Amyloid diseases are global epidemics characterized by the accumulative deposits of cross-beta amyloid fibrils and plaques. Despite decades of intensive research, few solutions are available for the diagnosis, treatment, and prevention of these debilitating diseases. Since the early work on the interaction of human β2-microglobulin and nanoparticles by Linse et al. in 2007, the field of amyloidosis inhibition has gradually evolved into a new frontier in nanomedicine offering numerous interdisciplinary research opportunities, especially for materials, chemistry and biophysics. In this review we summarise, for the first time, the in vitro and in vivo models employed thus far in the field of anti-amyloidosis nanomedicines. Based on this systematic summary, we bring forth the notion that, due to the complex and often overlapping physiopathologies of amyloid diseases, there is a crucial need for the appropriate use of in vitro and in vivo models for validating novel anti-amyloidosis nanomedicines, and there is a crucial need for the development of new animal models that reflect the behavioural, symptomatic and cross-talk hallmarks of amyloid diseases such as Alzheimer’s (AD), Parkinson’s (PD) diseases and type 2 diabetes (T2DM).Three dimensional (3D) DNA walkers hold great potential in serving as an ideal candidate for signal transduction and amplification in bio-assays. However, the autonomous operation of 3D DNA walkers inside living cells is still few and far between, which could be attributed to the lack of suitable driving forces and moderate efficiency in terms of the cellular uptake of such complex 3D DNA components. Herein, a newly updated autonomously operated and highly integrated 3D DNA walker on Au nanoparticles (Au NPs)/zeolitic imidazolate framework-8 (ZIF-8) was activated in a tumor microenviroment and its signal amplified assay capability in living cells was demonstrated using miRNA as a sensing model biomolecule. Specifically, we assembled a 3D DNA motor, including Zn2+-dependent DNAzyme and substrates on the AuNPs grafted on ZIF-8. After being delivered into a living cell, ZIF-8 was efficiently degraded in the tumor microenvironment (low pH value), locally releasing the Zn2+ and DNA motor. Then, a self-sufficient DNA motor autonomously performed the bio-analytical task of imaging miRNA-10b, with a low detection limit of 34 pM. Also, such self-sufficient 3D walkers allowed real-time imaging of MDA-MB-231 cells by intracellular operation. This method demonstrates the self-sufficient 3D DNA motor’s bioanalytical application in living cells which may inspire various other biological applications including gene delivery, therapy, etc.Causal gene networks model the flow of information within a cell. Reconstructing causal networks from omics data is challenging because correlation does not imply causation. When genomics and transcriptomics data from a segregating population are combined, genomic variants can be used to orient the direction of causality between gene expression traits. Instrumental variable methods use a local expression quantitative trait locus (eQTL) as a randomized instrument for a gene’s expression level, and assign target genes based on distal eQTL associations. Mediation-based methods additionally require that distal eQTL associations are mediated by the source gene. A detailed comparison between these methods has not yet been conducted, due to the lack of a standardized implementation of different methods, the limited sample size of most multi-omics datasets, and the absence of ground-truth networks for most organisms. Rhapontigenin inhibitor Here we used Findr, a software package providing uniform implementations of instrumental variable, men expression. Mediation suggests a new candidate gene, DNM1, for a hotspot on Chr XII, whereas instrumental variable methods could not distinguish between multiple genes located within the hotspot. In conclusion, causal inference from genomics and transcriptomics data is a powerful approach for reconstructing causal gene networks, which could be further improved by the development of methods to control for residual correlations in mediation analyses, and for genomic linkage and pleiotropic effects from transcriptional hotspots in instrumental variable analyses.Malaria is a life-threatening epidemic disease with half of the world’s population at risk. Although its incidence rate has fallen since 2010, this ratio dramatically stalled between 2014 and 2018. New fast and optimized tools in vaccine analysis and seroconversion testing are critically needed. We developed a clinical diagnostic device based on piezo-actuated nanoresonators that perform as quantitative in situ calibrated nano-bio sensors for specific detection of multiple target molecules in serum samples. The immunoassay successfully diagnoses humoral immune responses induced by malaria vaccine candidates and reveals the timeline and stage of the infection. We applied the newly developed strategy to a variety of different samples, from pure antibody/vaccine solutions, to blood samples from clinical trials on both naïve and pre-exposed malaria volunteers from sub-Saharan countries. Our nanomechanical assay provides a direct one-step label-free quantitative immunoassay that is on par with the gold-standard, multi-step enzyme-linked immunosorbent assay (ELISA). We achieve a limit of detection of few pg ml-1, or sub-pM concentrations. The 6 μl sample volume allows more than 50 experiments from one finger prick. Furthermore, we simultaneously detected multiple analytes by differential functionalization of multiple sensors in parallel. The inherent differential read-out with in situ controls reduces false positive results. Due to the faster turnaround time, the minimal volume required and the automatized handling system, this technique has great potential for miniaturization and routine diagnostics in pandemic emergencies.An unprecedented Ru(ii)-catalyzed Csp2-H bond activation and annulation reaction of phenylindazolones with diaryl-substituted alkynes and dialkyl-substituted alkynes provided efficient routes for the construction of all-carbon quaternary-centered indolo[1,2-a]quinazolinones and quaternary carbon-centered indazolo[1,2-a]indazolones, respectively. The indolo[1,2-a]quinazolinones were fomed via Csp2-H activation, alkyne insertion and a 1,2-phenyl shift. Indazolo[1,2-a]indazolones were formed through a cascade reaction via the formation of exocyclic double bonds containing indolo[1,2-a]quinazolinones.