In the past, water homeostasis of the brain was understood as a certain quantitative equilibrium of water content between intravascular, interstitial, and intracellular spaces governed mostly by hydrostatic effects i.e., strictly by physical laws. The recent achievements in molecular bioscience have led to substantial changes in this regard. Some new concepts elaborate the idea that all compartments involved in cerebral fluid homeostasis create a functional continuum with an active and precise regulation of fluid exchange between them rather than only serving as separate fluid receptacles with mere passive diffusion mechanisms, based on hydrostatic pressure. According to these concepts, aquaporin-4 (AQP4) plays the central role in cerebral fluid homeostasis, acting as a water channel protein. The AQP4 not only enables water permeability through the blood-brain barrier but also regulates water exchange between perivascular spaces and the rest of the glymphatic system, described as pan-cerebral fluid pathway interlacing macroscopic cerebrospinal fluid (CSF) spaces with the interstitial fluid of brain tissue. With regards to this, AQP4 makes water shift strongly dependent on active processes including changes in cerebral microcirculation and autoregulation of brain vessels capacity. In this paper, the role of the AQP4 as the gatekeeper, regulating the water exchange between intracellular space, glymphatic system (including the so-called neurovascular units), and intravascular compartment is reviewed. In addition, the new concepts of brain edema as a misbalance in water homeostasis are critically appraised based on the newly described role of AQP4 for fluid permeation. Finally, the relevance of these hypotheses for clinical conditions (including brain trauma and stroke) and for both new and old therapy concepts are analyzed.

Tissue engineering is an interdisciplinary field of science that has developed very intensively in recent years. The first part of this review describes materials with medical and dental applications from the following groups: metals, polymers, ceramics, and composites. Both positive and negative sides of their application are presented from the point of view of medical application and mechanical properties. A variety of techniques for the manufacture of biomedical components are presented in this review. The main focus of this work is on additive manufacturing and 3D printing, as these modern techniques have been evaluated to be the best methods for the manufacture of medical and dental devices. The second part presents devices for skull bone reconstruction. The materials from which they are made and the possibilities offered by 3D printing in this field are also described. The last part concerns dental transitional implants (scaffolds) for guided bone regeneration, focusing on polylactide–hydroxyapatite nanocomposite due to its unique properties. This section summarises the current knowledge of scaffolds, focusing on the material, mechanical and biological requirements, the effects of these devices on the human body, and their great potential for applications.

Previous research and clinical reports have shown that some individuals after COVID-19 infection may demonstrate symptoms of so-called brain fog, manifested by cognitive impairment and disorganization in behavior. Meanwhile, in several other conditions, related to intellectual function, a specific pattern of changes in electric brain activity, as recorded by quantitative electroencephalography (QEEG) has been documented. We hypothesized, that in post-COVID brain fog, the subjective complaints may be accompanied by objective changes in the QEEG profile. In order to test this hypothesis, we have performed an exploratory study on the academic staff of our University with previous records of QEEG originating in the pre-COVID-19 era. Among them, 20 subjects who revealed neurological problems in the cognitive sphere (confirmed as covid fog/brain fog by a clinical specialist) after COVID-19 infection were identified. In those individuals, QEEG was performed. We observed, that opposite to baseline QEEG records, increased Theta and Alpha activity, as well as more intensive sensimotor rhythm (SMR) in C4 (right hemisphere) in relation to C3 (left hemisphere). Moreover, a visible increase in Beta 2 in relation to SMR in both hemispheres could be documented. Summarizing, we could demonstrate a clear change in QEEG activity patterns in individuals previously not affected by COVID-19 and now suffering from post-COVID-19 brain fog. These preliminary results warrant further interest in delineating their background. Here, both neuroinflammation and psychological stress, related to Sars-CoV2-infection may be considered. Based on our observation, the relevance of QEEG examination as a supportive tool for post-COVID clinical workup and for monitoring the treatment effects is also to be explored.

Decompressive craniectomy has been widely used in patients with head trauma. The randomized clinical trial on an early decompression (DECRA) demonstrated that craniectomy did not improve the neurological outcome, in contrast to previous animal experiments. The goal of our study was to analyze the effect of decompressive craniectomy in a murine model of head injury. Male mice were assigned into the following groups: sham, decompressive craniectomy, closed head injury (CHI), and CHI followed by craniectomy. At 24 h post-trauma, animals underwent the Neurological Severity Score test (NSS) and Beam Balance Score test (BBS). At the same time point, magnetic resonance imaging was performed, and volume of edema and contusion was assessed, followed by histopathological analysis. According to NSS, animals undergoing both trauma and craniectomy presented the most severe neurological impairment. Also, balancing time was reduced in this group compared with sham animals. Both edema and contusion volume were increased in the trauma and craniectomy group compared with sham animals. Histopathological analysis showed that all animals that underwent trauma presented substantial neuronal loss. In animals treated with craniectomy after trauma, a massive increase of edema with hemorrhagic transformation of contusion was documented. Decompressive craniectomy applied after closed head injury in mice leads to additional structural and functional impairment. The surgical decompression via craniectomy promotes brain edema formation and contusional blossoming in our model. This additive effect of combined mechanical and surgical trauma may explain the results of the DECRA trial and should be explored further in experiments.