A Systematic Literature Review on Machine Learning in Shared Mobility

Shared mobility has emerged as a sustainable alternative to both private transportation and traditional public transport, promising to reduce the number of private vehicles on roads while offering users greater flexibility. Today, urban areas are home to a myriad of innovative services, including car-sharing, ride-sharing, and micromobility solutions like moped-sharing, bike-sharing, and e-scooter-sharing. Given the intense competition and the inherent operational complexities of shared mobility systems, providers are increasingly seeking specialized decision-support methodologies to boost operational efficiency. While recent research indicates that advanced machine learning methods can tackle the intricate challenges in shared mobility management decisions, a thorough evaluation of existing research is essential to fully grasp its potential and pinpoint areas needing further exploration. This paper presents a systematic literature review that specifically targets the application of Machine Learning for decision-making in Shared Mobility Systems. Our review underscores that Machine Learning offers methodological solutions to specific management challenges crucial for the effective operation of Shared Mobility Systems. We delve into the methods and datasets employed, spotlight research trends, and pinpoint research gaps. Our findings culminate in a comprehensive framework of Machine Learning techniques designed to bolster managerial decision-making in addressing challenges specific to Shared Mobility across various levels

Intradiscal Glucocorticoid Injection in Discogenic Back Pain and Influence on Modic Changes: A Systematic Review and Meta-analysis of RCTs.

BACKGROUND The benefit of intradiscal glucocorticoid injection (IGI) for discogenic low back pain (LBP) remains controversial. OBJECTIVES The objective of this study was to systematically assess and meta-analyze the efficacy of IGI compared with these control groups. STUDY DESIGN Systematic review and meta-analysis. METHODS A comprehensive literature search was performed screening PubMed and Embase through May 2022. Only randomized controlled trials (RCTs) comparing IGI to control groups in adult patients with discogenic lumbar back pain were included. A random effects model was used to pool mean differences of pain intensity (visual analaog scale [VAS] 0-100), and physical function assessed with the Oswestry Disability Index (ODI). Subgroup analyses were stratified by Modic magnetic resonance imaging findings. RESULTS Seven studies met inclusion criteria with a total of 626 patients. The short-term (= 6 months) follow-up. A subgroup analysis did not demonstrate an effect of Modic (type I) changes on the efficacy of IGI. LIMITATIONS A limited number of studies was available and consequently publication bias could not be evaluated using a funnel plot. Statistical heterogeneity was detected among the included studies. CONCLUSION We conclude that IGI reduces discogenic LBP intensity and improves physical function effectively at short-term follow-up, and continues to improve physical function at intermediate-term. However, 6 months posttreatment, outcomes are similar in comparison to the control groups. The type of Modic change does not appear to be related with the response to IGI. KEY WORDS Low back pain, lumbar back pain, intradiscal glucocorticoid injection, modic changes, meta-analysis

Severe dermatitis, multiple allergies, and metabolic wasting syndrome caused by a novel mutation in the N-terminal plakin domain of desmoplakin.

BackgroundSevere dermatitis, multiple allergies, and metabolic wasting (SAM) syndrome is a recently recognized syndrome caused by mutations in the desmoglein 1 gene (DSG1). To date, only 3 families have been reported.ObjectiveWe studied a new case of SAM syndrome known to have no mutations in DSG1 to detail the clinical, histopathologic, immunofluorescent, and ultrastructural phenotype and to identify the underlying molecular mechanisms in this rare genodermatosis.MethodsHistopathologic, electron microscopy, and immunofluorescent studies were performed. Whole-exome sequencing data were interrogated for mutations in desmosomal and other skin structural genes, followed by Sanger sequencing of candidate genes in the patient and his parents.ResultsNo mutations were identified in DSG1; however, a novel de novo heterozygous missense c.1757A>C mutation in the desmoplakin gene (DSP) was identified in the patient, predicting the amino acid substitution p.His586Pro in the desmoplakin polypeptide.ConclusionsSAM syndrome can be caused by mutations in both DSG1 and DSP. Knowledge of this genetic heterogeneity is important for both analysis of patients and genetic counseling of families. This condition and these observations reinforce the importance of heritable skin barrier defects, in this case desmosomal proteins, in the pathogenesis of atopic disease

Severe dermatitis, multiple allergies, and metabolic wasting syndrome caused by a novel mutation in the N-terminal plakin domain of desmoplakin

BackgroundSevere dermatitis, multiple allergies, and metabolic wasting (SAM) syndrome is a recently recognized syndrome caused by mutations in the desmoglein 1 gene (DSG1). To date, only 3 families have been reported.ObjectiveWe studied a new case of SAM syndrome known to have no mutations in DSG1 to detail the clinical, histopathologic, immunofluorescent, and ultrastructural phenotype and to identify the underlying molecular mechanisms in this rare genodermatosis.MethodsHistopathologic, electron microscopy, and immunofluorescent studies were performed. Whole-exome sequencing data were interrogated for mutations in desmosomal and other skin structural genes, followed by Sanger sequencing of candidate genes in the patient and his parents.ResultsNo mutations were identified in DSG1; however, a novel de novo heterozygous missense c.1757A>C mutation in the desmoplakin gene (DSP) was identified in the patient, predicting the amino acid substitution p.His586Pro in the desmoplakin polypeptide.ConclusionsSAM syndrome can be caused by mutations in both DSG1 and DSP. Knowledge of this genetic heterogeneity is important for both analysis of patients and genetic counseling of families. This condition and these observations reinforce the importance of heritable skin barrier defects, in this case desmosomal proteins, in the pathogenesis of atopic disease