Detection of Sybil attack in vehicular ad hoc networks by analyzing network performance

<span>Vehicular ad hoc network (VANET) is an emerging technology which can be very helpful for providing safety and security as well as for intelligent transportation services. But due to wireless communication of vehicles and high mobility it has certain security issues which cost the safety and security of people on the road. One of the major security concerns is the Sybil attack in which the attacker creates dummy identities to gain high influence in the network that causes delay in some services and fake voting in the network to misguide others. The early detection of this attack can prevent people from being misguided by the attacker and save them from getting into any kind of trap. In this research paper, Sybil attack is detected by first applying the Poisson distribution algorithm to predict the traffic on the road and in the second approach, analysis of the network performance for packet delivery ratio (PDR) is performed in malign and benign environment. The simulation result shows that PDR decreases in presence of fake vehicles in the network. Our approach is simple and effective as it does not require high computational overhead and also does not violate the privacy issues of people in the network.</span>

Manipulation of Skyrmion Motion Dynamics for Logical Device Application Mediated by Inhomogeneous Magnetic Anisotropy

Magnetic skyrmions are promising potential information carriers for future spintronic devices owing to their nanoscale size, non-volatility and high mobility. In this work, we demonstrate the controlled manipulation of skyrmion motion and its implementation in a new concept of racetrack logical device by introducing an inhomogeneous perpendicular magnetic anisotropy (PMA) via micromagnetic simulation. Here, the inhomogeneous PMA can be introduced by a capping nano-island that serves as a tunable potential barriers/well which can effectively modulate the size and shape of isolated skyrmion. Using the inhomogeneous PMA in skyrmion-based racetrack enables the manipulation of skyrmion motion behaviors, for instance, blocking, trapping or allowing passing the injected skyrmion. In addition, the skyrmion trapping operation can be further exploited in developing special designed racetrack devices with logic AND and NOT, wherein a set of logic AND operations can be realized via skyrmion–skyrmion repulsion between two skyrmions. These results indicate an effective method for tailoring the skyrmion structures and motion behaviors by using inhomogeneous PMA, which further provide a new pathway to all-electric skyrmion-based memory and logic devices.

Anti-high-mobility group box-1 (HMGB1) mediates the apoptosis of alveolar epithelial cells (AEC) by receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway in the rats of crush injuries

Objectives The lung injury is often secondary to severe trauma. In the model of crush syndrome, there may be secondary lung injury. We hypothesize that high-mobility group box 1 (HMGB1), released from muscle tissue, mediates the apoptosis of alveolar epithelial cells (AEC) via HMGB1/Receptor of advanced glycation end-products (RAGE)/c-Jun N-terminal kinase (JNK) pathway. The study aimed to investigate how HMGB1 mediated the apoptosis of AEC in the rat model. Methods Seventy-five SD male rats were randomly divided into five groups: CS, CS + vehicle, CS + Ethyl pyruvate (EP), CS + FPS-ZM1 group, and CS + SP600125 groups. When the rats CS model were completed after 24 h, the rats were sacrificed. We collected the serum and the whole lung tissues. Inflammatory cytokines were measured in serum samples. Western blot and RT-qPCR were used to quantify the protein and mRNA. Lastly, apoptotic cells were detected by TUNEL. We used SPSS 25.0 for statistical analyses. Results Nine rats died during the experiments. Dead rats were excluded from further analysis. Compared to the CS group, levels of HMGB1 and inflammatory cytokines in serum were downregulated in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups. Western blot and RT-qPCR analysis revealed a significant downregulation of HMGB1, RAGE, and phosphorylated-JNK in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups, compared with the CS groups, excluding total-JNK mRNA. Apoptosis of AEC was used TUNEL to assess. We found the TUNEL-positive cells were downregulated in CS + EP, CS + FPS-ZM1, and CS + SP600125 groups. Conclusion The remote lung injury begins early after crush injuries. The HMGB1/RAGE/JNK signaling axis is an attractive target to abrogate the apoptosis of AEC after crush injuries.

The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review

Background: High mobility group box 1 (HMGB1) protein is a damage-associated molecular pattern (DAMP) molecule that plays an important role in the repair and regeneration of tissue injury. It also acts as a pro-inflammatory cytokine through the activation of toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), to elicit the neuroinflammatory response. HMGB1 may aggravate several cellular responses which may lead to pathological inflammation and cellular death. Thus, there have been a considerable amount of research into the pathological role of HMGB1 in diseases. However, whether the mechanism of action of HMGB1 is similar in all neurodegenerative disease pathology remains to be determined. Objective: Therefore, this systematic review aimed to critically evaluate and elucidate the role of HMGB1 in the pathology of neurodegeneration based on the available literature. Methods: A comprehensive literature search was performed on four databases; EMBASE, PubMed, Scopus, and CINAHL Plus. Results: A total of 85 articles were selected for critical appraisal, after subjecting to the inclusion and exclusion criteria in this study. The selected articles revealed that HMGB1 levels were found elevated in most neurodegeneration except in Huntington’s disease and Spinocerebellar ataxia, where the levels were found decreased. This review also showcased that HMGB1 may act on distinctive pathways to elicit its pathological response leading to the various neurodegeneration processes/diseases. Conclusion: While there have been promising findings in HMGB1 intervention research, further studies may still be required before any HMGB1 intervention may be recommended as a therapeutic target for neurodegenerative diseases.

Remarkably High-Performance Nanosheet GeSn Thin-Film Transistor

High-performance p-type thin-film transistors (pTFTs) are crucial for realizing low-power display-on-panel and monolithic three-dimensional integrated circuits. Unfortunately, it is difficult to achieve a high hole mobility of greater than 10 cm2/V·s, even for SnO TFTs with a unique single-hole band and a small hole effective mass. In this paper, we demonstrate a high-performance GeSn pTFT with a high field-effect hole mobility (μFE), of 41.8 cm2/V·s; a sharp turn-on subthreshold slope (SS), of 311 mV/dec, for low-voltage operation; and a large on-current/off-current (ION/IOFF) value, of 8.9 × 106. This remarkably high ION/IOFF is achieved using an ultra-thin nanosheet GeSn, with a thickness of only 7 nm. Although an even higher hole mobility (103.8 cm2/V·s) was obtained with a thicker GeSn channel, the IOFF increased rapidly and the poor ION/IOFF (75) was unsuitable for transistor applications. The high mobility is due to the small hole effective mass of GeSn, which is supported by first-principles electronic structure calculations.

Tcf1 is essential for initiation of oncogenic Notch1-driven chromatin topology in T-ALL

NOTCH1 is a well-established lineage specifier for T cells and amongst the most frequently mutated genes throughout all subclasses of T cell acute lymphoblastic leukemia (T-ALL). How oncogenic NOTCH1 signaling launches a leukemia-prone chromatin landscape during T-ALL initiation is unknown. Here we demonstrate an essential role for the high-mobility-group transcription factor Tcf1 in orchestrating chromatin accessibility and topology allowing aberrant Notch1 signaling to convey its oncogenic function. Although essential, Tcf1 is not sufficient to initiate leukemia. The formation of a leukemia-prone epigenetic landscape at the distal Notch1-regulated Myc enhancer, which is fundamental to this disease, is Tcf1-dependent and occurs within the earliest progenitor stage even before cells adopt a T lymphocyte or leukemic fate. Moreover, we discovered a unique evolutionarily conserved Tcf1-regulated enhancer element in the distal Myc-enhancer, which is important for the transition of pre-leukemic cells to full-blown disease.

Human Resilience in the Face of Mid-Holocene Climate Change on the Central West Coast of South Africa

After the Last Glacial Maximum, important yet milder climatic trends continued to characterise the Holocene. None of them was more challenging to forager groups in the central west coast of South Africa than the mid-Holocene Altithermal (8200–4200 cal BP). Hot and dry weather and 1–3 m higher sea levels were thought once to have barred local foragers from this region because of a lack of sites dating to this period. Instead, this initial scenario reflected largely a sampling problem. Steenbokfontein Cave is one of a few sites with some of the largest mid-Holocene deposits, allowing insights into forager adaptations during this period. Results show high mobility over large distances and a terrestrial diet mostly dependant on small bovids, complemented with fewer coastal resources. Stone tool kits and lithic raw materials among various sites suggest that much evidence for mid-Holocene occupation is actually found near the local riparian systems.