• Biomedical Science Letters
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• v.12 no.2
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• pp.119-125
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• 2006

In relation to the tissue engineering, the cellular responses to the morphology of the scaffold surface are interesting topics. Human ligament fibroblasts (HLFs) were cultured on the micrpatterned silicone substrates subjected to cyclic stretch to simulate ligament motion. Groove and ridge width of silicone substrates was 10/50, 20/50, 20/10, and 20/20 ${\mu}m$ (groove/ridge ${\mu}m$) with a depth of $3{\mu}m$. Strain was applied over two days for 4 hours per day with a frequency of 0.5 Hz with the magnitudes of 4 or 8%. The purpose of this study was to evaluate ligament fibroblast alignment and cellular responses in relation to the pattern of microgrooved surface and stretching magnitude. Ligament fibroblasts in the microgrooved surface were elongated and aligned parallel to the microgrooves under no stretch. Uniaxial cyclic stretch induced cellular activities and their orientation rise in cellular response and the cells showed alignment and elongation perpendicular to the direction of the stretch. Biochemical analyses showed that the best cellular response was found on the $20/50{\mu}m$ under 8% stretch. The surface morphology and mechanical stretching were found to contribute to increase of proliferation, collagen production.

• The Journal of Advanced Prosthodontics
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• v.3 no.2
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• pp.63-68
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• 2011

PURPOSE. The object of this study was to investigate the effect of UV irradiation (by a general commercial UV sterilizer) on anodized titanium surface. Surface characteristics and cellular responses were compared between anodized titanium discs and UV irradiated anodized titanium discs. MATERIALS AND METHODS. Titanium discs were anodized and divided into the following groups: Group 1, anodized (control), and Goup 2, anodized and UV irradiated for 24 hours. The surface characteristics including contact angle, roughness, phase of oxide layer, and chemical elemental composition were inspected. The osteoblast-like human osteogenic sarcoma (HOS) cells were cultured on control and test group discs. Initial cellular attachment, MTS-based cell proliferation assay, and ALP synthesis level were compared between the two groups for the evaluation of cellular response. RESULTS. After UV irradiation, the contact angle decreased significantly (P<.001). The surface roughness and phase of oxide layer did not show definite changes, but carbon showed a considerable decrease after UV irradiation. Initial cell attachment was increased in test group (P=.004). Cells cultured on test group samples proliferated more actively (P=.009 at day 2, 5, and 7) and the ALP synthesis also increased in cells cultured on the test group (P=.016 at day 3, P=.009 at day 7 and 14). CONCLUSION. UV irradiation induced enhanced wettability, and increased initial cellular responses of HOS cells on anodized titanium surface.

• Steel and Composite Structures
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• v.5 no.2_3
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• pp.193-202
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• 2005

This paper describes recent developments in composite construction and their effect on codified design procedures in the UK. Areas of particular interest include: rules on shear connection, design of beams with web openings, serviceability limits, such as floor vibrations, and fire safe design. The design of cellular beams with regular circular openings now includes generalized rules for web-post buckling, and for the development of in-plane moment in the web-post for asymmetric sections. Closed solutions for the maximum shear force due to limits on web-post bending or buckling are presented. The fire resistance of cellular beams is also dependent on the temperature of the web-post, and for closely spaced openings. It is necessary to increase the thickness of fire protection to the web. For serviceability design of beams, deflection limits and natural frequency and response factor for vibration are presented. It may be necessary to use stricter limits for certain applications.

• Molecules and Cells
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• v.47 no.1
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• pp.100006.1-100006.10
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• 2024

Nitric oxide (NO) serves as an evolutionarily conserved signaling molecule that plays an important role in a wide variety of cellular processes. Extensive studies in Drosophila melanogaster have revealed that NO signaling is required for development, physiology, and stress responses in many different types of cells. In neuronal cells, multiple NO signaling pathways appear to operate in different combinations to regulate learning and memory formation, synaptic transmission, selective synaptic connections, axon degeneration, and axon regrowth. During organ development, elevated NO signaling suppresses cell cycle progression, whereas downregulated NO leads to an increase in larval body size via modulation of hormone signaling. The most striking feature of the Drosophila NO synthase is that various stressors, such as neuropeptides, aberrant proteins, hypoxia, bacterial infection, and mechanical injury, can activate Drosophila NO synthase, initially regulating cellular physiology to enable cells to survive. However, under severe stress or pathophysiological conditions, high levels of NO promote regulated cell death and the development of neurodegenerative diseases. In this review, I highlight and discuss the current understanding of molecular mechanisms by which NO signaling regulates distinct cellular functions and behaviors.

• Biotechnology and Bioprocess Engineering:BBE
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• v.6 no.4
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• pp.231-236
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• 2001

How much do we know about the biology of aging from cell culture studies Most normal somatic cells have a finite potential to divide due to a process termed cellular or replicative senescence. A growing body evidence suggests that senescence evolved to protect higher eu-karyotes, particularly mammals, from developing cancer, We now know that telomere shortening due to the biochemistry of DNA replication, induces replicative senescence in human cells. How-ever in rodent cells, replicative senescence occurs despite very long telomeres. Recent findings suggest that replicative senescence is just the tip of the iceberg of a more general process termed cellular senescence. It appears that cellular senescence is a response to potentially oncogenic in-sults, including oxidative damage. In young orgainsms, growth arrest by cell senescence sup-presses tumor development, but later in life, due to the accumulation of senescent cells which se-cret factors that can disrupt tissues during aging, cellular senescence promotes tumorigenesis. Therefore, antagonistic pleiotropy may explain, if not in whole the apparently paradoxical effects of cellular senescence, though this still remains an open question.

• Molecules and Cells
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• v.39 no.1
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• pp.60-64
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• 2016

Inflammation is a pathophysiological response to infection or tissue damage during which high levels of reactive oxygen and nitrogen species are produced by phagocytes to kill microorganisms. Reactive oxygen and nitrogen species serve also in the complex regulation of inflammatory processes. Recently, it has been proposed that peroxiredoxins may play key roles in innate immunity and inflammation. Indeed, peroxiredoxins are evolutionarily conserved peroxidases able to reduce, with high rate constants, hydrogen peroxide, alkyl hydroperoxides and peroxynitrite which are generated during inflammation. In this minireview, we point out different possible roles of peroxiredoxins during inflammatory processes such as cytoprotective enzymes against oxidative stress, modulators of redox signaling, and extracellular pathogen- or damage-associated molecular patterns. A better understanding of peroxiredoxin functions in inflammation could lead to the discovery of new therapeutic targets.

• Korean Journal of Veterinary Pathology
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• v.2 no.1
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• pp.37-46
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• 1998

It has been known that $\gamma$-irradiation usually induces cell death in regenerating stem cell in normal tissues like skin, intestine and hematopoietic organ. The experiment were carried out to evaluate the early response of radiation injury in radiosensitive and intermediate radiosensitive tissues in feeding and starving rats with the doses of 3.5 and 7.0 Gy. The results of the study showed that the histological phenomenon was apoptosis in the doses of the radiation as the early response of tissue injury. Apoptosis were showed organ-specific and cellular specific responses suggesting that the selection of apoptosis be exactly focused on highly renewal organs and cells. It was interesting that the rats starved for 72 hours prior to irradiation induced less apoptosis in liver than fed rats. As for cellular responses it appeared that apoptotic cells were mostly distributed in ductal or periportal cells in liver of feeding rats unlikely in liver of Starving rots which showed no difference in zonal distribution. In salivary gland apoptotic cells in fed rats were highly induced in intercalating and ductal cell population than in acinar cell population although unlikely in starved rats. This study showed the value of apoptosis using the detection system of TUNEL for evaluating cellular damage after radiation injury and the diminished effect of starvation on cell damage after ionizing irradiation.

• Journal of dental hygiene science
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• v.22 no.3
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• pp.164-170
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• 2022

Background: When cells are damaged by nicotine, cellular senescence due to oxidative stress accelerates. In addition, stress-induced inflammatory response and cellular senescence cause the accumulation of damaged organelles in cells, and autophagy appears to remove them. Conversely, when autophagy is reduced, harmful cell components accumulate, and aging is accelerated. This study aimed to determine the association between nicotine-induced cellular senescence and autophagy expression patterns in human gingival fibroblasts. Methods: Cells were treated with various concentrations of nicotine (0, 0.1, 0.5, 1, 2, and 5 mM) and 10 nM rapamycin was added to 1 mM nicotine to investigate the relationship between autophagy and cellular senescence. Cell viability was confirmed using WST-8 and the degree of cellular senescence was measured by SA-β-gal staining. The expression of the inflammatory proteins (COX-2 and iNOS) and autophagy markers (LC3-II, p62, and Beclin-1) was analyzed by western blotting. Results: The cell viability tended to decrease in a concentration-dependent manner. COX-2 showed no concentration-dependent expression and iNOS increased in the 0.5 mM nicotine treated group. The degree of cellular senescence was the highest in the 1 mM nicotine treatment group. In the group treated with rapamycin and nicotine, the conversion ratio of LC3-II to LC3-I was the highest, that of p62 was the lowest, and the level of Beclin-1 proteins was significantly increased. Furthermore, the degree of cellular senescence was reduced in the group in which rapamycin was added to nicotine compared to that in the group treated with nicotine alone. Conclusion: This study provides evidence that autophagy activated in an aging environment reduces cellular senescence to a certain some extent.

• Molecules and Cells
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• v.44 no.6
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• pp.384-391
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• 2021

The recent appearance of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people around the world and caused a global pandemic of coronavirus disease 2019 (COVID-19). It has been suggested that uncontrolled, exaggerated inflammation contributes to the adverse outcomes of COVID-19. In this review, we summarize our current understanding of the innate immune response elicited by SARS-CoV-2 infection and the hyperinflammation that contributes to disease severity and death. We also discuss the immunological determinants behind COVID-19 severity and propose a rationale for the underlying mechanisms.

• Journal of Korean Academy of Nursing
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• v.23 no.4
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• pp.528-543
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• 1993

Vitamin E, which has its advocates in the treatment of diabetes mellitus. autoimmune disease, cancer and peripheral vascular and thromboembolic disease, has now been alleged to have a powerful antioxident effect and to affect various biological activities such as fertility factor, inhibition of human platelet aggregation and stabilization of biological membranes. The present study was designed to test whether vitamin I(alpha-tocopherol) can : (1) enhance the hemagglutinin response to sheep red blood cells (SRBC), (2) modulate Arthus and delayed type hypersensitivity(DTH) to SRBC and contact hypersensitivity to dinitrofluorobenzene (DNFB). (3) enhance the mitogenic response of murine splenocyte, (4) decrease the recovery of Cryptococcus neoformans from brain, lung, liver, spleen and kidney of infected mice and (5) have an inhibitory or enhancing effect on the induction of active systemic anaphylaxis(ASA) induced by chicken-gamma globulin (CGG) in mice. Mice were given either intramuscular injections of 0.3ml (300mg) of vitamin I before immunization or were infection for 10 consecutive days or were given by vitamin I esophageal intubation, 0.1ml(100mg), for 20 days before sacrifice for the mitogenic response experiments. It was found that vitamin E treated mice showed a significant enhancement in hemagglutinin response, Arthus reaction and DTH to SRBC and contact hypersensitivity to DNFB. There was no significant difference in the mitogenic response to phytohemagglutinin(PHA), but the response to concanavalin A(ConA) or pokeweed mitogem(PWM) was increased in vitamin E-treated mice. Interestingly, the vitamin E administration before C. neoformans infection decreased significantly the recovery of C. neoformans from brain lung, liver, spleen and kidney of the infected mice as compared with that of the control mice, strongly suggesting that vitamin E pretreatment may increase the resistance of mice to the fungal infection. Unexpectedly, vitamin E administration enhanced the production of CGG -induced ASA. Taken together, it can be concluded that vitamin I administration may in-crease the humoral and cellular immune response and resistance. to C. neoformans infection, but enhance the induction of ASA to CGG. Further studies are necessary to clarify the underlying mechanism accounting for these effects.