Serological autoimmune profile of systemic lupus erythematosus in deep and non-deep endometriosis patients

Several studies have reported a high prevalence of autoimmune diseases such as systemic lupus erythematosus (SLE) in endometriosis patients. The aim of this study was to evaluate the SLE autoimmune antibody profile in patients with deep (DE) and non-deep endometriosis (Non-DE).Four groups of premenopausal patients were evaluated: patients with DE (n = 50); patients with ovarian endometriomas (Non-DE; n = 50); healthy patients without endometriosis (C group; n = 45); and SLE patients without endometriosis (SLE group; N = 46). Blood samples were obtained and the standard SLE autoimmune profile was evaluated in all patients. Pain symptoms related to endometriosis and clinical SLE manifestations were also recorded.The DE group presented a statistically significant higher proportion of patients with antinuclear antibodies (ANA) (20%) compared to the Non-DE group (4%) and C group (2.2%). Levels of complement were more frequently lower among DE and Non-DE patients although differences did not reach statistical significance. Similarly, anti-dsDNA antibodies and anticoagulant lupus were positive in more patients of the DE group but did not reach statistical significance. The DE group complained of more arthralgia and asthenia compared to the Non-DE and C groups.The results of this study showed higher positivity of ANA and greater arthralgia and asthenia in patients with DE compared with Non-DE patients and healthy controls, suggesting that they may have a higher susceptibility to autoimmune diseases and present more generalized pain.Copyright © 2023. Published by Elsevier B.V

Microwave-Assisted Synthesis and Evaluation of Antimicrobial Activity of 3-{3-(s-Aryl and s-Heteroaromatic)acryloyl}-2Hchromen-2-one Derivatives

The exploration of potential utilization of microwaves as an energy source for heterocyclic synthesis was herein investigated using condensation of 3-acetylcoumarin (1) with aromatic and heteroaromatic aldehydes to afford the corresponding aromatic chalcones (2a–j) and heteroaromatic chalcones (3a–e and 4a–e), respectively, in good to excellent yield within 1–3 min. The chemical structures were confirmed by analytical and spectral data. All the synthesized compounds were screened for their antibacterial activity and 3-{3-(4-dimethylaminophenyl)acryloyl}-2H-chromen-2-one (2i) was discovered to be the most active at minimum inhibitory concentration (MIC) value of 7.8 µg/m

3-{2-[2-(Diphenyl­methyl­ene)hydrazin­yl]thia­zol-4-yl}-2H-chromen-2-one

In the title compound, C25H17N3O2S, the coumarin ring system is essentially planar with a maximum deviation of 0.019 (2) Å. A weak intra­molecular C—H⋯O hydrogen bond stabilizes the mol­ecular structure, so that the coumarin plane is approximately coplanar with the thia­zole ring, making a dihedral angle of 2.5 (10)°. The two phenyl rings are nearly perpendicular to each other, with a dihedral angle of 81.44 (12)°. In the crystal structure, the mol­ecules are linked into an infinite chain along the b axis by inter­molecular C—H⋯O hydrogen bonds. Weak C—H⋯π inter­actions are observed between the chains

3-{2-[2-(2-Fluoro­benzyl­idene)hydrazin­yl]-1,3-thia­zol-4-yl}-2H-chromen-2-one

In the title compound, C19H12FN3O2S, the chromene ring system and the thia­zole ring are approximately planar [maximum deviations of 0.023 (3) Å and 0.004 (2) Å, respectively]. The chromene ring system is inclined at angles of 4.78 (10) and 26.51 (10)° with respect to the thia­zole and benzene rings, respectively, while the thia­zole ring makes a dihedral angle of 23.07 (12)° with the benzene ring. The mol­ecular structure is stabilized by an intra­molecular C—H⋯O hydrogen bond, which generates an S(6) ring motif. The crystal packing is consolidated by inter­molecular N—H⋯O hydrogen bonds, which link the mol­ecules into chains parallel to [100], and by C—H⋯π and π–π [centroid–centroid distance = 3.4954 (15) Å] stacking inter­actions

(E)-1-[1-(6-Bromo-2-oxo-2H-chromen-3-yl)ethyl­idene]thio­semicarbazide

The title compound, C12H10BrN3O2S, exists in an E configuration with respect to the C=N bond. The approximately planar 2H-chromene ring system [maximum deviation = 0.059 (1) Å] is inclined at a dihedral angle of 17.50 (5)° with respect to the mean plane through the thio­semicarbazide unit and an intra­molecular N—H⋯N hydrogen bond generates an S(5) ring. In the crystal structure, adjacent mol­ecules are linked by N—H⋯S hydrogen bonds, forming [010] chains built up from R 2 2(8) loops, such that each S atom accepts two such bonds. These chains are further inter­connected into sheets parallel to the ab plane via short Br⋯O inter­actions [3.0732 (13) Å] and a π–π aromatic stacking inter­action [3.7870 (8) Å] is also observed

3-{2-[2-(3-Hy­droxy­benzyl­idene)hydrazin-1-yl]-1,3-thia­zol-4-yl}-2H-chromen-2-one hemihydrate

In the title compound, C19H13N3O3S·0.5H2O, both organic mol­ecules (A and B) exist in E configurations with respect to the acyclic C=N bond and have similar overall conformations. In mol­ecule A, the essentially planar thia­zole ring [maximum deviation = 0.010 (2) Å] is inclined at inter­planar angles of 11.44 (10) and 32.50 (12)°, with the 2H-chromene ring system and the benzene ring, respectively. The equivalent values for mol­ecule B are 0.002 (2) Å, 7.71 (9) and 12.51 (12)°. In the crystal structure, neighbouring mol­ecules are inter­connected into infinite layers lying parallel to (010) by O—H⋯O, O—H⋯N, N—H⋯O and C—H⋯O hydrogen bonds. Further stabilization of the crystal structure is provided by weak inter­molecular C—H⋯π and π–π [centroid–centroid distance = 3.6380 (19) Å] inter­actions

Translating Pharmacogenomics: Challenges on the Road to the Clinic

Pharmacogenomics is one of the first clinical applications of the postgenomic era. It promises personalized medicine rather than the established “one size fits all” approach to drugs and dosages. The expected reduction in trial and error should ultimately lead to more efficient and safer drug therapy. In recent years, commercially available pharmacogenomic tests have been approved by the Food and Drug Administration (FDA), but their application in patient care remains very limited. More generally, the implementation of pharmacogenomics in routine clinical practice presents significant challenges. This article presents specific clinical examples of such challenges and discusses how obstacles to implementation of pharmacogenomic testing can be addressed