Malware forensic analytics framework using big data platform

The dramatically increased threats such as malware attacks to our cyber world have given us the vital sign to strengthen the security in a more proactive way. Thus, in recent research we proposed an integrated malware forensic analytics framework that will expose the future threats of malware attacks. This framework incorporates malware collections, malware analytics and visualization of discovered malware attacks. In this paper, we present the design and implementation of the framework which focuses on analytics and visualization, and utilized the emerging technology of big data platform. The implementation of the framework shows promising results in presenting descriptive analytics and predicting the future attacks using machine learning algorithms. We also demonstrate the feasibility of Hortonworks Cybersecurity Package (HCP) in supporting the proposed framework. Finally, we discussed the future work that can be further investigated in improving the implementation of the framework

Dynamic thiol/disulphide homeostasis metrics as a risk factor for peripheral arterial disease.

OBJECTIVE: To examine dynamic thiol/disulphide homeostasis metrics as a novel risk factor of oxidative stress in patients with peripheral arterial disease. METHODS: One hundred patients with lower extremity peripheral arterial disease (a study group) and 100 control subjects were included in this prospective case-control study. Participants' baseline clinical characteristics and laboratory data including some oxidant/antioxidant status parameters such as albumin, ferroxidase and myeloperoxidase, and thiol/disulphide homeostasis parameters such as native thiol, total thiol and disulphide, as well as native thiol/total thiol, disulphide/native thiol and disulphide/total thiol ratios were all recorded and then compared between the groups. RESULTS: Mean albumin and ferroxidase, and median myeloperoxidase levels were found to be significantly higher in patients with the peripheral arterial disease than in control group (p = 0.045, p = 0.000 and p = 0.000, respectively). Mean native thiol and total thiol, and median disulphide levels were found to be significantly lower in the study group as compared with the control group (p = 0.000, p = 0.000 and p = 0.037, respectively). According to the results of logistic regression analysis, systolic blood pressure, ferroxidase and myeloperoxidase levels were detected to be the independent predictors of peripheral arterial disease. CONCLUSION: Our report is the first one in the literature investigating dynamic thiol/disulphide homeostasis metrics as a novel risk factor of oxidative stress in peripheral arterial disease. Dynamic thiol/disulphide homeostasis metrics may be used as a valuable risk factor of oxidative stress in patients with the peripheral arterial disease since it is readily available, easily calculated and relatively cheap

Clinical Characteristics and Long-term Follow-up of Patients with Diabetes Due To PTF1A Enhancer Mutations

Context: Biallelic mutations in the PTF1A enhancer are the commonest cause of isolated pancreatic agenesis. These patients do not have severe neurological features associated with loss-of-function PTF1A mutations. Their clinical phenotype and disease progression have not been well characterized. Objective: To evaluate phenotype and genotype characteristics and long-term follow-up of patients with PTF1A enhancer mutations. Setting: Twelve tertiary pediatric endocrine referral centers. Patients: Thirty patients with diabetes caused by PTF1A enhancer mutations. Median follow-up duration was 4 years. Main outcome measures: Presenting and follow-up clinical (birthweight, gestational age, symptoms, auxology) and biochemical (pancreatic endocrine and exocrine functions, liver function, glycated hemoglobin) characteristics, pancreas imaging, and genetic analysis. Results: Five different homozygous mutations affecting conserved nucleotides in the PTF1A distal enhancer were identified. The commonest was the Chr10:g.23508437A>G mutation (n = 18). Two patients were homozygous for the novel Chr10:g.23508336A>G mutation. Birthweight was often low (median SDS = -3.4). The majority of patients presented with diabetes soon after birth (median age of diagnosis: 5 days). Only 2/30 presented after 6 months of age. All patients had exocrine pancreatic insufficiency. Five had developmental delay (4 mild) on long-term follow-up. Previously undescribed common features in our cohort were transiently elevated ferritin level (n = 12/12 tested), anemia (19/25), and cholestasis (14/24). Postnatal growth was impaired (median height SDS: -2.35, median BMI SDS: -0.52 SDS) with 20/29 (69%) cases having growth retardation. Conclusion: We report the largest series of patients with diabetes caused by PTF1A enhancer mutations. Our results expand the disease phenotype, identifying recurrent extrapancreatic features which likely reflect long-term intestinal malabsorption.This article is available to RD&E staff via NHS OpenAthens (subject to any publisher embargo). Click on the Publisher URL, and log in with NHS OpenAthens if prompted.Genetic testing for neonatal diabetes was funded through a Wellcome Trust Senior Investigator award (grant number: 098395/Z/12/Z). EDF is a Diabetes UK RD Law rence Fellow (19/005971), and SEF has a Sir Henry Dale Fellow ship jointly funded by the Wellcome Trust and the Royal Society (105636/Z/14/Z).published version, accepted version (12 month embargo), submitted versio