A Decomposition Approach to Multi-Vehicle Cooperative Control

We present methods that generate cooperative strategies for multi-vehicle control problems using a decomposition approach. By introducing a set of tasks to be completed by the team of vehicles and a task execution method for each vehicle, we decomposed the problem into a combinatorial component and a continuous component. The continuous component of the problem is captured by task execution, and the combinatorial component is captured by task assignment. In this paper, we present a solver for task assignment that generates near-optimal assignments quickly and can be used in real-time applications. To motivate our methods, we apply them to an adversarial game between two teams of vehicles. One team is governed by simple rules and the other by our algorithms. In our study of this game we found phase transitions, showing that the task assignment problem is most difficult to solve when the capabilities of the adversaries are comparable. Finally, we implement our algorithms in a multi-level architecture with a variable replanning rate at each level to provide feedback on a dynamically changing and uncertain environment.Comment: 36 pages, 19 figures, for associated web page see http://control.mae.cornell.edu/earl/decom

He-HTLC: Revisiting Incentives in HTLC

Hashed Time-Locked Contracts (HTLCs) are a widely used primitive in blockchain systems such as payment channels, atomic swaps, etc. Unfortunately, HTLC is incentive-incompatible and is vulnerable to bribery attacks. The state-of-the-art solution is MAD-HTLC (Oakland\u2721), which proposes an elegant idea that leverages miners\u27 profit-driven nature to defeat bribery attacks. In this paper, we show that MAD-HTLC is still vulnerable as it only considers a somewhat narrow set of passive strategies by miners. Through a family of novel reverse-bribery attacks, we show concrete active strategies that miners can take to break MAD-HTLC and profit at the loss of MAD-HTLC users. For these attacks, we present their implementation and game-theoretical profitability analysis. Based on the learnings from our attacks, we propose a new HTLC realization, He-HTLC (Our specification is lightweight and inert to incentive manipulation attacks. Hence, we call it He-HTLC where He stands for Helium.) that is provably secure against all possible strategic manipulation (passive and active). In addition to being secure in a stronger adversary model, He-HTLC achieves other desirable features such as low and user-adjustable collateral, making it more practical to implement and use the proposed schemes. We implemented He-HTLC on Bitcoin and the transaction cost of He-HTLC is comparative to average Bitcoin transaction fees

Neurocysticercosis with a single brain lesion in Germany: a case report

Neurocysticercosis is rare in Western Europe and a high degree of physician awareness is necessary for diagnosis. We describe a case of Neurocysticercosis with a single brain lesion acquired in Germany in which only surgical removal and subsequent histological examination allowed diagnosis whereas diagnostic investigation yielded no pathological findings

Topodiagnostic implications of hemiataxia: An MRI-based brainstem mapping analysis

The topodiagnostic implications of hemiataxia following lesions of the human brainstem are only incompletely understood. We performed a voxel-based statistical analysis of lesions documented on standardised MRI in 49 prospectively recruited patients with acute hemiataxia due to isolated unilateral brainstem infarction. For statistical analysis individual MRI lesions were normalised and imported in a three-dimensional voxel-based anatomical model of the human brainstem. Statistical analysis revealed hemiataxia to be associated with lesions of three distinct brainstem areas. The strongest correlation referred to ipsilateral rostral and dorsolateral medullary infarcts affecting the inferior cerebellar peduncle, and the dorsal and ventral spinocerebellar tracts. Secondly, lesions of the ventral pontine base resulted in contralateral limb ataxia, especially when ataxia was accompanied by motor hemiparesis. In patients with bilateral hemiataxia, lesions were located in a paramedian region between the upper pons and lower midbrain, involving the decussation of dentato-rubro-thalamic tracts. We conclude that ataxia following brainstem infarction may reflect three different pathophysiological mechanisms. (1) Ipsilateral hemiataxia following dorsolateral medullary infarctions results from a lesion of the dorsal spinocerebellar tract and the inferior cerebellar peduncle conveying afferent information from the ipsilateral arm and leg. (2) Pontine lesions cause contralateral and not bilateral ataxia presumably due to major damage to the descending corticopontine projections and pontine base nuclei, while already crossed pontocerebellar fibres are not completely interrupted. (3) Finally, bilateral ataxia probably reflects a lesion of cerebellar outflow on a central, rostral pontomesencephalic level. © 2007 Elsevier Inc. All rights reserved

Structural characterisation of the N-glycan moiety of the barnacle settlement-inducing protein complex (SIPC)

Many barnacle species are gregarious and their cypris larvae display a remarkable ability to explore surfaces before committing to permanent attachment. The chemical cue to gregarious settlement behaviour – the settlement-inducing protein complex (SIPC) – is an α2-macroglobulin-like glycoprotein. This cuticular protein may also be involved in cyprid reversible adhesion if its presence is confirmed in footprints of adhesive deposited during exploratory behaviour, which increase the attractiveness of surfaces and signal other cyprids to settle. The full-length open-reading frame of the SIPC gene encodes a protein of 1547 amino acids with seven potential N-glycosylation sites. In this study on Balanus amphitrite, glycan profiling of the SIPC via hydrophilic interaction liquid chromatography with fluorescence detection (HILIC-fluorescence) provided evidence of predominantly high mannose glycans (M2–9), with the occurrence of monofucosylated oligomannose glycans (F(6)M2–4) in lower proportions. The high mannose glycosylation found supports previous observations of an interaction with mannose-binding lectins and exogenous mannose increasing settlement in B. amphitrite cypris larvae. Transmission electron microscopy of the deglycosylated SIPC revealed a multi-lobed globular protein with a diameter of ∼8 nm. Obtaining a complete structural characterisation of the SIPC remains a goal that has the potential to inspire solutions to the age-old problem of barnacle fouling.No Full Tex

PROTECT VIII kids extension study: Long-term safety and efficacy of BAY 94-9027 (damoctocog alfa pegol) in children with severe haemophilia A

Introduction: BAY 94-9027 (damoctocog alfa pegol; an extended half-life PEGylated recombinant factor VIII [FVIII]) demonstrated efficacy and safety in previously treated paediatric patients (PTPs) aged <12 years with severe haemophilia A in the PROTECT VIII Kids study (NCT01775618). Aim: To evaluate the long-term safety of BAY 94-9027 in PTPs aged <12 years at enrolment. Methods: In the PROTECT VIII Kids study, boys <12 years with severe haemophilia A were enrolled in two age cohorts (6–<12 years and <6 years) and treated prophylactically twice weekly, every 5 days or every 7 days, with BAY 94-9027 for ≥50 exposure days (EDs). Patients who had completed ≥50 EDs and ≥6 months in the main study or 12-week safety expansion study were eligible to participate in the extension. Primary safety variable was frequency of inhibitor development; main efficacy variable was annualised bleeding rate (ABR). Results: Of 73 PTPs from the main/expansion studies, 59 (81%) entered the extension phase for a median (range) duration of 5.0 (0.4–5.9) years. Overall, 39 patients completed ≥5 years of treatment. No patients developed FVIII inhibitors/anti-PEG antibodies, and two patients aged <6 years discontinued. Median ABR for total bleeds was 1.5 (<6 years) and 1.9 (6–<12 years). Total ABR improved in the extension vs. the main study. In the last 12 months of treatment, median spontaneous ABR was 0.0 in both age groups. Conclusions: BAY 94-9027 showed long-term safety and efficacy for the prevention and treatment of bleeds in younger and older paediatric patients with severe haemophilia A

Extensive necrosis of visceral melanoma metastases after immunotherapy

<p>Abstract</p> <p>Background</p> <p>The prognosis for metastatic melanoma remains poor even with traditional decarbazine or interferon therapy. 5-year survival is markedly higher amongst patients undergoing metastatectomy. Unfortunately not all are suitable for metastatectomy. Alternative agents for systemic therapy have, to date, offered no greater rates of survival beyond traditional therapy. A toll-like receptor 9 agonist, PF-3512676 (formerly known as CPG 7909) is currently being evaluated for its potential.</p> <p>Case presentation</p> <p>We present the case of a 54-year-old Caucasian male with completely resected metastatic cutaneous melanoma after immunotherapy. The patient initially progressed during adjuvant high-dose interferon, with metastases to the liver, spleen, and pelvic lymph nodes. During an 18-month treatment period with PF-3512676 (formerly known as CPG 7909), a synthetic cytosine-phosphorothioate-guanine rich oligodeoxynucleotide, slow radiologic disease progression was demonstrated at the original disease sites. Subsequent excision of splenic and pelvic nodal metastases was performed, followed by resection of the liver metastases. Histologic examination of both hepatic and splenic melanoma metastases showed extensive necrosis. Subsequent disease-free status was demonstrated by serial positron emission tomography (PET).</p> <p>Conclusion</p> <p>Existing evidence from phase I/II trials suggests systemic treatment with PF-3512676 is capable of provoking a strong tumor-specific immune response and may account for the prolonged tumor control in this instance.</p

Structural alterations in functional neurological disorder and related conditions: A software and hardware problem?

Functional neurological (conversion) disorder (FND) is a condition at the interface of neurology and psychiatry. A “software” vs. “hardware” analogy describes abnormal neurobiological mechanisms occurring in the context of intact macroscopic brain structure. While useful for explanatory and treatment models, this framework may require more nuanced considerations in the context of quantitative structural neuroimaging findings in FND. Moreover, high co-occurrence of FND and somatic symptom disorders (SSD) as defined in DSM-IV (somatization disorder, somatoform pain disorder, and undifferentiated somatoform disorder; referred to as SSD for brevity in this article) raises the possibility of a partially overlapping pathophysiology. In this systematic review, we use a transdiagnostic approach to review and appraise the structural neuroimaging literature in FND and SSD. While larger sample size studies are needed for definitive characterization, this article highlights that individuals with FND and SSD may exhibit sensorimotor, prefrontal, striatal-thalamic, paralimbic, and limbic structural alterations. The structural neuroimaging literature is contextualized within the neurobiology of stress-related neuroplasticity, gender differences, psychiatric comorbidities, and the greater spectrum of functional somatic disorders. Future directions that could accelerate the characterization of the pathophysiology of FND and DSM-5 SSD are outlined, including “disease staging” discussions to contextualize subgroups with or without structural changes. Emerging neuroimaging evidence suggests that some individuals with FND and SSD may have a “software” and “hardware” problem, although if structural alterations are present the neural mechanisms of functional disorders remain distinct from lesional neurological conditions. Furthermore, it remains unclear whether structural alterations relate to predisposing vulnerabilities or consequences of the disorder. Keywords: Conversion disorder, Psychogenic, Neuroimaging, MRI, Functional neurological disorder, Somatic symptom disorde