Biocompatible, porous hydrogels composed of aliphatic polyesters and poly(2-isopropenyl-2-oxazoline). Their application as scaffolds for bone tissue regeneration.

In this study, porous networks were efficiently prepared by crosslinking hydrophilic poly(2-isopropenyl-2-oxazoline) (PiPOx) with dicarboxylic polyesters (HOOC-PLA-COOH or HOOC-PCL-COOH) in the presence of sodium chloride as a water-soluble porogen. Importantly, by using a relatively simple synthetic protocol, the resulting spongy materials were freely formed to the desired size and shape while maintaining stable dimensions. According to the SEM data, the porous 3D structure can be altered by the pore dimensions, which are dependent on the porogen crystal size. After porosity characterization, the mechanical properties were also evaluated via uniaxial compression and tensile tests. The porous networks formed hydrogels with a high water absorption capacity. Finally, after showing cytocompatibility by the MTT assay, we also demonstrated the applicability of the porous hydrogels as scaffolds for cell cultivation. The presented results suggest that this type of hydrogels is a promising material for tissue engineering.

Helicobacter pylori components increase the severity of metabolic syndrome and its hepatic manifestations induced by a high fat diet.

The metabolic syndrome, often accompanied by hepatic manifestations, is a high-risk factor for developing cardiovascular disease. Patients with metabolic dysfunction associated with steatohepatic disease (MASDL) are at significant risk of developing coronary artery disease. Atherosclerosis is a systemic inflammatory disorder in which several factors, including dietary or infectious factors, can cause an inflammatory response. Helicobacter pylori (HP) bacteria have been implicated in the progression of proatherogenic vascular endothelial lesions, moreover, our previous study in an experimental in vivo model of Cavia porcellus showed that HP components and high-fat substances acted synergistically in promoting vascular endothelial inflammation, leading to an early onset of a proatherogenic environment. In the present study, our goal was to determine the contribution of HP components to the development of hepatic manifestations of metabolic syndrome in an experimental model. Our results showed that HP infection in animals exposed to a high-fat diet increased oxidative stress and lipid peroxidation, followed by endothelial lipid deposition, impaired endothelial apoptosis, cell lysis, and increased vascular stiffness. Finally, histopathological analysis of liver tissue showed signs of MASLD development in HP-infected animals fed a high-fat diet.