Catalogue Number
BN-O1055
Analysis Method
Specification
98%(HPLC)
Storage
2-8°C
Molecular Weight
241.24
Appearance
Botanical Source
Structure Type
Category
SMILES
C1=CC=C(C(=C1)C(=O)C2=CC=CC=C2N)C(=O)O
Synonyms
2-Aminobenzophenone-2′-carboxylic acid/2-Anthraniloylbenzoic Acid/2-Aminobenzophenone-2'-carboxylic acid/2-(2-aminobenzoyl)benzoic acid/2'-Aminobenzophenone-2-carboxylic Acid
IUPAC Name
2-(2-aminobenzoyl)benzoic acid
Density
1.322 g/cm3
Solubility
Flash Point
268.8ºC
Boiling Point
520.9ºC at 760 mmHg
Melting Point
196-199 °C (dec.)(lit.)
InChl
InChl Key
KORKIRUGUNPQML-UHFFFAOYSA-N
WGK Germany
RID/ADR
HS Code Reference
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:1147-43-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
No Technical Documents Available For This Product.
29352099
Objective
To investigate whether cigarette smoking interacts with genes involved in individual susceptibility to xenobiotics for the risk of Parkinson disease (PD).
Methods
Two French population-based case-control studies (513 patients, 1,147 controls) were included as a discovery sample to examine gene-smoking interactions based on 3,179 single nucleotide polymorphisms (SNPs) in 289 genes involved in individual susceptibility to xenobiotics. SNP-by-cigarette smoking interactions were tested in the discovery sample through an empirical Bayes (EB) approach. Nine SNPs were selected for replication in a population-based case-control study from California (410 patients, 845 controls) with standard logistic regression and the EB approach. For SNPs that replicated, we performed pooled analyses including the discovery and replication datasets and computed pooled odds ratios and confidence intervals (CIs) using random-effects meta-analysis.
Results
Nine SNPs interacted with smoking in the discovery dataset and were selected for replication. Interactions of smoking with rs4240705 in the RXRA gene and rs1900586 in the SLC17A6 gene were replicated. In pooled analyses (logistic regression), the interactions between smoking and rs4240705-G and rs1900586-G were 1.66 (95% CI 1.28-2.14, p = 1.1 × 10−4, p for heterogeneity = 0.366) and 1.61 (95% CI 1.17-2.21, p = 0.003, p for heterogeneity = 0.616), respectively. For both SNPs, while smoking was significantly less frequent in patients than controls in AA homozygotes, this inverse association disappeared in G allele carriers.
Conclusions
We identified and replicated suggestive gene-by-smoking interactions in PD. The inverse association of smoking with PD was less pronounced in carriers of minor alleles of both RXRA-rs4240705 and SLC17A6-rs1900586. These findings may help identify biological pathways involved in the inverse association between smoking and PD.
Smoking and Parkinson disease: Evidence for gene-by-smoking interactions
Pei-Chen Lee, PhD,* Ismaïl Ahmed, PhD,* Marie-Anne Loriot, PhD, Claire Mulot, PhD, Kimberly C. Paul, PhD, Jeff M. Bronstein, MD, PhD, Beate Ritz, MD, PhD, and Alexis Elbaz, MD, PhDcorresponding author
2018 Feb 13
5874536
kushner, D. J. (National Research Council, Ottawa, Ontario, Canada). Lysis and dissolution of cells and envelopes of an extremely halophilic bacterium. J. Bacteriol. 87:1147-1156. 1964.—Envelopes of the extremely halophilic bacterium, Halobacterium cutirubrum, disintegrate in the absence of salt to form much smaller particles. Extensive proteolytic breakdown to compounds of low molecular weight is not involved in this process or in the lysis of cells in the absence of salt. NaCl is much more effective than KCl or NH4Cl in preserving the integrity of intact cells, but is only slightly more effective in preserving the integrity of mechanically prepared envelopes, of cells made permeable by treatment with acid, and of cells made permeable by formalin fixation followed by exposure to water. MgCl2 is much more effective in preserving the integrity of these preparations than of intact cells. The results suggest that the exterior cell surface has sites specifically requiring Na+ to maintain their integrity, whereas the interior surface has sites whose integrity is maintained at least as well by K+ or NH4+ as by Na+.
LYSIS AND DISSOLUTION OF CELLS AND ENVELOPES OF AN EXTREMELY HALOPHILIC BACTERIUM
D. J. Kushner
1964 May;
20857860
Study Objectives:
The sleep-deprivation-induced changes in delta power, an electroencephalographical correlate of sleep need, and brain transcriptome profiles have importantly contributed to current hypotheses on sleep function. Because sleep deprivation also induces stress, we here determined the contribution of the corticosterone component of the stress response to the electrophysiological and molecular markers of sleep need in mice.
Design:
N/A
Settings:
Mouse sleep facility.
Participants:
C57BL/6J, AKR/J, DBA/2J mice.
Interventions:
Sleep deprivation, adrenalectomy (ADX).
Measurements and Results:
Sleep deprivation elevated corticosterone levels in 3 inbred strains, but this increase was larger in DBA/2J mice; i.e., the strain for which the rebound in delta power after sleep deprivation failed to reach significance. Elimination of the sleep-deprivation-associated corticosterone surge through ADX in DBA/2J mice did not, however, rescue the delta power rebound but did greatly reduce the number of transcripts affected by sleep deprivation. Genes no longer affected by sleep deprivation cover pathways previously implicated in sleep homeostasis, such as lipid, cholesterol (e.g., Ldlr, Hmgcs1, Dhcr7, −24, Fkbp5), energy and carbohydrate metabolism (e.g., Eno3, G6pc3, Mpdu1, Ugdh, Man1b1), protein biosynthesis (e.g., Sgk1, Alad, Fads3, Eif2c2, −3, Mat2a), and some circadian genes (Per1, −3), whereas others, such as Homer1a, remained unchanged. Moreover, several microRNAs were affected both by sleep deprivation and ADX.
Conclusions:
Our findings indicate that corticosterone contributes to the sleep-deprivation-induced changes in brain transcriptome that have been attributed to wakefulness per se. The study identified 78 transcripts that respond to sleep loss independent of corticosterone and time of day, among which genes involved in neuroprotection prominently feature, pointing to a molecular pathway directly relevant for sleep function.
Citation:
Mongrain V; Hernandez SA; Pradervand S; Dorsaz S; Curie T; Hagiwara G; Gip P; Heller HC; Franken P. Separating the contribution of glucocorticoids and wakefulness to the molecular and electrophysiological correlates of sleep homeostasis. SLEEP 2010;33(9):1147-1157.
Sleep regulation, corticosterone, neuroprotection, microarray, microRNA
Separating the Contribution of Glucocorticoids and Wakefulness to the Molecular and Electrophysiological Correlates of Sleep Homeostasis
Valerie Mongrain, Susana A. Hernandez, Sylvain Pradervand, Stephane Dorsaz, Thomas Curie, Grace Hagiwara, Phung Gip, H. Craig Heller, Paul Franken
2010 Sep 1