Remote sensing and modeling of mosquito abundance and habitats in Coastal Virginia, USA

The increase in mosquito populations following extreme weather events poses a major threat to humans because of mosquitoes’ ability to carry disease-causing pathogens, particularly in low-lying, poorly drained coastal plains vulnerable to tropical cyclones. In areas with reservoirs of disease, mosquito abundance information can help to identify the areas at higher risk of disease transmission. Using a Geographic Information System (GIS), mosquito abundance is predicted across the City of Chesapeake, Virginia. The mosquito abundance model uses mosquito light trap counts, a habitat suitability model, and dynamic environmental variables (temperature and precipitation) to predict the abundance of the species Culiseta melanura, as well as the combined abundance of the ephemeral species, Aedes vexans and Psorophora columbiae, for the year 2003. Remote sensing techniques were used to quantify environmental variables for a potential habitat suitability index for the mosquito species. The goal of this study was to produce an abundance model that could guide risk assessment, surveillance, and potential disease transmission. Results highlight the utility of integrating field surveillance, remote sensing for synoptic landscape habitat distributions, and dynamic environmental data for predicting mosquito vector abundance across low-lying coastal plains. Limitations of mosquito trapping and multi-source geospatial environmental data are highlighted for future spatial modeling of disease transmission risk

Use of graphene as protection film in biological environments

Corrosion of metal in biomedical devices could cause serious health problems to patients. Currently ceramics coating materials used in metal implants can reduce corrosion to some extent with limitations. Here we proposed graphene as a biocompatible protective film for metal potentially for biomedical application. We confirmed graphene effectively inhibits Cu surface from corrosion in different biological aqueous environments. Results from cell viability tests suggested that graphene greatly eliminates the toxicity of Cu by inhibiting corrosion and reducing the concentration of Cu(2+) ions produced. We demonstrated that additional thiol derivatives assembled on graphene coated Cu surface can prominently enhance durability of sole graphene protection limited by the defects in graphene film. We also demonstrated that graphene coating reduced the immune response to metal in a clinical setting for the first time through the lymphocyte transformation test. Finally, an animal experiment showed the effective protection of graphene to Cu under in vivo condition. Our results open up the potential for using graphene coating to protect metal surface in biomedical application

Cholesterol Sulfotransferase SULT2B1b Modulates Sensitivity to Death Receptor Ligand TNFα in Castration-Resistant Prostate Cancer

Cholesterol sulfotransferase, SULT2B1b, has been demonstrated to modulate both androgen receptor activity and cell growth properties. However, the mechanism(s) by which SULT2B1b alters these properties within prostate cancer cells has not been described. Furthermore, specific advantages of SULT2B1b expression in prostate cancer cells is not understood. In these studies, single-cell mRNA sequencing (scRNA-seq) was conducted to compare the transcriptomes of SULT2B1b knockdown (KD) versus Control KD LNCaP cells. Over 2,000 differentially expressed (DE) genes were identified along with alterations in numerous canonical pathways, including the death receptor signaling pathway. The studies herein demonstrate that SULT2B1b KD increases tumor necrosis factor alpha (TNF) expression in prostate cancer cells and results in NF-κB activation in a TNF-dependent manner. More importantly, SULT2B1b KD significantly enhances TNF-mediated apoptosis in both TNF-sensitive LNCaP cells and TNF-resistant C4–2 cells. Overexpression of SULT2B1b in LNCaP cells also decreases sensitivity to TNF-mediated cell death, suggesting that SULT2B1b modulates pathways dictating the TNF sensitivity capacity of prostate cancer cells. Probing human prostate cancer patient datasets further support this work by providing evidence that SULT2B1b expression is inversely correlated with TNF-related genes, including TNF, CD40LG, FADD, and NFKB1. Together, these data provide evidence that SULT2B1b expression in prostate cancer cells enhances resistance to TNF and may provide a growth advantage. In addition, targeting SULT2B1b may induce an enhanced therapeutic response to TNF treatment in advanced prostate cancer

Use of graphene as protection film in biological environments

Corrosion of metal in biomedical devices could cause serious health problems to patients. Currently ceramics coating materials used in metal implants can reduce corrosion to some extent with limitations. Here we proposed graphene as a biocompatible protective film for metal potentially for biomedical application. We confirmed graphene effectively inhibits Cu surface from corrosion in different biological aqueous environments. Results from cell viability tests suggested that graphene greatly eliminates the toxicity of Cu by inhibiting corrosion and reducing the concentration of Cu2+ ions produced. We demonstrated that additional thiol derivatives assembled on graphene coated Cu surface can prominently enhance durability of sole graphene protection limited by the defects in graphene film. We also demonstrated that graphene coating reduced the immune response to metal in a clinical setting for the first time through the lymphocyte transformation test. Finally, an animal experiment showed the effective protection of graphene to Cu under in vivo condition. Our results open up the potential for using graphene coating to protect metal surface in biomedical application

Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Cholesterol accumulates in prostate lesions and has been linked to prostate cancer (PCa) incidence and progression. However, how accumulated cholesterol contributes to PCa development and progression is not completely understood. Cholesterol sulfate (CS), the primary sulfonation product of cholesterol sulfotransferase (SULT2B1b), accumulates in human prostate adenocarcinoma and precancerous prostatic intraepithelial neoplasia (PIN) lesions compared to normal regions of the same tissue sample. Given the enhanced accumulation of CS in these lesions, it was hypothesized that SULT2B1b-mediated production of CS provides a growth advantage to these cells. To address this, PCa cells with RNAi-mediated knockdown (KD) of SULT2B1b were used to assess the impact on cell growth and survival. SULT2B1b is expressed and functional in a variety of prostate cells and the data demonstrate that SULT2B1b KD, in LNCaP and other androgen-responsive (VCaP and C4-2) cells, results in decreased cell growth/viability and induces cell death. SULT2B1b KD also decreases androgen receptor (AR) activity and expression at mRNA and protein levels. While AR overexpression has no impact on SULT2B1b KD-mediated cell death, addition of exogenous androgen is able to partially rescue the growth inhibition induced by SULT2B1b KD in LNCaP cells. These results suggest that SULT2B1b positively regulates the AR either through alterations in ligand availability or by interaction with critical co-regulators that influence AR activity

Folate Receptor Beta Designates Immunosuppressive Tumor-Associated Myeloid Cells That Can Be Reprogrammed with Folate-Targeted Drugs

Although immunotherapies of tumors have demonstrated promise for altering the progression of malignancies, immunotherapies have been limited by an immunosuppressive tumor microenvironment (TME) that prevents infiltrating immune cells from performing their anticancer functions. Prominent among immunosuppressive cells are myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages (TAM) that inhibit T cells via release of immunosuppressive cytokines and engagement of checkpoint receptors. Here, we explore the properties of MDSCs and TAMs from freshly isolated mouse and human tumors and find that an immunosuppressive subset of these cells can be distinguished from the nonimmunosuppressive population by its upregulation of folate receptor beta (FRβ) within the TME and its restriction to the TME. This FRβ+ subpopulation could be selectively targeted with folate-linked drugs. Delivery of a folate-targeted TLR7 agonist to these cells (i) reduced their immunosuppressive function, (ii) increased CD8+ T-cell infiltration, (iii) enhanced M1/M2 macrophage ratios, (iv) inhibited tumor growth, (v) blocked tumor metastasis, and (vi) improved overall survival without demonstrable toxicity. These data reveal a broadly applicable strategy across tumor types for reprogramming MDSCs and TAMs into antitumorigenic immune cells using a drug that would otherwise be too toxic to administer systemically. The data also establish FRβ as the first marker that distinguishes immunosuppressive from nonimmunosuppressive subsets of MDSCs and TAMs. Because all solid tumors accumulate MDSCs and TAMs, a general strategy to both identify and reprogram these cells should be broadly applied in the characterization and treatment of multiple tumors

Interobserver reliability of classification and characterization of proximal humeral fractures: a comparison of two and three-dimensional CT

Interobserver reliability for the classification of proximal humeral fractures is limited. The aim of this study was to test the null hypothesis that interobserver reliability of the AO classification of proximal humeral fractures, the preferred treatment, and fracture characteristics is the same for two-dimensional (2-D) and three-dimensional (3-D) computed tomography (CT). Members of the Science of Variation Group--fully trained practicing orthopaedic and trauma surgeons from around the world--were randomized to evaluate radiographs and either 2-D CT or 3-D CT images of fifteen proximal humeral fractures via a web-based survey and respond to the following four questions: (1) Is the greater tuberosity displaced? (2) Is the humeral head split? (3) Is the arterial supply compromised? (4) Is the glenohumeral joint dislocated? They also classified the fracture according to the AO system and indicated their preferred treatment of the fracture (operative or nonoperative). Agreement among observers was assessed with use of the multirater kappa (κ) measure. Interobserver reliability of the AO classification, fracture characteristics, and preferred treatment generally ranged from "slight" to "fair." A few small but statistically significant differences were found. Observers randomized to the 2-D CT group had slightly but significantly better agreement on displacement of the greater tuberosity (κ = 0.35 compared with 0.30, p < 0.001) and on the AO classification (κ = 0.18 compared with 0.17, p = 0.018). A subgroup analysis of the AO classification results revealed that shoulder and elbow surgeons, orthopaedic trauma surgeons, and surgeons in the United States had slightly greater reliability on 2-D CT, whereas surgeons in practice for ten years or less and surgeons from other subspecialties had slightly greater reliability on 3-D CT. Proximal humeral fracture classifications may be helpful conceptually, but they have poor interobserver reliability even when 3-D rather than 2-D CT is utilized. This may contribute to the similarly poor interobserver reliability that was observed for selection of the treatment for proximal humeral fractures. The lack of a reliable classification confounds efforts to compare the outcomes of treatment methods among different clinical trials and reports

Publisher Correction: On the issue of transparency and reproducibility in nanomedicine

© 2019, Springer Nature Limited. In the version of this Correspondence originally published, Christine Dufès was incorrectly written as Christine Dufés. This has been corrected in the online versions of the Correspondence

On the issue of transparency and reproducibility in nanomedicine.

Following our call to join in the discussion over the suitability of implementing a reporting checklist for bio-nano papers, the community responds