Peroxidase-catalyzed copolymerization of syringaldehyde and bisphenol A

Syringaldehyde, one of the major derivatives of lignin, was copolymerized with bisphenol A via a CiP (Coprinus cinereus peroxidase)-catalyzed reaction. Although syringaldehyde was not polymerized to a solid polymer, the copolymer with bisphenol A was obtained as a dark brown powdery precipitate. The relatively hydrophobic solvent, 2-propanol, gave a better yield (yield = 95%) than hydrophilic solvents, such as methanol, ethanol or acetone. Characteristic signals corresponding to the aldehyde group of syringaldehyde in the copolymer were detected in the FT-IR and (13)C NMR spectrum. The ratio of syringaldehyde incorporated into the copolymer was estimated by measuring the amount of monomers consumed (syringaldehyde and bisphenol A), which proportionally increased up to 80 mol% on increasing the initial ratio of syringaldehyde to bisphenol A. TGA (thermogravimetric analysis) showed that the thermally crosslinked copolymer (syringaldehyde:bisphenol A = 1: 1, w/w) had a much higher thermal resistance to thermal degradation than poly(bisphenol A); 36% residue still remained under a nitrogen atmosphere, even over 800 degrees C. This implies that the copolymer of syringaldehyde and bisphenol A could be a new thermally stable material originating from renewable resources.clos

Adiponectin is a potential catabolic mediator in osteoarthritis cartilage

Introduction: Adiponectin has been implicated in the pathogenesis of osteoarthritis (OA). We studied the effects of adiponectin on the OA cartilage homeostasis. Methods: Immunohistochemical analysis was performed to evaluate differential expression of adiponectin receptors (AdipoRs) in nonlesional and lesional areas of OA cartilage. Cartilage and chondrocytes from the knee joints of primary OA patients were cultured in the presence of adiponectin (0 similar to 30 mu g/ml). The levels of total nitric oxide (NO), matrix metalloproteinase (MMP)-1, -3, and -13, and tissue inhibitor of metalloproteinase (TIMP)-1 were measured in the conditioned media. The levels of inducible NO synthase (iNOS) and MMPs were determined with the quantitative real-time reverse transcription-polymerase chain reaction. The concentrations of collagenase-cleaved type II collagen neoepitope (C1-2C) were determined in the supernatant of adiponectin-stimulated OA cartilage explants. The effects of kinase and NOS inhibitors were evaluated in the adiponectin-stimulated chondrocytes. Results: The expression levels of both AdipoR1 and AdipoR2 were significantly higher in lesional than in nonlesional areas of OA cartilage. The increased rate of AdipoR1-positive chondrocytes was twice that of AdipoR2-positive chondrocytes when compared between nonlesional and lesional areas. Adiponectin-stimulated OA chondrocytes showed increased total NO and MMP-1, -3, and -13 levels compared with nonstimulated cells. The TIMP-1 level was not affected. The C1-2C levels were increased by adiponectin in OA cartilage explant culture. AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) inhibitors (compound C and SP600125) significantly suppressed adiponectin-induced production of total NO and MMP-1, -3, and -13. Inducible NOS inhibitors enhanced the expression of the adiponectin-induced MMPs. Conclusions: Adiponectin causes matrix degradation in OA cartilage and increases MMPs and iNOS expression via the AMPK and JNK pathways in human OA chondrocytes. The catabolic effects of adiponectin may be counteracted by NO.Saxena NK, 2010, GASTROENTEROLOGY, V139, P1762, DOI 10.1053/j.gastro.2010.07.001Challa TD, 2010, MOL CELL ENDOCRINOL, V323, P282, DOI 10.1016/j.mce.2010.03.025Nishitani K, 2010, J CELL BIOCHEM, V109, P425, DOI 10.1002/jcb.22421HAO D, 2010, RHEUMATOL INTLaurberg TB, 2009, J RHEUMATOL, V36, P1885, DOI 10.3899/jrheum.080907Song HJ, 2009, TRANSL RES, V154, P18, DOI 10.1016/j.trsl.2009.04.003Huang CY, 2009, EUR J CLIN INVEST, V39, P417, DOI 10.1111/j.1365-2362.2009.02106.xFilkova M, 2009, ANN RHEUM DIS, V68, P295, DOI 10.1136/ard.2008.095737Yamauchi T, 2008, INT J OBESITY, V32, pS13, DOI 10.1038/ijo.2008.233Lago R, 2008, OSTEOARTHR CARTILAGE, V16, P1101, DOI 10.1016/j.joca.2007.12.008Lee YM, 2008, BIOCHEM BIOPH RES CO, V370, P641, DOI 10.1016/j.bbrc.2008.04.003Hattori Y, 2008, FEBS LETT, V582, P1719, DOI 10.1016/j.febslet.2008.04.037Haugen F, 2007, ENDOCRINOLOGY, V148, P5478, DOI 10.1210/en.2007-0370Tang CH, 2007, J IMMUNOL, V179, P5483Schober F, 2007, BIOCHEM BIOPH RES CO, V361, P968, DOI 10.1016/j.bbrc.2007.07.106Aigner T, 2007, NAT CLIN PRACT RHEUM, V3, P391, DOI 10.1038/ncprheum0534Legendre F, 2007, CLIN EXP RHEUMATOL, V25, P546Sharma L, 2007, ANN RHEUM DIS, V66, P141, DOI 10.1136/ard.2006.059931Pottie P, 2006, ANN RHEUM DIS, V65, P1403, DOI 10.1136/ard.2006.061994Chen TH, 2006, BBA-MOL BASIS DIS, V1762, P711, DOI 10.1016/j.bbadis.2006.06.008Presle N, 2006, OSTEOARTHR CARTILAGE, V14, P690, DOI 10.1016/j.joca.2006.01.009Neumeier M, 2006, J LEUKOCYTE BIOL, V79, P803, DOI 10.1189/jlb.0905521Luo XH, 2005, EXP CELL RES, V309, P99, DOI 10.1016/j.yexcr.2005.05.021Miyazaki T, 2005, BIOCHEM BIOPH RES CO, V333, P79, DOI 10.1016/j.bbrc.2005.05.076Ho LJ, 2005, BIOCHEM PHARMACOL, V70, P200, DOI 10.1016/j.bcp.2005.04.039Kadowaki T, 2005, ENDOCR REV, V26, P439, DOI 10.1210/er.2005-0005Meier U, 2004, CLIN CHEM, V50, P1511, DOI 10.1373/clinchem.2004.032482Englund M, 2004, ARTHRITIS RHEUM, V50, pS254Schaffler A, 2003, JAMA-J AM MED ASSOC, V290, P1709Tsao TS, 2002, J BIOL CHEM, V277, P29359, DOI 10.1074/jbc.C200312200Wang Y, 2002, J BIOL CHEM, V277, P19521, DOI 10.1074/jbc.M200601200Cooper C, 2000, ARTHRITIS RHEUM, V43, P995Chan ED, 1998, BIOCHEM BIOPH RES CO, V253, P790Hauselmann HJ, 1998, J IMMUNOL, V160, P1444StefanovicRacic M, 1997, J ORTHOPAED RES, V15, P442Tamura T, 1996, ENDOCRINOLOGY, V137, P3729StefanovicRacic M, 1996, J IMMUNOL, V156, P1213MURRELL GAC, 1995, BIOCHEM BIOPH RES CO, V206, P15REGINATO AM, 1994, ARTHRITIS RHEUM, V37, P1338HART DJ, 1993, J RHEUMATOL, V20, P331FELSON DT, 1992, ANN INTERN MED, V116, P535

Correlation between FDG uptake and glucose transporter type 1 expression in neuroendocrine tumors of the lung

Neuroendocrine (NE) lung tumors are subdivided into the following types; typical (TC) and atypical carcinoids (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell lung carcinoma (SCLC). Moreover, the determinants of the FDG uptakes of NE lung tumors have not been elucidated. Thus, the aim of the present study was to investigate the relationships between FDG uptake and glucose transporter type 1 (Glut-1) expression in these NE tumors. Tissue-proven NE lung tumor patients (n=32; age, mean+/-S.D.=67.8+/-10 years; male:female=28:4) who had undergone F-18 FDG-PET before treatment were enrolled in this study. There were 1 TC, 3 AC, 5 LCNEC, and 23 SCLC patients. FDG uptakes were quantified using maximum standardized uptake values (maxSUV). Paraffin sections of tumor tissues were immunostained using anti-Glut-1 antibody (Neomarkers, 1:50). Levels of Glut-1 expression are presented as percentages of tumor cells positively immunostained (%Glut-1). Relations between FDG uptakes and Glut-1 expression were assessed using Pearson correlation analysis. The maxSUVs of all NE lung tumors ranged from 0.6 to 29.5 (mean+/-S.D.=7.7+/-5.4) and %Glut-1 expression ranged from 0 to 100% (18+/-24%). The maxSUVs of all NE lung tumors were found to be significantly correlated with %Glut-1 expression (r=0.6471, p=0.0001). By subgroup analysis, maxSUV was also found to be significantly correlated with %Glut-1 expression in SCLC (n=23, r=0.6189, p=0.0016). FDG uptake was found to be highly correlated with Glut-1 expression in NE lung tumors. This result suggests that Glut-1 plays a crucial role in determining FDG uptake in these tumors

A qualitative study on the experience of acupuncture treatment in infertile women

Background: This study aimed to record and analyze the experiences of infertile women who underwent acupuncture treatment. Methods: This is a qualitative study in which in-depth interviews were conducted with women who underwent acupuncture as a treatment for infertility from the viewpoint of phenomenology, a method of understanding human behavior in the general human and social context, and grasping the nature of the experience in depth. The study participants were 12 women who had been receiving acupuncture treatment for infertility for more than 3 months. Results: After analyzing the statements of the participants’ experiences, the main concerns regarding infertility were ''embarrassed by unexpected infertility,'' ''overwhelmed with negative feelings,'' ''blocking and defense,'' “sex as a duty,” and “repeatition of expectations and failures.” Significant statements regarding acupuncture treatments were “body warmth,” “becoming a body,” “care of the mind,” “last trust and hope,” and “difficulties of waiting.” The experience with supporter was love-hate relationships, and the experience of the children’s meaning was expressed as “precious beings in life.” Conclusion: The results of this study suggest that acupuncture treatment for infertility in women results in positive thinking through changes in the body as well as through increased hope. Participants experienced a feeling of warmth in their bodies, regular menstrual cycle, and reduced fatigue through acupuncture treatment, indicating a state of psychological stability

Growth inhibitory, bactericidal, and morphostructural effects of dehydrocostus lactone from Magnolia sieboldii Leaves on antibiotic-susceptible and -resistant strains of Helicobacter pylori.

Helicobacter pylori is associated with various diseases of the upper gastrointestinal tract, such as gastric inflammation and duodenal and gastric ulcers. The aim of the study was to assess anti-H. pylori effects of the sesquiterpene lactone dehydrocostus lactone (DCL) from Magnolia sieboldii leaves, compared to commercial pure DCL, two previously known sesquiterpene lactones (costunolide and parthenolide), (-)-epigallocatechin gallate, and four antibiotics. The antibacterial activity of natural DCL toward antibiotic-susceptible H. pylori ATCC 700392 and H. pylori ATCC 700824 strains (MIC, 4.9 and 4.4 mg/L) was similar to that of commercial DCL and was more effective than costunolide, parthenolide, and EGCG. The activity of DCL was slightly lower than that of metronidazole (MIC, 1.10 and 1.07 mg/L). The antibacterial activity of DCL was virtually identical toward susceptible and resistant strains, even though resistance to amoxicillin (MIC, 11.1 mg/L for PED 503G strain), clarithromycin (49.8 mg/L for PED 3582GA strain), metronidazole (21.6 mg/L for H. pylori ATCC 43504 strain; 71.1 mg/L for 221 strain), or tetracycline (14.2 mg/L for B strain) was observed. This finding indicates that DCL and the antibiotics do not share a common mode of action. The bactericidal activity of DCL toward H. pylori ATCC 43504 was not affected by pH values examined (4.0-7.0). DCL caused considerable conversion to coccoid form (94 versus 49% at 8 and 4 mg/L of DCL for 48 h). The Western blot analysis revealed that urease subunits (UreA and UreB) of H. pylori ATCC 43504 were not affected by 10 mM of DCL, whereas UreA monomer band completely disappeared at 0.1 mM of (-)-epigallocatechin gallate. Global efforts to reduce the level of antibiotics justify further studies on M. sieboldii leaf-derived materials containing DCL as potential antibacterial products or a lead molecule for the prevention or eradication of drug-resistant H. pylori

Cross-talk between the TM4SF5/FAK and the IL6/STAT3 pathways renders immune escape of human liver cancer cells

TM4SF5 overexpressed in hepatocellular carcinoma activates FAK during tumor cell migration. However, it remains unknown how TM4SF5 in hepatocellular carcinoma cells compromise with immune actions initiated by extracellular cytokines. Normal and cancerous hepatocytes with or without TM4SF5 expression were analyzed for the effects of cytokine signaling activity on TM4SF5/FAK signaling and metastatic potential. We found that IL6 was differentially expressed in hepatocytes depending on cancerous malignancy and TM4SF5 expression. IL6 treatment activated FAK and STAT3 and enhanced focal adhesion (FA) formation in TM4SF5-null cells, but it decreased TM4SF6-dependent FAK activity and FAformation in SNU761-TM4SF5 cells. STAT3 suppression abolished the IL6-mediated effects in normal Chang cells, but it did not recover the TM4SF5-dependent FAK activity that was inhibited by IL6 treatment in cancerous SNU761-TM4SF5 cells. In addition, modulation of FAK activity did not change the IL6-mediated STAT3 activity in either the Chang or SNU761 cell system. TM4SF5 expression in SNU761 cells caused invasive extracellular matrix degradation negatively depending on IL6/IL6R signaling. Thus, it is likely that hepatic cancer cells might adopt TM4SF5-dependent FAK activation and metastatic potential by lowering IL6 expression and thus avoiding its immunological action through the IL6-STAT3pathway.OAIID:oai:osos.snu.ac.kr:snu2014-01/102/0000003910/7SEQ:7PERF_CD:SNU2014-01EVAL_ITEM_CD:102USER_ID:0000003910ADJUST_YN:NEMP_ID:A078142DEPT_CD:375CITE_RATE:5.372FILENAME:83jh-mcb.pdfDEPT_NM:약학과SCOPUS_YN:YCONFIRM:

Cross Talk between the TM4SF5/Focal Adhesion Kinase and the Interleukin-6/STAT3 Pathways Promotes Immune Escape of Human Liver Cancer Cells

TM4SF5 overexpressed in hepatocellular carcinoma activates focal adhesion kinase (FAK) during tumor cell migration. However, it remains unknown how TM4SF5 in hepatocellular carcinoma cells compromises with immune actions initiated by extracellular cytokines. Normal and cancerous hepatocytes with or without TM4SF5 expression were analyzed for the effects of cytokine signaling activity on TM4SF5/FAK signaling and metastatic potential. We found that interleukin-6 (IL-6) was differentially expressed in hepatocytes depending on cancerous malignancy and TM4SF5 expression. IL-6 treatment activated FAK and STAT3 and enhanced focal adhesion (FA) formation in TM4SF5-null cells, but it decreased TM4SF5-dependent FAK activity and FA formation in SNU761-TM4SF5 cells. STAT3 suppression abolished the IL-6-mediated effects in normal Chang cells, but it did not recover the TM4SF5-dependent FAK activity that was inhibited by IL-6 treatment in cancerous SNU761-TM4SF5 cells. In addition, modulation of FAK activity did not change the IL-6-mediated STAT3 activity in either the Chang or SNU761 cell system. TM4SF5 expression in SNU761 cells caused invasive extracellular matrix degradation negatively depending on IL-6/IL-6 receptor (IL-6R) signaling. Thus, it is likely that hepatic cancer cells adopt TM4SF5-dependent FAK activation and metastatic potential by lowering IL-6 expression and avoiding its immunological action through the IL-6-STAT3 pathway

A mutated recombinant subunit vaccine protects mice and guinea pigs against botulinum type A intoxication

Botulinum neurotoxins (BoNTs) are the most potent toxins to mammals. A toxoid vaccine was previously used for prevention of botulinum intoxication; however, this vaccine is no longer available. Currently, no approved botulinum vaccines are available from the Food and Drug Administration (FDA). Recently, a recombinant host cell receptor-binding subunit created for use as a potential vaccine completed phase 2 clinical trials. The current study designed a vaccine candidate against BoNT type A (BoNT/A) using a structural design. Our vaccine candidate was the BoNT/A heavy chain C-terminal region (HCR) that contained the point mutation BA15 (R1269A) within the ganglioside-binding site. A Biacore affinity test showed that the affinity of BA15 for ganglioside GT1b was 100 times lower than that of the HCR. A SNAP25 cleavage assay revealed that immunized sera blocked SNAP25 cleavage of the BoNT/A toxin via BA15. In an in vivo experiment, mice and guinea pigs immunized with BA15 produced neutralizing antibodies that protected against 3,000 LD50 of BoNT/A. In conclusion, the results of both in vitro and in vivo assays showed that our BA15 vaccine candidate was similar to the recombinant host cell receptor-binding subunit vaccine. The inability of BA15to bind ganglioside shows that BA15 is a potential safe vaccine candidate

Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases

Mitochondria are one of the organelles undergoing rapid alteration during the senescence process. Senescent cells show an increase in mitochondrial size, which is attributed to the accumulation of defective mitochondria, which causes mitochondrial oxidative stress. Defective mitochondria are also targets of mitochondrial oxidative stress, and the vicious cycle between defective mitochondria and mitochondrial oxidative stress contributes to the onset and development of aging and age-related diseases. Based on the findings, strategies to reduce mitochondrial oxidative stress have been suggested for the effective treatment of aging and age-related diseases. In this article, we discuss mitochondrial alterations and the consequent increase in mitochondrial oxidative stress. Then, the causal role of mitochondrial oxidative stress on aging is investigated by examining how aging and age-related diseases are exacerbated by induced stress. Furthermore, we assess the importance of targeting mitochondrial oxidative stress for the regulation of aging and suggest different therapeutic strategies to reduce mitochondrial oxidative stress. Therefore, this review will not only shed light on a new perspective on the role of mitochondrial oxidative stress in aging but also provide effective therapeutic strategies for the treatment of aging and age-related diseases through the regulation of mitochondrial oxidative stress