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Damping intra-area and interarea oscillations are critical to optimal power flow and stability in a power system. Power system stabilizers (PSSs) are effective damping devices, as they provide auxiliary control signals to the excitation systems of generators. The proper selection of PSS parameters to accommodate variations in the power system dynamics is important and is a challenging task particularly when several PSSs are involved. Two classical bio-inspired algorithms, which are small-population-based particle swarm optimization (SPPSO) and bacterial foraging algorithm (BFA), are presented in this paper for the simultaneous design of multiple optimal PSSs in two power systems. A classical PSO with a small population of particles is called SPPSO in this paper. The SPPSO uses the regeneration concept, introduced in this paper, to attain the same performance as a PSO algorithm with a large population. Both algorithms use time domain information to obtain the objective function for the determination of the optimal parameters of the PSSs. The effectiveness of the two algorithms is evaluated and compared for damping the system oscillations during small and large disturbances, and their robustness is illustrated using the transient energy analysis. In addition, the computational complexities of the two algorithms are also presented. Index Terms--Bacterial foraging, computational complexity, multimachine power systems, Nigerian power system, particle swarm optimization (PSO), power system stabilizers (PSSs), regeneration stability, small population, transient energy (TE) analysis.

During early summer 2019, the Netherlands experienced an outbreak of the exotic oak processionary caterpillar. The vast number of caterpillars, which live in large nests on oak trees before they turn into moths, possess thousands of small, barbed hairs (setae) that are disseminated with the wind. The hairs cause a range of primarily dermatologic problems. However, Dutch ophthalmologists started reporting patients with ophthalmologic complaints caused by the penetrating hairs of the oak processionary caterpillar. This paper focuses on the ophthalmologic complications caused by the caterpillar hairs. We collected a series of four cases with reports ranging from a corneal erosion with hairs lodged into the cornea, to a sterile endophthalmitis in which hairs were found in the vitreous. A literature review for similar cases was performed using the PubMed and Embase database. Together with the Dutch Ophthalmic Society (Nederlands Oogheelkundig Gezelschap, NOG), a national survey was issued to determine the scale of this new problem. This showed that oak processionary caterpillar related complaints are primarily limited to the south of the Netherlands. Suggested ophthalmic treatment guidelines are presented. With the next summer at the doorstep, and limited preventative measures against the caterpillar hairs, we expect a new wave of ophthalmologic complaints coming year as well. [ABSTRACT FROM AUTHOR]

Immune cell activation is a stringently regulated process, as exaggerated innate and adaptive immune responses can lead to autoinflammatory and autoimmune diseases. Perhaps the best-characterized molecular pathway promoting cell activation is the nuclear factor-κB (NF-κB) signaling pathway. Stimulation of this pathway leads to transcription of numerous pro-inflammatory and cell-survival genes. Several mechanisms tightly control NF-κB activity, including the key regulatory zinc finger (de)ubiquitinating enzyme A20/tumor necrosis factor α-induced protein 3 (TNFAIP3). Single nucleotide polymorphisms (SNPs) in the vicinity of the TNFAIP3 gene are associated with a spectrum of chronic systemic inflammatory diseases, indicative of its clinical relevance. Mice harboring targeted cell-specific deletions of the Tnfaip3 gene in innate immune cells such as macrophages spontaneously develop autoinflammatory disease. When immune cells involved in the adaptive immune response, such as dendritic cells or B-cells, are targeted for A20/TNFAIP3 deletion, mice develop spontaneous inflammation that resembles human autoimmune disease. Therefore, more knowledge on A20/TNFAIP3 function in cells of the immune system is beneficial in our understanding of autoinflammation and autoimmunity. Using the aforementioned mouse models, novel A20/TNFAIP3 functions have recently been described including control of necroptosis and inflammasome activity. In this review, we discuss the function of the A20/TNFAIP3 enzyme and its critical role in various innate and adaptive immune cells. Finally, we discuss the latest findings on TNFAIP3 SNPs in human autoinflammatory and autoimmune diseases and address that genotyping of TNFAIP3 SNPs may guide treatment decisions. [ABSTRACT FROM AUTHOR]

ABSTRACT The deployment of large language models (LLMs) on edge devices and non‐server environments presents significant challenges, primarily due to constraints in memory usage, computational power, and inference time. This article investigates the feasibility of running LLMs across such devices by focusing on optimising memory usage, employing quantization techniques, and reducing inference time. Specifically, we utilise LLaMA 2 for biomedical text summarization and implement low‐rank adaptation (LoRA) quantization to compress the model size to compress the model size and fine‐tune it using limited resources. Our study systematically evaluates memory consumption during both training and inference phases, demonstrating substantial reductions through efficient LoRA quantization. Our results indicate that with careful optimization, it is feasible to deploy sophisticated LLMs like LLaMA 2 on low powered devices, thereby broadening the scope of their application in resource‐constrained environments. [ABSTRACT FROM AUTHOR]

Chronic perivascular inflammation is a prominent feature in the lungs of idiopathic pulmonary arterial hypertension. Although the proportions of conventional dendritic cells (cDCs) and plasmacytoid DCs are increased in idiopathic pulmonary arterial hypertension lungs, it remains unknown whether activated cDCs play a pathogenic role. The Tnfaip3 gene encodes the ubiquitin-binding protein A20, which is a negative regulator of NF-κB, critically involved in DC activation. Targeting of Tnfaip3/A20 in cDCs was achieved by Clec9a (DNGR1)-Cre-mediated excision of the Tnfaip3 gene in Tnfaip3 DNGR1-KO mice. Mice were evaluated for signs of pulmonary hypertension (PH) using right heart catheterization, echocardiography, and measurement of the Fulton index. Inflammation was assessed by immunohistochemistry and flow cytometry. Pulmonary cDCs and monocyte-derived DCs from 31-week-old Tnfaip3 DNGR1-KO mice showed modulated expression of cell surface activation markers compared with Tnfaip3 DNGR1-WT mice. Tnfaip3 DNGR1-KO mice developed elevated right ventricular systolic pressure and right ventricular hypertrophy. The lungs of these mice displayed increased vascular remodeling and perivascular and peribronchial immune cell infiltration resembling tertiary lymphoid organs. Proportions of activated T cells and expression of IL-1β, IL-6, and IL-10 were enhanced in the lungs of Tnfaip3 DNGR1-KO mice. Autoreactive IgA and IgG1 was detected in BAL and autoreactive IgA recognizing pulmonary endothelial antigens was present in the serum of Tnfaip3 DNGR1-KO mice. All signs of PH were ameliorated in Tnfaip3 DNGR1-KO mice by anti - IL-6 antibody treatment. These results indicate that activation of the NF-κB pathway in DCs, through deletion of A20/ Tnfaip3 , leads to experimental PH with accompanied pulmonary inflammation in an IL-6-dependent fashion.