Using High-Level Construal and Perceptions of Changeability to Promote Self-Change Over Self-Protection Motives in Response to Negative Feedback

2015 ◽  
Vol 41 (6) ◽  
pp. 822-838 ◽  
Author(s):  
Jennifer N. Belding ◽  
Karen Z. Naufel ◽  
Kentaro Fujita
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Romina Giacometti ◽  
Vanesa Jacobi ◽  
Florencia Kronberg ◽  
Charalampos Panagos ◽  
Arthur S. Edison ◽  
...  

Abstract The stink bug Nezara viridula is one of the most threatening pests for agriculture in North and South America, and its oral secretion may be responsible for the damage it causes in soybean (Glycine max) crop. The high level of injury to seeds caused by pentatomids is related to their feeding behavior, morphology of mouth parts, and saliva, though information on the specific composition of the oral secretion is scarce. Field studies were conducted to evaluate the biochemical damage produced by herbivory to developing soybean seeds. We measured metabolites and proteins to profile the insect saliva in order to understand the dynamics of soybean-herbivore interactions. We describe the mouth parts of N. viridula and the presence of metabolites, proteins and active enzymes in the watery saliva that could be involved in seed cell wall modification, thus triggering plant defenses against herbivory. We did not detect proteins from bacteria, yeasts, or soybean in the oral secretion after feeding. These results suggest that the digestive activity and organic compounds of watery saliva may elicit a plant self-protection response. This study adds to our understanding of stink bug saliva plasticity and its role in the struggle against soybean defenses.


Author(s):  
JOHN R. KOZA ◽  
MARTIN A. KEANE ◽  
MATTHEW J. STREETER ◽  
THOMAS P. ADAMS ◽  
LEE W. JONES

Some designs are sufficiently creative that they are considered to be inventions. The invention process is typically characterized by a singular moment when the prevailing thinking concerning a long-standing problem is, in a “flash of genius,” overthrown and replaced by a new approach that could not have been logically deduced from what was previously known. This paper discusses such logical discontinuities using an example based on the history of one of the most important inventions of the 20th century in electrical engineering, namely, the invention of negative feedback by AT&T's Harold S. Black. This 1927 invention overthrew the then prevailing idiom of positive feedback championed by Westinghouse's Edwin Howard Armstrong. The paper then shows how this historically important discovery can be readily replicated by an automated design and invention technique patterned after the evolutionary process in nature, namely, genetic programming. Genetic programming employs Darwinian natural selection along with analogs of recombination (crossover), mutation, gene duplication, gene deletion, and mechanisms of developmental biology to breed an ever improving population of structures. Genetic programming rediscovers negative feedback by conducting an evolutionary search for a structure that satisfies Black's stated high-level goal (i.e., reduction of distortion in amplifiers). Like evolution in nature, genetic programming conducts its search probabilistically without resort to logic using a process that is replete with logical discontinuities. The paper then shows that genetic programming can routinely produce many additional inventive and creative results. In this regard, the paper discusses the automated rediscovery of numerous 20th-century patented inventions involving analog electrical circuits and controllers, the Sallen–Key filter, and six 21st-century patented inventions. In addition, two patentable new inventions (controllers) have been created in the same automated way by means of genetic programming. The paper discusses the promising future of automated invention by means of genetic programming in light of the fact that, to date, increased computer power has yielded progressively more substantial results, including numerous human-competitive results, in synchrony with Moore's law. The paper argues that evolutionary search by means of genetic programming is a promising approach for achieving creative, human-competitive, automated design because illogic and creativity are inherent in the evolutionary process.


mBio ◽  
2021 ◽  
Author(s):  
Yu Tang ◽  
Ramesh Rijal ◽  
David E. Zimmerhanzel ◽  
Jacquelyn R. McCullough ◽  
Louis A. Cadena ◽  
...  

Many mammalian tissues such as the liver have the remarkable ability to regulate their size and have their cells stop proliferating when the tissue reaches the correct size. One possible mechanism involves the cells secreting a signal that they all sense, and a high level of the signal tells the cells that there are enough of them and to stop proliferating.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zheng Yu ◽  
Meiying Zhang ◽  
Bin Luo ◽  
Hongyang Jing ◽  
Yue Yu ◽  
...  

Abstract Background Epilepsy is characterized by the typical symptom of seizure, and anti-seizure medications are the main therapeutic method in clinical, but the effects of these therapy have not been satisfactory. To find a better treatment, it makes sense to further explore the regulatory mechanisms of seizures at genetic level. Lrp4 regionally expresses in mice hippocampus where is key to limbic epileptogenesis. It is well known that neurons release a high level of glutamate during seizures, and it has been reported that Lrp4 in astrocytes down-regulates glutamate released from neurons. However, it is still unclear whether there is a relationship between Lrp4 expression level and seizures, and whether Lrp4 plays a role in seizures. Results We found that seizures induced by pilocarpine decreased Lrp4 expression level and increased miR-351-5p expression level in mice hippocampus. Glutamate reduced Lrp4 expression and enhanced miR-351-5p expression in cultured hippocampal astrocytes, and these effects can be partially attenuated by AP5. Furthermore, miR-351-5p inhibitor lessened the reduction of Lrp4 expression in glutamate treated hippocampal astrocytes. Local reduction of Lrp4 in hippocampus by sh Lrp4 lentivirus injection in hippocampus increased the threshold of seizures in pilocarpine or pentylenetetrazol (PTZ) injected mice. Conclusions These results indicated that high released glutamate induced by seizures down-regulated astrocytic Lrp4 through increasing miR-351-5p in hippocampal astrocytes via activating astrocytic NMDA receptor, and locally reduction of Lrp4 in hippocampus increased the threshold of seizures. Lrp4 in hippocampal astrocytes appears to serve as a negative feedback factor in seizures. This provides a new potential therapeutic target for seizures regulation.


2007 ◽  
Vol 51 (1) ◽  
pp. 181-187 ◽  
Author(s):  
Saeed M. Hashimi ◽  
Melisa K. Wall ◽  
Andrew B. Smith ◽  
Anthony Maxwell ◽  
Robert G. Birch

ABSTRACT Xanthomonas albilineans produces a family of polyketide-peptide compounds called albicidins which are highly potent antibiotics and phytotoxins as a result of their inhibition of prokaryotic DNA replication. Here we show that albicidin is a potent inhibitor of the supercoiling activity of bacterial and plant DNA gyrases, with 50% inhibitory concentrations (40 to 50 nM) less than those of most coumarins and quinolones. Albicidin blocks the religation of the cleaved DNA intermediate during the gyrase catalytic sequence and also inhibits the relaxation of supercoiled DNA by gyrase and topoisomerase IV. Unlike the coumarins, albicidin does not inhibit the ATPase activity of gyrase. In contrast to the quinolones, the albicidin concentration required to stabilize the gyrase cleavage complex increases 100-fold in the absence of ATP. The slow peptide poisons microcin B17 and CcdB also access ATP-dependent conformations of gyrase to block religation, but in contrast to albicidin, they do not inhibit supercoiling under routine assay conditions. Some mutations in gyrA, known to confer high-level resistance to quinolones or CcdB, confer low-level resistance or hypersensitivity to albicidin in Escherichia coli. Within the albicidin biosynthesis region in X. albilineans is a gene encoding a pentapeptide repeat protein designated AlbG that binds to E. coli DNA gyrase and that confers a sixfold increase in the level of resistance to albicidin in vitro and in vivo. These results demonstrate that DNA gyrase is the molecular target of albicidin and that X. albilineans encodes a gyrase-interacting protein for self-protection. The novel features of the gyrase-albicidin interaction indicate the potential for the development of new antibacterial drugs.


1986 ◽  
Vol 110 (2) ◽  
pp. 233-238 ◽  
Author(s):  
D. Gauthier ◽  
G. Coulaud

ABSTRACT This study was conducted to investigate the hypothesis that the low LH pulsatility induced by underfeeding may result from an altered negative-feedback response to testosterone in cattle. Eight 21-month-old Aubrac bulls were divided into two equal groups. The first group (group H) received a high level of nutrition (producing a gain in weight of 570 g/day) and the second group (group L) a low level of nutrition (producing a loss in weight of 330 g/day). After 52 days of underfeeding the bulls were hemicastrated, castrated 7 days later and then injected with 30 mg testosterone daily for 14 days, 10 mg daily for 7 days and 2·5 mg daily for 7 days. After hemicastration, LH pulsatility was higher (P < 0·001) in group H (9·0 pulses in 24 h) than in group L (5·3 pulses in 24 h). After castration this value was the same in the two groups (24 pulses in 24 h). When the bulls were injected daily with 30 or 10 mg testosterone, the number of LH pulses in 24 h was lower (P < 0·05) in group L (14·3 and 9·8 pulses in 24 h with 30 mg, and 17·3 pulses in 24 h with 10 mg) than in group H (27·8 and 25·5 pulses in 24 h with 30 mg, and 24·0 pulses in 24 h with 10 mg). When the animals received 2·5 mg testosterone daily, the number of LH pulses was the same in both groups (20·3 pulses in 24 h). These results indicate that the negative-feedback response of the LH-releasing system to testosterone is modified by underfeeding in the bull. J. Endocr. (1986) 110, 233–238


2020 ◽  
Author(s):  
Zheng Yu ◽  
Meiying Zhang ◽  
Bin Luo ◽  
Hongyang Jing ◽  
Yue Yu ◽  
...  

Abstract Backgroud Epilepsy is characterized by the typical symptom of seizure, and anti-seizure medications are the main therapeutic method in clinical, but the effects of these therapy have not been satisfactory. To find a better treatment, it makes sense to further explore the regulatory mechanisms of seizures at genetic level. LRP4 regionally expresses in mice hippocampus where is key to limbic epileptogenesis. It is well known that neurons release a high level of glutamate during seizures, and it has been reported that LRP4 in astrocytes down-regulates glutamate released from neurons. However, it is still unclear whether there is a relationship between LRP4 expression level and seizures, and whether LRP4 plays a role in seizures.Results We found that seizures induced by pilocarpine decreased LRP4 expression level and increased miR-351-5p expression level in mice hippocampus. Glutamate reduced LRP4 expression and enhanced miR-351-5p expression in cultured hippocampal astrocytes, and these effects can be partially attenuated by AP5. Furthermore, miR-351-5p inhibitor lessened the reduction of LRP4 expression in glutamate treated hippocampal astrocytes. Local reduction of LRP4 in hippocampus by sh Lrp4 lentivirus injection in hippocampus increased the threshold of seizures in pilocarpine or pentylenetetrazol (PTZ) injected mice. Conclutions These results indicated that high released glutamate induced by seizures down-regulated astrocytic LRP4 through increasing miR-351-5p in hippocampal astrocytes via activating astrocytic NMDA receptor, and locally reduction of LRP4 in hippocampus increased the threshold of seizures. LRP4 in hippocampal astrocytes appears to serve as a negative feedback factor in seizures. This provides a new potential therapeutic target for seizures regulation.


1998 ◽  
Vol 156 (1) ◽  
pp. 169-175 ◽  
Author(s):  
T Okabe ◽  
R Takayanagi ◽  
M Adachi ◽  
K Imasaki ◽  
H Nawata

Nur77 is a member of the steroid receptor superfamily and is known to be expressed in animals under stress. We studied the role of nur77 in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis during the stress response using a murine pituitary corticotrope cell line, AtT-20. Corticotropin-releasing hormone (CRH), a stress mediator in the HPA axis, induced the expression of nur77 transiently in AtT-20 cells. Gel shift assay showed that nur77 bound to negative glucocorticoid responsive element (nGRE) in the promoter of the human proopiomelanocortin (POMC) gene and the formation of the nur77-nGRE complex increased after treatment of the cells with CRH. Negative GRE is known to be necessary for the negative regulation by glucocorticoid of the POMC gene expression. In stable transformants of AtT-20 cells expressing a human homolog of nur77, NAK-1, at a high level, glucocorticoid-mediated inhibition of both POMC mRNA induction and ACTH secretion was significantly lower than that in the NAK-1-non-expressing cells (P < 0.001). These results strongly suggest that nur77 antagonizes the negative feedback effect of glucocorticoid on the synthesis and secretion of ACTH in pituitary corticotropes. This suggests that nur77 plays an important role in the pituitary gland in the biological adaptation to overcome stress.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Timon Cheng-Yi Liu ◽  
Yan-Ying Liu ◽  
En-Xiu Wei ◽  
Fang-Hui Li

Photobiomodulation (PBM) is a nondamaged modulation of laser irradiation or monochromatic light (LI) on a biosystem function. It depends on whether the function is in its function-specific homeostasis (FSH). An FSH is a negative-feedback response of a biosystem to maintain the function-specific conditions inside the biosystem so that the function is perfectly performed. A function in its FSH is called a normal function. A function far from its FSH is called a dysfunctional function. The process of a function from dysfunctional to normal is called a functional normalization. For a normal function in its FSH, there are FSH-essential subfunctions (FESs), FSH-nonessential subfunctions (FNSs), and an FES/FNS-specific homeostasis (FESH/FNSH). A FSH can resist internal/external disturbances under the threshold, but can be disrupted by an FSH-specific stress (FSS). A normal/dysfunctional FSS is called a successful/chronic stress. An FESH/FNSH-specific stress was called an extraordinary/ordinary stress. A low level LI (LLL) cannot directly affect a normal function, but can modulate a chronic stress. A normal function may have a chronic ordinary stress, and an LLL may modulate the chronic ordinary stress so that it promotes the normalization of the dysfunctional FNS and then upgrades the normal function. A high level LI can modulate a normal function and may be a successful stress.


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