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Small object detection is a challenging task in computer vision. We claim that the huge performance gap between the small object detectors and normal sized object detectors stems from two aspects, including the small object dataset and the small object itself. In terms of datasets, we build a large-scale dataset with high image resolution dubbed Small-PCB, in order to promote detection in semiconductor industry. For the small object itself, we utilize multi-scale feature learning and feature fusion strategy to help detect objects. More concretely, we devise two novel components to predict small objects better: re-parameterized module with channel shuffle (RMCS) and multi-scale feature enhanced convolution (MFEC). MFEC aims to split input channels into several parts and applies convolutions with different sizes to each part, and adopt point-by-point convolution to fuse individual channel features. RMCS not only use structural re-parameterization, but also channel shuffle. The usage of channel shuffle can be seen as a fusion of channel features. It strengthens feature information interaction between different channel groups, which bring more informative feature clues. Based on the RMCS and the MFEC, we introduce OIU-RMCS and M-MFEC, respectively. Finally, we build our I-YOLO via integrating these two components into a YOLO-based detector. A large number of qualitative and quantitative results in the experiments indicate that our proposed I-YOLO achieves the state-of-the-art performance on the popular AI-TODv2 and Small-PCB datasets. [ABSTRACT FROM AUTHOR]

Fully discrete potential-based finite element methods called $${\mathbf{A}-\phi}$$ methods are used to solve a transient eddy current problem in a three-dimensional convex bounded polyhedron. Using $${\mathbf{A}-\phi}$$ methods, fully discrete coupled and decoupled numerical schemes are developed. The existence and uniqueness of solutions for these schemes together with the energy-norm error estimates are provided. To verify the validity of both schemes, some computer simulations are performed for the model from TEAM Workshop Problem 7. [ABSTRACT FROM AUTHOR]

Lymphocytes express voltage-gated (Kv) and Ca2+-activated (IKCa1) K+ channels. Recently, we found that WEHI-231, an immature B cell line, expresses voltage-independent K+ channels called large-conductance background K + channels (LKbg). Arachidonic acid (AA) has attracted attention because of its potential regulatory roles in the apoptosis of immature B cells. To elucidate the functional targets of AA, we investigated the effects of AA on membrane currents, voltages, and cytoplasmic Ca2+ concentration ([Ca2+]c) of WEHI-231 and Bal-17 cells that represent immature and mature mouse B cells, respectively. In whole-cell patch clamp, both Kv and IKCa1 were inhibited by AA. On the other hand, AA activated LKbg current and non-selective cationic (NSC) current in WEHI-231 while only NSC current in Bal-17. Inside–out patch clamp study showed that AA directly activates LKbg. AA induced hyperpolarization of WEHI-231 and depolarization of Bal-17 cells, respectively. The selective functional expression of LKbg and their activation by AA were also confirmed in the immature B cells (B220+/AA4.1+) freshly isolated from mouse spleen. In fura-2 spectrofluorimetry, AA induced persistent increase in [Ca2+]c of WEHI-231 cells, which was attenuated by KCl-induced depolarization. In Bal-17 cell, however, AA induced only a transient increase of [Ca2+]c. In summary, the novel type of background K+ channels (LKbg) in immature B cells is strongly activated while the other K+ channels (Kv and IKCa1) commonly expressed in lymphocytes are inhibited by AA. The hyperpolarization and augmentation of Ca2+ influx by LKbg activation might play a role in the response of immature B cells to AA. [ABSTRACT FROM AUTHOR]

A posteriori error estimate of the discontinuous-streamline diffusion method for first-order hyperbolic equations was presented, which can be used to adjust space mesh reasonably. A numerical example is given to illustrate the accuracy and feasibility of this method. [ABSTRACT FROM AUTHOR]

Relaxation of the corpus cavernosum smooth muscle is an absolute prerequisite of penile erection. Potassium channels play a role in the physiologic regulation of corporal smooth muscle tone. Among the several subtypes of potassium channels, Ca2+-activated potassium channel (KCa channel) subtypes are thought to be the most physiologically relevant in the regulation of corporal smooth muscle tone. The purpose of this study was to investigate the effects of nitric oxide (NO) and sildenafil on the KCa channels and elucidate the mechanisms of action on the KCa channels in smooth muscle cells of the human corpus cavernosum. The conventional patch-clamp technique was applied to short-term cultured smooth muscle cells of the human corpus cavernosum. Single-channel currents were recorded in cell-attached or inside-out patches, and whole-cell currents were recorded in perforated-patches. In cell-attached patches, sildenafil alone did not activate the KCa channels but sildenafil enhanced the NO-induced activation of KCa channels. The open probability of KCa channels was increased significantly after application of NO donor, SIN-1 (100 µM) (47±7.1%, n=10, P=0.002). The application of sildenafil (100 nM) with SIN-1 (100 µM) markedly increased the open probability of KCa channels (148±24%, n=8, P<0.001). The activation by SIN-1 or sildenafil with SIN-1 was completely blocked by pretreatment of the soluble guanylate cyclase inhibitor, ODQ (10 µM). In inside-out patches, SIN-1 or sildenafil with SIN-1 failed to activate KCa channels at pCa 7.5 (n=5). SIN-1 increased the whole cell outward K+ currents in all holding potential. The increased IK by SIN-1 was inhibited by charybdotoxin (CTX) about 70%. These data provide compelling evidence consistent with the involvement of the KCa channel subtype in modulating NO-induced relaxation responses in human corporal smooth muscle. Furthermore, the activation of KCa channels is thought to be mediated by activation of soluble guanylate cyclase, leading to increased intracellular levels of cyclic GMP and the subsequent activation of protein kinase rather than direct NO effect. [ABSTRACT FROM AUTHOR]