• Structural Engineering and Mechanics
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• v.32 no.5
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• pp.685-699
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• 2009

Current research and development of high performance concrete, together with study of phenomena that are pertinent to impact resistance, have lead to a new generation of barriers with improved properties to resist impact loads. The paper reviews major properties and mechanisms that affect impact resistance of concrete barriers as per criteria that characterize the resistance. These criteria are the perforation limit, penetration depth and the amount of front and rear face damage. From the long-known, single strength parameter that used to represent the barriers' impact resistance, more of the concrete mix ingredients are now considered to be effective in determining it. It is shown that the size and hardness of the aggregates, use of steel fibers and micro-silica have different effects on performance under impact and on the resistance. Additional pertinent phenomena, such as the rate and size effects, confinement and local versus global response, are pointed out with their reference to possible future developments in the design of impact resisting concrete barriers.

• Journal of Surface Science and Engineering
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• v.20 no.3
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• pp.95-105
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• 1987

For the purpose of improving the hot corrosion resistance of Ni-base superalloy, Inconel 600, aluminide and chromium-aluminide coatings by pack cementation process were studied. The morphology of these coatings is dependent on the type of process employed. And their overall composition depends on the composition of the base alloy and on the nature of the cement. Therefore the different aluminide and chromium-aluminide coatings obtained on a superalloy do not possess the same resistance to oxidation and hot corrosion. The mechanisms governing the formation of the coatings and the composition of the coating were varied by pack composition and temperature, and cyclic hot corrosion resistance of the auluminide coating formed by one-step process was inferior to that of the coating formed by two-step process. and Cr-Al composite coating showed good resistance for cyclic hot corrosion.

• Journal of Microbiology and Biotechnology
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• v.34 no.7
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• pp.1365-1375
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• 2024

The rise of Candida auris, a multidrug-resistant fungal pathogen, across more than 40 countries, has signaled an alarming threat to global health due to its significant resistance to existing antifungal therapies. Characterized by its rapid spread and robust drug resistance, C. auris presents a critical challenge in managing infections, particularly in healthcare settings. With research on its biological traits and genetic basis of virulence and resistance still in the early stages, there is a pressing need for a concerted effort to understand and counteract this pathogen. This review synthesizes current knowledge on the epidemiology, biology, genetic manipulation, pathogenicity, diagnostics, and resistance mechanisms of C. auris, and discusses future directions in research and therapeutic development. By exploring the complexities surrounding C. auris, we aim to underscore the importance of advancing research to devise effective control and treatment strategies.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.9
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• pp.4807-4814
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• 2012

Purpose: The chemoresistance of human hepatocellular carcinoma (HCC) to cytotoxic drugs, especially intrinsic or acquired multidrug resistance (MDR), still remains a major challenge in the management of HCC. In the present study, possible mechanisms involved in MDR of HCC were identified using a 5-fluorouracil (5-FU)-resistant human HCC cell line. Methods: BEL-7402/5-FU cells were established through continuous culturing parental BEL-7402 cells, imitating the pattern of chemotherapy clinically. Growth curves and chemosensitivity to cytotoxic drugs were determined by MTT assay. Doubling times, colony formation and adherence rates were calculated after cell counting. Morphological alteration, karyotype morphology, and untrastructure were assessed under optical and electron microscopes. The distribution in the cell cycle and drug efflux pump activity were measured by flow cytometry. Furthermore, expression of potential genes involved in MDR of BEL-7402/5-FU cells were detected by immunocytochemistry. Results: Compared to its parental cells, BEL-7402/5-FU cells had a prolonged doubling time, a lower mitotic index, colony efficiency and adhesive ability, and a decreased drug efflux pump activity. The resistant cells tended to grow in clusters and apparent changes of ultrastructures occurred. BEL-7402/5-FU cells presented with an increased proportion in S and G2/M phases with a concomitant decrease in G0/G1 phase. The MDR phenotype of BEL-7402/5-FU might be partly attributed to increased drug efflux pump activity via multidrug resistance protein 1 (MRP1), overexpression of thymidylate synthase (TS), resistance to apoptosis by augmentation of the Bcl-xl/Bax ratio, and intracellular adhesion medicated by E-cadherin (E-cad). P-glycoprotein (P-gp) might play a limited role in the MDR of BEL-7402/5-FU. Conclusion: Increased activity or expression of MRP1, Bcl-xl, TS, and E-cad appear to be involved in the MDR mechanism of BEL-7402/5-FU.

• Journal of Ginseng Research
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• v.44 no.1
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• pp.161-167
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• 2020

Background: The ascomycete fungi Cylindrocarpon destructans (Cd) and Fusarium solani (Fs) cause ginseng root rot and significantly reduce the quality and yield of ginseng. Cd produces the secondary metabolite radicicol, which targets the molecular chaperone Hsp90. Fs is resistant to radicicol, whereas other fungal genera associated with ginseng disease are sensitive to it. Radicicol resistance mechanisms have not yet been elucidated. Methods: Transcriptome analyses of Fs and Cd mycelia treated with or without radicicol were conducted using RNA-seq. All of the differentially expressed genes (DEGs) were functionally annotated using the Fusarium graminearum transcript database. In addition, deletions of two transporter genes identified by RNA-seq were created to confirm their contributions to radicicol resistance. Results: Treatment with radicicol resulted in upregulation of chitin synthase and cell wall integrity genes in Fs and upregulation of nicotinamide adenine dinucleotide dehydrogenase and sugar transporter genes in Cd. Genes encoding an ATP-binding cassette transporter, an aflatoxin efflux pump, ammonium permease 1 (mep1), and nitrilase were differentially expressed in both Fs and Cd. Among these four genes, only the ABC transporter was upregulated in both Fs and Cd. The aflatoxin efflux pump and mep1 were upregulated in Cd, but downregulated in Fs, whereas nitrilase was downregulated in both Fs and Cd. Conclusion: The transcriptome analyses suggested radicicol resistance pathways, and deletions of the transporter genes indicated that they contribute to radicicol resistance.

• Journal of Gastric Cancer
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• v.24 no.3
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• pp.300-315
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• 2024

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions: These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

• Human Ecology Research
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• v.57 no.2
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• pp.171-183
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• 2019

Convergence between technology and financial services is ubiquitous and widespread. Virtual banks represent an important aspect of financial markets that can generate value added for consumers and enhance the quality of financial services. This study explores the effect of innovation characteristics (relative advantage, compatibility, and perceived risk), consumer characteristics (status quo bias), and social mechanisms (network externality: complementarity, numbers of peers) on consumers' adoption intention and resistance to virtual banks. This study adopted an innovation resistance model with two dependent variables: adoption intention and resistance to virtual banks. An online self-administered survey was conducted and 532 or non-users of virtual banks aged 20 to 69 years old were analyzed. Frequency analysis, descriptive analysis, and hierarchical multiple regression indicated that status quo bias, relative advantage, perceived risk, complementarity, and number of peers insignificantly influence the adoption intention regarding virtual banks. Furthermore, status quo bias, relative advantage, perceived risk, and number of peers insignificantly influence the resistance to virtual banks. Female respondents have a lower adoption intention and higher resistance to virtual banks than male respondents. The findings suggest that the innovation resistance model can be useful in understanding consumers'adoption and resistance behavior as well as reveal that innovation characteristics, consumer characteristics, and social mechanism are important antecedent variables of the innovation adoption decision.

• Transactions of the Korean Society of Automotive Engineers
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• v.13 no.5
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• pp.152-162
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• 2005

Coolant rubber hoses for automobile radiators can be degraded and thus failed due to the influence of contacting stresses of air and coolant liquid under the thermal and mechanical loadings. In this study, test analysis was carried out for evaluating the degradation and failure mechanisms of coolant hose materials. Two kinds of EPDM rubber materials applicable to the hoses were adopted: commonly-used ethylene-propylene diene monomer(EPDM) rubbers and EPDM rubbers with high resistance against electro-chemical degradation (ECD). An increase of surface hardness and a large reduction of failure strain were shown due to the formation of oxidation layer for the specimens which had been kept in a high temperature air chamber. Coolant ageing effects took place only by an amount of pure thermal degradation. The specimens degraded by ECD test showed a swelling behavior and a considerable increase in weight on account of the penetration of coolant liquid into the skin and interior of the rubber specimens. The ECD induced material softening as well as drastic reduction in strength and failure strain. However EPDM rubbers designed for high resistance against ECD revealed a large improvement in reduction of failure strain and weight. This study finally established a procedure for reliability analysis and evaluation of the degradation and failure mechanisms of EPDM rubbers used in coolant hoses for automobile radiators.

• Sleep Medicine and Psychophysiology
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• v.6 no.1
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• pp.19-25
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• 1999

Sleep alters both breathing pattern and the ventilatory responses to external stimuli. These changes during sleep permit the development or aggravation of sleep-related hypoxemia in patients with respiratory disease and contribute to the pathogenesis of apneas in patients with the sleep apnea syndrome. Fundamental effects of sleep on the ventilatory control system are 1) removal of wakefulness input to the upper airway leading to the increase in upper airway resistance, 2) loss of wakefulness drive to the respiratory pump, 3) compromise of protective respiratory reflexes, and 4) additional sleep-induced compromise of ventilatory control initiated by reduced functional residual capacity on supine position assumed in sleep, decreased $CO_2$ production during sleep, and increased cerebral blood flow in especially rapid eye movement(REM) sleep. These effects resulted in periodic breathing during unsteady non-rapid eye movement(NREM) sleep even in normal subjects, regular but low ventilation during steady NREM sleep, and irregular breathing during REM sleep. Sleep-induced breathing instabilities are divided due primarily to transient increase in upper airway resistance and those that involve overshoots and undershoots in neural feedback mechanisms regulating the timing and/or amplitude of respiratory output. Following ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include 1) hypocapnia, 2) inhibitory effect from lung stretch, 3) baroreceptor stimulation, 4) upper airway mechanoreceptor reflexes, 5) central depression by hypoxia, and 6) central system inertia. While the respiratory control system functions well during wakefulness, the control of breathing is commonly disrupted during sleep. These changes in respiratory control resulting in breathing instability during sleep are related with the pathophysiologic mechanisms of obstructive and/or central apnea, and have the therapeutic implications for nocturnal hypoventilation in patients with chronic obstructive pulmonary disease or alveolar hypoventilation syndrome.

• Parasites, Hosts and Diseases
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• v.38 no.4
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• pp.209-236
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• 2000

The last two decades witnessed significant advances in the efforts of immune-parasitologists to elucidate the nature and role of the host mucosal defence mechanisms against intestinal nematode parasites. Aided by recent advances in basic immunology and biotechnology with the concomitant development of well defined laboratory models of infection, immunoparasitologists have more precisely analyzed and defined the different immune effector mechanisms during the infection; resulting in great improvement in our current knowledge and understanding of protective immunity against gastrointestinal (GI) nematode parasites. Much of this current understanding comes from experimental studies in laboratory rodents, which have been used as models of livestock and human GI nematode infections. These rodent studies, which have concentrated on Heligmosomoides polygyrus, Nippostrongylus brasiliensis, Strongyloides ratti/5. venezuelensis. Trichinella spiralis and trichuris muris infections in mice and rats, have helped in defining the types of T cell responses that regulate effector mechanisms and the effector mechanisms responsible for worm expulsion. In addition, these studies bear indications that traditionally accepted mechanisms of resistance such as eosinophilia and IgE responses may not play as important roles in protection as were previously conceived. In this review, we shall, from these rodent studies, attempt an overview of the mucosal and other effector responses against intestinal nematode parasites beginning with the indices of immune protection as a model of the protective immune responses that may occur in animals and man.