A novel application of deep learning with image cropping: a smart city use case for flood monitoring

© 2020, The Author(s). Event monitoring is an essential application of Smart City platforms. Real-time monitoring of gully and drainage blockage is an important part of flood monitoring applications. Building viable IoT sensors for detecting blockage is a complex task due to the limitations of deploying such sensors in situ. Image classification with deep learning is a potential alternative solution. However, there are no image datasets of gullies and drainages. We were faced with such challenges as part of developing a flood monitoring application in a European Union-funded project. To address these issues, we propose a novel image classification approach based on deep learning with an IoT-enabled camera to monitor gullies and drainages. This approach utilises deep learning to develop an effective image classification model to classify blockage images into different class labels based on the severity. In order to handle the complexity of video-based images, and subsequent poor classification accuracy of the model, we have carried out experiments with the removal of image edges by applying image cropping. The process of cropping in our proposed experimentation is aimed to concentrate only on the regions of interest within images, hence leaving out some proportion of image edges. An image dataset from crowd-sourced publicly accessible images has been curated to train and test the proposed model. For validation, model accuracies were compared considering model with and without image cropping. The cropping-based image classification showed improvement in the classification accuracy. This paper outlines the lessons from our experimentation that have a wider impact on many similar use cases involving IoT-based cameras as part of smart city event monitoring platforms

SEDLIN forms homodimers: characterisation of SEDLIN mutations and their interactions with transcription factors MBP1, PITX1 and SF1

BACKGROUND SEDLIN, a 140 amino acid subunit of the Transport Protein Particle (TRAPP) complex, is ubiquitously expressed and interacts with the transcription factors c-myc promoter-binding protein 1 (MBP1), pituitary homeobox 1 (PITX1) and steroidogenic factor 1 (SF1). SEDLIN mutations cause X-linked spondyloepiphyseal dysplasia tarda (SEDT). METHODOLOGY/PRINCIPAL FINDINGS We investigated the effects of 4 missense (Asp47Tyr, Ser73Leu, Phe83Ser and Val130Asp) and the most C-terminal nonsense (Gln131Stop) SEDT-associated mutations on interactions with MBP1, PITX1 and SF1 by expression in COS7 cells. Wild-type SEDLIN was present in the cytoplasm and nucleus and interacted with MBP1, PITX1 and SF1; the SEDLIN mutations did not alter these subcellular localizations or the interactions. However, SEDLIN was found to homodimerize, and the formation of dimers between wild-type and mutant SEDLIN would mask a loss in these interactions. A mammalian SEDLIN null cell-line is not available, and the interactions between SEDLIN and the transcription factors were therefore investigated in yeast, which does not endogenously express SEDLIN. This revealed that all the SEDT mutations, except Asp47Tyr, lead to a loss of interaction with MBP1, PITX1 and SF1. Three-dimensional modelling studies of SEDLIN revealed that Asp47 resides on the surface whereas all the other mutant residues lie within the hydrophobic core of the protein, and hence are likely to affect the correct folding of SEDLIN and thereby disrupt protein-protein interactions. CONCLUSIONS/SIGNIFICANCE Our studies demonstrate that SEDLIN is present in the nucleus, forms homodimers and that SEDT-associated mutations cause a loss of interaction with the transcription factors MBP1, PITX1 and SF1.This work was supported by the Oliver Bird Fund (Studentship No. RHE/00029/G), The Nuffield Foundation (J.J.), Arthritis Research Campaign (Grant ID 16438) (M.A.N. and R.V.T.), European Community Framework 7 programme grant TREAT-OA (HEALTH-F2-2008-00) (M.A.N. and R.V.T.) and the Medical Research Council (J.J., M.A.N. and R.V.T.). J.J. was an Oliver Bird funded PhD student

Evaluation of fine needle aspiration cytology as the initial diagnostic test in cases of cervical lymphadenopathy

Background: Cervical lymph node enlargement is common amongst the various causes of neck swelling. Proper diagnosis and early treatment is necessary for cervical lymph node disease and it is also necessary to rule out potentially curable causes as against malignancy in which the treatment is generally palliative. Fine needle aspiration cytology (FNAC) is now a day the initial investigation in most of the cases of cervical lymph node enlargement. Aims and Objectives of the study were to evaluate the sensitivity and specificity of FNAC in the diagnosis of cervical lymph node disease with an emphasis on discordant cases between the cytology and the histopathology.Methods: Patients admitted with cervical lymph node enlargement in a tertiary hospital of western India (attached with a medical college) from October 2014 to September 2016 were prospectively studied. Detailed history, clinical examination and necessary investigations of all patients were done especially fine needle aspiration cytology and histopathology examination and inference was obtained after the diagnosis was confirmed.Results: The cytological diagnoses were found to be malignant in 48 cases (30.6%) and benign in 109 cases (69.4%). The overall diagnostic sensitivity, specificity, positive predictive value, and negative predictive value of FNAC of cervical lymph nodes were 90.9%, 67.2%, 82.6%, and 81.3%, respectively. The overall diagnostic accuracy was 82.2%, while the overall discordance rate was 17.8%.Conclusions: FNAC is the initial investigation of choice in the diagnostic approach to most of the cases of cervical lymphadenopathy and it has good diagnostic sensitivity and specificity

Disorders of the calcium-sensing receptor and partner proteins: insights into the molecular basis of calcium homeostasis

The extracellular calcium (Ca(2+)(o))-sensing receptor (CaSR) is a family C G protein-coupled receptor, which detects alterations in Ca(2+)(o) concentrations and modulates parathyroid hormone secretion and urinary calcium excretion. The central role of the CaSR in Ca(2+)(o) homeostasis has been highlighted by the identification of mutations affecting the CASR gene on chromosome 3q21.1. Loss-of-function CASR mutations cause familial hypocalciuric hypercalcaemia (FHH), whereas gain-of-function mutations lead to autosomal dominant hypocalcaemia (ADH). However, CASR mutations are only detected in ≤70% of FHH and ADH cases, referred to as FHH type 1 and ADH type 1, respectively, and studies in other FHH and ADH kindreds have revealed these disorders to be genetically heterogeneous. Thus, loss- and gain-of-function mutations of the GNA11 gene on chromosome 19p13.3, which encodes the G-protein α-11 (Gα(11)) subunit, lead to FHH type 2 and ADH type 2, respectively; whilst loss-of-function mutations of AP2S1 on chromosome 19q13.3, which encodes the adaptor-related protein complex 2 sigma (AP2σ) subunit, cause FHH type 3. These studies have demonstrated Gα(11) to be a key mediator of downstream CaSR signal transduction, and also revealed a role for AP2σ, which is involved in clathrin-mediated endocytosis, in CaSR signalling and trafficking. Moreover, FHH type 3 has been demonstrated to represent a more severe FHH variant that may lead to symptomatic hypercalcaemia, low bone mineral density and cognitive dysfunction. In addition, calcimimetic and calcilytic drugs, which are positive and negative CaSR allosteric modulators, respectively, have been shown to be of potential benefit for these FHH and ADH disorders

Toward Specification-Guided Active Mars Exploration for Cooperative Robot Teams

As a step towards achieving autonomy in space exploration missions, we consider a cooperative robotics system consisting of a copter and a rover. The goal of the copter is to explore an unknown environment so as to maximize knowledge about a science mission expressed in linear temporal logic that is to be executed by the rover. We model environmental uncertainty as a belief space Markov decision process and formulate the problem as a two-step stochastic dynamic program that we solve in a way that leverages the decomposed nature of the overall system. We demonstrate in simulations that the robot team makes intelligent decisions in the face of uncertainty

Examining citizens' perceived value of internet of things technologies in facilitating public sector services engagement

YesWith the advancement of disruptive new technologies, there has been a considerable focus on personalisation as an important component in nurturing users' engagement. In the context of smart cities, Internet of Things (IoT) offer a unique opportunity to help empower citizens and improve societies' engagement with their governments at both micro and macro levels. This study aims to examine the role of perceived value of IoT in improving citizens' engagement with public services. A survey of 313 citizens in the UK, engaging in various public services, enabled through IoT, found that the perceived value of IoT is strongly influenced by empowerment, perceived usefulness and privacy related issues resulting in significantly affecting their continuous use intentions. The study offers valuable insights into the importance of perceived value of IoT-enabled services, while at the same time, providing an intersectional perspective of UK citizens towards the use of disruptive new technologies in the public sector

Genetic Approaches to Metabolic Bone Diseases

Metabolic bone diseases comprise a diverse group of disorders characterized by alterations in skeletal homeostasis, and are often associated with abnormal circulating concentrations of calcium, phosphate or vitamin D metabolites. These diseases commonly have a genetic basis and represent either a monogenic disorder due to a germline or somatic single gene mutation, or an oligogenic or polygenic disorder that involves variants in more than one gene. Germline single gene mutations causing Mendelian diseases typically have a high penetrance, whereas the genetic variations causing oligogenic or polygenic disorders are each associated with smaller effects with additional contributions from environmental factors. Recognition of familial monogenic disorders is of clinical importance to facilitate timely investigations and management of the patient and any affected relatives. The diagnosis of monogenic metabolic bone disease requires careful clinical evaluation of the large diversity of symptoms and signs associated with these disorders. Thus, the clinician must pursue a systematic approach beginning with a detailed history and physical examination, followed by appropriate laboratory and skeletal imaging evaluations. Finally, the clinician must understand the increasing number and complexity of molecular genetic tests available to ensure their appropriate use and interpretation.</p

A G-protein Subunit-α11 Loss-of-Function Mutation, Thr54Met, Causes Familial Hypocalciuric Hypercalcemia Type 2 (FHH2)

Familial hypocalciuric hypercalcemia (FHH) is a genetically heterogeneous disorder with three variants, FHH1 to FHH3. FHH1 is caused by loss-of-function mutations of the calcium-sensing receptor (CaSR), a G-protein coupled receptor that predominantly signals via G-protein subunit alpha-11 (Gα11 ) to regulate calcium homeostasis. FHH2 is the result of loss-of-function mutations in Gα11 , encoded by GNA11, and to date only two FHH2-associated Gα11 missense mutations (Leu135Gln and Ile200del) have been reported. FHH3 is the result of loss-of-function mutations of the adaptor protein-2 σ-subunit (AP2σ), which plays a pivotal role in clathrin-mediated endocytosis. We describe a 65-year-old woman who had hypercalcemia with normal circulating parathyroid hormone concentrations and hypocalciuria, features consistent with FHH, but she did not have CaSR and AP2σ mutations. Mutational analysis of the GNA11 gene was therefore undertaken, using leucocyte DNA, and this identified a novel heterozygous GNA11 mutation (c.161C>T; p.Thr54Met). The effect of the Gα11 variant was assessed by homology modeling of the related Gαq protein and by measuring the CaSR-mediated intracellular calcium (Ca(2+) i ) responses of HEK293 cells, stably expressing CaSR, to alterations in extracellular calcium (Ca(2+) o ) using flow cytometry. Three-dimensional modeling revealed the Thr54Met mutation to be located at the interface between the Gα11 helical and GTPase domains, and to likely impair GDP binding and interdomain interactions. Expression of wild-type and the mutant Gα11 in HEK293 cells stably expressing CaSR demonstrate that the Ca(2+) i responses after stimulation with Ca(2+) o of the mutant Met54 Gα11 led to a rightward shift of the concentration-response curve with a significantly (p < 0.01) increased mean half-maximal concentration (EC50 ) value of 3.88 mM (95% confidence interval [CI] 3.76-4.01 mM), when compared with the wild-type EC50 of 2.94 mM (95% CI 2.81-3.07 mM) consistent with a loss-of-function. Thus, our studies have identified a third Gα11 mutation (Thr54Met) causing FHH2 and reveal a critical role for the Gα11 interdomain interface in CaSR signaling and Ca(2+) o homeostasis. © 2016 American Society for Bone and Mineral Research