Power Limiter with PIN Diode Embedded in Cavity to Minimize Parasitic Inductance

This letter introduces a power limiter that limits the input power to protect the receiver when a large power enters the radio frequency receiver. When the power limiter receives a large power signal, a positive-intrinsic-negative (PIN) diode is turned on to limit the input power by lowering the impedance. We analyzed the characteristics of the power limiter according to the method of connecting the PIN diode in parallel with the input and output transmission lines of the power limiter. By embedding a PIN diode into the cavity and minimizing the length of the wire, a power limiter was designed and implemented to minimize parasitic inductance. In the S-band, the proposed power limiter’s insertion loss was below 0.5 dB, and the reflection loss characteristics were below 15 dB. Furthermore, it achieved an output P1dB of 21.8 dBm at 3.5 GHz

LTCC-Based DC-DC Converter for Reduction of Switching Noise and Radiated Emissions

In this study, a low-temperature co-fired ceramic (LTCC)-based direct current (DC)-DC converter is proposed for reducing stray inductance and mitigating electromagnetic interference. The dominant radiating loop of the proposed LTCC-based DC-DC converter features a multilayer design, which helps suppress noise sources and reduce radiated emissions. The peak voltage of switching noise for the proposed DC-DC converter at the frequency of 500 kHz is approximately 8.98% lower than that of a conventional DC-DC converter. In addition, the radiated emission level of the proposed DC-DC converter is lower than that of the conventional DC-DC converter. In sum, the proposed LTCC-technology-based multilayer design reduces the peak voltage of switching noise and the radiated emission of the DC-DC converter

Nonuniformity-Immune Read-In Integrated Circuit for Infrared Sensor Testing Systems

In this study, a novel IR projector driver that can minimize nonuniformity in electric circuits, using a dual-current-programming structure, is proposed to generate high-quality infrared (IR) scenes for accurate sensor evaluation. Unlike the conventional current-mode structure, the proposed system reduces pixel-to-pixel nonuniformity by assigning two roles (data sampling and current driving) to a single transistor. A prototype of the proposed circuit was designed and fabricated using the SK-Hynix 0.18 µm CMOS process, and its performance was analyzed using post-layout simulation data. It was verified that nonuniformity, which is defined as the standard deviation divided by the mean radiance, could be reduced from 21% to less than 0.1%

N-terminus-independent activation of c-Src via binding to a tetraspan(in) TM4SF5 in hepatocellular carcinoma is abolished by the TM4SF5 C-terminal peptide application

Active c-Src non-receptor tyrosine kinase localizes to the plasma membrane via N-terminal lipid modification. Membranous c-Src causes cancer initiation and progression. Even though transmembrane 4 L six family member 5 (TM4SF5), a tetraspan(in), can be involved in this mechanism, the molecular and structural influence of TM4SF5 on c-Src remains unknown. Methods: Here, we investigated molecular and structural details by which TM4SF5 regulated c-Src devoid of its N-terminus and how cell-penetrating peptides were able to interrupt c-Src activation via interference of c-Src-TM4SF5 interaction in hepatocellular carcinoma models. Results: The TM4SF5 C-terminus efficiently bound the c-Src SH1 kinase domain, efficiently to the inactively-closed form. The complex involved protein tyrosine phosphatase 1B able to dephosphorylate Tyr530. The c-Src SH1 domain alone, even in a closed form, bound TM4SF5 to cause c-Src Tyr419 and FAK Y861 phosphorylation. Homology modeling and molecular dynamics simulation studies predicted the directly interfacing residues, which were further validated by mutational studies. Cell penetration of TM4SF5 C-terminal peptides blocked the interaction of TM4SF5 with c-Src and prevented c-Src-dependent tumor initiation and progression in vivo. Conclusions: Collectively, these data demonstrate that binding of the TM4SF5 C-terminus to the kinase domain of inactive c-Src leads to its activation. Because this binding can be abolished by cell-penetrating peptides containing the TM4SF5 C-terminus, targeting this direct interaction may be an effective strategy for developing therapeutics that block the development and progression of hepatocellular carcinoma.Y

Snail1 induced in breast cancer cells in 3D collagen I gel environment suppresses cortactin and impairs effective invadopodia formation

AbstractAlthough an in vitro 3D environment cannot completely mimic the in vivo tumor site, embedding tumor cells in a 3D extracellular matrix (ECM) allows for the study of cancer cell behaviors and the screening of anti-metastatic reagents with a more in vivo-like context. Here we explored the behaviors of MDA-MB-231 breast cancer cells embedded in 3D collagen I. Diverse tumor environmental conditions (including cell density, extracellular acidity, or hypoxia as mimics for a continuous tumor growth) reduced JNKs, enhanced TGFβ1/Smad signaling activity, induced Snail1, and reduced cortactin expression. The reduced JNKs activity blocked efficient formation of invadopodia labeled with actin, cortactin, or MT1-MMP. JNKs inactivation activated Smad2 and Smad4, which were required for Snail1 expression. Snail1 then repressed cortactin expression, causing reduced invadopodia formation and prominent localization of MT1-MMP at perinuclear regions. MDA-MB-231 cells thus exhibited less efficient collagen I degradation and invasion in 3D collagen I upon JNKs inhibition. These observations support a signaling network among JNKs, Smads, Snail1, and cortactin to regulate the invasion of MDA-MB-231 cells embedded in 3D collagen I, which may be targeted during screening of anti-invasion reagents