Correction: Structural, magnetic and hyperthermia properties and their correlation in cobalt-doped magnetite nanoparticles.

[This corrects the article DOI: 10.1039/D1RA07407E.].

Structural, magnetic and hyperthermia properties and their correlation in cobalt-doped magnetite nanoparticles.

Cobalt doped magnetite nanoparticles (Co x Fe3-x O4 NPs) are investigated extensively because of their potential hyperthermia application. However, the complex interrelation among chemical compositions and particle size means their correlation with the magnetic and heating properties is not trivial to predict. Here, we prepared Co x Fe3-x O4 NPs (0 ≤ x ≤ 1) to investigate the effects of cobalt content and particle size on their magnetic and heating properties. A detailed analysis of the structural features indicated the similarity between the crystallite and particle sizes as well as their non-monotonic change with the increase of Co content. Magnetic measurements for the Co x Fe3-x O4 NPs (0 ≤ x ≤ 1) showed that the blocking temperature, the saturation magnetization, the coercivity, and the anisotropy constant followed a similar trend with a maximum at x = 0.7. Moreover, 57Fe Mössbauer spectroscopy adequately explained the magnetic behaviour, the anisotropy constant, and saturation magnetization of low Co content samples. Finally, our study shows that the relaxation loss is a primary contributor to the SAR in Co x Fe3-x O4 NPs with low Co contents as well as their potential application in magnetic hyperthermia.

Role of chemokines and cytokines in a reactivation model of arthritis in rats induced by injection with streptococcal cell walls.

Intraarticular injection of streptococcal cell wall (SCW) antigen followed by intravenous challenge results in a T cell-mediated monoarticular arthritis ill female Lewis rats. Initial studies showed that this reactivation response to intravenous SCW antigen is dependent on the presence of interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-alpha) and that the early phase of swelling is neutrophil-dependent. Neutrophil depletion or passive immunization with antibodies to P-selectin or macrophage inflammatory protein-2 reduced the intensity of ankle edema and the influx of neutrophils. After the first few days, however, the arthritic response is mediated primarily by mononuclear cells. Joint tissues showed up-regulation of mRNA for monocyte chemotactic protein-1 (MCP-1), which could be inhibited in part by anti-IL-4; treatment of rats with antibodies to IL-4 or MCP-1 significantly suppressed development of ankle edema and histopathological evidence of inflammation. Antibodies to interferon-gamma or IL-10 had no effect. Treatment with anti-MCP-1 also suppressed influx of (111)In-labeled T cells into the ankle joint. These data suggest that the late, mononuclear-dependent phase of SCW-induced arthritis in female Lewis rats requires cytokines that up-regulate MCP-1, which in turn may facilitate recruitment and extravasation of mononuclear cells into the joint.

Streptococcal cell wall-induced arthritis. Requirements for neutrophils, P-selectin, intercellular adhesion molecule-1, and macrophage-inflammatory protein-2.

Immune arthritis in rat ankle joints was induced by intra-articular injection of streptococcal cell was extract (SCW), followed 21 days later by i.v. injection of SCW. This results in a monoarticular arthritis characterized by an influx of neutrophils and mononuclear cells, a 35-fold increase in urinary excretion of 8-hydroxy-deoxyguanosine (8-OH-dGUA; an index of free radical production), ankle edema, and joint damage/destruction. Neutrophil depletion substantially reduced the intensity of ankle edema. Ab-induced blockade of P-selectin or ICAM-1 also reduced the intensity of ankle edema and the influx of neutrophils. Blockade of TNF-alpha or IL-1 resulted in nearly complete and persistent reduction in ankle edema and profound reductions in the accumulation of neutrophils and mononuclear cells in affected joints. Finally, blocking of macrophage-inflammatory protein-2 reduced ankle edema and neutrophil accumulation during the first 2 days after i.v. challenge with SCW. These data indicate that SCW-induced arthritis is neutrophil dependent and that the recruitment of neutrophils and subsequent joint edema requires ICAM-1, P-selectin, and macrophage-inflammatory protein-2, as well as TNF-alpha and IL-1.

Leukocyte contribution to parenchymal cell death in an experimental model of inflammation.

The relationship between leukocyte migration and parenchymal cell death in vivo remains poorly documented. Accordingly, cell killing in the rat mesentery, as recorded by propidium iodide staining, was investigated with an intravital approach. Superfusion of platelet-activating factor (PAF, 10(-8) M) or N-formyl-methionyl-leucyl-phenylalanine (fMLP, 10(-8) M) led to extensive leukocyte extravasation but no significant cell death. In contrast, pretreatment with 10(-8) M PAF or fMLP for 1 h, followed by superfusion of PAF in combination with fMLP (both at 10(-8) M) led to an increase in cell death. Mesenteric parenchymal cells but no endothelial cells were killed. Some of the dead cells were identified as granulocytes/monocytes that were already in the tissue at the start of the experiment. The incidence of cell death was lower but not eliminated when leukocyte migration was blocked with a monoclonal antibody against CD18. A xanthine oxidase inhibitor, BOF-4272, failed to diminish cell death, whereas a hydroxyl radical scavenger, dimethylthiourea, attenuated cell killing without an effect on the number of adhering and migrating leukocytes. These observations demonstrate that leukocytes serve as a factor in the killing of extravascular cells only after the development of a level of stimulation that differs from that required to induce a migratory stimulus into the extravascular space.

Transvascular and interstitial migration of neutrophils in rat mesentery.

OBJECTIVE: The consequential implications of the leukocyte-endothelial cell adhesion reaction, as well as the subsequent migratory activity of the leukocytes within the interstitium proper, are currently known only in general phenomenological terms. Our objective was to carry out a detailed quantitative analysis of transendothelial and interstitial migration. METHOD: We incorporated several new features, such as the video recording of time-lapse photography in conjunction with the time history of individual leukocytes under the influence of representative stimulators and inhibitors. The mesentery was suffused with the chemical activator N-formyl-met-leu-phe (fMLP, 5 x 10(-8) M) and histamine (10(-6) M) for periods up to 3 h. This leads to an attachment of neutrophils preferentially to the walls of small postcapillary venules followed by migration into the adjacent interstitium. RESULTS: The time interval between the initial neutrophil adhesion to the luminal side of the venules and their first appearance on the abluminal side of the venule wall was about 25 min. The time interval for the actual physical migration across the endothelium was only about 1-2 min. There was an initial increase in the number of neutrophils migrating across the wall per unit time after the application of fMLP. However, this effect then gradually decreased over the course of 1 h. In the extravascular tissue, the neutrophils appeared to migrate along random pathways with an average trajectory away from the venular wall. When histamine (1 microM) was applied topically in conjunction with fMLP, the overall migratory flux across the venular wall increased, although the cells migrated comparatively short distances into the interstitium. After pretreatment with phalloidin (25 micrograms/kg), an actin cross-linking agent, neutrophil adhesion and migration in response to fMLP stimulation was reduced. The mast cell stimulator 48/80 (25 mg/ml) resulted in rapid degranulation, which was accompanied by an insignificant increase in neutrophil diapedesis. After fMLP stimulation there was reduced neutrophil emigration in the presence of mast cell inhibitors, such as lodoxamide (1 microgram/kg) and ketotifin (microgram/kg). CONCLUSIONS: Our results demonstrate that both the endothelial cells and interstitial mast cells are involved in the rate of transvascular migration of leukocytes across postcapillary venules and into the interstitium.

The effects of frequency and duration of controlled passive mobilization on tendon healing.

This study was designed to determine the effects of frequency and duration of controlled passive motion on the healing flexor tendon following primary repair. Adult mongrel dogs were divided into two groups based on frequency of controlled passive motion. In one group, motion was applied manually at a frequency of 12 cycles/min for 5 min/day; in the other group, a continuous passive motion machine was used to apply motion at a lower frequency of 1 cycle/min for 60 min/day, making the number of cycles each day for both groups identical. Gliding function and tensile properties of repaired tendons were evaluated biomechanically at 3 and 6 weeks postoperatively. Results showed that gliding function in both groups was similar, but tensile properties, as represented by linear slope, ultimate load, and energy absorption, were significantly improved in the higher frequency group. It was concluded that frequency of controlled passive motion rehabilitation is a significant factor in accelerating the healing response following tendon repair, and higher frequency-controlled passive motion has a beneficial effect.