ODG
目录号 : GC44493
A detergent used to solubilize membrane proteins
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
ODG is a detergent used to solubilize membrane proteins. It has a critical micelle concentration (CMC) of greater than 10 mM.
| Cas No. | SDF | ||
| Canonical SMILES | O[C@@H]([C@@H](O[C@H](CO)[C@H]1O)OCC(C)(CO[C@H]2[C@H](O)[C@@H](O)[C@@H]([C@H](O2)CO)O)NC(CCSCCCCCCCC)=O)[C@H]1O | ||
| 分子式 | C27H51NO13S | 分子量 | 629.8 |
| 溶解度 | DMF: 2mg/mL,DMSO: 10mg/mL,Ethanol: 10mg/mL,PBS (pH 7.2): 2mg/mL | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5878 mL | 7.939 mL | 15.8781 mL |
| 5 mM | 0.3176 mL | 1.5878 mL | 3.1756 mL |
| 10 mM | 0.1588 mL | 0.7939 mL | 1.5878 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
ODG: Omics database generator - a tool for generating, querying, and analyzing multi-omics comparative databases to facilitate biological understanding
BMC Bioinformatics 2017 Aug 10;18(1):367.PMID:28797229DOI:10.1186/s12859-017-1777-7.
Background: Rapid generation of omics data in recent years have resulted in vast amounts of disconnected datasets without systemic integration and knowledge building, while individual groups have made customized, annotated datasets available on the web with few ways to link them to in-lab datasets. With so many research groups generating their own data, the ability to relate it to the larger genomic and comparative genomic context is becoming increasingly crucial to make full use of the data. Results: The Omics Database Generator (ODG) allows users to create customized databases that utilize published genomics data integrated with experimental data which can be queried using a flexible graph database. When provided with omics and experimental data, ODG will create a comparative, multi-dimensional graph database. ODG can import definitions and annotations from other sources such as InterProScan, the Gene Ontology, ENZYME, UniPathway, and others. This annotation data can be especially useful for studying new or understudied species for which transcripts have only been predicted, and rapidly give additional layers of annotation to predicted genes. In better studied species, ODG can perform syntenic annotation translations or rapidly identify characteristics of a set of genes or nucleotide locations, such as hits from an association study. ODG provides a web-based user-interface for configuring the data import and for querying the database. Queries can also be run from the command-line and the database can be queried directly through programming language hooks available for most languages. ODG supports most common genomic formats as well as generic, easy to use tab-separated value format for user-provided annotations. Conclusions: ODG is a user-friendly database generation and query tool that adapts to the supplied data to produce a comparative genomic database or multi-layered annotation database. ODG provides rapid comparative genomic annotation and is therefore particularly useful for non-model or understudied species. For species for which more data are available, ODG can be used to conduct complex multi-omics, pattern-matching queries.
β-Caryophyllene suppresses ferroptosis induced by cerebral ischemia reperfusion via activation of the NRF2/HO-1 signaling pathway in MCAO/R rats
Phytomedicine 2022 Jul 20;102:154112.PMID:35550220DOI:10.1016/j.phymed.2022.154112.
Background: Ischemic stroke is a complex brain disease regulated by several cell death processes, including apoptosis, autophagy, and ferroptosis. β-Caryophyllene (BCP), a natural bicyclic sesquiterpene abundantly found in essential oils, has been demonstrated to have potential pharmacological benefits in many diseases, including ischemic stroke. Purpose: This research was to determine the existence of ferroptosis in the pathogenesis of acute ischemic stroke and investigate whether BCP can inhibit ferroptosis to improve cerebral ischemia injury by activating the NRF2/HO-1 signaling pathway in rats. Methods: First, we verified ferroptosis by assessing proferroptotic changes after middle cerebral artery occlusion reperfusion (MCAO/R), along with protein and lipid peroxidation levels. Then male rats were divided randomly into Sham, MCAO/R, ML385 (NRF2-specific inhibitor) and BCP groups. The effects of BCP on cerebral injury were detected by the modified neurological severity score, TTC staining, and hematoxylin-eosin staining. We conducted western blotting analyzes of proteins, including those involved in ferroptosis and related signaling pathways. To demonstrate the neuroprotective effect of BCP in vitro, primary astrocytes were pretreated with different concentrations of BCP (10, 20, and 40 μM) for 24 h before oxygen-glucose deprivation/re-oxygenation (ODG/R). Results: We concluded that ferroptosis was engaged in the process of I/R-induced neurological damage, implying that this novel type of cell death might provide new therapeutic options for the clinical treatment of ischemic stroke. In vivo study proved that BCP improved neurological scores, infarct volume, and pathological features after MCAO/R. We demonstrated that BCP evidently enhanced NRF2 nuclear translocation, activated the NRF2/HO-1 pathway, which protected against ferroptosis. In vitro investigation revealed the same results. BCP decreased OGD/R-induced ROS generation and iron accumulation. Furthermore, the neuroprotective effects of BCP were reversed by the NRF2 inhibitor ML385. Conclusion: Our results indicated the critical role of ferroptosis in cerebral I/R injury. For the first time, we showed that the significant neuroprotective effects of BCP in attenuating ischemic stroke injury are correlated with ferroptosis regulation, and its mechanism is associated with activation of the NRF2/HO-1 axis.
Survival outcomes after laparoscopy-assisted distal gastrectomy versus open distal gastrectomy with nodal dissection for clinical stage IA or IB gastric cancer (JCOG0912): a multicentre, non-inferiority, phase 3 randomised controlled trial
Lancet Gastroenterol Hepatol 2020 Feb;5(2):142-151.PMID:31757656DOI:10.1016/S2468-1253(19)30332-2.
Background: Laparoscopy-assisted distal gastrectomy (LADG) is increasingly being used as an alternative to open distal gastrectomy (ODG) for gastric cancer treatment. Retrospective studies have shown equivalent survival with the two procedures, but these studies are limited by selection bias because LADG is more technically difficult than ODG. We aimed to evaluate whether LADG was non-inferior to ODG in terms of long-term survival outcomes. Methods: We did an open-label, multicentre, non-inferiority, phase 3 randomised controlled trial at 33 institutions in Japan. Patients aged 20-80 years with histologically confirmed gastric adenocarcinoma (T1N0, T1N1, or T2[MP]N0), clinical stage I, in the middle or lower third of the stomach, Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, with a body-mass index of less than 30 kg/m2, were randomly assigned (1:1) to receive ODG or LADG. Randomisation was done by telephone, fax, or with a web-based system in the Japan Clinical Oncology Group Data Center; a minimisation method with a random component was used to adjust for institution and clinical stage (IA or IB). Only study-accredited surgeons performed ODG and LADG. The primary endpoint was relapse-free survival and was analysed according to the intention-to-treat principle. The non-inferiority margin (LADG vs ODG) was set at a hazard ratio (HR) of 1·54. The trial was registered with the UMIN Clinical Trials Registry, UMIN000003319. Findings: Between March 15, 2010, and Nov 29, 2013, 921 patients were enrolled and randomly assigned to receive ODG (n=459) or LADG (n=462). 912 (99%) participants had the assigned surgery. 5-year relapse-free survival was 94·0% (95% CI 91·4-95·9) in the ODG group and 95·1% (92·7-96·8) in the LADG group. LADG was non-inferior to ODG for relapse-free survival (HR 0·84 [90% CI 0·56-1·27]), p=0·0075). The most common grade 3 or 4 adverse event was bowel obstruction, occurring in 11 (2%) of 455 patients in the ODG group and five (1%) of 457 patients in the LADG group. There were no treatment-related deaths. Interpretation: This trial supports the non-inferiority of LADG compared with ODG for clinical stage I gastric cancer relapse-free survival, suggesting that LADG should be considered a standard treatment option when performed by experienced surgeons. Funding: Japan National Cancer Center, Ministry of Health, Labour and Welfare of Japan, Japan Agency for Medical Research and Development.
Assessment of Laparoscopic Distal Gastrectomy After Neoadjuvant Chemotherapy for Locally Advanced Gastric Cancer: A Randomized Clinical Trial
JAMA Surg 2019 Dec 1;154(12):1093-1101.PMID:31553463DOI:10.1001/jamasurg.2019.3473.
Importance: Laparoscopic distal gastrectomy and neoadjuvant chemotherapy are increasingly used to treat locally advanced gastric cancer. However, the safety and efficacy of the laparoscopic procedure after neoadjuvant chemotherapy remain unclear. Objective: To evaluate the short-term outcomes of patients with locally advanced gastric cancer who received either laparoscopic distal gastrectomy or open distal gastrectomy. Design, setting, and participants: Between April 23, 2015, and November 16, 2017, a phase 2, open-label, noninferiority randomized clinical trial was conducted at the Gastrointestinal Cancer Center of Peking University Cancer Hospital and Institute in Beijing, China. Patients (n = 96) between 18 and 80 years of age with locally advanced gastric cancer (cT2-4aN+M0) who were receiving neoadjuvant chemotherapy were enrolled and randomized. An as-treated population and a modified intention-to-treat (mITT) population were defined for the data analysis. Interventions: Patients were randomized to undergo either laparoscopy-assisted distal gastrectomy (LADG) with D2 lymphadenectomy or open distal gastrectomy (ODG) with D2 lymphadenectomy. Main outcomes and measures: The primary end point was 3-year recurrence-free survival rate. Secondary end points were surgical radicality, 30-day postoperative morbidity and mortality, 2-week postoperative recovery indexes, and adjuvant chemotherapy completion status. Results: In total, 95 patients were eligible for as-treated analyses (LADG: 45, of whom 13 were female [29%], with a median [interquartile range (IQR)] age of 59 [52-65] years; ODG: 50, of whom 16 were female [32%], with a median [IQR] age of 61 [55-64] years) and mITT analyses (LADG: 47, of whom 14 were female [30%], with a median [IQR] age of 59 [52-65] years; ODG: 48, of whom 15 were female [31%], with a median [IQR] age of 61 [55-64] years). In the as-treated analyses, the LADG group had a significantly lower postoperative complication rate than the ODG group (20% vs 46%; P = .007). The postoperative visual analog scale score for pain was 1.2 units lower on postoperative day 2 only in the LADG group (95% CI, -2.1 to -0.3; P = .008). Patients in the LADG group had better adjuvant chemotherapy completion (adjusted odds ratio, 4.39; 95% CI, 1.63-11.80; P = .003) and were less likely to terminate adjuvant chemotherapy because of adverse effects (10 [22%] vs 21 [42%]; P = .04). The mITT analyses showed similar results to as-treated analyses. Conclusions and relevance: This trial found that LADG appears to offer the benefits of better postoperative safety and adjuvant chemotherapy tolerance compared with ODG for patients with locally advanced gastric cancer who received neoadjuvant chemotherapy. Trial registration: ClinicalTrials.gov identifier: NCT02404753.
Neuronal chemokine-like-factor 1 (CKLF1) up-regulation promotes M1 polarization of microglia in rat brain after stroke
Acta Pharmacol Sin 2022 May;43(5):1217-1230.PMID:34385606DOI:10.1038/s41401-021-00746-w.
The phenotypic transformation of microglia in the ischemic penumbra determines the outcomes of ischemic stroke. Our previous study has shown that chemokine-like-factor 1 (CKLF1) promotes M1-type polarization of microglia. In this study, we investigated the cellular source and transcriptional regulation of CKLF1, as well as the biological function of CKLF1 in ischemic penumbra of rat brain. We showed that CKLF1 was significantly up-regulated in cultured rat cortical neurons subjected to oxygen-glucose deprivation/reoxygenation (ODG/R) injury, but not in cultured rat microglia, astrocytes and oligodendrocytes. In a rat model of middle cerebral artery occlusion, we found that CKLF1 was up-regulated and co-localized with neurons in ischemic penumbra. Furthermore, the up-regulated CKLF1 was accompanied by the enhanced nuclear accumulation of NF-κB. The transcriptional activity of CKLF1 was improved by overexpression of NF-κB in HEK293T cells, whereas application of NF-κB inhibitor Bay 11-7082 (1 μM) abolished it, caused by OGD/R. By using chromatin-immunoprecipitation (ChIP) assay we demonstrated that NF-κB directly bound to the promoter of CKLF1 (at a binding site located at -249 bp to -239 bp of CKLF1 promoter region), and regulated the transcription of human CKLF1. Moreover, neuronal conditional medium collected after OGD/R injury or CKLF1-C27 (a peptide obtained from secreted CKLF1) induced the M1-type polarization of microglia, whereas the CKLF1-neutralizing antibody (αCKLF1) or NF-κB inhibitor Bay 11-7082 abolished the M1-type polarization of microglia. Specific knockout of neuronal CKLF1 in ischemic penumbra attenuated neuronal impairments and M1-type polarization of microglia caused by ischemic/reperfusion injury, evidenced by inhibited levels of M1 marker CD16/32 and increased expression of M2 marker CD206. Application of CKLF1-C27 (200 nM) promoted the phosphorylation of p38 and JNK in microglia, whereas specific depletion of neuronal CKLF1 in ischemic penumbra abolished ischemic/reperfusion-induced p38 and JNK phosphorylation. In summary, CKLF1 up-regulation in neurons regulated by NF-κB is one of the crucial mechanisms to promote M1-type polarization of microglia in ischemic penumbra.