. A putative σ70-type promoter was found upstream of tr1. The p44 genes include a central hypervariable region flanked by conserved regions. The hypervariable region sequence in the p44 expression locus was duplicated and, regardless of the expression status, conserved at another locus in both low- and high-passage cell cultures of strain NY-37. No significant differences in the hypervariable region were found when we compared p44 sequences, at the level of cDNA, within the expression locus and within other loci in the genomes of strains NY-37 and HZ. Similarly, in cDNA isolated from patients and from assorted cultures of strains NY-31, NY-36, and NY-37, hypervariable regions of 450 deduced amino acid sequences of various p44s within each strain were found to be identical, as were those of p44 sequences in the genome of strain HZ. These data suggest that variations in p44 sequences at the level of the p44 expression locus occur through unidirectional conversion of the entire (nonsegmental) p44 hypervariable region including flanking regions with a corresponding sequence copied from one of the conserved donor p44 genomic loci. The data suggest that the P44 antigenic repertoire within the hypervariable region is restricted.

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19

de Boer, Marjan, Peter Bom, Frodo Kindt, Joost J. B. Keurentjes, Ientse van der Sluis, L. C. van Loon, and Peter A. H. M. Bakker. "Control of Fusarium Wilt of Radish by Combining Pseudomonas putida Strains that have Different Disease-Suppressive Mechanisms." Phytopathology® 93, no. 5 (May 2003): 626–32. http://dx.doi.org/10.1094/phyto.2003.93.5.626.

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Biological control of soilborne plant pathogens in the field has given variable results. By combining specific strains of microorganisms, multiple traits antagonizing the pathogen can be combined and this may result in a higher level of protection. Pseudomonas putida WCS358 suppresses Fusarium wilt of radish by effectively competing for iron through the production of its pseudobactin siderophore. However, in some bioassays pseudobactin-negative mutants of WCS358 also suppressed disease to the same extent as WCS358, suggesting that an, as yet unknown, additional mechanism may be operative in this strain. P. putida strain RE8 induced systemic resistance against fusarium wilt. When WCS358 and RE8 were mixed through soil together, disease suppression was significantly enhanced to approximately 50% as compared to the 30% reduction for the single strain treatments. Moreover, when one strain failed to suppress disease in the single application, the combination still resulted in disease control. The enhanced disease suppression by the combination of P. putida strains WCS358 and RE8 is most likely the result of the combination of their different disease-suppressive mechanisms. These results demonstrate that combining biocontrol strains can lead to more effective, or at least, more reliable biocontrol of fusarium wilt of radish.

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20

Ayala, Juan, Alberto Quesada, Santiago Vadillo, Jerónimo Criado, and Segundo Píriz. "Penicillin-binding proteins of Bacteroides fragilis and their role in the resistance to imipenem of clinical isolates." Journal of Medical Microbiology 54, no. 11 (November 1, 2005): 1055–64. http://dx.doi.org/10.1099/jmm.0.45930-0.

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In this study penicillin-binding proteins (PBPs) of Bacteroides fragilis and the resistance mechanisms of this micro-organism to 11 β-lactam antibiotics were analysed. The study focused on the role of PBP2Bfr and metallo-β-lactamase in the mechanism of resistance to imipenem. The mechanism of β-lactam resistance in B. fragilis was strain dependent. The gene encoding the orthologue of Escherichia coli PBP3 gene (pbpBBfr, which encodes the protein PBP2Bfr) was sequenced in five of the eight strains studied, along with the ccrA (cfiA) gene in strain 119, and their implications for resistance were examined. Differences were found in the amino-acid sequence of PBP2Bfr in strains AK-2 and 119, and the production of β-lactamases indicated that these differences may be involved in the mechanism of resistance to imipenem. In vitro binding competition assays with membrane extracts using imipenem indicated that the PBP that bound imipenem with the highest affinity was PBP2Bfr, and that increased affinity in strain 7160 may be responsible for the moderate susceptibility of this strain to imipenem. In the same way, the importance of the chromosomal class A β-lactamase CepA in the resistance mechanism of the B. fragilis strains NCTC 9344, 7160, 2013E, AK-4, 0423 and R-212 was studied. In these strains this is the principal resistance mechanism to antimicrobial agents studied other than imipenem.

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Wang, R. Z., Z. Suo, A. G. Evans, N. Yao, and I. A. Aksay. "Deformation mechanisms in nacre." Journal of Materials Research 16, no. 9 (September 2001): 2485–93. http://dx.doi.org/10.1557/jmr.2001.0340.

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Nacre (mother-of-pearl) from mollusc shells is a biologically formed lamellar ceramic. The inelastic deformation of this material has been experimentally examined, with a focus on understanding the underlying mechanisms. Slip along the lamellae tablet interface has been ascertained by testing in compression with the boundaries oriented at 45° to the loading axis. The steady-state shear resistance τss has been determined and inelastic strain shown to be as high as 8%. The inelastic deformation was realized by massive interlamellae shearing. Testing in tension parallel to the tablets indicates inelastic strain of about 1%, occurring at a steady-state stress, σsss ≈ 110 MPa. The strain was associated with the formation of multiple dilatation bands at the intertablet boundaries accompanied by interlamellae sliding. Nano-asperities on the aragonite tablets and their interposing topology provide the resistance to interfacial sliding and establish the level of the stress needed to attain the inelastic strain. Detailed mechanisms and their significance for the design of robust ceramics are discussed.

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22

Hu, Zhiqiang, and Kaikun Wang. "Evolution of Dynamic Recrystallization in 5CrNiMoV Steel during Hot Forming." Advances in Materials Science and Engineering 2020 (January 9, 2020): 1–13. http://dx.doi.org/10.1155/2020/4732683.

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The dynamic recrystallization (DRX) behavior of 5CrNiMoV steel was investigated through hot compression at temperatures of 830–1230°C and strain rates of 0.001–10 s−1. From the experimental results, most true stress-strain curves showed the typical nature of DRX that a single peak was reached at low strains followed by a decrease of stress and a steady state finally at relatively high strains. The constitutive behavior of 5CrNiMoV steel was analyzed to deduce the operative deformation mechanisms, and the correlation between flow stress, temperature, and strain rate was expressed as a sine hyperbolic type constitutive equation. Based on the study of characteristic stresses and strains on the true stress-strain curves, a DRX kinetics model was constructed to characterize the influence of true strain, temperature, and strain rate on DRX evolution, which revealed that higher temperatures and lower strain rates had a favorable influence on improving the DRX volume fraction at the same true strain. Microstructure observations indicated that DRX was the main mechanism and austenite grains could be greatly refined by reducing the temperature of hot deformation or increasing the strain rate when complete recrystallization occurred. Furthermore, a DRX grain size model of 5CrNiMoV was obtained to predict the average DRX grain size during hot forming.

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Liu, Keming, Xiaochun Sheng, Qingpeng Li, Mengcheng Zhang, Ningle Han, Guangyu He, Jin Zou, Wei Chen, and Andrej Atrens. "Microstructure and Strengthening Model of Cu–Fe In-Situ Composites." Materials 13, no. 16 (August 6, 2020): 3464. http://dx.doi.org/10.3390/ma13163464.

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The tensile strength evolution and strengthening mechanism of Cu–Fe in-situ composites were investigated using both experiments and theoretical analysis. Experimentally, the tensile strength evolution of the in-situ composites with a cold deformation strain was studied using the model alloys Cu–11Fe, Cu–14Fe, and Cu–17Fe, and the effect of the strain on the matrix of the in-situ composites was studied using the model alloys Cu–3Fe and Cu–4.3Fe. The tensile strength was related to the microstructure and to the theoretical strengthening mechanisms. Based on these experimental data and theoretical insights, a mathematical model was established for the dependence of the tensile strength on the cold deformation strain. For low cold deformation strains, the strengthening mechanism was mainly work hardening, solid solution, and precipitation strengthening. Tensile strength can be estimated using an improved rule of mixtures. For high cold deformation strains, the strengthening mechanism was mainly filament strengthening. Tensile strength can be estimated using an improved Hall–Petch relation.

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24

Arunkumar, G., and P. S. S. Srinivasan. "Design of displacement amplifying compliant mechanisms with integrated strain actuator using topology optimization." Proceedings of the Institution of Mechanical Engineers, Part C: Journal of Mechanical Engineering Science 220, no. 8 (August 1, 2006): 1219–28. http://dx.doi.org/10.1243/09544062jmes261.

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Compliant mechanisms are the focus of active research because of the stability, robustness, and ease of manufacturing endowed by their unitized construction. However, despite significant advances in the development of systematic design techniques for these mechanisms, currently compliant mechanisms are not capable of performing certain kinematic tasks that rigid body mechanisms can readily perform. This work explores the various advantages of the compliant mechanism and some of the difficulties in the design of the compliant mechanisms, and designing a compliant mechanism for displacement amplification of piezoelectric actuator is developed using a topological optimization approach. The overall stroke amplification of geometrical advantage of the mechanism and overall mechanical efficiency of the mechanism are considered as objective functions. The maximization of these objectives is accomplished using two different solution methods: a sequential linear programming and an optimality criteria method.

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25

Robinson, J. H., Martin A. Rust, and Richard I. Todd. "Mechanisms of Microsuperplasticity." Materials Science Forum 551-552 (July 2007): 135–45. http://dx.doi.org/10.4028/www.scientific.net/msf.551-552.135.

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After superplastic deformation of Al-7475 and some other aluminium alloys, straininduced cavities are seen to be associated with long fibres parallel to the tensile direction. These fibres, whiskers or filaments are also observed on the fracture surface. This effect has become known as microsuperplasticity. The whisker characteristics are affected by the deformation conditions, particularly temperature and strain rate. To study the effect of these variables more fully, tensile samples of Al 7475 have been strained to failure at temperatures ranging from 480OC to 530OC and strain rates from 1.0E- 04s-1 to 5.0E-03s-1. Additional samples were deformed at 450OC and 420OC and a single strain rate. Some whiskering was observed under all testing conditions. The longest whiskers were generally seen at high temperatures and low strain rates. A TEM study of macroscopic whiskers produced under conditions of around 540OC and 1.0E-04 /s showed an amorphous structure. Annealing prior to deformation was shown to have little effect on whisker formation. EDX analysis showed the whole surface of the alloy to be enriched in alloying elements compared with the bulk alloy. The high levels of Mg detected were connected with the formation of magnesia as the surface oxide verified using Cr3+ fluorescence microscopy. Use of the differential scanning calorimeter (DSC) showed no conclusive evidence of partial melting below the testing temperatures. Considerations of capillarity and the DSC analysis suggest whiskering did not occur by a mechanism of viscous flow.

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26

Najafi, Hamidreza, and Sirous Asgari. "Strain hardening mechanisms in aged AEREX350 superalloy." Materials Science and Engineering: A 398, no. 1-2 (May 2005): 204–8. http://dx.doi.org/10.1016/j.msea.2005.03.015.

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27

Hinterstein, M., M. Hoelzel, J. Rouquette, J. Haines, J. Glaum, H. Kungl, and M. Hoffman. "Interplay of strain mechanisms in morphotropic piezoceramics." Acta Materialia 94 (August 2015): 319–27. http://dx.doi.org/10.1016/j.actamat.2015.04.017.

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Fichten, Catherine S., Kristen Robillard, and Stéphane Sabourin. "The attentional mechanisms model of interaction strain." Journal of Developmental and Physical Disabilities 6, no. 3 (September 1994): 239–54. http://dx.doi.org/10.1007/bf02578413.

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Glaeser, W. A. "High strain wear mechanisms in ferrous alloys." Wear 123, no. 2 (April 1988): 155–69. http://dx.doi.org/10.1016/0043-1648(88)90097-x.

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30

Danard, Y., G. Martin, L. Lilensten, F. Sun, A. Seret, R. Poulain, S. Mantri, et al. "Accommodation mechanisms in strain-transformable titanium alloys." Materials Science and Engineering: A 819 (July 2021): 141437. http://dx.doi.org/10.1016/j.msea.2021.141437.

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31

Luo, J. F., S. C. Mao, X. D. Han, G. Chen, Z. Zhang, and M. H. Wu. "High-Cycle Fatigue Mechanisms of a NiTi Shape Memory Alloy under Different Mean Strains." Materials Science Forum 610-613 (January 2009): 1120–27. http://dx.doi.org/10.4028/www.scientific.net/msf.610-613.1120.

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The high-cycle fatigue mechanisms of a NiTi shape memory alloy (SMA) under three different mean strains were investigated. Cold-rolled NiTi SMA specimens were heat treated at 600°C for 30min was selected to perform the fatigue test. Three samples were conducted cyclic deformation up to 2×105 cycles with three mean strains that subjected at full austenite, total stress-induced martensite (SIM) and austenite-martensite coexist status with the same strain amplitude of 0.25%. The cyclic stress-strain (CSS) curves show different cyclic softening and hardening at different mean strains. The S-S curves also reveal that cyclic deformation strain mainly occurred in martensite phase although austenite and martensite (A-M) coexisted. The transmission electron microscopy (TEM) investigation shows that slip dislocations with habit plane and basal plane dislocations were induced during the cycling, and these microstructure evolutions contribute to the cyclic softening and hardening.

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32

Huang, Liang, Yu Feng, and Zhiyong Zong. "Heterogeneous resistance to colistin in Enterobacter cloacae complex due to a new small transmembrane protein." Journal of Antimicrobial Chemotherapy 74, no. 9 (June 6, 2019): 2551–58. http://dx.doi.org/10.1093/jac/dkz236.

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Abstract Background Enterobacter strains can display heterogeneous resistance (heteroresistance) to colistin but the mechanisms remain largely unknown. We investigated potential mechanisms of colistin heteroresistance in an Enterobacter clinical strain, WCHECl-1060, and found a new mechanism. Methods Strain WCHECl-1060 was subjected to WGS to identify known colistin resistance mechanisms. Tn5 insertional mutagenesis, gene knockout and complementation and shotgun cloning were employed to investigate unknown colistin heteroresistance mechanisms. RNA sequencing was performed to link the newly identified mechanism with known ones. Results We showed that the phoP gene [encoding part of the PhoP-PhoQ two-component system (TCS)], the dedA(Ecl) gene (encoding an inner membrane protein of the DedA family) and the tolC gene (encoding part of the AcrAB-TolC efflux pump) are required for colistin heteroresistance. We identified a new gene, ecr, encoding a 72 amino acid transmembrane protein, which was able to mediate colistin heteroresistance. We then performed RNA sequencing and transcriptome analysis and found that in the presence of ecr the expression of phoP and the arnBCADTEF operon, which synthesizes and transfers l-Ara4N to lipid A, was increased significantly. Conclusions The small protein encoded by ecr represents a new colistin heteroresistance mechanism and is likely to mediate colistin heteroresistance via the PhoP-PhoQ TCS to act on the arnBCADTEF operon.

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Cosic, Mladen, and Stanko Brcic. "The development of controlled damage mechanisms-based design method for nonlinear static pushover analysis." Facta universitatis - series: Architecture and Civil Engineering 12, no. 1 (2014): 25–40. http://dx.doi.org/10.2298/fuace1401025c.

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This paper presents the original method of controlled building damage mechanisms based on Nonlinear Static Pushover Analysis (NSPA-DMBD). The optimal building damage mechanism is determined based on the solution of the Capacity Design Method (CDM), and the response of the building is considered in incremental situations. The development of damage mechanism of a system in such incremental situations is being controlled on the strain level, examining the relationship of current and limit strains in concrete and reinforcement steel. Since the procedure of the system damage mechanism analysis according to the NSPA-DMBD method is being iteratively implemented and designing checked after the strain reaches the limit, for this analysis a term Iterative-Interactive Design (IID) has been introduced. By selecting, monitoring and controlling the optimal damage mechanism of the system and by developed NSPA-DMBD method, damage mechanism of the building is being controlled and the level of resistance to an early collapse is being increased.

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34

Miao, Yinggang, He He, and Zhihui Li. "Strain hardening behaviors and mechanisms of polyurethane under various strain rate loading." Polymer Engineering & Science 60, no. 5 (March 2, 2020): 1083–92. http://dx.doi.org/10.1002/pen.25364.

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35

Guo, Yi, Yun Rong Luo, and Qing Yuan Wang. "Mean Strain Effect on the Cyclic Stress-Strain Behavior of Steel Structure Materials Q235." Advanced Materials Research 602-604 (December 2012): 430–34. http://dx.doi.org/10.4028/www.scientific.net/amr.602-604.430.

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The low cycle fatigue (LCF) behavior of Q235 steel under mean strain control has been investigated. A serious of the strain controlled cyclic loading experiments with several combinations of strain amplitudes and mean strains have been performed. Significant cyclic hardening and mean stress relaxation were observed in all cases. Fractography by scanning electron microscopy (SEM) was used to determine the LCF failure mechanisms and fatigue crack propagation modes of the Q235 steel.

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Yarushina, Victoria M., and Yuri Y. Podladchikov. "Plastic yielding as a frequency and amplitude independent mechanism of seismic wave attenuation." GEOPHYSICS 75, no. 3 (May 2010): N51—N63. http://dx.doi.org/10.1190/1.3420734.

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We have developed a mathematical formulation of two mechanisms of compressional wave attenuation, which can occur within the solid rock frame prestressed up to its yield stress in part of its volume. Energy losses are attributed to two distinct processes: irreversible plastic yielding and formation of radial microfractures around microscopic cavities. Small-amplitude waves propagating through the rocks prestressed at their yield point would cause nonelastic strain to avoid building local stresses above the yield limit and attenuate some fraction of their energy per every loading cycle. New mechanisms of microscale yielding and microfracturing give rise to frequency-independent attenuation due to rate-independence of plasticity formulation. Quality factor [Formula: see text] predicted by the model is independent of strain amplitude for small strains and decreases with increasing amplitude for large strains. We found that attenuation can be high even for small seismic strains [Formula: see text]. Thus, [Formula: see text] is achieved at effective pressures greater than twice the yield strength of the solid matrix for the plastic yielding mechanism and at overpressures exceeding half tensile strength for microfracturing.

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37

Kuramae, Eiko E., Stan Derksen, Thiago R. Schlemper, Maurício R. Dimitrov, Ohana Y. A. Costa, and Adriana P. D. da Silveira. "Sorghum Growth Promotion by Paraburkholderia tropica and Herbaspirillum frisingense: Putative Mechanisms Revealed by Genomics and Metagenomics." Microorganisms 8, no. 5 (May 13, 2020): 725. http://dx.doi.org/10.3390/microorganisms8050725.

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Bacteria from the genera Paraburkholderia and Herbaspirillum can promote the growth of Sorghum bicolor, but the underlying mechanisms are not yet known. In a pot experiment, sorghum plants grown on sterilized substrate were inoculated with Paraburkholderia tropica strain IAC/BECa 135 and Herbaspirillum frisingense strain IAC/BECa 152 under phosphate-deficient conditions. These strains significantly increased Sorghum bicolor cultivar SRN-39 root and shoot biomass. Shotgun metagenomic analysis of the rhizosphere revealed successful colonization by both strains; however, the incidence of colonization was higher in plants inoculated with P. tropica strain IAC/BECa 135 than in those inoculated with H. frisingense strain IAC/BECa 152. Conversely, plants inoculated with H. frisingense strain IAC/BECa 152 showed the highest increase in biomass. Genomic analysis of the two inoculants implied a high degree of rhizosphere fitness of P. tropica strain IAC/BECa 135 through environmental signal processing, biofilm formation, and nutrient acquisition. Both genomes contained genes related to plant growth-promoting bacterial (PGPB) traits, including genes related to indole-3-acetate (IAA) synthesis, nitrogen fixation, nodulation, siderophore production, and phosphate solubilization, although the P. tropica strain IAC/BECa 135 genome contained a slightly more extensive repertoire. This study provides evidence that complementary mechanisms of growth promotion in Sorghum might occur, i.e., that P. tropica strain IAC/BECa 135 acts in the rhizosphere and increases the availability of nutrients, while H. frisingense strain IAC/BECa 152 influences plant hormone signaling. While the functional and taxonomic profiles of the rhizobiomes were similar in all treatments, significant differences in plant biomass were observed, indicating that the rhizobiome and the endophytic microbial community may play equally important roles in the complicated plant-microbial interplay underlying increased host plant growth.

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38

Hoeksema, Marten A., Zeyang Shen, Inge R. Holtman, An Zheng, Nathan J. Spann, Isidoro Cobo, Melissa Gymrek, and Christopher K. Glass. "Mechanisms underlying divergent responses of genetically distinct macrophages to IL-4." Science Advances 7, no. 25 (June 2021): eabf9808. http://dx.doi.org/10.1126/sciadv.abf9808.

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Mechanisms by which noncoding genetic variation influences gene expression remain only partially understood but are considered to be major determinants of phenotypic diversity and disease risk. Here, we evaluated effects of >50 million single-nucleotide polymorphisms and short insertions/deletions provided by five inbred strains of mice on the responses of macrophages to interleukin-4 (IL-4), a cytokine that plays pleiotropic roles in immunity and tissue homeostasis. Of >600 genes induced >2-fold by IL-4 across the five strains, only 26 genes reached this threshold in all strains. By applying deep learning and motif mutation analyses to epigenetic data for macrophages from each strain, we identified the dominant combinations of lineage-determining and signal-dependent transcription factors driving IL-4 enhancer activation. These studies further revealed mechanisms by which noncoding genetic variation influences absolute levels of enhancer activity and their dynamic responses to IL-4, thereby contributing to strain-differential patterns of gene expression and phenotypic diversity.

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39

Cizek, P. "Softening Mechanisms in Two Duplex Stainless Steels Deformed in Hot Torsion." Materials Science Forum 467-470 (October 2004): 1157–62. http://dx.doi.org/10.4028/www.scientific.net/msf.467-470.1157.

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The aim of the present work was to undertake a detailed investigation of the softening mechanisms during hot deformation of a 21Cr-10Ni-3Mo (steel A) and a 21Cr-8Ni-3Mo (steel B) austenite/ferrite duplex stainless steels containing about 60% and 30% of austenite, respectively. The steels were subjected to hot deformation in torsion performed at 900 °C and 1200 °C using a strain rate of 0.7 s-1 to several strain levels. Quantitative optical and transmission electron microscopy were used in the investigation. Austenite was observed to soften via dynamic recovery (DRV) and dynamic recrystallisation (DRX) accompanied by DRV for the deformation temperatures of 900 °C and 1200 °C, respectively, for the both steels studied. DRX of austenite largely occurred through strain-induced grain boundary migration, complemented by (multiple) twinning, and developed significantly faster in steel A than in steel B, indicating that considerably larger strains partitioned into austenite in the former steel during deformation at 1200 °C. The above softening mechanism was accompanied by the formation of DRX grains from subgrains along the austenite/ferrite interface and by large-scale subgrain coalescence. At 900°C, stressassisted phase transitions between austenite and ferrite were observed, characterised by dissolution of the primary austenite, formation of Widmanstätten secondary austenite and gradual globularisation of the microstructure with increasing strain. These processes appeared to be significantly more widespread in steel B. The softening mechanism within ferrite for the both steels studied was classified as “continuous DRX”, characterised by a gradual increase in misorientations between neighbouring subgrains with strain, for the both deformation temperatures.

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40

Belyakov, Andrey, Marina Odnobokova, Iaroslava Shakhova, and Rustam Kaibyshev. "Regularities of Microstructure Evolution and Strengthening Mechanisms of Austenitic Stainless Steels Subjected to Large Strain Cold Working." Materials Science Forum 879 (November 2016): 224–29. http://dx.doi.org/10.4028/www.scientific.net/msf.879.224.

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The deformation microstructures and their effects on mechanical properties of austenitic stainless steels processed by cold rolling at ambient temperature to various total strains were studied. The cold working was accompanied by the development of strain-induced martensitic transformation because of meta-stable austenite at room temperature. The strain-induced martensitic transformation and deformation twinning promoted the grain refinement during cold rolling, leading to nanocrystalline structures consisting of a mixture of austenite and martensite grains with their transverse grain sizes of 50-150 nm containing high dislocation densities. The rolled samples experienced substantial strengthening resulted from high density of strain induced grain/phase boundaries and dislocations. The yield strength of austenitic stainless steels could be increased to 2000 MPa after rolling to total strains of about 4. The martensite and austenite provided almost the same contribution to overall yield strength. The dislocation strengthening was much higher than the grain boundary strengthening at small to moderate strains of about 2, whereas the latter gradually increased approaching the level of dislocation strengthening with increasing the strain.

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41

Fernández Zenoff, V., F. Siñeriz, and M. E. Farías. "Diverse Responses to UV-B Radiation and Repair Mechanisms of Bacteria Isolated from High-Altitude Aquatic Environments." Applied and Environmental Microbiology 72, no. 12 (October 20, 2006): 7857–63. http://dx.doi.org/10.1128/aem.01333-06.

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ABSTRACT Acinetobacter johnsonii A2 isolated from the natural community of Laguna Azul (Andean Mountains at 4,560 m above sea level), Serratia marcescens MF42, Pseudomonas sp. strain MF8 isolated from the planktonic community, and Cytophaga sp. strain MF7 isolated from the benthic community from Laguna Pozuelos (Andean Puna at 3,600 m above sea level) were subjected to UV-B (3,931 J m−2) irradiation. In addition, a marine Pseudomonas putida strain, 2IDINH, and a second Acinetobacter johnsonii strain, ATCC 17909, were used as external controls. Resistance to UV-B and kinetic rates of light-dependent (UV-A [315 to 400 nm] and cool white light [400 to 700 nm]) and -independent reactivation following exposure were determined by measuring the survival (expressed as CFU) and accumulation of cyclobutane pyrimidine dimers (CPD). Significant differences in survival after UV-B irradiation were observed: Acinetobacter johnsonii A2, 48%; Acinetobacter johnsonii ATCC 17909, 20%; Pseudomonas sp. strain MF8, 40%; marine Pseudomonas putida strain 2IDINH, 12%; Cytophaga sp. strain MF7, 20%; and Serratia marcescens, 21%. Most bacteria exhibited little DNA damage (between 40 and 80 CPD/Mb), except for the benthic isolate Cytophaga sp. strain MF7 (400 CPD/Mb) and Acinetobacter johnsonii ATCC 17909 (160 CPD/Mb). The recovery strategies through dark and light repair were different in all strains. The most efficient in recovering were both Acinetobacter johnsonii A2 and Cytophaga sp. strain MF7; Serratia marcescens MF42 showed intermediate recovery, and in both Pseudomonas strains, recovery was essentially zero. The UV-B responses and recovery abilities of the different bacteria were consistent with the irradiation levels in their native environment.

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42

Vozniak, Alina, and Zbigniew Bartczak. "Deformation of Poly-l-lactid acid (PLLA) under Uniaxial Tension and Plane-Strain Compression." Polymers 13, no. 24 (December 17, 2021): 4432. http://dx.doi.org/10.3390/polym13244432.

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The ability of PLLA, either amorphous or semicrystalline, to plastic deformation to large strain was investigated in a wide temperature range (Td = 70–140 °C). Active deformation mechanisms have been identified and compared for two different deformation modes—uniaxial drawing and plane-strain compression. The initially amorphous PLLA was capable of significant deformation in both tension and plane-strain compression. In contrast, the samples of crystallized PLLA were found brittle in tensile, whereas they proved to be ductile and capable of high-strain deformation when deformed in plane-strain compression. The main deformation mechanism identified in amorphous PLLA was the orientation of chains due to plastic flow, followed by strain-induced crystallization occurring at the true strain above e = 0.5. The oriented chains in amorphous phase were then transformed into oriented mesophase and/or oriented crystals. An upper temperature limit for mesophase formation was found below Td = 90 °C. The amount of mesophase formed in this process did not exceed 5 wt.%. An additional mesophase fraction was generated at high strains from crystals damaged by severe deformation. After the formation of the crystalline phase, further deformation followed the mechanisms characteristic for the semicrystalline polymer. Interlamellar slip supported by crystallographic chain slip has been identified as the major deformation mechanism in semicrystalline PLLA. It was found that the contribution of crystallographic slip increased notably with the increase in the deformation temperature. The most probable active crystallographic slip systems were (010)[001], (100)[001] or (110)[001] slip systems operating along the chain direction. At high temperatures (Td = 115–140 °C), the α→β crystal transformation was additionally observed, leading to the formation of a small fraction of β crystals.

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van der Ende, Arie, Carla T. P. Hopman, and Jacob Dankert. "Multiple Mechanisms of Phase Variation of PorA inNeisseria meningitidis." Infection and Immunity 68, no. 12 (December 1, 2000): 6685–90. http://dx.doi.org/10.1128/iai.68.12.6685-6690.2000.

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ABSTRACT Previously, we reported that PorA expression in Neisseria meningitidis is modulated by variation in the length of the homopolymeric tract of guanidine residues between the −35 and −10 regions of the promoter or by deletion of porA. To reveal additional mechanisms of variation in PorA expression, the meningococcal isolates from 41 patients and 19 carriers were studied. In addition, at least 3 meningococcal isolates from different body parts of each of 11 patients were analyzed. Sequence analysis of theporA promoter showed that the spacer between the −35 and −10 regions varies in length between 14 and 24 bp. PorA expression was observed in strains with a porA promoter spacer of 16 to 24 bp. All but one strain with a porA promoter spacer of 16 to 20 bp and undetectable PorA expression have a homopolymeric tract of 8 or 6 instead of 7 adenine residues in the porA coding region. The other PorA-negative strain had a single-base-pair deletion in the coding region. The highest level of PorA expression was observed in strains with a promoter spacer of 17 or 18 bp. PorA expression was reduced twofold in strains with a porA promoter spacer of 16 or 19 bp. Strains with a 16-bp promoter spacer with substitutions in the polyguanidine tract displayed increased levels of PorA expression compared to strains with a homopolymeric tract of guanidine residues in the porA promoter. In conclusion, meningococci display multiple mechanisms for varying PorA expression.

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44

Hugaas, Eivind, and Andreas T. Echtermeyer. "Filament wound composite fatigue mechanisms investigated with full field DIC strain monitoring." Open Engineering 11, no. 1 (January 1, 2021): 401–13. http://dx.doi.org/10.1515/eng-2021-0041.

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Abstract Fatigue of filament wound materials was investigated using Digital Image Correlation DIC monitoring every 50th cycle of a high cycle fatigue test of a split disk ring sample. The ring was cut from a filament wound glass fiber reinforced polymer pressure vessel and had a hole. The strain field redistributed over time, lowering and moving strain concentrations. The redistributive behavior was most extensive in areas that later developed local fiber failure, which soon led to catastrophic failure. Microscopy was carried out on partially fatigued material. Damage evolved as matrix cracks and matrix splitting of groups of fibers and complete debonding of single fibers. This occurred at borders of voids and matrix cracks, easing progressive fiber failure. It was concluded that fatigue in filament wound composites has an extensive matrix damage phase before final failure. Fibers could locally withstand strains close to and above the static failure strain for considerable number of cycles if little local strain field redistribution was observed. The used method was able to detect changes in the strain fields that preceded catastrophic failure. It was concluded that DIC combined with the post processing methods presented may serve as a valuable tool for structural integrity monitoring of composite pressure vessels over time.

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45

Hassan, Hamizah, Mahmud Tengku Muda Mohamed, Siti Fairuz Yusoff, Erneeza Mohd Hata, and Nor Elliza Tajidin. "Selecting Antagonistic Yeast for Postharvest Biocontrol of Colletotrichum gloeosporioides in Papaya Fruit and Possible Mechanisms Involved." Agronomy 11, no. 4 (April 13, 2021): 760. http://dx.doi.org/10.3390/agronomy11040760.

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Colletotrichum gloeosporioides causes anthracnose disease in papaya fruit resulting in tremendous economic loss due to its latent infection. This study aimed to evaluate the biocontrol activity of antagonistic yeasts against C. gloeosporioides in papaya and determine the possible mechanism involved. One hundred and ten yeast strains were isolated from different parts of the papaya plant. Among them, only five strains, namely F001, F006, L003, FL013 and LP010, showed more than 55% radial growth inhibition of C. gloeosporioides. These five potent yeast strains were further evaluated in vitro and in vivo. The results indicated that strain F001 had the strongest biocontrol activity based on spore germination and fungal growth inhibition. In vivo, the strain F001 caused 66.7% and 25% reductions in disease incidence and severity, respectively. Based on molecular identification, the strain F001 was confirmed as Trichosporon asahii. Despite there was no significant induction of defense enzyme activities found on the treated fruits, SEM observation showed direct attachment of T. asahii with the fungal hyphae and interfere in their establishment to the fruit surface. Based on these findings, the antagonistic yeast T. asahii strain F001 may be used as a potential natural biological control agent against anthracnose disease in papaya fruit.

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46

Soldati, L. P., B. R. Barber, S. Salardi, I. Molinari, and G. Bianchi. "A new rat model for studying the calpain-calpastatin system." Laboratory Animals 29, no. 4 (October 1, 1995): 420–26. http://dx.doi.org/10.1258/002367795780740032.

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A recombinant rat strain-Milan low-calpastatin strain (MLCS)-was derived from Milan hypertensive (MHS/Gib) and Milan normotensive (MNS/Gib) strains. The MLCS rats have normal blood pressure and low calpastatin activity, and this strain is proposed as a model for studies of the calpain-calpastatin system, which is involved in important cellular mechanisms. Calpastatin polymorphism was observed in 10 different strains of laboratory rats and a single locus hypothesis is suggested as the mode of inheritance.

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47

Chen, Xinchi, Xiaoyong Zhang, Chao Chen, and Kechao Zhou. "Mechanical Response and Deformation Mechanisms of TB17 Titanium Alloy at High Strain Rates." Processes 9, no. 3 (March 8, 2021): 484. http://dx.doi.org/10.3390/pr9030484.

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The mechanical response and deformation mechanisms of TB17 titanium alloy were studied at room temperature by the split-Hopkinson pressure bar test. The ultimate compression strength increases from 1050 MPa to 1400 MPa, as the strain rate increases from 2000 s−1 to 2800 s−1. The adiabatic shear failure occurred at strain rate 2800 s−1. When the strain rate was 2000 s−1, only {10 9 3}<331>β type II high index deformation twins, a small number of α” martensite, and interfacial ω phase were detected. When the strain rate was 2400 s−1 and above, multiple deformation mechanisms, including the primary {10 9 3}<331>β type II high index deformation twins, secondary {332}<113>β deformation twins, and α” martensite were identified. The deformation mechanism changes from primary deformation twins and α” martensite to multiple deformation mechanisms (primary and secondary deformation structure) with the increase of strain rates.

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Rittberg, Dawn A. H., and Jim A. Wright. "Relationships between sensitivity to hydroxyurea and 4-methyl-5-amino-1-formylisoquinoline thiosemicarbazone (MAIQ) and ribonucleotide reductase RNR2 mRNA levels in strains of Saccharomyces cerevisiae." Biochemistry and Cell Biology 67, no. 7 (July 1, 1989): 352–57. http://dx.doi.org/10.1139/o89-055.

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Ribonucleotide reductase is responsible for providing the deoxyribonucleotide precursors for DNA synthesis. In most species the enzyme consists of a large and a small subunit, both of which are required for activity. In mammalian cells, the small subunit is the site of action of several antitumor agents, including hydroxyurea and 4-methyl-5-amino-1-formylisoquinoline thiosemicarbazone (MAIQ). The mRNA levels for the small subunit of ribonucleotide reductase (RNR2) and sensitivity to hydroxyurea and MAIQ were determined in four strains of the yeast, Saccharomyces cerevisiae. Two strains exhibited significantly different sensitivities to both hydroxyurea and MAIQ, which closely correlated with differences in the levels of RNR2 mRNA. These results are consistent with recent observations with mammalian cells in culture, and indicate that a common mechanism of resistance to hydroxyurea and related drugs occurs through the elevation in ribonucleotide reductase message levels. A transplason mutagenized strain with marked structural modifications in RNR2 DNA and mRNA showed an extreme hypersensitivity to hydroxyurea but not to MAIQ, providing evidence that the two drugs do not inhibit the RNR2 subunit by the same mechanism. In addition, a yeast strain isolated for low but reproducible resistance to MAIQ exhibited a sensitivity to hydroxyurea similar to the parental wild-type strain, supporting the idea that the two drugs inhibit the activity of RNR2 by unique mechanisms. These yeast strains provide a useful approach for further studies into the regulation of eucaryotic ribonucleotide reduction and drug resistance mechanisms involving a key rate-limiting step in DNA synthesis.Key words: Saccharomyces cerevisiae, reductase, messenger RNA, hydroxyurea, thiosemicarbazone.

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49

Carro, David, Enric Bartra, and Benjamin Piña. "Karyotype Rearrangements in a Wine Yeast Strain by rad52-Dependent and rad52-Independent Mechanisms." Applied and Environmental Microbiology 69, no. 4 (April 2003): 2161–65. http://dx.doi.org/10.1128/aem.69.4.2161-2165.2003.

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ABSTRACT Yeast strains isolated from the wild may undergo karyotype changes during vegetative growth, a characteristic that compromises their utility in genetic improvement projects for industrial purposes. Karyotype instability is a dominant trait, segregating among meiotic derivatives as if it depended upon only a few genetic elements. We show that disrupting the RAD52 gene in a hypervariable strain partially stabilizes its karyotype. Specifically, RAD52 disruption eliminated recombination at telomeric and subtelomeric sequences, had no influence on ribosomal DNA rearrangement rates, and reduced to 30% the rate of changes in chromosomal size. Thus, there are at least three mechanisms related to karyotype instability in wild yeast strains, two of them not requiring RAD52-mediated homologous recombination. When utilized for a standard sparkling-wine second fermentation, Δrad52 strains retained the enological properties of the parental strain, specifically its vigorous fermentation capability. These data increase our understanding of the mechanisms of karyotype instability in yeast strains isolated from the wild and illustrate the feasibility and limitations of genetic remediation to increase the suitability of natural strains for industrial processes.

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50

Bisset, J. A., M. M. Rodriguez, C. Diaz, E. Ortiz, M. C. Marquetti, and J. Hemingway. "The mechanisms of organophosphate and carbamate resistance in Culex quinquefasciatus (Diptera: Culicidae) from Cuba." Bulletin of Entomological Research 80, no. 3 (September 1990): 245–50. http://dx.doi.org/10.1017/s0007485300050434.

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AbstractTwo field-collected strains of Culex quinquefasciatus Say, collected 50 km apart in Havana City, Cuba, were both resistant to malathion and propoxur, while one population also showed low level resistance to temephos. Laboratory selection of the latter population with malathion for 22 generations increased the malathion resistance 1050-fold, temephos resistance 24-fold and propoxur resistance 453-fold compared to the standard laboratory susceptible strain. Synergist studies and biochemical tests indicated that two mechanisms, an elevated esterase and an insensitive acetylcholinesterase, were operative in these strains. The esterase mechanism conferred resistance to malathion, but not to temephos or propoxur. The acetylcholinesterase mechanism increased the level of malathion resistance and extended the cross-resistance spectrum to temephos and propoxur.

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