Purpose: This study aimed to verify the reliability and validity of the Pain Assessment in Advanced Dementia Scale-Korean version (PAINAD-K) for assessing pain in patients unable to communicate in the post-anesthesia care unit (PACU). Methods: The study included 205 patients, aged >65 years, admitted to the PACU following general surgery. Reliability was assessed using Cronbach’s ⍺, test-retest, intraclass correlation coefficient (ICC), and kappa coefficients. Criterion validity was evaluated with concurrent validity, and receiver operating characteristic (ROC) analysis assessed sensitivity and specificity. Convergent and discriminant validity were analyzed to verify the construct of the scale. Results: The Cronbach’s ⍺, ICC, and test-retest correlation values were .78, .95~.98, and .56~.74, respectively, indicating good reliability. At baseline, the correlation coefficient was .93 with the Algoplus scale in the non-communicative group and .82 with the numeric rating scale in the communicative group. Further establishing criterion validity in the nonverbal group, the area under the ROC curve was 0.995 (sensitivity=98.4%, specificity=97.5%) at baseline and .95 (sensitivity=96.4%, specificity=93.2%) at the 30-minute follow-up. The correlation coefficient with the Critical-Care Pain Observation Tool was .69~.96, showing convergent validity, and there was a significant interaction effect between time and group, indicating discriminant validity. Conclusion The study findings suggest that the PAINAD-K is a psychometrically valid scale for assessing pain in PACU patients aged >65 years who are unable to communicate.

The mechanism of Western medicine that is commonly used for pain relief is well-known. However, very little is known for oriental herbs, and even less is known for mixture of the two. We investigated the combinational effect of 3 kinds of oriental herbs, usually used for the control of headache, and acetaminophen to relieve headache in microglia cell line, BV2. Lipopolysaccharide (LPS) stimulation induced to produce nitrite and increased the expression of inflammation-related factors like inducible nitric oxide synthase and cyclooxygenase-2 (COX-2) in murine microglia cell line, BV2. Oriental herbs such as Angelica tenuissima, Angelica dahurica, and Scutellaria baicalensis reduced the production of nitric oxide and the expression of COX-2. Moreover, a treatment of acetaminophen combined with oriental herbs was more decreased the COX-2 expression, and its product, prostaglandin E2 production in BV2 cells. Therefore, a combined treatment of oriental herbs such as A. tenuissima, A. dahurica, and S. baicalensis and Western medicine like acetaminophen has a synergistic effect on the decrease of LPS-induced inflammation in microglia.
Acetaminophen* ; Angelica ; Cell Line* ; Cyclooxygenase 2 ; Dinoprostone ; Headache ; Inflammation ; Microglia* ; Nitric Oxide ; Nitric Oxide Synthase Type II ; Scutellaria baicalensis

Asthma is a well-known inflammatory lung disease; however, the specific underlying mechanism is largely unknown. We previously demonstrated that alloferon effectively downregulates pulmonary inflammation. In this study, we examined whether alloferon has a therapeutic effect on asthma. Alloferon remarkably decreased the number of eosinophils, macrophages, and neutrophils in the bronchoalveolar lavage fluid (BALF) from ovalbumin (OVA)-induced asthma mice. It was synergistically decreased with 2.5 mg/kg prednisolone (PDA). Inflammatory cell infiltration around the bronchioles and in the alveolus of OVA-induced asthma mice was effectively prevented by alloferon alone and combined treatment with alloferon and PDS. The production of IL-5 and IL-17 was decreased by alloferon alone and combined treatment with alloferon and PDS. There was no change the level of total immunoglobulin (Ig) following alloferon administration; however, total Ig was decreased by PDS. IgG2a levels were not changed by either alloferon alone or alloferon in combination with PDS. However, the levels of OVA-specific IgG1 and IgE were decreased by alloferon and PDS. In conclusion, our results suggest that a combination of alloferon and prednisolone is effective for the treatment of asthma, as it prevents inflammatory cell infiltration via the down-regulation of IL-5 and IL-17 production and decreases IgG1 and IgE production via the suppression of T helper type 2 immune response.
Animals ; Asthma* ; Bronchioles ; Bronchoalveolar Lavage Fluid ; Down-Regulation ; Eosinophils ; Immunoglobulin E ; Immunoglobulin G ; Immunoglobulins ; Interleukin-17 ; Interleukin-5 ; Lung Diseases ; Macrophages ; Mice ; Neutrophils ; Ovalbumin ; Pneumonia ; Prednisolone

Dysfunction of gut immune regulation is involved in mucosal damage in inflammatory bowel disease (IBD). However, there is still no efficacious immune-regulator for the treatment of IBD. Alloferon is a novel immune-modulatory peptide that was originally isolated from infected insects. It shows anti-inflammatory effects by the regulation of cytokine production by immune cells and their activities. Therefore, we investigated the effect of alloferon in a mouse model of colitis using dextran sulfate sodium (DSS). Colitis was induced by administration of DSS in drinking water for 7 consecutive days. It was confirmed by the presence of weight loss, diarrhea, hematochezia, and colon contraction. Alloferon was injected 4 days after DSS administration. We found that alloferon improved the pathogenesis of IBD based on the reduced disease activity index (DAI) and colon contraction. Edema, epithelial erosion, and immune cell infiltration were found in mice administered DSS, but the phenomena were reduced following alloferon treatment. The plasma level of IL-6, a classical pro-inflammatory cytokine in colitis, was also decreased by alloferon. Moreover, alloferon inhibited the TNF-alpha-induced degradation and phosphorylation of IkappaB in Colo205 colon cancer cells. Taken together, these results show that alloferon has anti-inflammatory effects and attenuates DSS-induced colitis.
Animals ; Colitis* ; Colon ; Colonic Neoplasms ; Dextran Sulfate* ; Diarrhea ; Drinking Water ; Edema ; Gastrointestinal Hemorrhage ; Inflammatory Bowel Diseases ; Insects ; Interleukin-6 ; Mice ; Phosphorylation ; Plasma ; Weight Loss

BACKGROUND: Ultraviolet B (UVB) induces multiple inflammatory and carcinogenic reactions. In skin, UVB induces to secrete several kinds of inflammatory cytokines from keratinocytes and also increases angiogenic process via the modulation of vascular endothelial growth factor (VEGF) production. Interleukin-21 (IL-21) is an inflammatory cytokine and produced by activated T cells. The biologic functions of IL-21 have not yet extensively studied. METHODS: In the present study, we investigate the production of IL-21 from human keratinocyte cell line, HaCaT and its biological effect after exposure to UVB. RESULTS: First, we confirmed the IL-21 production and its receptor expression in HaCaT. And then, the change of IL-21 and VEGF production in HaCaT by UVB irradiation was examined. Not only IL-21 but also VEGF production was enhanced by UVB irradiation. Next, to determine relationship of enhanced production of IL-21 and VEGF, we detected VEGF production after neutralization of IL-21. VEGF production was reduced by IL-21 neutralization, which indicates that the IL-21 is involved in the VEGF production. CONCLUSION: Taken together, our results suggest that IL-21 and VEGF production is enhanced by UVB irradiation in HaCaT. In addition, it seems that IL-21 plays a role in the angiogenic process in skin via the modulation of VEGF production.
Cell Line ; Cytokines ; Humans ; Interleukins ; Keratinocytes ; Skin ; T-Lymphocytes ; Vascular Endothelial Growth Factor A

Primary or secondary anaplastic large-cell lymphoma (ALCL) is an uncommon type of T-cell lymphoma and is extremely rare.1-3 It was said that only 15-20 cases of primary CNS-ALCLs have been reported in the literature.3 ALCL may present with a variety of symptoms and MRI findings. We report a case of a 10-year-old girl who presented with meningitis and later developed optic neuritis. She was initially diagnosed as tuberculosis meningitis after a positive interferon-γ test. Clinicians should be

BACKGROUND: Vitamin C is an essential nutrient for maintaining human life. Vitamin C insufficiency in the plasma is closely related with the development of scurvy. However, in vivo kinetics of vitamin C regarding its storage and consumption is still largely unknown. METHODS: We used Gulo-/- mice, which cannot synthesize vitamin C like human. Vitamin C level in plasma and organs from Gulo-/- mice was examined, and it compared with the level of wild-type mice during 5 weeks. RESULTS: The significant weight loss of Gulo-/- mice was shown at 3 weeks after vitamin C withdrawal. However, there was no differences between wild-type and vitamin C-supplemented Gulo-/- mice (3.3 g/L in drinking water). The concentration of vitamin C in plasma and organs was significantly decreased at 1 week after vitamin C withdrawal. Vitamin C is preferentially deposited in adrenal gland, lymph node, lung, and brain. There were no significant changes in the numbers and CD4/CD8 ratio of splenocytes in Gulo-/- mice with vitamin C withdrawal for 4 weeks. And the architecture of spleen in Gulo-/- mice was disrupted at 5 weeks after vitamin C withdrawal. CONCLUSION: The vitamin C level of Gulo-/- mice was considerably decreased from 1 week after vitamin C withdrawal. Vitamin C is preferentially stored in some organs such as brain, adrenal gland and lung.
Adrenal Glands ; Animals ; Ascorbic Acid ; Brain ; Drinking ; Humans ; Kinetics ; Lung ; Lymph Nodes ; Mice ; Plasma ; Scurvy ; Spleen ; Vitamins ; Weight Loss

BACKGROUND: It is already known that high concentration of vitamin C induces apoptosis on tumor cells. However, there is no report regarding the function of vitamin C on the modulation of immune susceptibility of cancer. Therefore, we investigated whether vitamin C can modulate immune susceptibility of tumor cells, especially on the induction of Fas-mediated apoptosis. METHODS: First, the optimal concentration of vitamin C, which cannot induce damages on tumor cells for 36 hrs. We found that 2 mM of vitamin C did not show harmful effect. In addition, the optimal concentration of agonistic anti-Fas Abs for 18 hrs was examined. RESULTS: As a result, 400 ng/ml of agonistic anti-Fas Abs did not induce apoptosis on tumor cells. Next, we tried to find the effect of 2 mM of vitamin C on the modulation of the susceptibility to agonistic anti-Fas Abs. When tumor cells were cultured with 400 ng/ml of agonistic anti-Fas Abs for 18 hrs, after pre-treatment with 2 mM of vitamin C for 24 hrs, viability of cells was decreased. Interestingly, we found that the expression of Fas (CD95) and MHC class I was increased by the treatment of vitamin C. CONCLUSION: Taken together, vitamin C increases the susceptibility of tumor cells to anti-Fas Abs and the expression of Fas (CD95) and MHC class I on tumor cells.
Apoptosis ; Ascorbic Acid ; Cell Line ; Humans ; Stomach ; Stomach Neoplasms ; Vitamins

Hyperoxic ventilation induces detrimental effects on the respiratory system, and ambient oxygen may be harmful unless compensated by physiological anti-oxidants, such as vitamin C. Here we investigate the changes in electrolyte transport of airway epithelium in mice exposed to normobaric hyperoxia and in gulonolacton oxidase knock-out (gulo[-/-]) mice without vitamin C (Vit-C) supplementation. Short-circuit current (Isc) of tracheal epithelium was measured using Ussing chamber technique. After confirming amiloride-sensitive Na+ absorption (DeltaIsc,amil), cAMP-dependent Cl- secretion (DeltaIsc,forsk) was induced by forskolin. To evaluate Ca2+-dependent Cl- secretion, ATP was applied to the luminal side (DeltaIsc,ATP). In mice exposed to 98% PO2 for 36 hr, DeltaIsc,forsk decreased, DeltaIsc,amil and DeltaIsc,ATP was not affected. In gulo(-/-) mice, both DeltaIsc,forsk and DeltaIsc,ATP decreased from three weeks after Vit-C deprivation, while both were unchanged with Vit-C supplementation. At the fourth week, tissue resistance and all electrolyte transport activities were decreased. An immunofluorescence study showed that the expression of cystic fibrosis conductance regulator (CFTR) was decreased in gulo(-/-) mice, whereas the expression of KCNQ1 K+ channel was preserved. Taken together, the CFTR-mediated Cl- secretion of airway epithelium is susceptible to oxidative stress, which suggests that supplementation of the antioxidant might be beneficial for the maintenance of airway surface liquid.
Animals ; Ascorbic Acid Deficiency/*metabolism ; Biological Transport/drug effects ; Chlorides/*metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/antagonists & inhibitors/drug ; Forskolin/pharmacology ; Hyperbaric Oxygenation ; Hyperoxia/*physiopathology ; Ion Transport/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Inbred ICR ; Mice, Knockout/metabolism ; Mice, Transgenic ; Microscopy, Fluorescence ; Oxidative Stress ; Oxygen/adverse effects/pharmacology ; Potassium Channels/metabolism ; Respiratory Mucosa/drug effects/*metabolism/secretion ; Sodium ; Sugar Acids/metabolism

Vitamin C is an essential water-soluble nutrient which primarily exerts its effect on host defense mechanisms and immune homeostasis, but the mechanism related to immune-potentiation is poorly understood. Since dendritic cells (DCs) are known as a potent antigen presenting cell (APC) that could enhance the antigen specific immune responses, we investigate the effects of vitamin C on activation of DCs and its related mechanism by using dendritic cell lines, DC-1. First, we found that there was no damage on DC-1 by 2.5 mM of vitamin C. In the presence of vitamin C, the expression of CD80, CD86, and MHC molecules was increased, but it was decreased by the pre-treatment of SB203580, p38 MAPK-specific inhibitor. We confirmed the phosphorylation of p38 MAPK was increased by the treatment of vitamin C. Taken together, these results suggest that vitamin C could enhance the activity of dendritic cells via the up-regulation of the expression of CD80, CD86, and MHC molecules and the activation of p38 MAPK is related to this process.
Ascorbic Acid ; Defense Mechanisms ; Dendritic Cells ; Homeostasis ; Imidazoles ; p38 Mitogen-Activated Protein Kinases ; Phosphorylation ; Pyridines ; Up-Regulation ; Vitamins