Computational shelf-life dating : complex systems approaches to food quality and safety

Shelf-life is defined as the time that a product is acceptable and meets the consumers expectations regarding food quality. It is the result of the conjunction of all services in production, distribution, and consumption. Shelf-life dating is one of the most difficult tasks in food engineering. Market pressure has lead to the implementation of shelf-life by sensory analyses, which may not reflect the full quality spectra. Moreover, traditional methods for shelf-life dating and small-scale distribution chain tests cannot reproduce in a laboratory the real conditions of storage, distribution, and consumption on food quality. Today, food engineers are facing the challenges to monitor, diagnose, and control the quality and safety of food products. The advent of nanotechnology, multivariate sensors, information systems, and complex systems will revolutionize the way we manage, distribute, and consume foods. The informed consumer demands foods, under the legal standards, at low cost, high standards of nutritional, sensory, and health benefits. To accommodate the new paradigms, we herein present a critical review of shelf-life dating approaches with special emphasis in computational systems and future trends on complex systems methodologies applied to the prediction of food quality and safety.Fundo Europeu de Desenvolvimento Regional (FEDER) - Programa POS-ConhecimentoFundação para a Ciência e a Tecnologia (FCT) - SFRH/BPD/26133/2005, SFRH/ BPD/20735/200

Pan-cancer whole-genome analyses of metastatic solid tumours

Contains fulltext : 215492.pdf (publisher's version ) (Open Access)Metastatic cancer is a major cause of death and is associated with poor treatment efficacy. A better understanding of the characteristics of late-stage cancer is required to help adapt personalized treatments, reduce overtreatment and improve outcomes. Here we describe the largest, to our knowledge, pan-cancer study of metastatic solid tumour genomes, including whole-genome sequencing data for 2,520 pairs of tumour and normal tissue, analysed at median depths of 106x and 38x, respectively, and surveying more than 70 million somatic variants. The characteristic mutations of metastatic lesions varied widely, with mutations that reflect those of the primary tumour types, and with high rates of whole-genome duplication events (56%). Individual metastatic lesions were relatively homogeneous, with the vast majority (96%) of driver mutations being clonal and up to 80% of tumour-suppressor genes being inactivated bi-allelically by different mutational mechanisms. Although metastatic tumour genomes showed similar mutational landscape and driver genes to primary tumours, we find characteristics that could contribute to responsiveness to therapy or resistance in individual patients. We implement an approach for the review of clinically relevant associations and their potential for actionability. For 62% of patients, we identify genetic variants that may be used to stratify patients towards therapies that either have been approved or are in clinical trials. This demonstrates the importance of comprehensive genomic tumour profiling for precision medicine in cancer

Who wants to talk to terrorists?

Interviewing terrorists or former terrorists has become an increasingly popular research method in terrorism studies. What terrorists say can shed light on motivations, decision-making processes and operational details that without first-hand testimony could only be inferred. In this chapter, a selection of these studies is reviewed alongside a consideration of global trends in terrorism and developments in terrorism research

SARS-CoV-2 Omicron-B.1.1.529 leads to widespread escape from neutralizing antibody responses

On 24th November 2021, the sequence of a new SARS-CoV-2 viral isolate Omicron-B.1.1.529 was announced, containing far more mutations in Spike (S) than previously reported variants. Neutralization titers of Omicron by sera from vaccinees and convalescent subjects infected with early pandemic Alpha, Beta, Gamma, or Delta are substantially reduced, or the sera failed to neutralize. Titers against Omicron are boosted by third vaccine doses and are high in both vaccinated individuals and those infected by Delta. Mutations in Omicron knock out or substantially reduce neutralization by most of the large panel of potent monoclonal antibodies and antibodies under commercial development. Omicron S has structural changes from earlier viruses and uses mutations that confer tight binding to ACE2 to unleash evolution driven by immune escape. This leads to a large number of mutations in the ACE2 binding site and rebalances receptor affinity to that of earlier pandemic viruses

Evidence of escape of SARS-CoV-2 variant B.1.351 from natural and vaccine-induced sera

The race to produce vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) began when the first sequence was published, and this forms the basis for vaccines currently deployed globally. Independent lineages of SARS-CoV-2 have recently been reported: UK, B.1.1.7; South Africa, B.1.351; and Brazil, P.1. These variants have multiple changes in the immunodominant spike protein that facilitates viral cell entry via the angiotensin-converting enzyme-2 (ACE2) receptor. Mutations in the receptor recognition site on the spike are of great concern for their potential for immune escape. Here, we describe a structure-function analysis of B.1.351 using a large cohort of convalescent and vaccinee serum samples. The receptor-binding domain mutations provide tighter ACE2 binding and widespread escape from monoclonal antibody neutralization largely driven by E484K, although K417N and N501Y act together against some important antibody classes. In a number of cases, it would appear that convalescent and some vaccine serum offers limited protection against this variant