Local Cyber-physical Attack with Leveraging Detection in Smart Grid

A well-designed attack in the power system can cause an initial failure and then results in large-scale cascade failure. Several works have discussed power system attack through false data injection, line-maintaining attack, and line-removing attack. However, the existing methods need to continuously attack the system for a long time, and, unfortunately, the performance cannot be guaranteed if the system states vary. To overcome this issue, we consider a new type of attack strategy called combinational attack which masks a line-outage at one position but misleads the control center on line outage at another position. Therefore, the topology information in the control center is interfered by our attack. We also offer a procedure of selecting the vulnerable lines of its kind. The proposed method can effectively and continuously deceive the control center in identifying the actual position of line-outage. The system under attack will be exposed to increasing risks as the attack continuously. Simulation results validate the efficiency of the proposed attack strategy.Comment: Accepted by IEEE SmartGridComm 201

Local Cyber-Physical Attack for Masking Line Outage and Topology Attack in Smart Grid

Malicious attacks in the power system can eventually result in a large-scale cascade failure if not attended on time. These attacks, which are traditionally classified into \emph{physical} and \emph{cyber attacks}, can be avoided by using the latest and advanced detection mechanisms. However, a new threat called \emph{cyber-physical attacks} which jointly target both the physical and cyber layers of the system to interfere the operations of the power grid is more malicious as compared with the traditional attacks. In this paper, we propose a new cyber-physical attack strategy where the transmission line is first physically disconnected, and then the line-outage event is masked, such that the control center is misled into detecting as an obvious line outage at a different position in the local area of the power system. Therefore, the topology information in the control center is interfered by our attack. We also propose a novel procedure for selecting vulnerable lines, and analyze the observability of our proposed framework. Our proposed method can effectively and continuously deceive the control center into detecting fake line-outage positions, and thereby increase the chance of cascade failure because the attention is given to the fake outage. The simulation results validate the efficiency of our proposed attack strategy.Comment: accepted by IEEE Transactions on Smart Grid. arXiv admin note: text overlap with arXiv:1708.0320

Modeling Spatial Relations of Human Body Parts for Indexing and Retrieving Close Character Interactions

Retrieving pre-captured human motion for analyzing and synthesizing virtual character movement have been widely used in Virtual Reality (VR) and interactive computer graphics applications. In this paper, we propose a new human pose representation, called Spatial Relations of Human Body Parts (SRBP), to represent spatial relations between body parts of the subject(s), which intuitively describes how much the body parts are interacting with each other. Since SRBP is computed from the local structure (i.e. multiple body parts in proximity) of the pose instead of the information from individual or pairwise joints as in previous approaches, the new representation is robust to minor variations of individual joint location. Experimental results show that SRBP outperforms the existing skeleton-based motion retrieval and classification approaches on benchmark databases

The impact of universal newborn hearing screening on long-term literacy outcomes: a prospective cohort study

Objective: To determine whether the benefits of universal newborn hearing screening (UNHS) seen at age 8?years persist through the second decade.Design: Prospective cohort study of a population sample of children with permanent childhood hearing impairment (PCHI) followed up for 17?years since birth in periods with (or without) UNHS.Setting: Birth cohort of 100?000 in southern England.Participants: 114 teenagers aged 13-19?years, 76 with PCHI and 38 with normal hearing. All had previously their reading assessed aged 6-10?years.Interventions: Birth in periods with and without UNHS; confirmation of PCHI before and after age 9?months.Main outcome measure: Reading comprehension ability. Regression modelling took account of severity of hearing loss, non-verbal ability, maternal education and main language.Results: Confirmation of PCHI by age 9?months was associated with significantly higher mean z-scores for reading comprehension (adjusted mean difference 1.17, 95% CI 0.36 to 1.97) although birth during periods with UNHS was not (adjusted mean difference 0.15, 95% CI -0.75 to 1.06). The gap between the reading comprehension z-scores of teenagers with early compared with late confirmed PCHI had widened at an adjusted mean rate of 0.06 per year (95% CI -0.02 to 0.13) during the 9.2-year mean interval since the previous assessment.Conclusions: The benefit to reading comprehension of confirmation of PCHI by age 9?months increases during the teenage years. This strengthens the case for UNHS programmes that lead to early confirmation of permanent hearing loss

Quantitative proteomic profiling of white matter in cases of cerebral amyloid angiopathy reveals upregulation of extracellular matrix proteins and clusterin

Aims: Cerebral amyloid angiopathy (CAA) is the accumulation of amyloid beta (Aβ) in the walls of cerebral arterioles, arteries and capillaries. Changes in the white matter in CAA are observed as hyperintensities and dilated perivascular spaces on MRI suggesting impairment of fluid drainage but the pathophysiology behind these changes is poorly understood. We tested the hypothesis that proteins associated with clearance of Aβ peptides are upregulated in the white matter in cases of CAA.Methods: In this study, we compare the quantitative proteomic profile of white matter from post-mortem brains of patients with CAA and age-matched controls in order to gain insight into the cellular processes and key molecules involved in the pathophysiology of CAA.Results: Our proteomic analysis resulted in the profiling of 3,734 proteins (peptide FDR p<0.05). Of these, 189 were differentially expressed in CAA vs. control. Bioinformatics analysis of these proteins showed significant enrichment of proteins related to cell adhesion | cell-matrix interaction, mitochondrial dysfunction and hypoxia. Upregulated proteins in CAA included EMILIN2, COL4A2, TLN1, CLU, HSPG2. Downregulated proteins included DSP, IDE, HBG1.Conclusions: The present study reports an in-depth quantitative proteomic profiling of white matter from patients with CAA, highlighting extracellular matrix proteins and clusterin as key molecules in the pathophysiology of white matter changes in cases of CAA

Health-related quality of life, functional impairment and comorbidity in people with mild-to-moderate chronic kidney disease: a cross-sectional study

Objectives: To determine the associations between comorbidities, health-related quality of life (HRQoL) and functional impairment in people with mild-to-moderate chronic kidney disease (CKD) in primary care.Design: Cross-sectional analysis at 5-year follow-up in a prospective cohort study.Setting: Thirty-two general practitioner surgeries in England.Participants: 1008 participants with CKD stage 3 (of 1741 people recruited at baseline in the Renal Risk in Derby study) who survived to 5?years and had complete follow-up data for HRQoL and functional status (FS).Primary and secondary outcome measures HRQoL assessed using the 5-level EQ-5D version (EQ-5D-5L, with domains of mobility, self-care, usual activities, pain/discomfort and anxiety/depression and index value using utility scores calculated from the English general population), and FS using the Karnofsky Performance Status scale (functional impairment defined as Karnofksy score ?70). Comorbidity was defined by self-reported or doctor-diagnosed condition, disease-specific medication or blood result.Results: Mean age was 75.8 years. The numbers reporting some problems in EQ-5D-5L domains were: 582 (57.7%) for mobility, 166 (16.5%) for self-care, 466 (46.2%) for usual activities, 712 (70.6%) for pain/discomfort and 319 (31.6%) for anxiety/depression. Only 191 (18.9%) reported no problems in any domain. HRQoL index values showed greater variation among those with lower FS (eg, for those with Karnofsky score of 60, the median (IQR) EQ-5D index value was 0.45 (0.24 to 0.68) compared with 0.94 (0.86 to 1) for those with Karnofsky score of 90). Overall, 234 (23.2%) had functional impairment.In multivariable logistic regression models, functional impairment was independently associated with experiencing problems for all EQ-5D-5L domains (mobility: OR 16.87 (95% CI 8.70 to 32.79, p < 0.001, self-care: OR 13.08 (95% CI 8.46 to 20.22), p< 0.001, usual activities: OR 8.27 (95% CI 5.43 to 12.58), p< 0.001, pain/discomfort: OR 2.94 (95% CI 1.86 to 4.67), p< 0.001, anxiety/depression: 3.08 (95% CI 2.23 to 4.27), p< 0.001). Higher comorbidity count and obesity were independently associated with problems in mobility, self-care, usual activities and pain/discomfort: for three or more comorbidities versus none: (mobility: OR 2.10 (95% CI 1.08 to 4.10, p for trend 0.002), self-care: OR 2.64 (95% CI 0.72 to 9.67, p for trend 0.05), usual activities: OR 4.20 (95% CI 2.02 to 8.74, p for trend < 0.001), pain/discomfort: OR 3.06 (95% CI 1.63 to 5.73, p for trend < 0.001)), and for obese (body mass index (BMI) ?30?kg/m2) versus BMI < 25?kg/m2: (mobility: OR 2.44 (95% CI 1.61 to 3.69, p for trend < 0.001), self-care: OR 1.98 (95% CI 1.06 to 3.71, p for trend 0.003), usual activities: OR 1.82 (95% CI 1.19 to 2.76, p for trend 0.019), pain/discomfort: OR 2.37 (95% CI 1.58 to 3.55, p for trend < 0.001)). Female sex, lower FS and lower educational attainment were independently associated with anxiety/depression (ORs 1.60 (95% CI 1.18 to 2.16, p 0.002), 3.08 (95% CI 2.23 to 4.27, p< 0.001) and 1.67 (95% CI 1.10 to 2.52, p 0.009), respectively). Older age, higher comorbidity count, albuminuria (?30?mg/mmol vs < 3?mg/mmol), lower educational attainment (no formal qualifications vs degree level) and obesity were independently associated with functional impairment (ORs 1.07 (95% CI 1.04 to 1.09, p< 0.001), 2.18 (95% CI 0.80 to 5.96, p for trend < 0.001), 1.74 (95% CI 0.82 to 3.68, p for trend 0.005), 2.08 (95% CI 1.26 to 3.41, p for trend < 0.001) and 4.23 (95% CI 2.48 to 7.20), respectively).Conclusions: The majority of persons with mild-to-moderate CKD reported reductions in at least one HRQoL domain, which were independently associated with comorbidities, obesity and functional impairment

Vascular α1A Adrenergic Receptors as a Potential Therapeutic Target for IPAD in Alzheimer’s Disease

Drainage of interstitial fluid from the brain occurs via the intramural periarterial drainage (IPAD) pathways along the basement membranes of cerebral capillaries and arteries against the direction of blood flow into the brain. The cerebrovascular smooth muscle cells (SMCs) provide the motive force for driving IPAD, and their decrease in function may explain the deposition of amyloid-beta as cerebral amyloid angiopathy (CAA), a key feature of Alzheimer's disease. The α-adrenoceptor subtype α1A is abundant in the brain, but its distribution in the cerebral vessels is unclear. We analysed cultured human cerebrovascular SMCs and young, old and CAA human brains for (a) the presence of α1A receptor and (b) the distribution of the α1A receptor within the cerebral vessels. The α1A receptor was present on the wall of cerebrovascular SMCs. No significant changes were observed in the vascular expression of the α1A-adrenergic receptor in young, old and CAA cases. The pattern of vascular staining appeared less punctate and more diffuse with ageing and CAA. Our results show that the α1A-adrenergic receptor is preserved in cerebral vessels with ageing and in CAA and is expressed on cerebrovascular smooth muscle cells, suggesting that vascular adrenergic receptors may hold potential for therapeutic targeting of IPAD.</p

The Pattern of AQP4 Expression in the Ageing Human Brain and in Cerebral Amyloid Angiopathy

In the absence of lymphatics, fluid and solutes such as amyloid-β (Aβ) are eliminated from the brain along basement membranes in the walls of cerebral capillaries and arteries-the Intramural Peri-Arterial Drainage (IPAD) pathway. IPAD fails with age and insoluble Aβ is deposited as plaques in the brain and in IPAD pathways as cerebral amyloid angiopathy (CAA); fluid accumulates in the white matter as reflected by hyperintensities (WMH) on MRI. Within the brain, fluid uptake by astrocytes is regulated by aquaporin 4 (AQP4). We test the hypothesis that expression of astrocytic AQP4 increases in grey matter and decreases in white matter with onset of CAA. AQP4 expression was quantitated by immunocytochemistry and confocal microscopy in post-mortem occipital grey and white matter from young and old non-demented human brains, in CAA and in WMH. Results: AQP4 expression tended to increase with normal ageing but AQP4 expression in severe CAA was significantly reduced when compared to moderate CAA (p = 0.018). AQP4 expression tended to decline in the white matter with CAA and WMH, both of which are associated with impaired IPAD. Adjusting the level of AQP4 activity may be a valid therapeutic target for restoring homoeostasis in the brain as IPAD fails with age and CAA.</p

Deposition of amyloid β in the walls of human leptomeningeal arteries in relation to perivascular drainage pathways in cerebral amyloid angiopathy

Deposition of amyloid beta (AB) in the walls of cerebral arteries as cerebral amyloid angiopathy (CAA) suggests an age-related failure of perivascular drainage of soluble A? from the brain. As CAA is associated with Alzheimer's disease and with intracerebral haemorrhage, the present study determines the unique sequence of changes that occur as A? accumulates in artery walls. Paraffin sections of post-mortem human occipital cortex were immunostained for collagen IV, fibronectin, nidogen 2, AB and smooth muscle actin and the immunostaining was analysed using Image J and confocal microscopy. Results showed that nidogen 2 (entactin) increases with age and decreases in CAA. Confocal microscopy revealed stages in the progression of CAA: AB initially deposits in basement membranes in the tunica media, replaces first the smooth muscle cells and then the connective tissue elements to leave artery walls completely or focally replaced by AB. The pattern of development of CAA in the human brain suggests expansion of AB from the basement membranes to progressively replace all tissue elements in the artery wall. Establishing this full picture of the development of CAA is pivotal in understanding the clinical presentation of CAA and for developing therapies to prevent accumulation of AB in artery walls. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock