Comprehensive study of physical unclonable functions on FPGAs: correlation driven Implementation, deep learning modeling attacks, and countermeasures

For more than a decade and a half, Physical Unclonable Functions (PUFs) have been presented as a promising hardware security primitive. The idea of exploiting variabilities in hardware fabrication to generate a unique fingerprint for every silicon chip introduced a more secure and cheaper alternative. Other solutions using non-volatile memory to store cryptographic keys, require additional processing steps to generate keys externally, and secure environments to exchange generated keys, which introduce many points of attack that can be used to extract the secret keys. PUFs were addressed in the literature from different perspectives. Many publications focused on proposing new PUF architectures and evaluation metrics to improve security properties like response uniqueness per chip, response reproducibility of the same PUF input, and response unpredictability using previous input/response pairs. Other research proposed attack schemes to clone the response of PUFs, using conventional machine learning (ML) algorithms, side-channel attacks using power and electromagnetic traces, and fault injection using laser beams and electromagnetic pulses. However, most attack schemes to be successful, imposed some restrictions on the targeted PUF architectures, which make it simpler and easier to attack. Furthermore, they did not propose solid and provable enhancements on these architectures to countermeasure the attacks. This leaves many open questions concerning how to implement perfect secure PUFs especially on FPGAs, how to extend previous modeling attack schemes to be successful against more complex PUF architectures (and understand why modeling attacks work) and how to detect and countermeasure these attacks to guarantee that secret data are safe from the attackers. This Ph.D. dissertation contributes to the state of the art research on physical unclonable functions in several ways. First, the thesis provides a comprehensive analysis of the implementation of secure PUFs on FPGAs using manual placement and manual routing techniques guided by new performance metrics to overcome FPGAs restrictions with minimum hardware and area overhead. Then the impact of deep learning (DL) algorithms is studied as a promising modeling attack scheme against complex PUF architectures, which were reported immune to conventional (ML) techniques. Furthermore, it is shown that DL modeling attacks successfully overcome the restrictions imposed by previous research even with the lack of accurate mathematical models of these PUF architectures. Finally, this comprehensive analysis is completed by understanding why deep learning attacks are successful and how to build new PUF architectures and extra circuitry to thwart these types of attacks. This research is important for deploying cheap and efficient hardware security primitives in different fields, including IoT applications, embedded systems, automotive and military equipment. Additionally, it puts more focus on the development of strong intrinsic PUFs which are widely proposed and deployed in many security protocols used for authentication, key establishment, and Oblivious transfer protocols

The role of the P2X7 nucleotide receptor in salivary gland inflammation

Salivary gland inflammation is a hallmark of Sjogren's syndrome (SS), a common autoimmune disease characterized by lymphocytic infiltration and the consequent impairment of the salivary gland and loss of saliva secretion, predominantly in women. The current therapeutic management of SS is relatively ineffective and does not address the underlying inflammatory processes contributing to the pathology of SS. In this study, two novel therapeutic approaches were evaluated to limit salivary gland inflammation and improve secretory function, i.e., antagonism of the P2X7 nucleotide receptor (P2X7R), which prevents salivary gland inflammation and activation of the P2Y[subscript2] nucleotide receptor (P2Y[subscript2]R) which stimulates the regeneration of damaged salivary glands. The P2X7R is an ATP-gated non-selective cation channel that regulates inflammatory responses in cells and tissues, including salivary gland epithelium. The P2X7R contributes to the pathology of a variety of inflammatory diseases, including rheumatoid arthritis and inflammatory bowel disease. In immune cells, P2X7R activation induces the production of pro-inflammatory cytokines, including IL-1[beta] and IL-18, by inducing the oligomerization of the multiprotein complex NLRP3-type inflammasome. This study (Chapter II) sheds light on the role of the P2X7R in salivary gland inflammation and hyposalivation. Our results show that in primary mouse submandibular gland (SMG) epithelial cells, P2X7R activation induces the assembly of the NLRP3 inflammasome and the maturation and release of IL-1[beta], responses that are absent in SMG cells isolated from mice devoid of P2X7Rs (P2X7R[superscript-/-]). P2X7R-mediated IL-1[beta] release in SMG epithelial cells is dependent on downhill transmembrane Na[superscript+] and/or K[superscript+] fluxes, the activation of heat shock protein 90 (HSP90), a protein required for the activation and stabilization of the NLRP3 inflammasome, and the generation of mitochondrial ROS. In vivo administration of the P2X7R antagonist A438079 in the CD28[superscript-/-], IFN[superscript][superscript-/-], NOD.H-2[superscripth4] mouse model of salivary gland exocrinopathy ameliorated salivary gland inflammation and enhanced carbachol-induced saliva secretion. These findings demonstrate that P2X7R antagonism in vivo represents a promising therapeutic strategy to limit salivary gland inflammation and improve secretory function. The P2Y[subscript2]R, a G protein-coupled receptor equipotently activated by ATP and UTP, is upregulated in a variety of tissues, including salivary gland epithelium, in response to injury or stress and is proposed to play a role in tissue regeneration. The results indicated that P2Y2R activation with UTP enhances the migration, aggregation and self-organization of dispersed salivary epithelial cells forming spheres that display characteristics similar to differentiated acini in salivary glands. One of the consequences of the chronic inflammatory disease SS is the fibrosis of the salivary gland. The role of transforming growth factor- [beta] (TGF-[beta]) is well established in the fibrosis and regeneration of various organs, including the liver, lung and kidney. In this study, results with a submandibular gland (SMG) duct ligation-induced mouse model of fibrosis indicated that 7 days of SMG duct ligation resulted in upregulation of TGF-β signaling components which correlated with the upregulation of the fibrosis markers collagen 1 and fibronectin, responses that were inhibited by administration of the TGF-[beta] receptor 1 inhibitors. These results suggest that TGF-[beta] signaling contributes to duct ligation-induced changes in salivary epithelium that correlate with glandular fibrosis.Includes biblographical reference

An Epidemiological Study of Sheep and Goat pox Outbreaks in the Sudan

Sheep and goat pox Outbreaks occurred in different geographic areas of Sudan and most strikingly, were highly species specific. Two outbreaks in Gedarif State in June. 2013 affected no goats and outbreak in Khartoum state in March. 2015 affected no sheep despite communal herding; affected goats were vaccinated with 0240 strain. Clinically, the disease was characterized by fever, depression and eruption of generalized pox lesions. Mortality rate ranged between 5.2 and 6.7% with a mean of 6.1%. Isolation of viruses succeed on Lamb testes cell culture at passage four, the diseases were diagnosed using virus neutralisation test and polymerase chain reaction. Sheeppox and goatpox isolates grew well in lamb testes and Vero cells. In MDBK however, both viruses induced slight CPE that reached 60% in 9 days. On the other hand, both isolates induced no CPE in chick embryo fibroblast cells. Virus isolation attempts failed on chorioallantoic membrane of embryonated chicken eggs

Association Between Hemoglobin A1C and the Severity of Acute Ischemic Stroke in Sudanese Patients in Omdurman Military Hospital

Background: Hemoglobin A1C (HbA1c) levels are known to be linked to a higher risk of stroke. However, no research data is available on the impact of HbA1C on the severity of acute ischemic stroke in Sudan. Methods: This study is a descriptive, cross-sectional hospital-based study of 40 cases of acute ischemic stroke. Ischemic stroke was confirmed using computed tomography (CT) scan at admission; all subjects’ blood HbA1C levels were also measured. Participants were divided into two subgroups based on HbA1C at admission, good glycemic control (GGC) (<7 HbA1C) and poor glycemic control (PGC) (>7 HbA1C), and neurological impairment was assessed using the National Institutes of Health Stroke Scale (NIHSS). Results: The age distribution of the participants was 45-85 years, with an average age of 63.5±9.2 years with the highest frequency (67.5%) in the age group of 55-75 years. PGC had a statistically significant high HbA1C value of 8.9±1.3 (P=0.000), when compared to GGC subgroups 5.1±0. The association between stroke severity and HbA1C levels on admission in this study was statistically significant (P value=0.005), on admission (78.6%) PGC had moderate to severe stroke (> 18.8 NIHSS) versus (33.3%) that of the GGC (>10.4NIHSS). The frequency of elevated HbA1C levels in patients with acute ischemic stroke was 70% in this study. Conclusion: PGC was shown to be linked to the occurrence of stroke and to its severity

Zoonotic pathogens of dromedary camels in Kenya:a systematised review

Kenya is home to Africa’s third largest population of dromedary camels, and production at commercial and local levels are increasingly important. In pastoral and nomadic communities in the arid and semi-arid lands (ASALs), camels play a vital role in food security, while commercial milk production and formalized export markets are rapidly emerging as camel populations expand into non-traditional areas. Until recently, little focus was placed on camels as hosts of zoonotic disease, but the emergence of Middle Eastern respiratory coronavirus (MERS-CoV) in 2012, and the discovery of exposure to the virus in Kenyan camels, highlighted the need for further understanding of this area. This systematised review utilised a robust search strategy to assess the occurrence of camel-associated zoonoses in Kenya and to evaluate the quality of the published literature. Seventy-four studies were identified, covering sixteen pathogens, with an increasing number of good quality studies in recent years. Despite this, the area remains under-researched and there is a lack of robust, high-quality research. Trypanosome spp., Echinococcus granulosus and Brucella spp. appeared most frequently in the literature. Pathogens with the highest reported prevalence were MERS-CoV (0–100%), Echinococcus granulosa (7–60%) and Rift Valley fever virus (7–57%). Exposure to Brucella spp., Coxiella burnetii and Crimean-Congo haemorrhagic fever virus showed higher levels in camel or camel-associated vectors than other livestock species, although brucellosis was the only disease for which there was robust evidence linking camel and human exposure. Zoonotic agents with less severe human health outcomes, such as Dermatophilosus congolensis and contagious ecthyma, were also represented in the literature. This review provides an important summary of the scope and quality of current knowledge. It demonstrates that further research, and improved adherence to robust study design and reporting are essential if the zoonotic risk from camels in Kenya, and elsewhere, is to be better understood

Physical and chemical processes of Abu Rusheid cataclastic rocks for recovering niobium, zirconium and uranium compounds

Cataclastic rocks of Abu Rushied area (South Eastern Desert, Egypt) characterized by the presence of niobium, tantalum, zirconium minerals as well as uranium-thorium minerals. Physical upgrading process was applied using gravity and magnetic separation techniques to concentrate these economic minerals mainly to obtain the magnetic niobium concentrate at 0.2- 0.5 ampere, beside the non-magnetic Zr and U at 1.5 ampere. The chemical processing upon niobium concentrate was performed using NH4F roasting process at 250ºC followed by selective precipitation of Nb as Nb-sulfide. An alkaline fusion using NaOH was applied upon zirconium concentrate at the optimum conditions of: zircon concentrate/ NaOH mass ratio 1/2, fusion temperature of 650ºC and 2.5h fusion time followed by selective precipitation of Zr as Zr- tartrate. Finally, two flowsheets were drawn summarizing the whole recovery processes

Acute ammonia exposure combined with heat stress impaired the histological features of gills and liver tissues and the expression responses of immune and antioxidative related genes in Nile tilapia

Ammonia exposure can be considered more stressful for aquatic animals when it coincides with high temperature. This study was conducted to detect the effects of ammonia exposure and heat stress and their interactions on the histological features of gills and liver tissues and the expression responses of immune and antioxidative related genes in Nile tilapia. Thus, 180 fish were divided into four groups (triplicates), where the first and third groups were kept in clean water without total ammonium nitrogen (TAN) exposure. At the same time, the second and fourth groups were exposed to 5 mg TAN/L. After seven days, the water temperature was raised in the third (without ammonia toxicity) and fourth (exposed with 5 mg TAN/L) groups up to 32 °C and kept under these conditions for 24 h. While the first (without ammonia toxicity) and second (exposed with 5 mg TAN/L) groups were kept under optimum water temperature (27.28 °C) then gills and liver tissues were dissected. Marked upregulation of keap1 was seen in the gills of fish exposed to ammonia/heat stress. The expression of mRNA levels for nrf2, nqo-1, cat, and gpx genes were downregulated in all stressed groups, with the lowest was recorded in the ammonia/heat stress group. The transcription of ho-1 was upregulated in the ammonia and heat stress groups while downregulated in the ammonia/heat stress group. The transcription of the complement C3 gene was downregulated in the livers of heat stress and ammonia/heat stress groups, while the lysozyme gene was downregulated in the ammonia/heat stress group. The mRNA expression levels of nf-κB, il-1β, and tnf-α genes were higher in the ammonia group than in the heat stress group. The highest transcription level of nf-κB, il-1β, tnf-α, il-8, and hsp70 genes and the lowest C3 and lysozyme genes were observed in fish exposed to ammonia/heat stress. The co-exposure to ammonia with heat stress triggered degeneration of primary and secondary gill filaments with telangiectasia and vascular congestion of secondary epithelium while, the liver showed hepatic vascular congestion and visible necrotic changes with nuclear pyknosis. In conclusion, the combined exposure of ammonia and heat stress induced oxidative stress, immunosuppression, and inflammation in Nile tilapia

Dietary Lactobacillus acidophilus ATCC 4356 Relieves the Impacts of Aflatoxin B1 Toxicity on the Growth Performance, Hepatorenal Functions, and Antioxidative Capacity of Thinlip Grey Mullet (Liza ramada) (Risso 1826)

Dietary Lactobacillus acidophilus ATCC 4356 was used to relieve the impacts of aflatoxin B1 toxicity on the performances of Liza ramada. The control diet was without any additives, while the second and third diets were supplemented with aflatoxin B1 at 0.5 and 1 mg/kg. The fourth diet was supplemented with Lb. acidophilus ATCC 4356 at 1 × 106 CFU/mL per kg diet, while the fifth with aflatoxin B1 at 1 mg/kg and Lb. acidophilus ATCC 4356 at 1 × 106 CFU/mL per kg diet. The growth performance markedly increased (p \u3c 0.05) in L. ramada fed Lb. acidophilus ATCC 4356, while aflatoxin B1 at 0.5 and 1 mg/kg groups showed a severe reduction. The red blood cells, hemoglobulin, hematocrit, and white blood cells were markedly increased in L. ramada fed Lb. acidophilus ATCC 4356 while decreased (p \u3c 0.05) in fish fed aflatoxin B1 at 0.5 and 1 mg/kg. The blood total protein and albumin were markedly increased (p \u3c 0.05) in L. ramada fed Lb. acidophilus ATCC 4356 while reduced in aflatoxin B1 at 0.5 and 1 mg/kg groups. The levels of total cholesterol and triglycerides were meaningfully increased in fish of the Lb. acidophilus ATCC 4356 and aflatoxin B1 at 1 mg/kg groups while decreased in aflatoxin B1 at 0.5 and 1 mg/kg groups. Alanine aminotransferase, aspartate aminotransferase, creatinine, and urea levels were markedly decreased (p \u3c 0.05) in fish-fed Lb. acidophilus ATCC 4356 while increased in aflatoxin B1 at 0.5 and 1 mg/kg groups. The highest levels of blood glucose and cortisol were seen in fish contaminated with aflatoxin B1 at 1 mg/kg, while the lowest levels were observed in the fish fed Lb. acidophilus ATCC 4356 group (p \u3c 0.05). The catalase and superoxide dismutase were markedly enhanced in the Lb. acidophilus ATCC 4356 group and severely declined in aflatoxin B1 at 0.5 and 1 mg/kg groups (p \u3c 0.05). The malondialdehyde level was markedly reduced in fish fed Lb. acidophilus ATCC 4356 with or without aflatoxin B1 at 1 mg/kg diets while increased in fish contaminated with aflatoxin B1 at 0.5 and 1 mg/kg (p \u3c 0.05). The control group had lower malondialdehyde levels than the aflatoxin B1 at 1 mg/kg group and higher than the Lb. acidophilus ATCC 4356 with or without aflatoxin B1 toxicity (p \u3c 0.05). Histopathological examination revealed impaired intestines and livers in fish contaminated with aflatoxin B1 while Lb. acidophilus ATCC 4356 relieves the inflammation and protected the intestines and livers. In conclusion, dietary Lb. acidophilus ATCC 4356 is recommended to relieve the impacts of aflatoxicosis-induced hepatorenal failure and oxidative stress in L. ramada

Development and Study of a New Keynesian Small Open Economy Model for Policy Analysis in Sudan, Evidence from DSGE Model

The purpose of this paper is to create a small open economy model for monetary policy discussion and analysis. A new Keynesian model for the Sudanese economy is developed using the DSGE technique. The paper made use of annual data from the period (1998 - 2021). The paper demonstrates that, in the case of a fully-fledged Islamic monetary system, the exchange rate can be used as a proxy for the policy rate and yield results that are consistent with what was expected.  The main findings are that when monetary policy shocks occur, an increase in the exchange rate directly leads to a contraction in aggregate demand, the fluctuations in output in the short run are primarily driven by output, inflation, and exchange rate shocks, that the response of the variables to policy shocks is consistent with economic theory and what is expected from the variables, and that the empirical findings of the model demonstrate how models can help in policy discussion and analysis. The policy implications were that Sudanese authorities can use the exchange rate to track the dynamics in monetary policy DSGE models that can be used for discussion and policy analysis, and Sudanese monetary authorities must pay close attention to output fluctuations based on variance decomposition analysis