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<p><b> Provides the foundations and principles needed for addressing the various challenges of developing smart cities </b> <p> Smart cities are emerging as a priority for research and development across the world. They open up significant opportunities in several areas, such as economic growth, health, wellness, energy efficiency, and transportation, to promote the sustainable development of cities. This book provides the basics of smart cities, and it examines the possible future trends of this technology. <i>Smart Cities: Foundations, Principles, and Applications</i> provides a systems science perspective in presenting the foundations and principles that span multiple disciplines for the development of smart cities. <p> Divided into three parts&mdash;foundations, principles, and applications&mdash;<i>Smart Cities</i> addresses the various challenges and opportunities of creating smart cities and all that they have to offer. It also covers smart city theory modeling and simulation, and examines case studies of existing smart cities from all around the world. In addition, the book: <ul> <li>Addresses how to develop a smart city and how to present the state of the art and practice of them all over the world</li> <li>Focuses on the foundations and principles needed for advancing the science, engineering, and technology of smart cities&mdash;including system design, system verification, real-time control and adaptation, Internet of Things, and test beds</li> <li>Covers applications of smart cities as they relate to smart transportation/connected vehicle (CV) and Intelligent Transportation Systems (ITS) for improved mobility, safety, and environmental protection</li> </ul> <br> <p><i> Smart Cities: Foundations, Principles, and Applications</i> is a welcome reference for the many researchers and professionals working on the development of smart cities and smart city-related industries.

IgA nephropathy (IgAN) in children is no longer considered a rare and benign disease but a nephritis with different presentations and various outcomes. The decision to initiate a treatment and the therapeutic choice depend on the individual risk of progression. The Kidney Disease: Improving Global Outcomes (KDIGO) clinical guidelines in 2012 considered that the risk factors for progression of IgAN were similar in both children and adults and suggested in some conditions to follow the adult schedules. In 2017 a KDIGO Controversies Conference on management and treatment of glomerular diseases decided not to include an update in children with IgAN since the level of evidence of treatments in children was too scarce. Children can follow the indications for adults as far as the disease is similar in the various ages. This review is aimed at discussing why the KDIGO guidelines are poorly suitable to treat children with IgAN, and there is a need to develop new prediction models for progression of IgAN in children to guide selection of the cases to be treated. The identification of different risk levels in children with IgAN may personalize the choice of available drugs and support the use of new targeted therapies.

IgA Nephropathy (IgAN) is the most prevalent glomerular disease worldwide. Complement system activation is crucial in its pathogenesis. Few studies correlated serum C3 and C4 with disease activity and prognosis. This retrospective study investigated the prognostic value of serum complement at the time of diagnosis in patients with IgAN. Specifically we evaluated whether adding serum C3 and C4 levels to established predictive models-one based on variables related to chronic kidney disease (CKD) progression and another incorporating variables from the International IgA Prediction Tool (IntIgAPT)-enhances the accuracy of outcome prediction. A composite renal outcome was defined as 50% decline in eGFR or onset of kidney failure. 101 patients were stratified according to baseline C3 levels in three groups (Low, Medium and High). During a median follow-up of 54 months, the Low group exhibited higher incidence of primary outcome (16.3 events vs 2.9 and 1.7 events × 100 pts/year, p = 0.0026). Model-1 (M1), consisting of CKD progression variables, and Model-3 (M3), comprising IntIgANPT variables, were implemented with baseline C3 and C4 to create Model-2 (M2) and Model-4 (M4), respectively. M2 demonstrated better predictive performance over M1, showing higher discrimination (lower AIC and BIC, higher C-index and NR2). Similarly, M4 outperformed M3, showing enhanced outcome prediction when C3 and C4 levels were added. Implementation of serum C3 and C4 can enhance prediction accuracy of already-validated prognostic models in IgAN. Lower C3 and higher C4 levels were associated with poorer prognosis, highlighting a more 'Complement-Pathic' subset of patients.

Background Cell invasion is a hallmark of metastatic cancer, leading to unfavorable clinical outcomes. In this study, we established two highly invasive lung cancer cell models (A549-i8 and H1299-i8) and identified mesoderm-specific transcript (MEST) as a novel invasive regulator of lung cancer. We aim to characterize its biological function and clinical significance in lung cancer metastasis. Methods Transwell invasion assay was performed to establish high-invasive lung cancer cell model. Immunohistochemistry (IHC) was used to detect MEST expression in tumor tissues. Mass spectrometry and bioinformatic analyses were used to identify MEST-regulated proteins and binding partners. Co-immunoprecipitation assay was performed to detect the interaction of MEST and VCP. The biological functions of MEST were investigated in vitro and in vivo. Immunofluorescence staining was conducted to explore the colocalization of MEST and VCP. Results MEST overexpression promoted metastasis of lung cancer cells in vivo and in vitro by activating NF-κB signaling. MEST increased the interaction between VCP and IκBα, which accelerated IκBα degradation and NF-κB activation. Such acceleration was abrogated by VCP silencing, indicating that MEST is an upstream activator of the VCP/IκBα/NF-κB signaling pathway. Furthermore, high expressions of MEST and VCP were associated with poor survival of lung cancer patients. Conclusion Collectively, these results demonstrate that MEST plays an important role in driving invasion and metastasis of lung cancer by interacting with VCP to coordinate the IκBα/NF-κB pathway. Targeting the MEST/VCP/IκBα/NF-κB signaling pathway may be a promising strategy to treat lung cancer.

Background IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide. While studies have primarily focused on identifying risk factors for disease progression, very few data exist on the likelihood of achieving complete recovery from the disease. Methods We conducted a single-center retrospective study on all consecutive patients with biopsy-proven IgAN diagnosed between 1986 and 2018 in our pediatric center. Biopsies were classified according to the MEST-C Oxford classification score. “Complete clinical remission” was defined as the absence of proteinuria, hematuria, and hypertension in patients with normal kidney function who had been off therapy for more than 2 years. Results Overall, 153 patients with age at onset of 10.6 ± 4 years were enrolled in the study. Of these, 41 achieved “complete clinical remission.” The estimated probability of complete clinical remission at 10 years was 43% (95%CI 33–54). However, seven patients relapsed within 10 years. Multivariable analysis showed that higher age at onset (HR 0.89, 95%CI 0.80–0.98, p  = 0.017) and segmental glomerulosclerosis lesions (HR 0.28, 95%CI 0.10–0.79, p  = 0.017) decreased significantly the chances of achieving complete clinical remission. Immunosuppressive therapy was not significantly associated with clinical outcomes. Conclusions Approximately one-third of patients with pediatric-onset IgAN achieve prolonged remission, in particular, very young children at disease onset without sclerotic glomerular lesions. Longer term follow-up is needed to assess if these patients have achieved permanent remission. Graphical abstract A higher resolution version of the Graphical abstract is available as Supplementary information

The imprinted isoform of the Mest gene in mice is involved in key mammalian traits such as placental and fetal growth, maternal care and mammary gland maturation. The imprinted isoform has a distinct differentially methylated region (DMR) at its promoter in eutherian mammals but in marsupials, there are no differentially methylated CpG islands between the parental alleles. Here, we examined similarities and differences in the MEST gene locus across mammals using a marsupial, the tammar wallaby, a monotreme, the platypus, and a eutherian, the mouse, to investigate how imprinting of this gene evolved in mammals. By confirming the presence of the short isoform in all mammalian groups (which is imprinted in eutherians), this study suggests that an alternative promoter for the short isoform evolved at the MEST gene locus in the common ancestor of mammals. In the tammar, the short isoform of MEST shared the putative promoter CpG island with an antisense lncRNA previously identified in humans and an isoform of a neighbouring gene CEP41. The antisense lncRNA was expressed in tammar sperm, as seen in humans. This suggested that the conserved lncRNA might be important in the establishment of MEST imprinting in therian mammals, but it was not imprinted in the tammar. In contrast to previous studies, this study shows that MEST is not imprinted in marsupials. MEST imprinting in eutherians, therefore must have occurred after the marsupial-eutherian split with the acquisition of a key epigenetic imprinting control region, the differentially methylated CpG islands between the parental alleles.

The Oxford Classification was proposed as an independent prognostic indicator in IgA nephropathy (IgAN). However, most studies on the subject focus on adults instead of children. Using a meta-analysis to appraise the predictive roles of the Oxford classification for the prognosis of pediatric patients with IgAN. All cohort studies regarding the analysis of the association between poor kidney-related prognosis (GFR categories G2-G5) according to the Kidney Disease Improving Global Outcomes (KDIGO) Guideline in pediatric patients with IgAN and five pathologic lesions in the Oxford Classification were included. Hazard ratios (HRs) regarding the association between the Oxford classification and prognosis of pediatric patients with IgAN were synthesized using random effect models. The risk of bias in studies was assessed based on the Newcastle-Ottawa scale. Fourteen articles were included with 5679 IgAN patients and 710 endpoint outcome events occurred. M1 was associated with a higher risk of poor kidney-related prognosis compared with M0, pooled HR (1.79; 95%CI, 1.46-2.19;  < 0.001, random effect model). S1 and T1 or T2 increased the risk of poor kidney-related prognosis (pooled HR, 2.13; 95%CI, 1.68-2.70;  < 0.001; pooled HR, 2.64; 95%CI, 1.81-3.86;  < 0.001, respectively, estimated by random effect model). Compared with C0, C1, or C2 was also associated with an increased risk of poor kidney-related prognosis in the subgroup analysis of Asian and other populations. Evidence to indicate that E1 increased the risk of poor kidney-related prognosis was marginal.

There is evidence that expression and methylation of the imprinted paternally expressed gene 1/mesoderm-specific transcript homologue (PEG1/MEST) gene may be affected by assisted reproductive technologies (ARTs) and infertility. In this study, we sought to assess the imprinting status of the MEST gene in a large cohort of in vitro-derived human preimplantation embryos, in order to characterise potentially adverse effects of ART and infertility on this locus in early human development. Embryonic genomic DNA from morula or blastocyst stage embryos was screened for a transcribed AflIII polymorphism in MEST and imprinting analysis was then performed in cDNA libraries derived from these embryos. In 10 heterozygous embryos, MEST expression was monoallelic in seven embryos, predominantly monoallelic in two embryos, and biallelic in one embryo. Screening of cDNA derived from 61 additional human preimplantation embryos, for which DNA for genotyping was unavailable, identified eight embryos with expression originating from both alleles (biallelic or predominantly monoallelic). In some embryos, therefore, the onset of imprinted MEST expression occurs during late preimplantation development. Variability in MEST imprinting was observed in both in vitro fertilization and intracytoplasmic sperm injection-derived embryos. Biallelic or predominantly monoallelic MEST expression was not associated with any one cause of infertility. Characterisation of the main MEST isoforms revealed that isoform 2 was detected in early development and was itself variably imprinted between embryos. To our knowledge, this report constitutes the largest expression study to date of genomic imprinting in human preimplantation embryos and reveals that for some imprinted genes, contrasting imprinting states exist between embryos.

Assisted reproductive technologies are fertility treatments used by subfertile couples to conceive their biological child. Although generally considered safe, these pregnancies have been linked to genomic imprinting disorders, including Beckwith–Wiedemann and Silver–Russell Syndromes. Silver–Russell Syndrome is a growth disorder characterized by pre- and post-natal growth retardation. The Mest imprinted domain is one candidate region on chromosome 7 implicated in Silver–Russell Syndrome. We have previously shown that maintenance of imprinted methylation was disrupted by superovulation or embryo culture during pre-implantation mouse development. For superovulation, this disruption did not originate in oogenesis as a methylation acquisition defect. However, in comparison to other genes, Mest exhibits late methylation acquisition kinetics, possibly making Mest more vulnerable to perturbation by environmental insult. In this study, we present a comprehensive evaluation of the effects of superovulation and in vitro culture on genomic imprinting at the Mest gene. Superovulation resulted in disruption of imprinted methylation at the maternal Mest allele in blastocysts with an equal frequency of embryos having methylation errors following low or high hormone treatment. This disruption was not due to a failure of imprinted methylation acquisition at Mest in oocytes. For cultured embryos, both the Fast and Slow culture groups experienced a significant loss of maternal Mest methylation compared to in vivo-derived controls. This loss of methylation was independent of development rates in culture. These results indicate that Mest is more susceptible to imprinted methylation maintenance errors compared to other imprinted genes.