Distributed C2 System Recovery Mechanisms

1988 ◽  
Author(s):  
William T. Wood ◽  
Helmut K. Berg ◽  
Anand R. Tripathi ◽  
Jonathan Silverman ◽  
Elaine N. Frankowski
Keyword(s):  
Recovery Mechanisms

scholarly journals Maturation, inactivation, and recovery mechanisms of soluble guanylyl cyclase

2021 ◽  
Vol 296 ◽  
pp. 100336
Author(s):  
Dennis J. Stuehr ◽  
Saurav Misra ◽  
Yue Dai ◽  
Arnab Ghosh
Keyword(s):  
Guanylyl Cyclase ◽  
Soluble Guanylyl Cyclase ◽  
Recovery Mechanisms

scholarly journals Enhanced oil recovery mechanisms of polymer flooding in a heterogeneous oil reservoir

2021 ◽  
Vol 48 (1) ◽  
pp. 169-178
Author(s):  
Xiangguo LU ◽  
Bao CAO ◽  
Kun XIE ◽  
Weijia CAO ◽  
Yigang LIU ◽  
...  
Keyword(s):  
Enhanced Oil Recovery ◽  
Oil Recovery ◽  
Polymer Flooding ◽  
Oil Reservoir ◽  
Recovery Mechanisms

scholarly journals Simulating lesion-dependent functional recovery mechanisms

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Noor Sajid ◽  
Emma Holmes ◽  
Thomas M. Hope ◽  
Zafeirios Fountas ◽  
Cathy J. Price ◽  
...  
Keyword(s):  
Functional Recovery ◽  
Model Performance ◽  
Neuronal System ◽  
Learning Capacity ◽  
Word Repetition ◽  
Alternative System ◽  
Long Term Effect ◽  
Different Types ◽  
Recovery Mechanisms ◽  
Incomplete Damage

AbstractFunctional recovery after brain damage varies widely and depends on many factors, including lesion site and extent. When a neuronal system is damaged, recovery may occur by engaging residual (e.g., perilesional) components. When damage is extensive, recovery depends on the availability of other intact neural structures that can reproduce the same functional output (i.e., degeneracy). A system’s response to damage may occur rapidly, require learning or both. Here, we simulate functional recovery from four different types of lesions, using a generative model of word repetition that comprised a default premorbid system and a less used alternative system. The synthetic lesions (i) completely disengaged the premorbid system, leaving the alternative system intact, (ii) partially damaged both premorbid and alternative systems, and (iii) limited the experience-dependent plasticity of both. The results, across 1000 trials, demonstrate that (i) a complete disconnection of the premorbid system naturally invoked the engagement of the other, (ii) incomplete damage to both systems had a much more devastating long-term effect on model performance and (iii) the effect of reducing learning capacity within each system. These findings contribute to formal frameworks for interpreting the effect of different types of lesions.

scholarly journals ESRFuzzer: an enhanced fuzzing framework for physical SOHO router devices to discover multi-Type vulnerabilities

Cybersecurity ◽  
2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu Zhang ◽  
Wei Huo ◽  
Kunpeng Jian ◽  
Ji Shi ◽  
Longquan Liu ◽  
...  
Keyword(s):  
Web Server ◽  
Test Cases ◽  
Communication Model ◽  
Home Office ◽  
Security Vulnerabilities ◽  
Testing Environment ◽  
Semantic Models ◽  
Recovery Mechanisms ◽  
General Mode ◽  
Soho Router

AbstractSOHO (small office/home office) routers provide services for end devices to connect to the Internet, playing an important role in cyberspace. Unfortunately, security vulnerabilities pervasively exist in these routers, especially in the web server modules, greatly endangering end users. To discover these vulnerabilities, fuzzing web server modules of SOHO routers is the most popular solution. However, its effectiveness is limited due to the lack of input specification, lack of routers’ internal running states, and lack of testing environment recovery mechanisms. Moreover, existing works for device fuzzing are more likely to detect memory corruption vulnerabilities.In this paper, we propose a solution ESRFuzzer to address these issues. It is a fully automated fuzzing framework for testing physical SOHO devices. It continuously and effectively generates test cases by leveraging two input semantic models, i.e., KEY-VALUE data model and CONF-READ communication model, and automatically recovers the testing environment with power management. It also coordinates diversified mutation rules with multiple monitoring mechanisms to trigger multi-type vulnerabilities. With the guidance of the two semantic models, ESRFuzzer can work in two ways: general mode fuzzing and D-CONF mode fuzzing. General mode fuzzing can discover both issues which occur in the CONF and READ operation, while D-CONF mode fuzzing focus on the READ-op issues especially missed by general mode fuzzing.We ran ESRFuzzer on 10 popular routers across five vendors. In total, it discovered 136 unique issues, 120 of which have been confirmed as 0-day vulnerabilities we found. As an improvement of SRFuzzer, ESRFuzzer have discovered 35 previous undiscovered READ-op issues that belong to three vulnerability types, and 23 of them have been confirmed as 0-day vulnerabilities by vendors. The experimental results show that ESRFuzzer outperforms state-of-the-art solutions in terms of types and number of vulnerabilities found.

Possible reason for preferential damage to renal tubular epithelial cells evoked by amphotericin B.

1996 ◽  
Vol 40 (5) ◽  
pp. 1116-1120 ◽  
Author(s):  
I Walev ◽  
S Bhakdi
Keyword(s):  
Epithelial Cells ◽  
Amphotericin B ◽  
Important Determinant ◽  
Major Complication ◽  
Toxic Action ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Recovery Mechanisms ◽  
Renal Tubular

An important determinant of nephrotoxicity, which is the major complication of long-term amphotericin B treatment, is dysfunction of distal tubular epithelial cells. The underlying cause for this rather selective damage to the cells is unknown. In the present investigation, it was shown that kidney epithelial cells were initially damaged by amphotericin B at concentrations of 2.5 to 10 micrograms/ml, as demonstrable by a dramatic drop in cellular K+ levels. Cells could recover from the initial toxic action of the polyene if they were kept in medium of neutral pH, and cellular K+ levels returned to normal after 6 h. However, the recovery mechanisms failed at lower pHs of 5.6 to 6.0. At low pHs, cells became progressively depleted of ATP; they leaked lactate dehydrogenase and became irreversibly damaged after approximately 6 h. The possibility that the low pH characteristic of the distal tubulus lumen renders the renal epithelial cells particularly vulnerable to the toxic action of amphotericin B is raised. The concept is in line with an earlier report that alkalization ameliorates amphotericin B nephrotoxicity in rats.

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