An Explanatory Model of Motivation for Cyber-Attacks Drawn from Criminological Theories

A new influence model for Cyber Security is presented that deals with security attacks and implementation of security measures from an attacker's perspective. The underlying hypothesis of this model is that Criminological theories of Rational Choice, Desire for Control, and Low Self-Control are relevant to cybercrime and thereby aid in the understanding its basic Motivation. The model includes the roles of Consequences, Moral Beliefs such as Shame and Embarrassment together with Formal Sanctions in deterring cybercrime, as well as role of Defense Posture to limit the Opportunity to attack and increase the likelihood that an attacker will be detected and exposed. One of the motivations of the study was the observation that few attempts have been made to understand cybercrime, in the context of typical crime because: (a) an attacker may consider his actions as victimless due to remoteness of the victim; (b) ease to commit cybercrimes due to opportunities afforded by the Internet and its accessibility, and readily available tools and knowledge for an attack; and (c) vagueness of cybercrime laws that makes prosecution difficult. In developing the model, information from studies in classical crime was related to Cybercrime allowing for analysis of past cyber-attacks, and subsequently preventing future IS attacks, or mitigating their effects. The influence model's applicability is demonstrated by applying it to case studies of actual information attacks which were prosecuted through the United States Courts, and whose judges' opinions are used for statements of facts. Additional, demonstration of the use and face validity of the model is through the mapping of the model to major annual surveys' and reports' results of computer crime. The model is useful in qualitatively explaining "best practices" in protecting information assets and in suggesting emphasis on security practices based on similar results in general criminology

Vascular co-option in lung cancer metastatic to the eye after treatment with bevacizumab

Abstract Background Chemotherapy with bevacizumab alters the angiogenic environment, and therefore, the growth and spread of metastases. We present a patient with metastatic lung adenocarcinoma to the eye with findings suggestive of retinal vascular co-option. Methods Case report. Results A 57-year-old male, receiving systemic bevacizumab for metastatic lung adenocarcinoma, presented with vitreous opacities and clumped deposits adherent to the retinal vessels. No choroidal metastases were present. Diagnostic vitrectomy yielded cellular evidence of adenocarcinoma, with thyroid transcription factor-1 staining confirming a lung primary. Conclusion The perivascular growth of small foci of metastatic vitreous cells suggests vascular co-option from the native retinal circulation. Similar modification of metastatic disease by bevacizumab has been observed in animal models and selected human cases

High-Resolution Optical Coherence Tomography Retinal Imaging: A Case Series Illustrating Potential and Limitations

Purpose. To present a series of retinal disease cases that were imaged by spectral domain optical coherence tomography (SD-OCT) in order to illustrate the potential and limitations of this new imaging modality. Methods. The series comprised four selected cases (one case each) of age-related macular degeneration (ARMD), diabetic retinopathy (DR), central retinal artery occlusion (CRAO), and branch retinal vein occlusion (BRVO). Patients were imaged using the Heidelberg Spectralis (Heidelberg Engineering, Germany) in SD-OCT mode. Patients also underwent digital fundus photography and clinical assessment. Results. SD-OCT imaging of a case of age-related macular degeneration revealed a subfoveal choroidal neovascular membrane with detachment of the retinal pigment epithelium (RPE) and neurosensory retina. Using SD-OCT, the cases of DR and BRVO both exhibited macular edema with cystoid spaces visible in the outer retina. Conclusions. The ability of SD-OCT to clearly and objectively elucidate subtle morphological changes within the retinal layers provides information that can be used to formulate diagnoses with greater confidence

Autoimmune and autoinflammatory mechanisms in uveitis

The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders

Toxic epidermal necrolysis and Stevens-Johnson syndrome

Toxic epidermal necrolysis (TEN) and Stevens Johnson Syndrome (SJS) are severe adverse cutaneous drug reactions that predominantly involve the skin and mucous membranes. Both are rare, with TEN and SJS affecting approximately 1or 2/1,000,000 annually, and are considered medical emergencies as they are potentially fatal. They are characterized by mucocutaneous tenderness and typically hemorrhagic erosions, erythema and more or less severe epidermal detachment presenting as blisters and areas of denuded skin. Currently, TEN and SJS are considered to be two ends of a spectrum of severe epidermolytic adverse cutaneous drug reactions, differing only by their extent of skin detachment. Drugs are assumed or identified as the main cause of SJS/TEN in most cases, but Mycoplasma pneumoniae and Herpes simplex virus infections are well documented causes alongside rare cases in which the aetiology remains unknown. Several drugs are at "high" risk of inducing TEN/SJS including: Allopurinol, Trimethoprim-sulfamethoxazole and other sulfonamide-antibiotics, aminopenicillins, cephalosporins, quinolones, carbamazepine, phenytoin, phenobarbital and NSAID's of the oxicam-type. Genetic susceptibility to SJS and TEN is likely as exemplified by the strong association observed in Han Chinese between a genetic marker, the human leukocyte antigen HLA-B*1502, and SJS induced by carbamazepine. Diagnosis relies mainly on clinical signs together with the histological analysis of a skin biopsy showing typical full-thickness epidermal necrolysis due to extensive keratinocyte apoptosis. Differential diagnosis includes linear IgA dermatosis and paraneoplastic pemphigus, pemphigus vulgaris and bullous pemphigoid, acute generalized exanthematous pustulosis (AGEP), disseminated fixed bullous drug eruption and staphyloccocal scalded skin syndrome (SSSS). Due to the high risk of mortality, management of patients with SJS/TEN requires rapid diagnosis, evaluation of the prognosis using SCORTEN, identification and interruption of the culprit drug, specialized supportive care ideally in an intensive care unit, and consideration of immunomodulating agents such as high-dose intravenous immunoglobulin therapy. SJS and TEN are severe and life-threatening. The average reported mortality rate of SJS is 1-5%, and of TEN is 25-35%; it can be even higher in elderly patients and those with a large surface area of epidermal detachment. More than 50% of patients surviving TEN suffer from long-term sequelae of the disease

Branch Retinal Vein Occlusion: Pathogenesis, Visual Prognosis, and Treatment Modalities

In branch retinal vein occlusion (BRVO), abnormal arteriovenous crossing with vein compression, degenerative changes of the vessel wall and abnormal hematological factors constitute the primary mechanism of vessel occlusion. In general, BRVO has a good prognosis: 50–60% of eyes are reported to have a final visual acuity (VA) of 20/40 or better even without treatment. One important prognostic factor for final VA appears to be the initial VA. Grid laser photocoagulation is an established treatment for macular edema in a particular group of patients with BRVO, while promising results for this condition are shown by intravitreal application of steroids or new vascular endothelial growth factor inhibitors. Vitrectomy with or without arteriovenous sheathotomy combined with removal of the internal limiting membrane may improve vision in eyes with macular edema which are unresponsive to or ineligible for laser treatment