Cyber-physical LPG debutanizer distillation columns: machine-learning-based soft sensors for product quality monitoring

Summarization: Refineries execute a series of interlinked processes, where the product of one unit serves as the input to another process. Potential failures within these processes affect the quality of the end products, operational efficiency, and revenue of the entire refinery. In this context, implementation of a real-time cognitive module, referring to predictive machine learning models, enables the provision of equipment state monitoring services and the generation of decision-making for equipment operations. In this paper, we propose two machine learning models: (1) to forecast the amount of pentane (C5) content in the final product mixture; (2) to identify if C5 content exceeds the specification thresholds for the final product quality. We validate our approach using a use case from a real-world refinery. In addition, we develop a visualization to assess which features are considered most important during feature selection, and later by the machine learning models. Finally, we provide insights on the sensor values in the dataset, which help to identify the operational conditions for using such machine learning models.Παρουσιάστηκε στο: Applied Science

Disruption of ALX1 Causes Extreme Microphthalmia and Severe Facial Clefting: Expanding the Spectrum of Autosomal-Recessive ALX-Related Frontonasal Dysplasia

We present an autosomal-recessive frontonasal dysplasia (FND) characterized by bilateral extreme microphthalmia, bilateral oblique facial cleft, complete cleft palate, hypertelorism, wide nasal bridge with hypoplasia of the ala nasi, and low-set, posteriorly rotated ears in two distinct families. Using Affymetrix 250K SNP array genotyping and homozygosity mapping, we mapped this clinical entity to chromosome 12q21. In one of the families, three siblings were affected, and CNV analysis of the critical region showed a homozygous 3.7 Mb deletion containing the ALX1 (CART1) gene, which encodes the aristaless-like homeobox 1 transcription factor. In the second family we identified a homozygous donor-splice-site mutation (c.531+1G > A) in the ALX1 gene, providing evidence that complete loss of function of ALX1 protein causes severe disruption of early craniofacial development. Unlike loss of its murine ortholog, loss of human ALX1 does not result in neural-tube defects; however, it does severely affect the orchestrated fusion between frontonasal, nasomedial, nasolateral, and maxillary processes during early-stage embryogenesis. This study further expands the spectrum of the recently recognized autosomal-recessive ALX-related FND phenotype in humans