Automatic Verification and Execution of Cyber Attack on IoT Devices.

Internet of Things (IoT) devices are becoming a part of our daily life; from health monitors to critical infrastructure, they are used everywhere. This makes them ideal targets for malicious actors to exploit for nefarious purposes. Recent attacks like the Mirai botnet are just examples in which default credentials were used to exploit thousands of devices. This raises major concerns about IoT device security. In this work, we aimed to investigate security of IoT devices through performing automatic penetration test on IoT devices. A penetration test is a way of detecting security problems, but manually testing billions of IoT devices is infeasible. This work has therefore examined autonomous penetration testing on IoT devices. In recent studies, automated attack execution models were developed for modeling automated attacks in cyber ranges. We have (1) investigated how such models can be applied for performing autonomous IoT penetration testing. Furthermore, we have (2) investigated if some well known and severe Wi-Fi related vulnerabilities still exist in IoT devices. Through a case study, we have shown that the such models can be used to model and design autonomous penetration testing agents for IoT devices. In addition, we have demonstrated that well-known vulnerabilities are present in deployed and currently sold products used in IoT devices, and that they can be both autonomously revealed through our developed system.

Virtual medical student education and recruitment during the COVID-19 pandemic.

Due to the immediate need for social distancing, as well as widespread disruption in clinical practices, brought on by the novel severe acute respiratory syndrome coronavirus 2 (COVID-19) pandemic, medical student education rapidly shifted to a virtual format, which resulted in a variety of innovative and remotely accessible practices to address new restrictions on face-to-face education. Educators approached curriculum design seeking to replicate as much of the in-person experience as possible, and were faced with overcoming the challenges of replacing the innately hands-on nature of surgery with virtual operative and skills experiences. Restrictions on in-person visiting electives expedited the role of virtual education as a notable opportunity for medical student education and recruitment, with a variety of approaches to engaging undergraduate medical learners, including the use of live-streaming operative cases, virtual didactic curricula, and a rise in podcasts; web-based conferences; and virtual journal clubs. In addition to education, virtual outreach to medical students has become an essential tool in trainee recruitment and selection, and ongoing application of novel educational platforms will allow for new opportunities in multi-institutional collaboration and exchange with a multitude of benefits to future vascular surgery trainees. Our aim was to outline the resources and practices used to virtually teach and recruit medical students and the benefits of virtual rotations to the program and students.

Racial differences in utilization and outcomes of hemodialysis access in the Unites States.

OBJECTIVE: To evaluate patterns of use and outcomes of arteriovenous fistulas and prosthetic grafts within racial categories in a large population based cohort of hemodialysis (HD) patients in the United States. METHODS: A retrospective analysis of white, black, and Hispanic patients in the prospectively maintained United States Renal Database System who had an autogenous fistula or prosthetic graft placed for HD access between January 2007 and December 2014 was performed. Analysis of variance, χ2, t-tests, Kaplan-Meier, log-rank tests, multivariable logistic, and Cox regression analyses were used to evaluate maturation, patency, infection, and mortality. RESULTS: This study of 359,942 patients, composed of 285,781 autogenous fistulas (79.4%) and 74,161 prosthetic grafts (20.6%) placed in 213,877 white (59.4%), 115,727 black (32.2%), and 30,338 Hispanic (8.4%) patients. There was a 11% increase in the risk-adjusted odds of HD catheter use as bridge to autogenous fistula placement in blacks (adjusted odds ratio, 1.11; 95% confidence interval [CI], 1.08-1.14; P < .001) and a 9% increase in Hispanics (adjusted odds ratio, 1.09; 95% CI, 1.05-1.14; P < .001) compared with whites. Fistula maturation for HD access for whites vs blacks vs Hispanics was 77.0% vs 76.3% vs 77.8% (P = .35). After adjusting for covariates, fistula maturation was higher for blacks (adjusted hazard ratio, 1.09; 95% CI, 1.06-1.13; P < .001) and Hispanics (adjusted hazard ratio, 1.13; 95% CI, 1.06-1.20; P < .001) compared with whites. There was no significant difference in prosthetic graft maturation for blacks and Hispanics compared with whites. Primary, primary-assisted, and secondary patency were highest for Hispanic and least for black autogenous fistula recipients. Primary, primary-assisted, and secondary patency was also highest for Hispanic patients who received prosthetic grafts. Prosthetic grafts were associated with a decrease in patency and patient survival compared with fistulas in all racial categories. Mortality was lower for blacks and Hispanics relative to white patients. Initiation of HD with a catheter and conversion to autogenous fistula was associated with decrease in patency and patient survival compared with initiation with a fistula in all racial groups. CONCLUSIONS: Autogenous fistulas are associated with better patency and patient survival compared with prosthetic grafts for all races studied. The use of HD catheter before fistula placement is more prevalent in Hispanic and black patients and is associated with worse patency and patient survival irrespective of race. Fistula and graft patency is highest for Hispanic patients. Patient survival is higher for Hispanic and black patients relative to whites. These associations suggest potential benefit with initiation of HD via autogenous fistula and minimizing temporizing catheter use, irrespective of race.

Hemodynamic events during carotid stenting are associated with significant periprocedural stroke and adverse events.

BACKGROUND: There are limited data on the impact of carotid angioplasty and stenting (CAS)-related changes in blood pressure, heart rate, and preprocedural medications on periprocedural stroke in contemporary, real-world practice. This study evaluates the risk attributable to the CAS-related hemodynamic events and the impact preprocedural medications have on mitigating this risk in a large, population-based cohort. METHODS: We studied all patients in the Vascular Quality Initiative who underwent CAS between January 2006 and December 2016. Kaplan-Meier, multivariable logistic, and Cox regression analyses were used to evaluate the impact of periprocedural hypertension, hypotension, bradycardia, and medication use on immediate periprocedural stroke (IPPS), 30-day, and 1-year stroke. RESULTS: Of the 13,698 CAS procedures studied, 1239 (9.1%), 1824 (13.3%), and 1333 (9.7%) patients experienced periprocedural hypertension, hypotension, and bradycardia, respectively. IPPS was 3.2% vs 2.1% vs 0.65% (P < .001), comparing patients with periprocedural hypertension vs hypotension vs normotension and 1.4 vs 1.0% (P = .19) for bradycardic vs nonbradycardic patients. Periprocedural hypertension was associated with a four-fold increase in IPPS (adjusted odd ratio [aOR], 3.97; 95% confidence interval [CI], 2.63-5.99; P < .001). periprocedural hypotension and bradycardia were associated with 5.5-fold (aOR, 5.56; 95% CI, 3.24-9.52; P < .001) and 2.3-fold (aOR, 2.31; 95% CI, 1.26-4.25; P = .007) increases in IPPS among patients with carotid symptoms. There was 76% decrease in IPPS for patients who did not experience a periprocedural hemodynamic event (aOR, 0.24; 95% CI, 0.16-0.35; P < .001). Unlike preprocedural beta-blockers and angiotensin-converting enzyme inhibitors, prophylactic antibradyarrhythmic agents conferred a 58% reduction in IPPS among patients with carotid symptoms (aOR, 0.42; 95% CI, 0.23-0.78; P = .006). The periprocedural hemodynamic events were also associated with 7.7-fold increase in myocardial infarction (aOR, 7.70; 95% CI, 4.77-12.45; P < .001), a 2.2-fold increase in 30-day mortality (aOR, 2.24; 95% CI, 1.61-3.12; P < .001), and a 16% increase in length of stay (aOR, 1.16; 95% CI, 0.04-2.28; P = .042). The occurrence of these hemodynamic events is higher in patients with prior cardiac disease and the difference in periprocedural outcomes extended to 1 year. CONCLUSIONS: Periprocedural hemodynamic events are associated with an increase in periprocedural stroke, myocardial infarction, death, and length of stay. Periprocedural hypertension in all patients; hypotension and bradycardia in patients with symptomatic carotid disease are associated with significant increase in IPPS. Prophylactic antibradyarrhythmic agents are associated with decrease in bradycardia and IPPS. These results heighten the need to anticipate and promptly address these CAS-related hemodynamic events, especially in susceptible patients.

Systemic vasoprotection by inhaled carbon monoxide is mediated through prolonged alterations in monocyte/macrophage function.

Carbon monoxide (CO) is anti-inflammatory and protective in models of disease. Its actions in vitro are short-lived but are sustained in vivo. We hypothesize that systemic CO can mediate prolonged phenotype changes in vivo, with a focus on macrophages (Mφs). Mφs isolated from CO treated rats responded to lipopolysaccharide (LPS) with increased IL6, IL10 and iNOS expression but decreased TNF. Conditioned media (CM) collected from peritoneal Mφs isolated from CO treated rats stimulated endothelial cell (EC) proliferation versus CM from Mφs from air treated rats. This effect was mediated by Mφ released VEGF and HMGB1. Inhaled CO reduced LPS induced Mφ M1 inflammatory phenotype for up to 5 days. Mitochondrial oxygen consumption in LPS treated Mφs from CO treated mice was preserved compared to LPS treated Mφs from control mice. Finally, transient reduction of inflammatory cells at the time of inhaled CO treatment eliminated the vasoprotective effect of CO in a rodent carotid injury model. Thus, inhaled CO induces a prolonged mixed phenotype change in Mφs, and potentially other inflammatory cells, that contribute to vasoprotection. These findings demonstrate the ability of inhaled CO to modify Mφs in a sustained manner to mediate its therapeutic actions, supporting the translational potential of inhaled CO.

P2Y2 nucleotide receptor mediates arteriogenesis in a murine model of hind limb ischemia.

OBJECTIVE: Arteriogenesis represents the maturation of preformed vascular connections in response to flow changes and shear stress. These collateral vessels can restore up to 60% of the native blood flow. Shear stress and vascular injury can induce the release of nucleotides from vascular smooth muscle cells and platelets that can serve as signaling ligands, suggesting they may be involved in mediating arteriogenesis. The P2Y2 nucleotide receptor (P2Y2R) has also been shown to mediate smooth muscle migration and arterial remodeling. Thus, we hypothesize that P2Y2R mediates arteriogenesis in response to ischemia. METHODS: Hind limb ischemia was induced by femoral artery ligation (FAL) in C57Bl/6NJ or P2Y2R negative mice (P2Y2(-/-)). Hind limb perfusion was measured with laser Doppler perfusion imaging and compared with the sham-operated contralateral limb immediately and at 3, 7, 14, 21, and 28 days after ligation. Collateral vessel size was measured by Microfil casting. Muscle specimens were harvested and analyzed with immunohistochemistry for Ki67, vascular cell adhesion molecule, macrophages, and muscle viability by hematoxylin and essoin stain. RESULTS: Hind limb ischemia induced by FAL in C57Bl/6NJ mice resulted in significant ischemia as measured by laser Doppler perfusion imaging. There was rapid recovery to nearly normal levels of perfusion by 2 weeks. FAL in P2Y2(-/-) mice resulted in severe ischemia with greater tissue loss. Recovery of perfusion was impaired, achieving only 40% compared with wild-type mice by 28 days. Collateral vessels in the P2Y2(-/-) mice were underdeveloped, with reduced vascular cell proliferation and smaller vessel size. The collaterals were ∼65% the size of wild-type collateral vessels (P = .011). Angiogenesis at 28 days in the ischemic muscle, however, was greater in the P2Y2(-/-) mice (P < .001), possibly related to persistent ischemia leading and angiogenic drive. Early macrophage recruitment was reduced by nearly 70% in P2Y2(-/-) despite significantly more myocyte necrosis. However, inflammation was greater at 28 days in the P2Y2(-/-) mice. CONCLUSIONS: P2Y2R deficiency does not alter baseline collateral vessel formation but does significantly impair collateral maturation, with resultant persistent limb ischemia despite enhanced angiogenesis. These findings reinforce the importance of arteriogenesis in the recovery of perfusion in ischemic tissues compared with angiogenesis. They also support the role of P2Y2R in mediating this process. The mechanism by which P2Y2R mediates arteriogenesis may involve the recruitment of inflammatory cells to the ischemic tissues, which is essential to arteriogenesis. Approaches to target P2Y2R may yield new therapeutic strategies for the treatment of arterial occlusive disease.

Xanthine Oxidoreductase Function Contributes to Normal Wound Healing.

Chronic, nonhealing wounds result in patient morbidity and disability. Reactive oxygen species (ROS) and nitric oxide (NO) are both required for normal wound repair, and derangements of these result in impaired healing. Xanthine oxidoreductase (XOR) has the unique capacity to produce both ROS and NO. We hypothesize that XOR contributes to normal wound healing. Cutaneous wounds were created in C57Bl6 mice. XOR was inhibited with dietary tungsten or allopurinol. Topical hydrogen peroxide (H2O2, 0.15%) or allopurinol (30 µg) was applied to wounds every other day. Wounds were monitored until closure or collected at d 5 to assess XOR expression and activity, cell proliferation and histology. The effects of XOR, nitrite, H2O2 and allopurinol on keratinocyte cell (KC) and endothelial cell (EC) behavior were assessed. We identified XOR expression and activity in the skin and wound edges as well as granulation tissue. Cultured human KCs also expressed XOR. Tungsten significantly inhibited XOR activity and impaired healing with reduced ROS production with reduced angiogenesis and KC proliferation. The expression and activity of other tungsten-sensitive enzymes were minimal in the wound tissues. Oral allopurinol did not reduce XOR activity or alter wound healing but topical allopurinol significantly reduced XOR activity and delayed healing. Topical H2O2 restored wound healing in tungsten-fed mice. In vitro, nitrite and H2O2 both stimulated KC and EC proliferation and EC migration. These studies demonstrate for the first time that XOR is abundant in wounds and participates in normal wound healing through effects on ROS production.

Contemporary outcomes of intact and ruptured visceral artery aneurysms.

OBJECTIVE: The treatment outcomes of ruptured visceral artery aneurysms (rVAAs) have been sparsely characterized, with no clear comparison between different treatment modalities. The purpose of this paper was to review the perioperative and long-term outcomes of open and endovascular interventions for intact visceral artery aneurysms (iVAAs) and rVAAs. METHODS: This was a retrospective review of all treated VAAs at one institution from 2003 to 2013. Patient demographics, aneurysm characteristics, management, and subsequent outcomes (technical success, mortality, reintervention) and complications were recorded. RESULTS: The study identified 261 patients; 181 patients were repaired (77 ruptured, 104 intact). Pseudoaneurysms were more common in rVAAs (81.8% vs 35.3% for iVAAs; P < .001). The rVAAs were smaller than the iVAAs (20.7 mm vs 27.5 mm; P = .018), and their most common presentation was abdominal pain; 29.7% were hemodynamically unstable. Endovascular intervention was the initial treatment modality for 67.4% (75.3% for rVAAs, 61.5% for iVAAs). The perioperative complication rate was higher for rVAAs (13.7% vs 1% for iVAAs; P = .003), as was mortality at 30 days (13% vs 0% for iVAAs; P = .001), 1 year (32.5% for rVAAs vs 4.1% for iVAAs; P < .001), and 3 years (36.4% for rVAAs vs 8.3% for iVAAs; P < .001). Lower 30-day mortality was noted with endovascular repair for rVAAs (7.4% vs 28.6% open; P = .025). Predictors of mortality for rVAAs included age (odds ratio, 1.04; P = .002), whereas endovascular repair was protective (odds ratio, 0.43; P = .037). Mean follow-up was 26.2 months, and Kaplan-Meier estimates of survival were higher for iVAAs at 3 years (88% vs 62% for rVAAs; P = .045). The 30-day reintervention rate was higher for rVAAs (7.7% vs 19.5% for iVAAs; P = .019) but was similar between open and endovascular repair (8.2% vs 15%; P = NS). CONCLUSIONS: rVAAs have significant mortality. Open and endovascular interventions are equally durable for elective repair of VAAs, but endovascular interventions for rVAAs result in lower morbidity and mortality. Aggressive treatment of pseudoaneurysms is electively recommended at diagnosis regardless of size.

Glycation-assisted synthesized gold nanoparticles inhibit growth of bone cancer cells.

This study presents a novel approach to synthesize glycogenic gold nanoparticles (glycogenic GNps) capped with glycated products (Schiff's base, Heyns products, fructosylamine etc.). These glycogenic GNps have been found to be active against human osteosarcoma cell line (Saos-2) with an IC50 of 0.187 mM, while the normal human embryonic lung cell line (L-132) remained unaffected up to 1mM concentration. The size of glycogenic GNps can also be controlled by varying the time of incubation of gold solution. Glycation reactions involving a combination of fructose and HSA (Human Serum Albumin) were found to be effective in the reduction of gold to glycogenic GNps whereas glucose in combination with HSA did not result in the reduction of gold. The progress of the reaction was followed using UV-visible spectroscopy and NBT (Nitroblue tetrazolium) assay. The glycogenic GNps were found to be spherical in shape with an average size of 24.3 nm, in a stable emulsion. These GNps were characterized using UV-visible spectroscopy, zeta potential analysis, transmission electron microscopy (TEM) and scanning electron microscopy (SEM).

Evolution of treatment for traumatic thoracic aortic injuries.

OBJECTIVE: To review the evolution of traumatic thoracic aortic injury (TTAI) treatment at a single institution. METHODS: Retrospective analysis of all patients included in an institutional trauma registry and vascular surgery database who underwent treatment of TTAI between January 1999 and January 2011. RESULTS: Ninety-one patients (69 males) were treated for TTAI. The mean age was 38.5 years (range, 16-79 years). Forty-one patients underwent open repair (OR) and 50 thoracic endovascular repair (TEVAR), 37 with thoracic stent grafts (TSG) alone, 11 with infrarenal aortic extender cuffs (AEC), and two with a combination of TSG and AEC. OR was performed exclusively until 2004; the last one was performed in January 2007. All TTAIs have since been treated with TEVAR. The left subclavian artery (LSA) was fully covered in 10 patients (20%) and partially covered in eight patients, with revascularization in only two cases. The use of AEC and avoidance of LSA coverage increased after 2007. Baseline characteristics and injury severity scores were similar between groups. The mortality rate was higher in the OR group (19.5% vs 6.0%; P = .06), although it did not reach statistical significance. The overall incidence of morbidities was similar between the two groups (42% OR vs 50% TEVAR). Two patients developed paraplegia (4.4%) after OR compared with none after TEVAR. In the TEVAR group, a pseudoaneurysm, an iliac artery thrombosis, and a retroperitoneal hematoma developed in one patient each. Overall, eight patients (16%) developed stent graft-related complications (SRC), with two developing early (within 30 days) complications. All complications were related to poor apposition, requiring 10 reinterventions. Four patients underwent open conversions with no mortality. Nine out of 10 SRCs were associated with the use of thoracic stent graft malapposition. No patient treated with AEC had endoleaks or SRC. CONCLUSIONS: TEVAR for TTAI has superior survival outcomes and has replaced OR. SRC requiring reintervention is associated with malapposition and the use of TSG. Until TTAI-specific endografts become available, use of AEC may minimize malapposition and reduce reinterventions. Routine overstenting of the LSA is not necessary and may increase SRC.

Late collapse of a thoracic endoprosthesis.

Thoracic stent graft collapse is a rare complication of thoracic endovascular aortic repair that is mostly asymptomatic and occurs ≤ 3 months of the procedure. We describe the case of a 36-year-old man who presented with symptomatic endograft collapse 38 months after an initial thoracic endovascular aortic repair that was performed for traumatic aortic transection. He had sudden and complete loss of bilateral lower extremity motor and sensory functions (spinal cord ischemia) and anal sphincter tone. The patient was successfully treated with redo thoracic endovascular aortic repair, followed by open conversion and device explantation.

Tumor necrosis factor-alpha and the early vein graft.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-alpha activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-alpha therapy would inhibit NIH. METHODS: Rabbits underwent bilateral vein grafting using jugular vein. All distal branches except the occipital artery were unilaterally ligated to create distinct flow environments between the bilateral grafts. Vein grafts were harvested sequentially up to 28 days for TNF-alpha messenger RNA (mRNA) quantitation. In separate experiments, animals received short-term or long-term dosing with pegylated soluble TNF-alpha type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. RESULTS: Quantitative mRNA assay (TaqMan) revealed shear-dependent (P < .001) and time-dependent (P < .001) TNF-alpha expression. TNF-alpha induction was maximal at day 1 and gradually decreased over time, but was persistently elevated even 4 weeks later (P < .001). Low shear (associated with increased NIH) resulted in significantly higher TNF-alpha mRNA expression (P = .03). PEG sTNF-RI was found in high concentrations in the serum and localized to NIH. The high-flow and low-flow vein grafts from treated animals demonstrated similar volumes of NIH compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling (P = .064) and anti-Ki-67 (P = .12) assays. CONCLUSIONS: Placement of a vein into the arterial circulation acutely upregulates TNF-alpha; this expression level correlates with the degree of subsequent NIH. Pharmacologic interruption of this signaling pathway has no significant impact on NIH or wall cellular proliferation/apoptosis, suggesting that early vein graft adaptations can proceed via TNF-alpha-independent mechanisms.