Unraveling Atopic Dermatitis: Insights into Pathophysiology, Therapeutic Advances, and Future Perspectives.

Atopic dermatitis (AD) is an inflammatory skin condition that frequently develops before the onset of allergic rhinitis or asthma. More than 10% of children are affected by this serious skin condition, which is painful for the sufferers. Recent research has connected the environment, genetics, the skin barrier, drugs, psychological factors, and the immune system to the onset and severity of AD. The causes and consequences of AD and its cellular and molecular origins are reviewed in this paper. The exploration of interleukins and their influence on the immunological pathway in AD has been facilitated by using relevant biomarkers in clinical trials. This approach enables the identification of novel therapeutic modalities, fostering the potential for targeted translational research within the realm of personalized medicine. This review focuses on AD's pathophysiology and the ever-changing therapeutic landscape. Beyond the plethora of biologic medications in various stages of approval or development, a range of non-biologic targeted therapies, specifically small molecules, have emerged. These include Janus kinase (JAK) inhibitors like Baricitinib, Upadacitinib, and Abrocitinib, thus expanding the spectrum of therapeutic options. This review also addresses the latest clinical efficacy data and elucidates the scientific rationale behind each targeted treatment for atopic dermatitis.

Tailoring the dimensionality of metal complexes via ligand modifications.

A series of CuII complexes obtained under the same reaction conditions has been analyzed to gain insight into the effect of the ligand composition on the final reaction product. Dipodal ligands containing N-donor imidazole rings and a benzene ring as a spacer with different numbers of methyl substituents on the aromatic rings were selected for the study such as 1,3-bis(imidazol-1-ylmethyl)benzene (L1), 1,3-bis(imidazol-1-ylmethyl)-5-methylbenzene (L2), 1,3-bis(imidazol-1-ylmethyl)-2,4,6-trimethylbenzene (L3), 1,3-bis(2-methylimidazol-1-ylmethyl)-2,4,6-trimethylbenzene (L4). L4 has not been reported previously and was synthesized for this study. The formed metal complexes show the presence of polymeric (ligand with no or one methyl substituent; 1-4), or discrete motifs (3- or 5-methyl substituents; 5-7). The new metal complexes 3, 5 and 6 were analyzed using single-crystal X-ray diffraction and powder diffraction. In addition, the structural analyses were supported by computational methods.

Solvent-induced polymorphism in dipodal N-donor ligands containing a biphenyl core.

Polymorph screenings for two related dipodal N-donor ligands containing a biphenyl core, namely 4,4'-bis(pyridin-4-ylmethyl)-1,1'-biphenyl (1) and 4,4'-bis(1H-imidazol-1-ylmethyl)-1,1'-biphenyl (2) were performed, and the new phases were isolated and their crystal structures analysed. Profiling included methods such as PXRD and thermal analysis. Hirshfeld surface analyses, as well as crystal lattice energy calculations provided deeper insight in the interplay of the intermolecular forces and the stability of the isolated phases. Furthermore, our studies revealed the presence of solvent-induced polymorphism, whereby the metastable phase is dominant upon crystallisation from THF (1a) and EtOH (2c). Upon heating, these phases transform into a more stable form, whereby the transformations were followed by PXRD studies (1, 2).