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Synthesis and Crystal Structure of Asymmetric Dimer of 1,2-Benzothiazine Derivatives Using Silver Oxide (Silver Oxide를 이용한 1,2-벤조티아진 유도체의 비대칭 중합체 합성 및 결정 구조)

  • Park, Myung Suk
    • Journal of the Korean Chemical Society
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    • v.42 no.6
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    • pp.657-663
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    • 1998
  • New asymmetric dimer, 7,7'-substituted (or H)-4-oxo-2,2'- dialkyl-l,l',2,2'-dibenzothiazine-3,3'dicarboxylic acid methyl ester-1,1,1',1'-tetraoxide 3,4'-yl ethers 2a-d were synthesized through the oxidative dimerization of 7-substituted (or H)-4-hydroxy-2-alkyl-1,2-benzothiazine-3-carboxylic acid methyl ester 1,1-dioxides la-d using silver oxide($Ag_2O$). 4-Oxo-2,2'-dialkyl-1,1'2,2'-dibenzothiazine-3,3'-dicarboxylic acid methyl ester-1,1,1',l'-tetraoxide 3,4'-yl ether 2c was identified by X-ray crystal structure determination.

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Salinity and sodicity disturbs growth of medicinal crop Guar (Cyanoposisa tetragonoloba)

  • Ullah, Muhammad Arshad;Rasheed, Muhammad;Mahmood, Imdad Ali
    • The Korean Journal of Food & Health Convergence
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    • v.4 no.2
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    • pp.7-11
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    • 2018
  • Salinity is one of the major and increasing problems in irrigated agriculture in Pakistan. Salinity stress negatively affects the growth and yield of plants guar (Cyanoposisa tetragonoloba). This experiment was conducted to evaluate the effects of ($4dSm^{-1}+13.5(mmol\;L^{-1})^{1/2}$, $5dSm^{-1}+25(mmol \;L^{-1})^{1/2}$, $5dSm^{-1}+30(mmol\;L^{-1})^{1/2}$, $10dSm^{-1}+25(mmol\;L^{-1})^{1/2}$ and $10dSm^{-1}+30(mmol \;L^{-1})^{1/2}$) on biomass yield of guar against salinity tolerance. Maximum biomass yield ($54.50gpot^{-1}$) was produced by $4dSm^{-1}+13.5(mmol\;L^{-1})^{1/2}$ treatment. Biomass produce was reduced with the increase of the salts toxicity. Minimum biomass yield ($30.17gpot^{-1}$) was attained under $10dSm^{-1}+30(mmol \;L^{-1})^{1/2}$. $5dSm^{-1}+25(mmol\;L^{-1})^{1/2}$ treatment exhibited improved outcome i.e. the least diminution % over control (18.66). Salinity cum sodicity showed staid effect on the growth reduction from 18.66% to 44.64%. This reduction fissure was impacted by the toxic effect of salinity and sodicity on Guar growth. Salinity- sodicity behaved toxic impact on the growth reduction from 18.66% to 44.64%. Based on the findings, guar (Cyanoposisa tetragonoloba) grows better at $4dSm^{-1}+13.5(mmol \;L^{-1})^{1/2}$ treatment.

Effect of Genistein on the Benzo(k)fluoranthene Regulated CYP1B1 Gene Expression (Genistein이 Benzo(k)fluoranthene에 의한 CYP1B1 유전자조절 작용에 미치는 영향)

  • Seo, Mi-Jung;Sheen, Yhun-Yhong
    • Environmental Mutagens and Carcinogens
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    • v.24 no.4
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    • pp.163-170
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    • 2004
  • CYP1B1 enzyme metabolize PAHs and estradiol. CYP1B1 metabolize estradiol to 4-hydroxyestradiol that is considered as carcinogenic metabolite. Luciferase activity was induced about 20 folds over that control by 1 nM TCDD (2,3,7,8-tetrchlorodibenzo-p-dioxin) and these inductions were dose-dependent. Recent industrialized society, human hasbeen widely been exposed to widespread environmental contaminants such as PAHs (polycyclic aromatic hydrocarbon) that are originated from the incomplete combustion of hydrocarbons. PAHs are known to be ligands of the AhR (aryl hydrocarbon receptor). Induction of cytochrome P4501B1(CYP1B1) in cell culture is widely used as a biomarket for PAHs. Therefore we have studied the effect of PAHs in the human breast cancer cells MCF-7 to evaluate bioactivity of PAHs. Cytochrome P4501B1(CYP1B1) is known to be inducible by xenobiotic compounda such as policyclic aromatic hydrocarbon (PAH) and dioxins such as 2,3,7,8-tetrachloro-dibenzo-p-dioxin(TCDD). And these induction of CYP1B1 is also regulated by many categories of chemicals. In order to investigate the effects of several chemicals on CYP1B1 gene expression in luciferase gene, and then transfected into these cells. After treatment of chemicals, the luciferase activity was measured. We examined effects of PAHs on the CYP1B1-lucifrease reporter gene and CYP1B1 mRNA level. Benzo(k)fluoranthene showed strong response to CYP1B1 promoter activity stimulation, and also CYP1B1 mRNAs increase in MCF-7 cells in a concentration-dependent manner. flvonoids such as genistein decreased B(k)F induced luciferase activity at low concentration. it exhibited stimulatory effect at high concentration.

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Nutrient Turnover by Fine Roots in Temperate Hardwood and Softwood Forest Ecosystems Varying in Calcium Availability

  • Park, Byung Bae
    • Journal of Korean Society of Forest Science
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    • v.96 no.2
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    • pp.214-221
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    • 2007
  • The effect of nutrient availability and forest type on the nutrient turnover of fine roots is important in terrestrial nutrient cycling, but it is poorly understood. I measured nutrient turnover of hardwoods and softwoods at three well studied sites in the northeastern US: Sleepers River, VT; Hubbard Brook, NH; Cone Pond, NH. Significant differences in nutrient turnover by fine roots were observed among sites, but not between forest types. The magnitude of differences for each element ranged from 3 times for P and N to 8 times for Ca and Mg between sites. Smaller differences of 0.2 to 0.8 times were observed between forest types. In hardwoods, the Sleepers River 'new' site had $23kg\;ha^{-1}\;yr^{-1}$ Ca, $7kg\;ha^{-1}\;yr^{-1}$ Mg, and $16kg\;ha^{-1}\;yr^{-1}$ K turnover, owing to high root nutrient contents and turnover. Cone Pond had the highest turnover for Mn ($0.8kg\;ha^{-1}\;yr^{-1}$) and Al ($16kg\;ha^{-1}\;yr^{-1}$), owing to high nutrient contents. The Hubbard Brook hardwood site exhibited the lowest turnover of these elements. In softwoods, the variation in turnover of Ca, Mg, and K was lower than in hardwoods. The Hubbard Brook had the highest turnover for P ($1.6kg\;ha^{-1}\;yr^{-1}$), N ($31kg\;ha^{-1}\;yr^{-1}$), Mn ($0.4kg\;ha^{-1}\;yr^{-1}$), Al ($10kg\;ha^{-1}\;yr^{-1}$), Fe ($6.4kg\;ha^{-1}\;yr^{-1}$), Zn ($0.3kg\;ha^{-1}\;yr^{-1}$), Cu ($34g\;ha^{-1}\;yr^{-1}$), and C ($1.1Mg\;ha^{-1}\;yr^{-1}$). Root Ca turnover exponentially increased as soil percentage Ca saturation increased because of greater root nutrient contents and more rapid turnover at the higher Ca sites. These results imply that nutrient inputs by root turnover significantly increase as soil Ca availability improves in temperate forest ecosystems.

Hypoxia-inducible factor 1α inhibitor induces cell death via suppression of BCR-ABL1 and Met expression in BCR-ABL1 tyrosine kinase inhibitor sensitive and resistant chronic myeloid leukemia cells

  • Masanobu Tsubaki;Tomoya Takeda;Takuya Matsuda;Akihiro Kimura;Remi Tanaka;Sakiko Nagayoshi;Tadafumi Hoshida;Kazufumi Tanabe;Shozo Nishida
    • BMB Reports
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    • v.56 no.2
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    • pp.78-83
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    • 2023
  • Chronic myeloid leukemia (CML) has a markedly improved prognosis with the use of breakpoint cluster region-abelson 1 (BCR-ABL1) tyrosine kinase inhibitors (BCR-ABL1 TKIs). However, approximately 40% of patients are resistant or intolerant to BCR-ABL1 TKIs. Hypoxia-inducible factor 1α (HIF-1α) is a hypoxia response factor that has been reported to be highly expressed in CML patients, making it a therapeutic target for BCR-ABL1 TKI-sensitive CML and BCR-ABL1 TKI-resistant CML. In this study, we examined whether HIF-1α inhibitors induce cell death in CML cells and BCR-ABL1 TKI-resistant CML cells. We found that echinomycin and PX-478 induced cell death in BCR-ABL1 TKIs sensitive and resistant CML cells at similar concentrations while the cell sensitivity was not affected with imatinib or dasatinib in BCR-ABL1 TKIs resistant CML cells. In addition, echinomycin and PX-478 inhibited the c-Jun N-terminal kinase (JNK), Akt, and extracellular-regulated protein kinase 1/2 (ERK1/2) activation via suppression of BCR-ABL1 and Met expression in BCR-ABL1 sensitive and resistant CML cells. Moreover, treatment with HIF-1α siRNA induced cell death by inhibiting BCR-ABL1 and Met expression and activation of JNK, Akt, and ERK1/2 in BCR-ABL1 TKIs sensitive and resistant CML cells. These results indicated that HIF-1α regulates BCR-ABL and Met expression and is involved in cell survival in CML cells, suggesting that HIF-1α inhibitors induce cell death in BCR-ABL1 TKIs sensitive and resistant CML cells and therefore HIF-1α inhibitors are potential candidates for CML treatment.

IL-1 Receptor Dynamics in Immune Cells: Orchestrating Immune Precision and Balance

  • Dong Hyun Kim;Won-Woo Lee
    • IMMUNE NETWORK
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    • v.24 no.3
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    • pp.21.1-21.16
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    • 2024
  • IL-1, a pleiotropic cytokine with profound effects on various cell types, particularly immune cells, plays a pivotal role in immune responses. The proinflammatory nature of IL-1 necessitates stringent control mechanisms of IL-1-mediated signaling at multiple levels, encompassing transcriptional and translational regulation, precursor processing, as well as the involvement of a receptor accessory protein, a decoy receptor, and a receptor antagonist. In T-cell immunity, IL-1 signaling is crucial during both the priming and effector phases of immune reactions. The fine-tuning of IL-1 signaling hinges upon two distinct receptor types; the functional IL-1 receptor (IL-1R) 1 and the decoy IL-1R2, accompanied by ancillary molecules such as the IL-1R accessory protein (IL-1R3) and IL-1R antagonist. IL-1R1 signaling by IL-1β is critical for the differentiation, expansion, and survival of Th17 cells, essential for defense against extracellular bacteria or fungi, yet implicated in autoimmune disease pathogenesis. Recent investigations emphasize the physiological importance of IL-1R2 expression, particularly in its capacity to modulate IL-1-dependent responses within Tregs. The precise regulation of IL-1R signaling is indispensable for orchestrating appropriate immune responses, as unchecked IL-1 signaling has been implicated in inflammatory disorders, including Th17-mediated autoimmunity. This review provides a thorough exploration of the IL-1R signaling complex and its pivotal roles in immune regulation. Additionally, it highlights recent advancements elucidating the mechanisms governing the expression of IL-1R1 and IL-1R2, underscoring their contributions to fine-tuning IL-1 signaling. Finally, the review briefly touches upon therapeutic strategies targeting IL-1R signaling, with potential clinical applications.

Ginsenoside Contents of Korean White Ginseng and Taegeuk Ginseng with Various Sizes and Cultivation Years (국내산 백삼과 태극삼의 크기 및 연근별 인삼사포닌 함량)

  • Hwang, Jin-Bong;Ha, Jae-Ho;Hawer, Woo-Derck;NahmGung, Bae;Lee, Boo-Yong
    • Korean Journal of Food Science and Technology
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    • v.37 no.3
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    • pp.508-512
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    • 2005
  • Ginsenoside composition and contents of Korean white and taegeuk ginsengs were investigated to establish Chinese pharmaceutical standards for import of Korean ginseng. Total ginsenoside-Rg1, Re, and Rb1 of all Korean white and taegeuk ginseng samples were higher than guideline of Chinese standard of 0.4%, $Mean{\pm}S.D.$ values of Rg1, Re, and Rb1 of Korean white ginseng were $232.7{\pm}110.2,\;235.3{\pm}101.5,\;and\;280.1{\pm}121.3\;mg%$, respectively. Ratio of Rg1 to Re of Korean white ginseng was 1.02. $Mean{\pm}S.D.$ values of Rg1, Re, and Rb1 of Korean taeguek ginseng were $262.1{\pm}127.2,\;213.1{\pm}55.7,\;and\;279.9{\pm}92.1\;mg%$, respectively.

Distribution of HLA-DQA1*01, *03, *05 and DQB1*02 Subtypes and the Associated Haplotypes in the Korean Population

  • Pyo, Chul-Woo;Chung, Seo-Young;Hur, Seong-Suk;Kim, Hyoung-Jae;Choi, Jee-Yeoun;Kim, Yang-Kyum;Yoo, Ha-Jung;Choi, Hee-Baeg;Kim, Tai-Gyu
    • IMMUNE NETWORK
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    • v.3 no.2
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    • pp.103-109
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    • 2003
  • Background: As all HLA class II genes, the DQ genes show their polymorphic variation mainly in the second exon, which encodes the first extracellular domain of the molecule. PCR-SSOP (Polymerase chain reaction-Sequence specific oligonucleotide probe) techniques were frequently used for HLA-DQA1 and DQB1 typing but certain alleles, $DQA1^*0101/0104/0105$, $^*302/0303$, $*0501/0505$ and $DQB1^*0201/^*0202$ which differ from each other in segment other than exon 2, could not be unequivocally assigned. Methods: To overcome this problem, we applied additional PCR-SSP (PCR-Sequence specific primer) method to analyze DQA1 exons 1, 3 and 4 and DQB1 exon 3. And we investigated the distributions and haplotypes of HLA-DRB1, DQA1 and DQB1 alleles in 406 unrelated Korean healthy individuals. Results: Using this method the indistinguishable alleles of DQA1 and DQB1 in PCR-SSOP were typed definitively. We also found several important associations between DQA1 and DQB1 alleles in the Korean population; $DQA1^*0101-DQB1^*0501$, $DQA1^*0104-DQB1^*0502$ or $-^*0503$, $DQA1^*0105-DQB1^*0501$, $DQA1^*0302-DQB1^*0303$, $DQA1^*0303-DQB1^*0401$ or $-^*0402$, $DQA1^*0501-DQB1^*0201$, $DQA1^*0505-DQB1^*0301$, and $DQA1^*0201-DQB1^*0202$. The haplotypes of DRB1-DQA1-DQB1 associated with $DQA1^*01$, $^*03$, $^*05$, and $DQB1^*02$ subtypes were investigated. Several haplotypes associated with these alleles were observed in the Korean population. Conclusion: Our results can be helpful to find potential unrelated donors for bone marrow registries and study the HLA-associated disease and anthropology at high-resolution allelic level.

The Synthesis of 6-Fluoroquinolone Carboxamidopenicillin Derivatives (6-Fluoroquinolone Carboxamidopenicillin 유도체의 합성)

  • 임철부;김정주
    • YAKHAK HOEJI
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    • v.31 no.2
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    • pp.92-97
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    • 1987
  • The N-[1H-6-fluoro-1,4-dihydro-4-oxo-7-chloroquinoline-3-carboxy] succinimide was reacted with amoxicillin, ampicillin and 6-APA to give 6-[D-(-)-$\alpha$-{1H-6-fluoro-1,4-dihydro-4-oxo-7-chloroguinoline-3-carboxamido} p-hydroxyphanyl acetamido] penicillanic acid [1], 6-[D-(-)-$\alpha$-{1H-6-fluoro-1,4-dihydro-4-oxo-7-chloroquinoline-3-carboxamido} phenylacetamido] penicillanic acid [10] and 6-[1H-6-fluoro-1,4-dihydro-4-oxo-7-chloroquinoline-3-carboxamido] penicillanic acid [19]. The 1-alkyl-6-fluoro-1,4-dihydro-4-oxo-7-substituted quinoline-3-carboxylic acids were reacted with ethyl chloroformate for making mixed anhydride; these mixed anhydrides were reacted with amoxicillin, ampilcillin and 6-APA to give 6-[D-(-)-$\alpha$-{1-alkyl-6-fluoro-1,4-dihydro-4-oxo-7-substituted quinoline-3-carboxamido} p-hydroxyphenylacetamido] penicillanic acid [2-9], 6-[D-(1)-$\alpha$-{1-alkyl-6-fluoro-1,4-dihydro-4-oxo-7-substituted quinoline-3-carboxamido} phenylacetamidod penicillanic acid [11-18] and 6-[1-alkyl-6-fluoro-1,4-dihydro-4-oxo-7-substituted quinoline-3-carboxamido] penicillanic acid [20-27].

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