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ObjectiveSjögren’s syndrome (SS) is a systemic autoimmune disease that targets the exocrine glands, resulting in impaired saliva and tear secretion. To date, type I interferons (I-IFNs) are increasingly recognized as pivotal mediators in SS, but their endogenous drivers have not been elucidated. This study investigates the role of mitochondrial double-stranded RNAs (mt-dsRNAs) in regulating I-IFN response in SS.MethodsSaliva and tear from SS patients and controls (n=73 for saliva and n=16 for tear), the salivary glands of the SS-prone-non-obese-diabetic mouse, and primary human salivary glandular cells were screened for mt-dsRNAs by RT-qPCR. The human salivary cell line (NS-SV-AC) grown as three-dimensional spheroids were subject to dsRNA stress to measure mt-dsRNA induction and recapitulation of SS glandular inflammatory features. Acetylcholine, SS-IgG, upadacitinib (JAK1 inhibitor), or 2-C′-methyladenosine (mitochondrial transcription inhibitor) were applied to characterize the roles of mt-dsRNAs. To identify endogenous dsRNA-sensor and confirm the mitochondrial origin of cytoplasmic dsRNAs, the immunoprecipitation of dsRNAs was performed.Resultsmt-dsRNAs were elevated in the SS specimens with salivary ND5 and tear CYTB1 being statistically associated with secretory dysfunction/inflammation and corneal/conjunctival damage, respectively. Stimulation of the spheroids with dsRNA stress of poly I:C induced mt-dsRNAs, p-PKR, and I-IFNS via the JAK1/STAT pathway whereas the inhibition of mt-RNA synthesis or JAK1 attenuated the glandular signature. The inhibitory effect of acetylcholine on mt-dsRNAs and I-IFNS induction was reversed by SS-IgG.Conclusionmt-dsRNAs amplify the impact of dsRNA stress on SS glandular signaturesin vitro, potentially propagating a pseudo-viral signal in the SS target tissue.SummaryMitochondrial double-stranded RNA levels were elevated in the tear and saliva of SS patients, which was associated with secretory dysfunction and tissue inflammation. These RNAs amplified type I interferon signature as well as glandular phenotypes reported in SS. Inhibitors of mitochondrial RNA transcription or JAK1 in salivary gland acinar cell spheroids attenuated the mitochondrial RNA-mediated changes.

Fucoxanthin (FX), a natural carotenoid present in edible brown seaweed, is known for its therapeutic potential in various diseases, including bone disease. However, its underlying regulatory mechanisms in osteoclastogenesis remain unclear. In this study, we investigated the effect of FX on osteoclast differentiation and its regulatory signaling pathway. In vitro studies were performed using osteoclast-like RAW264.7 cells stimulated with the soluble receptor activator of nuclear factor-κB ligand or tumor necrosis factor-alpha/interleukin-6. FX treatment significantly inhibited osteoclast differentiation and bone resorption ability, and downregulated the expression of osteoclast-specific markers such as nuclear factor of activated T cells 1, dendritic cell-specific seven transmembrane protein, and matrix metallopeptidase 9. Intracellular signaling pathway analysis revealed that FX specifically decreased the activation of the extracellular signal-regulated kinase and p38 kinase, and increased the nuclear translocation of phosphonuclear factor erythroid 2-related factor 2 (Nrf2). Our results suggest that FX regulates the expression of mitogen-activated protein kinases and Nrf2. Therefore, FX is a potential therapeutic agent for osteoclast-related skeletal disorders including osteoporosis and rheumatoid arthritis.

Background Preconditioning with lipopolysaccharide (LPS) is used to improve the secretion of anti-inflammatory agents in B cells. However, there are only a few studies on canine B cells. Objective This study aimed to evaluate the immune regulatory capacity of canine peripheral blood mononuclear cell-derived B cells pretreated with LPS. Methods Canine B cells were isolated from canine peripheral blood mononuclear cells, which were obtained from three healthy canine donors. The B cells were preconditioned with LPS, and then cell viability and the expression of the regulatory B cell marker were assessed. Finally, RNA extraction and immunofluorescence analysis were performed. Results LPS primed B cells expressed the interleukin (IL)-10 surface marker and immunoregulatory gene expression, such as IL-10, programmed death-ligand 1, and transforming growth factor beta. Macrophages in the inflammatory condition cocultured with primed B cells were found to have significantly down-regulated pro-inflammatory cytokine, such as tumor necrosis factor-α, and up-regulated anti-inflammatory cytokines such as IL-10. Additionally, it was revealed that co-culture with primed B cells re-polarized M1 macrophages to M2 macrophages. Conclusions This study revealed that LPS-primed B cells have an anti-inflammatory effect and can re-polarize macrophages, suggesting the possibility of using LPS-primed B cells as a therapeutic agent for its anti-inflammatory effects and immune modulation.

Background Mesenchymal stem/stromal cells (MSCs) are effective therapeutic agents that ameliorate inflammation through paracrine effect; in this regard, extracellular vesicles (EVs) have been frequently studied. To improve the secretion of anti-inflammatory factors from MSCs, preconditioning with hypoxia or hypoxia-mimetic agents has been attempted and the molecular changes in preconditioned MSC-derived EVs explored. In this study, we aimed to investigate the increase of hypoxia-inducible factor 1-alpha (HIF-1α)/cyclooxygenase-2 (COX-2) in deferoxamine (DFO)-preconditioned canine MSC (MSCDFO) and whether these molecular changes were reflected on EVs. Furthermore, we focused on MSCDFO derived EVs (EVDFO) could affect macrophage polarization via the transfer function of EVs. Results In MSCDFO, accumulation of HIF-1α were increased and production of COX-2 were activated. Also, Inside of EVDFO were enriched with COX-2 protein. To evaluate the transferring effect of EVs to macrophage, the canine macrophage cell line, DH82, was treated with EVs after lipopolysaccharide (LPS) stimulation. Polarization changes of DH82 were evaluated with quantitative real-time PCR and immunofluorescence analyses. When LPS-induced DH82 was treated with EVDFO, phosphorylation of signal transducer and transcription3 (p-STAT3), which is one of key factor of inducing M2 phase, expression was increased in DH82. Furthermore, treated with EVDFO in LPS-induced DH82, the expression of M1 markers were reduced, otherwise, M2 surface markers were enhanced. Comparing with EVDFO and EVnon. Conclusion DFO preconditioning in MSCs activated the HIF-1α/COX-2 signaling pathway; Transferring COX-2 through EVDFO could effectively reprogram macrophage into M2 phase by promoting the phosphorylation of STAT3.

Background As a co-receptor for fibroblast growth factor 23, klotho plays a pivotal role in phosphate metabolism. The kidney is known to be the main source of soluble alpha-klotho and the principal regulator of its concentration. Previous studies in human participants showed that the concentration of soluble alpha-klotho in serum and urine decreased in chronic kidney disease (CKD) patients. However, no previous study has assessed soluble alpha-klotho levels in dogs. This study aimed to measure serum and urinary alpha-klotho levels in CKD dogs and identify their associations with International Renal Interest Society (IRIS) CKD stages and other parameters known to be associated with CKD. Results Serum and urinary alpha klotho concentrations were measured by a commercially available canine-specific sandwich enzyme-linked immunosorbent assay kit and compared between groups by a nonparametric Kruskal–Wallis test. Spearman’s correlation coefficient was used to evaluate the relationships between variables. A stepwise multiple regression analysis was performed to estimate the effects of independent predictors on klotho concentrations. The urine klotho-to-creatinine ratio (UrKl/Cr) was significantly lower in stage 3 dogs than the control group and was significantly lower in dogs with stage 3 and 4 CKD than in those with stage 1 and 2 disease. UrKl/Cr was negatively correlated with serum symmetric dimethylarginine (sSDMA), blood urea nitrogen (BUN), creatinine, and phosphorus concentration. Serum alpha-klotho concentration in dogs with stages 2 and 3 CKD was significantly lower than those in the control group. There was no significant correlation between serum alpha-klotho and BUN, creatinine, and phosphorus concentrations. No statistically significant differences were observed in UrKl/Cr and serum alpha-klotho concentration between groups based on sex, age, urine protein-to-creatinine ratio (UPC), or blood pressure. Conclusions UrKl/Cr decreased in dogs with advanced CKD, and it was negatively correlated with sSDMA, BUN, creatinine, and phosphorus concentrations. Thus, klotho is associated with CKD and its clinical consequences, including CKD-mineral bone disorder, in dogs. Although serum klotho concentration was negatively correlated with sSDMA levels, it was not apparently related to IRIS CKD stage or other parameters known to be associated with CKD.

La1−xSrxVO3 (0 ≤ x ≤ 1) films can be transparent conducting oxides such as n-type SrVO3 and p-type La2/3Sr1/3VO3 films. They also show a semiconductor-to-metal transition (SMT) near x = 0.2. The optical and electrical properties of La1−xSrxVO3 (0 ≤ x ≤ 1) films grown on (LaAlO3)0.3(Sr2AlTaO6)0.7 (LSAT) substrates using RF sputtering deposition were investigated. Resistivities of La1−xSrxVO3 showed SMT near x = 0.2. La1−xSrxVO3 films grown on LSAT substrates were found to have high crystallinity using θ−2θ scan and grazing incidence x-ray diffraction measurements. Dielectric functions of La1−xSrxVO3 films were measured using spectroscopic ellipsometry. The evolution of optical spectra of La1−xSrxVO3 films from LaVO3 to SrVO3 was compared to the electronic band structures as a function of Sr composition, which was either experimentally observed or theoretically calculated in the literature. With increasing Sr composition, the interband transition energies of O 2p to V 3d states near 4 eV changed linearly as a function of Sr content.

Novel red phosphorescent iridium(III) complexes, namely (MN-Q)2Ir(tmd), (MN-MQ)2Ir(tmd), (PT-P)2Ir(tmd) and (PT-MP)2Ir(tmd) were synthesized for the red phosphorescent organic lightemitting diodes (phOLEDs). The ligands have sites of both the electron donor and acceptor in a molecule. The main ligands were synthesized by the Suzuki coupling reaction, and comprised an electron donor and an electron acceptor group. Subsequently, the iridium(III) complexes were synthesized by the Nonoyama reaction and their photochemical luminescence properties were investigated by ultraviolet-visible and photoluminescence spectroscopy. The manufactured devices were characterized by current density-voltage-luminance, power efficiency, external quantum efficiency, as well as their electroluminescence spectra. Finally, the effects of the trifluoromethyl group on the emission efficiency of the organic light-emitting diodes were investigated by comparing the energy levels and luminescence efficiency of the three iridium complexes.

Although the transition from B-DNA to the A-form is essential for many biological concerns, the properties of this transition have not been resolved. The B to A equilibrium can be analyzed conveniently because of the significant changes in circular dichroism (CD) and absorption spectrum. CD and linear dichroism (LD) methods were used to examine the binding of water-soluble meso-tetrakis(N-methylpyridinium-4-yl)porphyrin (TMPyP) and its derivatives, Co-TMPyP, with B- and A-calf thymus DNA. B- to A-transitions occurred when the physiological buffer was replaced with a water-ethanol mixture (∼80 v/v %), and the fluorescence emission spectra of TMPyP bound to DNA showed a different pattern under ethanol–water conditions and water alone. The featureless broad emission bands of TMPyP were split into two peaks near at 658 and 715 nm in the presence of DNA under an aqueous solution. In the case of an ethanol–water system, however, the emission bands are split in two peaks near at 648 and 708 nm and 656 and 715 nm with and without DNA, respectively. This may be due to a change in the solution polarity. On the basis of the CD and LD data, TMPyP interacts with B-DNA via intercalation at a low ratio under a low ionic strength, 1 mM sodium phosphate. On the other hand, the interaction with A-DNA (80 v/v % ethanol–water system) occurs in a nonintercalating manner. This difference might be because the structural conformations, such as the groove of A-DNA, are not as deep as in B-DNA and the bases are much more tilted. In the case of Co-TMPyP, porphyrin binds preferably via an outside self-stacking mode with B- and A-DNA.

New red phosphorescent iridium(III) complex, (TP-MQ)2Ir(tmd) was synthesized for red emitter of the phosphorescent organic light-emitting diodes (phOLEDs). The ligands have sites of both the electr...

Most photonic crystal films have been studied with various ionic liquids. The object of our research was to examine the expression of one-dimensional lamellar photonic crystal color with different ...

Novel red phosphorescent iridium(III) complexes, (DPAP-MQ)2Ir(tmd), (DMAP-MQ)2Ir(tmd), (PN-MQ)2Ir(tmd) were synthesized for red emitter of the phosphorescent organic light-emitting diodes (phOLEDs)...

The object of our research is to observe the expression of 1D lamellar photonic crystal color depending on difference molecular weight of PolyStyrene-Block-2-Vinyl Pyridine(PS-b-P2VP) (52k-57k, 84K...

The spectral properties of meso-tetrakis (N-methylpyridinium-4-yl)porphyrin (TMPyP) in the presence of parallel and antiparallel G-quadruplexes formed from a thrombin-binding aptamer G-quadruplex (...

Limb-sparing surgery is one of the surgical options for dogs with distal radial osteosarcoma (OSA). This case report highlights the novel application of a three-dimensional (3D)-printed patient-specific polycaprolactone/β-tricalcium phosphate (PCL/β-TCP) scaffold in limb-sparing surgery in a dog with distal radial OSA. The outcomes evaluated included postoperative gait analysis, complications, local recurrence of tumor, metastasis, and survival time. Post-operative gait evaluation showed significant improvement in limb function, including increased weight distribution and decreased asymmetry. The implant remained well in place and increased bone opacity was observed between the host bone and the scaffold. There was no complication due to scaffold or surgery. Significant improvement in limb function and quality of life was noted postoperatively. Local recurrence and pulmonary metastasis were identified at 8 weeks postoperatively. The survival time from diagnosis of OSA to death was 190 days. The PCL/β-TCP scaffold may be an effective alternative to cortical allograft in limb-sparing surgery for bone tumors.

Amorphous gallium/titanium (Ga,Ti) co-doped indium oxide (In2O3) (GTiIO) films present significant potential as transparent conducting electrodes for use in flexible electronic devices. Amorphous GTiIO films were grown on silicon and glass substrates using linear-facing target sputtering and various oxygen flow rates. Transmittance was as high as 80% in the visible range for O2 flow rates of 0.3, 0.7, and 1.0 SCCM. The lowest resistivity was obtained at f(O2) = 0.3 SCCM with 0.47 mΩ cm. Dielectric functions were determined, and optical gap energies were estimated as close to 3.4 eV using a Tauc formula. We show that Drude tail amplitude is proportional to the carrier density. An electronic transition was found at 2.7 eV from the optical spectra of the thin film at f(O2) = 0 SCCM; this transition was designated to be an inter-conduction band transition from the first to the second conduction band. Using Hall parameters and Drude tail amplitudes in dielectric functions, the effective mass of GTiIO films was determined as 0.398 m0 at f(O2) = 0.3 SCCM.

Recently, the flexibility and stability of perovskite solar cells (PSCs) with high power-conversion efficiency (PCE) have attracted the interest of many research. Reliable flexible transparent conductive electrodes (TCEs) and high stability at the perovskite/transport layers interface are vital for increasing the performance of flexible- and stable-PSCs. Herein, we develop PSCs with two-dimensional graphene (Gr) TCEs and MoS2 electron transport layers (ETLs). By modulating the number of layers (L) of Gr (LGr) and MoS2 (LMoS2), the maximum PCE of PSCs were 14.42 and 12.92% was achieved for PSCs fabricated on glass and polyethylene terephthalate substrates, respectively, at LGr = 2 and LMoS2 = 1. PSCs showed excellent stability as it lost only 18% of the initial PCE after 500 h. This is attributed to the improved ETL/perovskite interface. Moreover, the flexible PSCs retained 84% and 63% of the original PCE value after 1000 inner- and outer-bending cycles at a radius of curvature of 2 mm; thus, it is suitable for flexible devices.

Angiogenesis is critical for local tumor growth. This study aimed to develop a three-dimensional two-layer co-culture system to investigate effects of cancer cells on the growth of endothelial cells (ECs). Poly(&epsilon, caprolactone) (PCL) nanofibrous membranes were generated via electrospinning of PCL in chloroform (C-PCL-M) and chloroform and dimethylformamide (C/DMF-PCL-M). We assembled a two-layer co-culture system using C-PCL-M and C/DMF-PCL-M for EC growth in the upper layer with co-cultured cancer cells in the lower layer. In the absence of vascular endothelial growth factor (VEGF), growth of bEND.3 ECs decreased on C/DMF-PCL-M but not on C-PCL-M with time. Growth of bEND.3 cells on C/DMF-PCL-M was enhanced through co-culturing of CT26 cancer cells and enhanced growth of bEND.3 cells was abrogated with anti-VEGF antibodies and sorafenib. However, EA.hy926 ECs displayed steady growth and proliferation on C/DMF-PCL-M, and their growth was not further increased through co-culturing of cancer cells. Moreover, chemical hypoxia in CT26 cancer cells upon treatment with CoCl2 enhanced the growth of co-cultured bEND.3 cells in the two-layer system. Thus, EC growth on the nanofibrous scaffold is dependent on the types of ECs and composition of nanofibers and this co-culture system can be used to analyze EC growth induced by cancer cells.

Background Sildenafil citrate, a highly selective phosphodiesterase type 5 inhibitor, is used to treat pulmonary hypertension (PH) in veterinary medicine. The objective of this study was to investigate pharmacokinetic profiles by oral administration of orally disintegrating film (ODF) and film coated tablet (FCT) formulations and rectal administration of ODF formulation in healthy dogs. Twelve healthy beagle dogs were administered four separate doses of sildenafil: FCT formulation 2 mg/kg orally, ODF formulation 2 mg/kg orally, ODF formulation 2 mg/kg rectally, and ODF formulation 10 mg/kg rectally. For 24 hours following administration, blood samples were collected and the plasma concentrations of sildenafil were assayed by liquid chromatography-tandem mass spectrometry. Results There were no significant differences in all the pharmacokinetic parameters between FCT and ODF formulations when administrated orally. Cmax at the time of rectal administration was lower when the same dose was given as that orally administered. No serious systemic adverse events (AEs) were observed. Conclusions These findings suggest that sildenafil ODF formulation can be used as an alternative to FCT formulation in the treatment of canine PH patients; additionally, rectal administration of sildenafil ODF may be a beneficial treatment option for canine patients who are unable to receive medication orally.

Author(s): Lim, Eunsoo; Hyun, Sunah; Lee, Jae Myeong; Kim, Seirhan; Lee, Min-Jeong; Lee, Sun-Mi; Oh, Ye-Sung; Park, Inwhee; Shin, Gyu-Tae; Kim, Heungsoo; Morisky, Donald E; Jeong, Jong Cheol | Abstract: Background:For phosphate control, patient education is essential due to the limited clearance of phosphate by dialysis. However, well-designed randomized controlled trials about dietary and phosphate binder education have been scarce. Methods:We enrolled maintenance hemodialysis patients and randomized them into an education group (n = 48) or a control group (n = 22). We assessed the patients' drug compliance and their knowledge about the phosphate binder using a questionnaire. Results:The primary goal was to increase the number of patients who reached a calcium-phosphorus product of lower than 55. In the education group, 36 (75.0%) patients achieved the primary goal, as compared with 16 (72.7%) in the control group (P = 0.430). The education increased the proportion of patients who properly took the phosphate binder (22.9% vs. 3.5%, P = 0.087), but not to statistical significance. Education did not affect the amount of dietary phosphate intake per body weight (education vs. control: -1.18 ± 3.54 vs. -0.88 ± 2.04 mg/kg, P = 0.851). However, the dietary phosphate-to-protein ratio tended to be lower in the education group (-0.64 ± 2.04 vs. 0.65 ± 3.55, P = 0.193). The education on phosphate restriction affected neither the Patient-Generated Subjective Global Assessment score (0.17 ± 4.58 vs. -0.86 ± 3.86, P = 0.363) nor the level of dietary protein intake (-0.03 ± 0.33 vs. -0.09 ± 0.18, P = 0.569). Conclusion:Education did not affect the calcium-phosphate product. Education on the proper timing of phosphate binder intake and the dietary phosphate-to-protein ratio showed marginal efficacy.

Meso-tetrakis(N-methyl pyridinium-4-yl)porphyrin (TMPyP) intercalates between the base-pairs of DNA at a low [TMPyP]/[DNA base] ratio in aqueous solutions and molecular crowding conditions, which is induced by the addition of Poly(ethylene glycol) (PEG). Studied DNA-binding drugs, including TMPyP, 9-aminoacridine, ethidium bromide, and DAPI (4′,6-diamidino-2-phenylindole) showed similar binding properties in the presence or absence of PEG molecules which is examined by circular and linear dichroism. According to the LDr (reduced linear dichroism) results of the binding drugs examined in this work, PEG molecules induced no significant change compared to their binding properties in aqueous buffering systems. These results suggest that the transition moments are not expected to be perturbed significantly by PEG molecules. In this study, the experimental conditions of PEG 8000 were maintained at 35% (v/v) of total reaction volume, which is equal to the optimal molar concentration (0.0536 M as final concentration for PEG 8000) to maintain suitable cell-like conditions. Therefore, there was no need to focus on the conformational changes of the DNA helical structure, such as forming irregular aggregate structures, induced by large quantities of molecular crowding media itself at this stage.

Helicobacter pylori (H. pylori) infection causes chronic gastritis and gastric cancer. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) is a key enzyme that catalyzes the oxidation of prostaglandin E2 (PGE2) to 15-keto-PGE2. 15-PGDH is speculated as a tumor suppressor as its expression has been frequently down-regulated in diverse human malignancies including gastric cancer. However, the molecular mechanisms underlying 15-PGDH down-regulation in tumorigenesis remain largely unknown. In the present study, we found that the 15-PGDH expression was down-regulated in rat gastric mucosa (RGM)-1 cells infected with H. pylori. H. pylori induced hypermethylation of 15-PGDH promoter. The hypermethylation level of 15-PGDH was higher in the stomach biopsy from H. pylori-infected patients with gastritis than those without H. pylori infection. Notably, H. pylori induced the expression of DNA methyl transferase (DNMT) 1 through generation of reactive oxygen species (ROS). In H. pylori-infected C57BL/6 mice, 15-PGDH expression was reduced while DNMT1 expression was increased in the stomach tissues. In conclusion, H. pylori induces DNA methylation of CpG islands in the 15-PGDH promoter through up-regulation of DNMT1 expression, which is attributable to the generation of ROS.

Helicobacter pylori (H. pylori) have been known to cause gastritis and promote gastric cancer development. H.pylori infection causes overproduction of prostaglandin E2 (PGE2), which has been implicated in inflammation and carcinogenesis. The intracellular level of PGE2 is regulated not only by its biosynthesis, but also by degradation. 15-Hydroxyprostaglandin dehydrogenase (15-PGDH) is the key enzyme that catalyzes the first step of PGE2 degradation. In the present study, we have observed that H. pylori suppressed the expression of 15-PGDH in rat gastric mucosa (RGM)-1 cells. By using deletion constructs of 15-PGDH promoter, we found that the Ets-binding site is the most essential determinant of 15-PGDH expression in RGM-1 cells. H. pylori infection suppressed the phosphorylation of Elk-1, a major transcription factor of the Ets family. Notably, curcumin, a yellow coloring agent present in the rhizome of Curcuma longa Linn (Zingiberaceae) with anti-inflammatory activity, induced expression of 15-PGDH in RGM-1 cells. We have found that activator protein-1 (AP-1) is the most critical transcription factor responsible for curcumin-induced upregulation of 15-PGDH expression. Curcumin enhanced the expression of c-Jun and c-Fos, which are functional subunits of AP-1, in the nuclear fraction of RGM-1 cells. Knockdown of c-jun abrogated curcumin-induced expression of 15-PGDH. Curcumin induced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and c-Jun NH2-terminal kinase (JNK1/2), but did not affect the phosphorylation of p38 mitogen-activated protein kinase (MAPK) in RGM-1 cells. Pharmacologic inhibition of each of above kinases abolished the curcumin-induced expression of c-Jun and 15-PGDH in RGM-1 cells. In another study, tetrahydrocurcumin which lacks the α,β-unsaturated carbonyl group failed to upregulate the expression 15-PGDH, suggesting that the electrophilic carbonyl moiety of curcumin plays a critical role in its induction of 15-PGDH expression in RGM-1 cells. Moreover, oral administration of curcumin increased the expression of 15-PGDH in the total protein lysate and enhanced the expression of c-Jun, c-Fos and CREB in the nuclear fraction of the mouse stomach. Curcumin again induced phosphorylation of ERK1/2 and JNK1/2, but did not affect that of p38 MAPK in the mouse stomach in vivo. Taken together, our study suggests that down-regulation of 15-PGDH expression induced by H. pylori infection may contribute, at least in part, to development of gastritis and gastric cancer, and upregulation of 15-PGDH expression by curcumin can account for the chemopreventive effect of this phytochemical on inflammation-associated gastric carcinogenesis. Citation Format: Ye-Sung Oh, Jeong-hwa Woo, Ji-Hye Jang, Young Wook Lee, Jong-Min Park, Young-Joon Surh, Hye-Kyung Na. Suppression of 15-Hydroxyprostaglandin Dehydrogenase in Helicobacter pylori-infected rt gastric mucosa cells and its restoration by curcumin. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3665. doi:10.1158/1538-7445.AM2013-3665