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A novel simple cosine-shaped resonator is proposed in this paper, intended to reduce mutual coupling between units. The proposed methodology is based on resisting the propagation of surface waves. Initially, a configuration consisting of 2 × 3 cosine-shaped resonators placed between two patch antennas is designed, resulting in a reduction of over 13.5 dB at the frequency of 5.8 GHz. Subsequently, a fractal microstrip array antenna is employed as a test case to demonstrate the efficacy of the proposed strategy. The radiating element is designed using a Koch snowflake fractal structure. A 4 × 4 microstrip array prototype antenna, fed by an aperture-coupled, corporate feeding structure, was designed, fabricated, and evaluated. Periodic arrangement of the cosine-shaped resonators around the radiation elements results in a 3.28% increase in impedance bandwidth. The measured results indicate an impedance bandwidth of 9.83% (5.54–6.11 GHz), an improvement in peak gain up to 20.46 dBi at the operating frequency, and a 3-dB gain bandwidth of 19.14% (5.21–6.32 GHz). [ABSTRACT FROM AUTHOR]

Aplastic anemia (AA) is a T cell immune-mediated autoimmune disease. Overactivated CD8+ T cells play a leading role in the pathogenesis of AA, which may be due to disbalance in costimulatory and coinhibitory signals in T cells. In this study, we firstly investigated the expression of OX40, 4–1BB, GITR, ICOS, CTLA-4, LAG-3, and TIM-3 on CD8+ T cells from untreated patients with AA and healthy individuals (HIs) by flow cytometry. Moreover, we further analyzed the phenotype and functional characteristics of CD8+GITR+ T cells to more fully assess the T cell activation dysfunction in AA. We for the first time demonstrated significantly decreased percentage of CD8+GITR+ T cells in AA, and CD8+GITR+CTLA-4+ T cells were significantly higher in patients with AA compared with HIs. Conversely, the percentage of CD8+GITR+granzyme B+ and CD8+GITR+perforin+ T cells in AA patients was significantly reduced. Our preliminary data illustrate that the CD8+GITR+ T cell population might negatively regulate overactive T cell activation in AA. [ABSTRACT FROM AUTHOR]

Let L = { L (t , x) , t ≥ 0 , x ∈ R } be the local time of a G-Brownian motion B on a sublinear expectation space (Ω , H , E ˆ). In this paper, we show that the local time L is a rough path of roughness p quasi-surely for any 2

In this paper, we consider the optimal approximation of a Rosenblatt process based on semimartingales of the formwhere (y1,y2)↦a(y1,y2) is a square integrable process andBis a standard Brownian motion. We show that there exists a unique semimartingale closest to Rosenblatt process ifais deterministic. [ABSTRACT FROM PUBLISHER]

As a core scaffold protein, Cullin 7 (Cul7) forms Skp1-Cullin-F-box (SCF) E3 ubiquitin ligase complexes with the regulator of cullins-1 (ROC1), S-phase kinase associated protein 1 (Skp1) and F-Box, and WD repeat domain containing 8 (Fbxw8). Alternatively, Cul7 can form a CRL7SMU1 complex with suppressor of Mec-8 and Unc-52 protein homolog (SMU1), damage-specific DNA binding protein 1 (DDB1), and ring finger protein 40 (RNF40), to promote cell growth. The mutations of Cul7 cause the 3-M dwarf syndrome, indicating Cul7 plays an important role in growth and development in humans and mice. Moreover, Cul7 regulates cell transformation, tumor protein p53 activity, cell senescence, and apoptosis, mutations in Cul7 are also involved in the development of tumors, indicating the characteristics of an oncogene. Cul7 is highly expressed in breast cancer, lung cancer, hepatocellular carcinoma, pancreatic cancer, ovarian cancer, and other malignant tumors where Cul7 promotes tumor development, cell transformation, and cell survival by regulating complex signaling pathways associated with protein degradation. In this review, we discuss the roles of Cul7 in malignant tumor development and its involvement in oncogenic signaling. We finally discuss the potential of Cul7 as a potential significant anti-cancer target.

Aplastic anemia (AA) is a T cell immune-mediated autoimmune disease. Overactivated CD8 + T cells play a leading role in the pathogenesis of AA, which may be due to disbalance in costimulatory and coinhibitory signals in T cells. In this study, we firstly investigated the expression of OX40, 4-1BB, GITR, ICOS, CTLA-4, LAG-3, and TIM-3 on CD8 + T cells from untreated patients with AA and healthy individuals (HIs) by flow cytometry. Moreover, we further analyzed the phenotype and functional characteristics of CD8 + GITR + T cells to more fully assess the T cell activation dysfunction in AA. We for the first time demonstrated significantly decreased percentage of CD8 + GITR + T cells in AA, and CD8 + GITR + CTLA-4 + T cells were significantly higher in patients with AA compared with HIs. Conversely, the percentage of CD8 + GITR + granzyme B + and CD8 + GITR + perforin + T cells in AA patients was significantly reduced. Our preliminary data illustrate that the CD8 + GITR + T cell population might negatively regulate overactive T cell activation in AA.