Intelligent Control and Security of Fog Resources in Healthcare Systems via a Cognitive Fog Model

There have been significant advances in the field of Internet of Things (IoT) recently, which have not always considered security or data security concerns: A high degree of security is required when considering the sharing of medical data over networks. In most IoT-based systems, especially those within smart-homes and smart-cities, there is a bridging point (fog computing) between a sensor network and the Internet which often just performs basic functions such as translating between the protocols used in the Internet and sensor networks, as well as small amounts of data processing. The fog nodes can have useful knowledge and potential for constructive security and control over both the sensor network and the data transmitted over the Internet. Smart healthcare services utilise such networks of IoT systems. It is therefore vital that medical data emanating from IoT systems is highly secure, to prevent fraudulent use, whilst maintaining quality of service providing assured, verified and complete data. In this paper, we examine the development of a Cognitive Fog (CF) model, for secure, smart healthcare services, that is able to make decisions such as opting-in and opting-out from running processes and invoking new processes when required, and providing security for the operational processes within the fog system. Overall, the proposed ensemble security model performed better in terms of Accuracy Rate, Detection Rate, and a lower False Positive Rate (standard intrusion detection measurements) than three base classifiers (K-NN, DBSCAN and DT) using a standard security dataset (NSL-KDD)

Lrig2 and Hpse2, mutated in urofacial syndrome, pattern nerves in the urinary bladder.

Mutations in leucine-rich-repeats and immunoglobulin-like-domains 2 (LRIG2) or in heparanase 2 (HPSE2) cause urofacial syndrome, a devastating autosomal recessive disease of functional bladder outlet obstruction. It has been speculated that urofacial syndrome has a neural basis, but it is unknown whether defects in urinary bladder innervation are present. We hypothesized that urofacial syndrome features a peripheral neuropathy of the bladder. Mice with homozygous targeted Lrig2 mutations had urinary defects resembling those found in urofacial syndrome. There was no anatomical blockage of the outflow tract, consistent with a functional bladder outlet obstruction. Transcriptome analysis revealed differential expression of 12 known transcripts in addition to Lrig2, including 8 with established roles in neurobiology. Mice with homozygous mutations in either Lrig2 or Hpse2 had increased nerve density within the body of the urinary bladder and decreased nerve density around the urinary outflow tract. In a sample of 155 children with chronic kidney disease and urinary symptoms, we discovered novel homozygous missense LRIG2 variants that were predicted to be pathogenic in 2 individuals with non-syndromic bladder outlet obstruction. These observations provide evidence that a peripheral neuropathy is central to the pathobiology of functional bladder outlet obstruction in urofacial syndrome, and emphasize the importance of LRIG2 and heparanase 2 for nerve patterning in the urinary tract

Generation and Analysis of Striated Muscle Selective LINC Complex Protein Mutant Mice

The linker of nucleoskeleton and cytoskeleton (LINC) complex mediates intracellular cross talk between the nucleus and the cytoplasm. In striated muscle, the LINC complex provides structural support to the myocyte nucleus and plays an essential role in regulating gene expression and mechanotransduction. A wide range of cardiac and skeletal myopathies have been linked to mutations in LINC complex proteins. Studies utilizing tissue-specific knockout and mutant mouse models have revealed important insights into the roles of the LINC complex in striated muscle. In this chapter, we describe several feasible approaches for generating striated muscle-specific gene knockout and mutant mouse models to study LINC complex protein function in cardiac and skeletal muscle. The experimental procedures used for phenotyping and analysis of LINC complex knockout mice are also described