Size-dependent magnetic and magnetothermal properties of gadolinium silicide nanoparticles

Gadolinium silicide (Gd₅Si₄) nanoparticles are an interesting class of materials due to their high magnetization, low Curie temperature, low toxicity in biological environments and their multifunctional properties. We report the magnetic and magnetothermal properties of gadolinium silicide (Gd₅Si₄) nanoparticles prepared by surfactant-assisted ball milling of arc melted bulk ingots of the compound. Using different milling times and speeds, a wide range of crystallite sizes (13–43 nm) could be produced and a reduction in Curie temperature (T_C) from 340 K to 317 K was achieved, making these nanoparticles suitable for self-controlled magnetic hyperthermia applications. The magnetothermal effect was measured in applied AC magnetic fields of amplitude 164–239 Oe and frequencies 163–519 kHz. All particles showed magnetic heating with a strong dependence of the specific absorption rate (SAR) on the average crystallite size. The highest SAR of 3.7 W g⁻¹ was measured for 43 nm sized nanoparticles of Gd₅Si₄. The high SAR and low T_C, (within the therapeutic range for magnetothermal therapy) makes the Gd₅Si₄ behave like self-regulating heat switches that would be suitable for self-controlled magnetic hyperthermia applications after biocompatibility and cytotoxicity tests.

Gadolinium silicide (Gd₅Si₄) nanoparticles prepared by surfactant-assisted ball milling exhibit a size-dependent reduction in magnetic ordering temperature and a high magnetothermal effect making them suitable for magnetic hyperthermia applications.     

Effect of mouthwashes on the discoloration of bracket-bonded tooth surfaces: an in vitro study

Clinical Oral Investigations - This in vitro study aimed to investigate the color changes of the bracket-bonded tooth surfaces after the use of 4 different mouthwashes. A total of 100 human...     

Convalescent plasma therapy in patients with COVID-19

IntroductionPassive antibody therapy has been used to immunize vulnerable people against infectious agents. In this study, we aim to investigate the efficacy of convalescent plasma (CP) in the treatment of severe and critically ill patients diagnosed with COVID-19.MethodThe data of severe or critically ill COVID-19 patients who received anti-SARS-CoV-2 antibody-containing CP along with the antiviral treatment (n = 888) and an age-gender, comorbidity, and other COVID-19 treatments matched severe or critically ill COVID-19 patients at 1:1 ratio (n = 888) were analyzed retrospectively.ResultsDuration in the intensive care unit (ICU), the rate of mechanical ventilation (MV) support and vasopressor support were lower in CP group compared with the control group (p = 0.001, p = 0.02, p = 0.001, respectively). The case fatality rate (CFR) was 24.7 % in the CP group, and it was 27.7 % in the control group. Administration of CP 20 days after the COVID-19 diagnosis or COVID-19 related symptoms were associated with a higher rate of MV support compared with the first 3 interval groups (≤5 days, 6?10 days, 11?15 days) (p=0.001).ConclusionCP therapy seems to be effective for a better course of COVID-19 in severe and critically ill patients.     

Brain Neuronal Degeneration Caused by Episodic Alcohol Intoxication in Rats: Effects of Nimodipine, 6,7-Dinitro-quinoxaline-2,3-dione, and MK-801

Rats repeatedly intoxicated with alcohol (ethanol, three times daily) over a 4-day period display neuronal degeneration in the dentate gyrus; entorhinal, piriform, insular, orbital, and perirhinal cortices; and in the olfactory nerve fibers and terminals in the olfactory bulb. Postulating a role for excitotoxicity, we have attempted to prevent the degeneration using antagonists that are neuroprotective in this type of brain damage. In an initial study, continuous subcutaneous infusion of a high dose of the glutamate/NMDA receptor antagonist MK-801 (2 mg/kg/day) by itself caused extensive neuronal degeneration in several brain regions and severe behavioral intoxication that precluded survival if combined with high blood alcohol levels (～300 mg/dl). Moreover, the lower, nonneurotoxic blood alcohol levels (～150 mg/dl) that were compatible with survival worsened the MK-801-induced brain damage. In a subsequent experiment, daily intraperitoneal injections of a lower dose of MK-801 (1 mg/kg/day) resulted in no MK-801 toxicity and, when combined with neurotoxic levels of alcohol, no reduction in alcohol-induced neurotoxicity. Nimodipine, a voltage-gated Ca²⁺ channel blocker, reduced the neuronal damage in the dentate gyrus, but greatly increased it in the piriform cortex when administered intragastrically at 600 mg/kg/day; it provided no protection from alcohol-dependent degeneration when given intragastrically at 100 mg/kg/day. Continuous intracere-broventricular delivery of 0.24 to 0.29 mg/day of 6,7-dinitro-quinoxa-line-2,3-dione, a glutamate/α-amino-3-hydroxy-5-methyl-4-isoxazole receptor antagonist, failed to diminish alcohol-dependent neuronal damage in any brain region. We conclude that brain damage from episodic “binge” alcohol intoxication is not primarily mediated by excitotoxic mechanisms, implying that other, nonexcrtotoxic pathophysiological mechanisms, are involved. Furthermore, MK-801, far from protecting from the alcohol-induced damage, at high doses causes widespread neuropathology that is significantly potentiated by alcohol.