A review on impedimetric immunosensors for pathogen and biomarker detection

Since the discovery of antibiotics in the first quarter of the twentieth century, their use has been the principal approach to treat bacterial infection. Modernized medicine such as cancer therapy, organ transplantation or advanced major surgeries require effective antibiotics to manage bacterial infections. However, the irresponsible use of antibiotics along with the lack of development has led to the emergence of antimicrobial resistance which is considered a serious global threat due to the rise of multidrug-resistant bacteria (Wang et al. in Antibiotic resistance: a rundown of a global crisis, pp. 1645–1658, 2018). Currently employed diagnostics techniques are microscopy, colony counting, ELISA, PCR, RT-PCR, surface-enhanced Raman scattering and others. These techniques provide satisfactory selectivity and sensitivity (Joung et al. in Sens Actuators B Chem 161:824–831, 2012). Nevertheless, they demand specialized personnel and expensive and sophisticated machinery which can be labour-intensive and time-consuming, (Malvano et al. in Sensors (Switzerland) 18:1–11, 2018; Mantzila et al. in Anal Chem 80:1169–1175, 2008). To get around these problems, new technologies such as biosensing and lab-on-a-chip devices have emerged in the last two decades. Impedimetric immunosensors function by applying electrochemical impedance spectroscopy to a biosensor platform using antibodies or other affinity proteins such as Affimers (Tiede et al. in Elife 6(c):1–35, 2017) or other binding proteins (Weiss et al. in Electrochim Acta 50:4248–4256, 2005) as bioreceptors, which provide excellent sensitivity and selectivity. Pre-enrichment steps are not required and this allows miniaturization and low-cost. In this review different types of impedimetric immunosensors are reported according to the type of electrode and their base layer materials, either self-assembled monolayers or polymeric layers, composition and functionalization for different types of bacteria, viruses, fungi and disease biomarkers. Additionally, novel protein scaffolds, both antibody derived and non-antibody derived, used to specifically target the analyte are considered

Correlation between magnetic interactions and domain structure in A1 FePt ferromagnetic thin films

We have investigated the relationship between the domain structure and the magnetic interactions in a series of FePt ferromagnetic thin films of varying thickness. As-made films grow in the magnetically soft and chemically disordered A1 phase that may have two distinct domain structures. Above a critical thickness $d_{cr}\sim 30$ nm the presence of an out of plane anisotropy induces the formation of stripes, while for $d<d_{cr}$ planar domains occur. Magnetic interactions have been characterized using the well known DCD-IRM remanence protocols, $\delta M$ plots, and magnetic viscosity measurements. We have observed a strong correlation between the domain configuration and the sign of the magnetic interactions. Planar domains are associated with positive exchange-like interactions, while stripe domains have a strong negative dipolar-like contribution. In this last case we have found a close correlation between the interaction parameter and the surface dipolar energy of the stripe domain structure. Using time dependent magnetic viscosity measurements, we have also estimated an average activation volume for magnetic reversal, $\langle V_{ac}\rangle \sim 1.37\times 10^{4}$ nm$^{3},$ which is approximately independent of the film thickness or the stripe period.Comment: 25 pages, 11 figure

Zur Lehre des Morbus Addisonii

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Distribución de las precipitaciones en Rafaela y Esperanza, Santa Fe

p.85-89Para determinar el modelo estadístico que provea el mejor ajuste para la distribución de precipitaciones en las localidades de Rafaela y Esperanza (Santa Fe), se utilizaron los registros de precipitaciones mensuales de Esperanza (1929 - 1975) y Rafaela (1937 - 1998). Las distribuciones empíricas se compararon con las teóricas Normal y Logaritmica (LN), Normal Raíz Cúbica (NR) y Gamma Incompleta (GI). Según la prueba de Lilliefors, NR y GI presentaron el mejor ajuste para todos los meses (p menor 0,01). LN presentó buen ajuste (p menor 0,05) para todas las estaciones del año, excepto el invierno

Repression of Esophageal Neoplasia and Inflammatory Signaling by Anti-miR-31 Delivery In Vivo.

BACKGROUND: Overexpression of microRNA-31 (miR-31) is implicated in the pathogenesis of esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary zinc deficiency. Using a rat model that recapitulates features of human ESCC, the mechanism whereby Zn regulates miR-31 expression to promote ESCC is examined. METHODS: To inhibit in vivo esophageal miR-31 overexpression in Zn-deficient rats (n = 12-20 per group), locked nucleic acid-modified anti-miR-31 oligonucleotides were administered over five weeks. miR-31 expression was determined by northern blotting, quantitative polymerase chain reaction, and in situ hybridization. Physiological miR-31 targets were identified by microarray analysis and verified by luciferase reporter assay. Cellular proliferation, apoptosis, and expression of inflammation genes were determined by immunoblotting, caspase assays, and immunohistochemistry. The miR-31 promoter in Zn-deficient esophagus was identified by ChIP-seq using an antibody for histone mark H3K4me3. Data were analyzed with t test and analysis of variance. All statistical tests were two-sided. RESULTS: In vivo, anti-miR-31 reduced miR-31 overexpression (P = .002) and suppressed the esophageal preneoplasia in Zn-deficient rats. At the same time, the miR-31 target Stk40 was derepressed, thereby inhibiting the STK40-NF-κΒ-controlled inflammatory pathway, with resultant decreased cellular proliferation and activated apoptosis (caspase 3/7 activities, fold change = 10.7, P = .005). This same connection between miR-31 overexpression and STK40/NF-κΒ expression was also documented in human ESCC cell lines. In Zn-deficient esophagus, the miR-31 promoter region and NF-κΒ binding site were activated. Zn replenishment restored the regulation of this genomic region and a normal esophageal phenotype. CONCLUSIONS: The data define the in vivo signaling pathway underlying interaction of Zn deficiency and miR-31 overexpression in esophageal neoplasia and provide a mechanistic rationale for miR-31 as a therapeutic target for ESCC