relictum exhibits very low genetic diversity in its Western Palearctic transmission area. This is likely the result of a recent introduction event or a selective sweep.The results corroborate earlier findings derived from a limited dataset that the globally transmitted malaria parasite P. relictum exhibits very low genetic diversity in its Western Palearctic transmission area. This is likely the result of a recent introduction event or a selective sweep. Brain ischemia compromises natural killer (NK) cell-mediated immune defenses by acting on neurogenic and intracellular pathways. Less is known about the posttranscriptional mechanisms that regulate NK cell activation and cytotoxicity after ischemic stroke. Using a NanoString nCounter® miRNA array panel, we explored the microRNA (miRNA) profile of splenic NK cells in mice subjected to middle cerebral artery occlusion. Differential gene expression and function/pathway analysis were applied to investigate the main functions of predicted miRNA target genes. miR-1224 inhibitor/mimics transfection and passive transfer of NK cells were performed to confirm the impact of miR-1224 in NK cells after brain ischemia. We observed striking dysregulation of several miRNAs in response to ischemia. Among those miRNAs, miR-1224 markedly increased 3 days after ischemic stroke. Transfection of miR-1224 mimics into NK cells resulted in suppression of NK cell activity, while an miR-1224 inhibitor enhanced NK cell activity and cytotoxicity, especially in the periphery. Passive transfer of NK cells treated with an miR-1224 inhibitor prevented the accumulation of a bacterial burden in the lungs after ischemic stroke, suggesting an enhanced immune defense of NK cells. Mizoribine The transcription factor Sp1, which controls cytokine/chemokine release by NK cells at the transcriptional level, is a predicted target of miR-1224. The inhibitory effect of miR-1224 on NK cell activity was blocked in Sp1 knockout mice. These findings indicate that miR-1224 may serve as a negative regulator of NK cell activation in an Sp1-dependent manner; this mechanism may be a novel target to prevent poststroke infection specifically in the periphery and preserve immune defense in the brain.These findings indicate that miR-1224 may serve as a negative regulator of NK cell activation in an Sp1-dependent manner; this mechanism may be a novel target to prevent poststroke infection specifically in the periphery and preserve immune defense in the brain.The purpose of this letter to the Editor is to report some shortcomings in the statistical analysis and variable grouping in the recent publication of the article "Clinical outcomes of chondroblastoma treated using synthetic bone substitute risk factors for developing radiographic joint degeneration," and to further explore some of the factors that may affect the clinical prognosis of chondroblastoma patients. We also suggest future prospective controlled studies with large samples to improve the limitations encountered by Outani et al. (World J Surg Oncol. 18(1)47, 2020) due to insufficient statistical power of variables and lack of controls.Pruritus is one of the most common symptoms experienced by neoplastic patients. The pathogenesis of neoplastic itch is complex and multifactorial and could be due to an unbalanced production of humoral mediators by altered immune effector cells. IL-31 is a pro-inflammatory cytokine produced by CD4 + T helper cells. The aim of this review was to evaluate the role of this Th2 cytokine and its receptor IL-31RA, in the onset of neoplastic pruritus. We analysed scientific literature looking for the most relevant original articles linking IL-31to itch in oncologic diseases. Interleukin-31 seems to be a main itch mediator in several hematologic disease such as Cutaneous T cells lymphomas. In these patients IL-31 was positively linked to itch level, and IL-31 matched with disease stage. IL-31 seems to play an important role in the signalling pathway involved in pruritus, but it is also suggested to play a proinflammatory and immunomodulatory role which could play a part in the progression of the neoplastic disease. Further studies will be fundamental in facing pruritus in oncologic patients, since this problem compromise their quality of life worsening an already critic picture. Gelatinous zooplankton can be difficult to preserve morphologically due to unique physical properties of their cellular and acellular components. The relatively large volume of mesoglea leads to distortion of the delicate morphology and poor sample integrity in specimens prepared with standard aldehyde or alcohol fixation techniques. Similar challenges have made it difficult to extend standard laboratory methods such as in situ hybridization to larger juvenile ctenophores, hampering studies of late development. We have found that a household water repellant glass treatment product commonly used in laboratories, Rain-X®, alone or in combination with standard aldehyde fixatives, greatly improves morphological preservation of such delicate samples. We present detailed methods for preservation of ctenophores of diverse sizes compatible with long-term storage or detection and localization of target molecules such as with immunohistochemistry and in situ hybridization and show that this fixation might be broadly useful for preservation of other delicate marine specimens. This new method will enable superior preservation of morphology in gelatinous specimens for a variety of downstream goals. Extending this method may improve the morphological fidelity and durability of museum and laboratory specimens for other delicate sample types.This new method will enable superior preservation of morphology in gelatinous specimens for a variety of downstream goals. Extending this method may improve the morphological fidelity and durability of museum and laboratory specimens for other delicate sample types. Previous work in HEK-293 cells demonstrated the importance of amino acid-induced mTORC1 translocation to the lysosomal surface for stimulating mTORC1 kinase activity and protein synthesis. This study tested the conservation of this amino acid sensing mechanism in human skeletal muscle by treating subjects with chloroquine-a lysosomotropic agent that induces in vitro and in vivo lysosome dysfunction. mTORC1 signaling and muscle protein synthesis (MPS) were determined in vivo in a randomized controlled trial of 14 subjects (10M, 4F; 26 ± 4year) that ingested 10g of essential amino acids (EAA) after receiving 750mg of chloroquine (CHQ, n = 7) or serving as controls (CON, n = 7; no chloroquine). Additionally, differentiated C2C12 cells were used to assess mTORC1 signaling and myotube protein synthesis (MyPS) in the presence and absence of leucine and the lysosomotropic agent chloroquine. mTORC1, S6K1, 4E-BP1 and rpS6 phosphorylation increased in both CON and CHQ 1h post EAA ingestion (P < 0.05). MPS increased similarly in both groups (CON, P = 0.