Galectins-Potential Therapeutic Targets for Neurodegenerative Disorders.

Advancements in medicine have increased the longevity of humans, resulting in a higher incidence of chronic diseases. Due to the rise in the elderly population, age-dependent neurodegenerative disorders are becoming increasingly prevalent. The available treatment options only provide symptomatic relief and do not cure the underlying cause of the disease. Therefore, it has become imperative to discover new markers and therapies to modulate the course of disease progression and develop better treatment options for the affected individuals. Growing evidence indicates that neuroinflammation is a common factor and one of the main inducers of neuronal damage and degeneration. Galectins (Gals) are a class of ß-galactoside-binding proteins (lectins) ubiquitously expressed in almost all vital organs. Gals modulate various cellular responses and regulate significant biological functions, including immune response, proliferation, differentiation, migration, and cell growth, through their interaction with glycoproteins and glycolipids. In recent years, extensive research has been conducted on the Gal superfamily, with Gal-1, Gal-3, and Gal-9 in prime focus. Their roles have been described in modulating neuroinflammation and neurodegenerative processes. In this review, we discuss the role of Gals in the causation and progression of neurodegenerative disorders. We describe the role of Gals in microglia and astrocyte modulation, along with their pro- and anti-inflammatory functions. In addition, we discuss the potential use of Gals as a novel therapeutic target for neuroinflammation and restoring tissue damage in neurodegenerative diseases.

Drying-Induced Self-Similar Assembly of Megamolecular Polysaccharides through Nano and Submicron Layering.

We propose a self-similar assembly to generate planar orientation of megamolecular polysaccharides on the nanometer scale and submicron scale. Evaporating the aqueous liquid crystalline (LC) solution on a planar air-LC interface induces polymer layering by self-assembly and rational action of macroscopic capillary forces between the layers. To clarify the mechanisms of nanometer- and submicron-scale layering, the polymer films are investigated by electron microscopy.

Photoexpansion of Biobased Polyesters: Mechanism Analysis by Time-Resolved Measurements of an Amorphous Polycinnamate Hard Film.

Cinnamate-based polyesters were synthesized, including poly(4-hydroxycinnamic acid), poly(4-hydroxy-3-methoxycinnamic acid), poly(3-hydroxycinnamic acid) (P3HCA), and hyperbranched poly(3,4-dihydroxycinnamic acid) (PdHCA). These materials were further processed into hard and dry membranes by casting and underwent photoreactions by ultraviolet (UV) light. The photodeformation behavior of the linear and hyperbranched polyester containing membranes with cinnamate derivatives in the main chain was observed macroscopically and microscopically. The PdHCA and P3HCA membranes were amorphous and exhibited photodeformations. The PdHCA surface visibly contracts, which is a typically observed phenomenon in photoresponsive polymers; however, the P3HCA surface showed a unique photoexpansion behavior. Time-resolution infrared spectroscopy of the P3HCA film revealed trans-to-cis isomerism in the polymer main chains that bent convexly as a result of photoexpansion of the UV-irradiated regions. Furthermore, photomasking created a micropattern on the P3HCA film, which supported the photoexpansion mechanism of the P3HCA film.

Sox2: A Regulatory Factor in Tumorigenesis and Metastasis.

The transcription factor Sox2 plays an important role in various phases of embryonic development, including cell fate and differentiation. These key regulatory functions are facilitated by binding to specific DNA sequences in combination with partner proteins to exert their effects. Recently, overexpression and gene amplification of Sox2 has been associated with tumor aggression and metastasis in various cancer types, including breast, prostate, lung, ovarian and colon cancer. All the different roles for Sox2 involve complicated regulatory networks consisting of protein-protein and protein-nucleic acid interactions. Their involvement in the EMT modulation is possibly enabled by Wnt/ ß-catenin and other signaling pathways. There are number of in vivo models which show Sox2 association with increased cancer aggressiveness, resistance to chemo-radiation therapy and decreased survival rate suggesting Sox2 as a therapeutic target. This review will focus on the different roles for Sox2 in metastasis and tumorigenesis. We will also review the mechanism of action underlying the cooperative Sox2- DNA/partner factors binding where Sox2 can be potentially explored for a therapeutic opportunity to treat cancers.