This work is devoted to unbuffered and buffered water treatment by means of atmospheric pressure cold plasma of electrical discharges. The interest in the activation of these two liquids by plasma-induced, gaseous-phase chemistry ranges over a wide area of potential applications and interdisciplinary scientific fields. These include biology, medicine, sanitation, environmental restoration, agriculture, etc. Atmospheric pressure cold plasma is here produced in the form of a plasma jet and set into physical contact with the liquid specimens. The operational window of the treatment, in terms of plasma reactivity, is determined by means of UV-NIR optical emission spectroscopy, and the treated liquids are probed in a variety of respects. Evaporation rate, temperature, acidity and basicity, resistivity, and oxidation-reduction potential are measured as a function of the treatment time, either in-situ or ex-situ. The formation of principal reactive oxygen species, i.e., ^•OH, H₂O₂ and ${\mathrm{O}}_2^{•-}$, with a plasma jet mean power lower than 400 mW, is eventually demonstrated and their concentration is measured with original methods borrowed from the biology field. The experimental results are linked to reports published over the last ten years, which are compiled in a brief but meaningful review.

The critical arguments for radiofrequency radiation exposure limits are currently based on the principle that radio frequencies (RF) and electromagnetic fields (EMFs) are non-ionising, and their exposure limits are even 100-fold lower than those emitted from the Sun in the whole RF-EMF spectrum. Nonetheless, this argument has been challenged by numerous experimental and theoretical studies on the diverse biological effects of RF-EMF at much lower power density (W/m²) levels than today’s exposing limits. On the other hand, less attention has been given to counterarguments based on the differences in the physics concepts underlying man-made versus natural electromagnetic radiation (EMR) and on the fact that man’s biology has been adapted to the natural EMR levels reaching Earth’s surface at single EMF wavelengths, which are the natural limits of man’s exposure to EMFs. The article highlights the main points of interaction of natural and man-made radiation with biomatter and reveals the physical theoretical background that explains the effects of man-made microwave radiation on biological matter. Moreover, the article extends its analysis on experimental quantum effects, establishing the “ionising-like” effects of man-made microwave radiation on biological matter.

Obesity in children and adolescents has been associated with oxidative stress (OS). The lipid hydroperoxides (LOOH) and the malondialdehyde (MDA) and thiobarbituric reactive substances (TBARS) that oxidatively modify proteins (Pr) (i.e., PrMDA and PrTBARS, respectively) represent markers of OS-associated lipid peroxidation. We aimed to assess OS in children and adolescents with obesity using—for the first time—markers involved in the early and late lipid oxidation process. LOOH, PrMDA, and PrTBARS were investigated in 41 children and adolescents with obesity and 31 controls. Obesity was defined as BMI > 95% for age and sex. The PrMDA/PrTBARS pair, which reflects a late peroxidation stage, was found to be significantly high (39%/180%) in children and adolescents with obesity compared to controls (p < 0.001). Similarly, the early LOOH peroxidation stage marker was increased by 30%. The studied OS parameters were not influenced by sex or age. Our study introduces LOOH, PrTBARS, and PrMDA as markers for evaluating OS in children and adolescents with obesity. LOOH, PrTBARS, and PrMDA may also hold promise as prognostic markers for potential obesity-associated long-term complications.

Introduction: Tourniquet use in total knee arthroplasty (TKA) can cause ischaemia-reperfusion (I-R) injury via oxidative stress. This study evaluated whether combined administration of the antioxidant N-acetylcysteine (NAC) and the iron-chelator Deferiprone can mitigate oxidative damage and improve clinical outcomes. Materials and methods: Twenty TKA patients were randomized into two groups, one group receiving NAC (600 mg, 6 h pre-op) and Deferiprone (1000 mg, 2 h pre-op) (intervention group) and the other group serving as placebo (control). Lipid hydroperoxides (LOOH) and protein malondialdehyde (PrMDA) were measured from quadriceps muscle tissue samples at 5 min (T1) and 40 min (T2) after tourniquet inflation, and 5 min after deflation (T3). Blood markers including serum ferritin, white blood cell (WBC) count, and polymorphonuclear neutrophils (PMNs) were assessed along with tissue PrMDA and LOOH as primary outcome measurements, while pain scores and knee flexion were recorded postoperatively as secondary outcome measurements. Results: LOOH levels were significantly lower in the intervention group at T2 and T3. PrMDA levels showed no significant differences. Ferritin levels rose by 69% in controls vs. 18% in the intervention group. WBC and PMNs normalized faster, with reduced pain and improved range of motion in the intervention group. Conclusion: The attenuation of LOOH elevation, the faster PMN deactivation, the inhibition of ferritin release from the cells along with the improved clinical outcomes suggest that combined NAC and Deferiprone administration may reduce tourniquet-related oxidative stress and inflammation, enhancing early recovery in TKA patients.

Thyrotropin (TSH) suppression is required in the management of patients with papillary thyroid carcinoma (PTC) to improve their outcomes, inevitably causing iatrogenic thyrotoxicosis. Nevertheless, the evidence supporting this practice remains limited and weak, and in vitro studies examining the mitogenic effects of TSH in cancerous cells used supraphysiological doses of bovine TSH, which produced conflicting results. Our study explores, for the first time, the impact of human recombinant thyrotropin (rh-TSH) on human PTC cell lines (K1 and TPC-1) that were transformed to overexpress the thyrotropin receptor (TSHR). The cells were treated with escalating doses of rh-TSH under various conditions, such as the presence or absence of insulin. The expression levels of TSHR and thyroglobulin (Tg) were determined, and subsequently, the proliferation and migration of both transformed and non-transformed cells were assessed. Under the conditions employed, rh-TSH was not adequate to induce either the proliferation or the migration rate of the cells, while Tg expression was increased. Our experiments indicate that clinically relevant concentrations of rh-TSH cannot induce proliferation and migration in PTC cell lines, even after the overexpression of TSHR. Further research is warranted to dissect the underlying molecular mechanisms, and these results could translate into better management of treatment for PTC patients.