Traumatic brain injury (TBI) is one of the leading causes of death and disability in children and adults and is a major risk factor for the development of posttraumatic epilepsy (PTE). Recent studies have provided significant insight into the pathophysiological mechanisms underlying the development of epilepsy. Although the link between brain trauma and epilepsy is well recognized, the complex biological mechanisms that result in PTE following TBI have not been fully elucidated. Therefore, this study investigated in order to identify whether or not the abnormal expression of calcium-binding proteins in the lesioned hippocampus plays a role in neuronal damage by brain trauma and whether or not the expressions may change in the contralateral hippocampus during the adaptive stage as early time point following TBI. During early time point following TBI, both parvalbumin (PV) and calbindin D-28k (CB) immunoreactivities were decreased with in the lesioned hippocampus. However, these expressions were recovered to control levels as depend on time courses. On the other hand, PV immunoreactivity in contralateral hippocampus was transiently reduced as compared to the control levels, whereas CB expression was unchanged. These findings indicate that the alterations of the calcium-binding proteins, especially PV and CB, may contribute to the neuronal death and/or damage induced by abnormal inhibitory neurotransmission at early time period following brain trauma and the development of epileptogenesis in patients with traumatic brain injury.
Cathepsin K (cat K) is the major cysteine protease expressed in osteoclasts and was thought to play a key role in matrix degradation during bone resorption. It was shown that the intracellular maturation of cat K was prevented by the cAMP antagonist, Rp-cAMP, and the protein kinase A (PKA) inhibitors of KT5720 and H89. In contrast, forskolin, a adenylate cyclase agonist, rather induced Cat K processing and maturation in osteoclasts. Furthermore, to determine whether cat K processing and maturation signaling involves protein kinase C (PKC), mouse total bone cells were treated with calphostin C, a specific inhibitor of PKC, however, no effect was observed, indicating that calphostin C did not affect to osteoclast-mediated cat K processing and maturation. Thus, it is indicated that the cAMP-PKA signaling pathway regulates cat K maturation in osteoclasts. Since secreted proenzymes have the potential to reenter the cell via M6P receptor, to prevent this possibility, it was tested cAMP antagonist Rp-cAMP and the PKA inhibitors KT5720 and H89 in the absence or presence of M6P. Inhibition of cat K processing by Rp-cAMP, KT5720, or H89 was observed in a dose-dependent manner. Furthermore, the addition of M6P resulted in enhanced potency of Rp-cAMP, KT5720 and H89. These dose-dependently inhibited in vitro bone resorption with a potency similar to that observed for inhibition of cat K processing.
This study investigated the anti-inflammatory activity of barley leaf extract in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and hairless mice. Pre-treatment with barley leaf extract significantly inhibited the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-II (COX-II) in a dose-dependent manner in LPS-stimulated RAW264.7 cells. Barley leaf extract also significantly inhibited the secretion of inflammatory cytokines, such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$), and interleukin-6 (IL-6). Moreover, phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear translocation of nuclear factor-kappa B (NF-${\kappa}B$) were strongly suppressed by barley leaf extract in LPS-stimulated cells. In hairless mice, barley extract significantly decreased the pathological phenotypes of contact dermatitis, such as erythema, edema, and scabs. These results indicate that barley leaf extract has an anti-inflammatory effect and therefore a possible role in the treatment of inflammatory diseases or in functional cosmetics.
Journal of Korea Entertainment Industry Association
/
v.13
no.2
/
pp.197-205
/
2019
This study was to compare arterial stiffness and hemodynamic responses between male smokers and non-smokers. This study also investigates the influences of smoking before exercise on arterial stiffness and hemodynamic responses. 24 male subjects of age 20-29 without history of cardiorespiratory disease were divided into smokers and non-smokers. Smokers had more than 5 years of smoking experience. In order to evaluate the effects of pre-exercise smoking, smokers were tested twice, once with a cigarette before the exercise and the other once without one. Data was collected from bio-impedance analysis, SphygmoCor XCEL, graded exercise test, and fitness test. Main results of this study are as follows: First, there are differences between smokers and non-smokers in cardiorespiratory and hemodynamic response functions, as shown by maximal oxygen consumption, exercise duration, and heart rate. Second, the although the arterial stiffness between smokers and non-smokers showed statistically significant differences in the speed of the pulse wave velocity and augmentation index, smoker had a faster rate. It shows that smoking behavior has a negative impact on the cardiovascular system. Third, pre-exercise smoking behavior does have an impact on cardiorespiratory and hemodynamic response functions, as shown by exercise duration and heart rate. Lastly, arterial stiffness between smokers and non-smokers showed statistically not significant in the speed of the pulse wave velocity and augmentation index. However, the difference was not statistically significant. Brachial systolic pressure, a component of pulse wave analysis, on the other hand, was significantly dependent on pre-exercise smoking behavior. Subjects who participated in this study are college students in early 20s. Given their relatively short history of smoking, it is possible that their smoking habits are not severe enough to develop into cardiorespiratory or cardiovascular diseases. But Smokers showed lower levels of cardiopulmonary functions, as maximal oxygen consumption and exercise duration than nonsmokers.
Purpose : Seoul National University Hospital developed a group counseling program for the terminal cancer patients and their family members. This program consists of each of doctor, nutritionist, nurse, pharmacist, and social worker to provide them with the information and to enhance their ability to cope with terminal cancer. This research aims to introduce this new program per se, and to appreciate its validity and applicability to the terminal cancer patients and their family members by analyzing the concerns and specific questions of the participants. Methods : The methodological approach employed in this research is 1996 content analysis of the group counseling reports, and interview of the 312 participants. The analysis includes the general characteristics of the subjects, family relationship to the patients, times of attendance to the group session, source of information to the program. Results : The participants consist of 261 family members(84%) and 51 patients(16%). Majority responded to the program with a single-attendance. Diagnosis are mainly lung cancer, stomach cancer, liver cancer. The ratio of participants by family members is decreased in the order of spouse, children, daughter-in-law, brothers and sisters, and parents. The source of information to the program is largely through medical staff(69%) as compared with posters in the hospital (26%). The participants are interested primarily in the medical information. Their interests are various, such as pain control, patient care, nutrition, psychosocial problem and etc. Conclusion : This program is characterized largely as a family-supporting program which primarily offers information for terminal cancer. This program is a sort of a hospice program, which maximizes the present quality of living of the terminal cancer patients as long as life continues by encouraging them to live with terminal cancer. Thus, this group program can be employed as an active support network for the patients and their family. In order to develop comprehensive care-giving services, it is required to have 24-hour telephone service, hospice facilities, home care service, and communication between the referral hospitals and the primary care physicians, in particular. Such a development of services is the ultimate goal for improving care. But the immediate goal of the program is to make possible better education for the patients and their family to live with terminal cancer.
Persistent organic pollutants (POPs) can affect epigenetic mechanisms and obesity development. Polybrominated diphenyl ethers (PBDEs)-widely used to make flames-are one of the important POPs. Prenatal exposure to endocrine disrupting chemicals (EDCs), such as POPs, may affect global DNA methylation in long interspersed nuclear elements (LINE-1), increasing the risk of obesity later in life. Therefore, pregnant Sprague-Dawley (SD) rats were used to elucidate whether BDE-47 and BDE-209 transferred through placenta and breast milk cause epigenetic changes in LINE-1 and increase genetic susceptibility to obesity as obesogen during the developmental periods. Global DNA methylation in LINE-1 and gene expression related to obesity were measured in dams and offspring, using a methylation-sensitive high resolution melting analysis (MS-HRM) and direct bisulfite sequencing and quantitative real time polymerase chain reaction (qPCR), respectively. The results of MS-HRM showed global DNA hypomethylation patterns in LINE-1 of exposed offspring (2 of total 4) at PND 4, but bisulfite sequencing showed no difference in both the exposed and non-exposed groups. Gene expression in dams related to ${\beta}$-oxidation pathway and those related to adipokines showed different patterns between the two groups. On the contrary, gene expressions of offspring showed a similar pattern. Gene expressions related to ${\beta}$-oxidation pathway and obesity were significantly increased when compared with 'at birth', but not $PPAR-{\alpha}$. In conclusion, this study demonstrated the possibility that co-exposure to BDE-47 and BDE-209-via the placenta and breast milk-may affect epigenetic changes and modulate gene expression levels related to obesity.
Air-borne pollen, biogenically created aerosol particle, influences Earth's radiative balance, visibility impairment, and human health. The importance of pollens has resulted in numerous experimental studies aimed at characterizing their dispersion and transport, as well as health effects. There is, however, limited scientific information concerning the optical properties of airborne pollen particles contributing to total ambient aerosols. In this study, for the first time, optical characteristics of pollen such as aerosol backscattering coefficient, aerosol extinction coefficient, and depolarization ratio at 532 nm and their effect to the atmospheric aerosol were studied by lidar remotes sensing technique. Dual-Lidar observations were carried out at the Gwangju Institute of Science & Technology (GIST) located in Gwagnju, Korea ($35.15^{\circ}E$, $126.53^{\circ}N$) for a spring pollen event from 5 to 7 May 2009. The pollen concentration was measured at the rooftop of Gwangju Bohoon hospital where the building is located 1.0 km apart from lidar site by using Burkard trap sampler. During intensive observation period, high pollen concentration was detected as 1360, 2696, and $1952m^{-3}$ in 5, 6, and 7 May, and increased lidar return signal below 1.5km altitude. Pollen optical depth retrieved from depolarization ratio was 0.036, 0.021, and 0.019 in 5, 6, and 7 May, respectively. Pollen particles mainly detected in daytime resulting increased aerosol optical depth and decrease of Angstrom exponent.
Transovarial transmission of cytoplamic polyhedrosis virus in the silkworm was studied by observing the phenomena of induction, interference and virulence enhancement in the larvae from moths inoculated with hexagonal Polyhedra of cytoplasmic polythedrosis virus. The experimental results obtained are as followings. 1. The effect of inoculation with tetragonal polyhedra of cytoplasmic polyhedrosis virus on the rate of infective induction with hexagonal polyhedron virus and with hexagonal plus tetragonal polyhedron viruses in the larvae from moths infected with hexagonal polyhedron virus was studied. Infection rate was higher by 40 to 60 percent in the larvae from infected female group than in tile larvae from noninfected female group. 2. In the studies of the effect of formalin-feeding on the induction of infection with hexagonal polyhedron virus, infection rate was higher by 40 percent in the larvae from infected female group than in the larvae from noninfected female group. However, there was no significant difference in the infection rates between the two formalin-concentration groups. 3. The effect of cold treatment on the induction of infection with hexagonal polyhedron virus was studied. Infection rate was higher by 50 percent in the larvae from infected female group than ill the larvae from noninfected female group. No difference was found in the infection rates of the two treatment groups of 12 and 48 hours. 4. The phenomena of induction and interference were studied by observing rate of infection with hexagonal polyhedron virus induced by the inoculation with tetragonal polyhedron virus. The degree of interference of primary hexagonal polyhedron virus by secondary tetragonal Ployhedron virus was increased as the dosage of secondary virus was increased. At the concentration of 1${\times}$10$\^$8/m1 of the secondary virus, the degree of interference was similar to. that of control group. On the other hand, infection with tetragonal polyhedron virus at low concentration was interfered by the primary virus. At the concentration of 1N10f/m1 of tetragonal polyhedron virus, however, the rate of infection with tetragonal polyhedron virus was increased sharply, which is still lower by 30 percent than that of control group. 5. In the studies of induction and virulence enhancement, based on the 1ate of mixed infection with hexagonal and tetragonal polyhedron viruses, the highest difference of infection rate between experimental group and control group exceeded 40 percent when the concentration of tetragonal polyhedron virus was 1${\times}$10$\^$7/m1. However, the infection rate of control group was not affected by concentrations of tetragonal polyhedron virus.
Background : Arsenic trioxide ($As_2O_3$) has been used to treat acute promyelocytic leukemia, and it induces apoptosis in a variety of solid tumor cell lines including non-small cell lung cancer cells. However, nonsteroidal antiinflammatory drugs (NSAID) can enhance tumor response to chemotherapeutic drugs or radiation. It was previously demonstrated that a combination treatment with $As_2O_3$ and sulindac induces the apoptosis of NCI-H157 human lung carcinoma cells by activating the caspase cascade. This study aimed to determine if a combination treatment augmented its apoptotic potential through other pathways except for the activation of the caspase cascade. Material and Methods : The NCI-H157 cells were treated with $As_2O_3$, sulindac and antioxidants such as glutathione (GSH) and N-acetylcysteine (NAC). The cell viability was measured by a MTT assay, and the level of intracellular hydrogen peroxide ($H_2O_2$) generation was monitored fluorimetrically using a scopoletin-horse radish peroxidase (HRP) assay. Western blotting and mitochondrial membrane potential transition analysis were performed in order to define the mechanical basis of apoptosis. Results : The viability of the cells was decreased by a combination treatment of $As_2O_3$ and sulindac, and the cells were protected using antioxidants in a dose-dependent manner. The increased $H_2O_2$ generation by the combination treatment was inhibited by antioxidants. The combination treatment induced changes in the mitochondrial transmembrane potential as well as the expression of the Bcl-2 family proteins, and increased cytochrome c release into the cytosol. However, the antioxidants inhibited the effects of the combination treatment. Conclusion : Combination treatment with $As_2O_3$ and sulindac induces apoptosis in NCI-H157 human lung carcinoma cells via ROS generation with a mitochondrial dysfunction.
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