Hi all,

I am having trouble plotting the IIp3 of gilber RF mixer I made

I have plotted 1 dB compression point using QPSS and QPAC simulation. flo=2.42GHz and frf=2.4GHz , 20 MHz IF

However my IIp3 simulation shows strange results

QPSS and QPAC setup

This Metasploit module exploits a stack buffer overflow in ASX to MP3 converter 3.1.3.7. By constructing a specially crafted ASX file and attempting to convert it to an MP3 file in the application, a buffer is overwritten, which allows for running shellcode. Tested on: Microsoft Windows 7 Enterprise, 6.1.7601 Service Pack 1 Build 7601, x64-based PC Microsoft Windows 10 Pro, 10.0.18362 N/A Build 18362, x64-based PC.

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China’s Ministry of Commerce (“MOFCOM”) has refused approval for the proposed P3 joint venture between shipping companies Maersk Line, Mediterranean Shipping Company (“MSC”) and CMA CGM (“the Companies”). &n...

MCP33131D-05

MCP33131-05

MCP33121-05

MCP33111-05

MCP33121-10

MCP33111-10

MCP33131-10

MCP33141-05

MCP33141-10

MCP33141D-05

MCP33141D-10

MCP33151-05

MCP33151-10

MCP33151D-05

MCP33151D-10

MCP3426

MCP3427

MCP3428

MCP3561

MCP3464

MCP3462

MCP3461

MCP3564

MCP3562

MCP3909

MCP3901

MCP3903

MCP3911

MCP39F501

MCP3910

MCP3918

MCP3912

MCP3919

MCP39F511N

MCP39F511

MCP39F521

MCP39F511A

Mycoplasma gallisepticum is the primary etiological agent of chronic respiratory disease in chickens. Live attenuated vaccines are most commonly used in the field to control the disease, but current vaccines have some limitations. Vaxsafe MG (strain ts-304) is a new vaccine candidate that is efficacious at a lower dose than the current commercial vaccine strain ts-11, from which it is derived. In this study, the transcriptional profiles of the trachea of unvaccinated chickens and chickens vaccinated with strain ts-304 were compared 2 weeks after challenge with M. gallisepticum strain Ap3AS during the chronic stage of infection. After challenge, genes, gene ontologies, pathways, and protein classes involved in inflammation, cytokine production and signaling, and cell proliferation were upregulated, while those involved in formation and motor movement of cilia, formation of intercellular junctional complexes, and formation of the cytoskeleton were downregulated in the unvaccinated birds compared to the vaccinated birds, reflecting immune dysregulation and the pathological changes induced in the trachea by infection with M. gallisepticum. Vaccination appears to protect the structural and functional integrity of the tracheal mucosa 2 weeks after infection with M. gallisepticum.

Nuclear import of viral genomes is an important step during the life cycle of adenoviruses (AdV), requiring soluble cellular factors as well as proteins of the nuclear pore complex (NPC). We addressed the role of the cytoplasmic nucleoporin Nup358 during adenoviral genome delivery by performing depletion/reconstitution experiments and time-resolved quantification of adenoviral genome import. Nup358-depleted cells displayed reduced efficiencies of nuclear import of adenoviral genomes, and the nuclear import receptor transportin 1 became rate limiting under these conditions. Furthermore, we identified a minimal N-terminal region of Nup358 that was sufficient to compensate for the import defect. Our data support a model where Nup358 functions as an assembly platform that promotes the formation of transport complexes, allowing AdV to exploit a physiological protein import pathway for accelerated transport of its DNA.

IMPORTANCE Nuclear import of viral genomes is an essential step to initiate productive infection for several nuclear replicating DNA viruses. On the other hand, DNA is not a physiological nuclear import substrate; consequently, viruses have to exploit existing physiological transport routes. Here, we show that adenoviruses use the nucleoporin Nup358 to increase the efficiency of adenoviral genome import. In its absence, genome import efficiency is reduced and the transport receptor transportin 1 becomes rate limiting. We show that the N-terminal half of Nup358 is sufficient to drive genome import and identify a transportin 1 binding region. In our model, adenovirus genome import exploits an existing protein import pathway and Nup358 serves as an assembly platform for transport complexes.

Yen-Ling Lian, Kuan-Wei Chen, Yu-Ting Chou, Ting-Ling Ke, Bi-Chang Chen, Yu-Chun Lin, and Linyi Chen

Myoblast fusion is required for myotube formation during myogenesis, and defects in myoblast differentiation and fusion have been implicated in a number of diseases, including human rhabdomyosarcoma. Although transcriptional regulation of the myogenic program has been studied extensively, the mechanisms controlling myoblast fusion remain largely unknown. This study identified and characterized the dynamics of a distinct class of blebs, termed bubbling blebs, which are smaller than those that participate in migration. The formation of these bubbling blebs occurred during differentiation and decreased alongside a decline in phosphatidylinositol-(3,4,5)-trisphosphate (PIP3) at the plasma membrane before myoblast fusion. In a human rhabdomyosarcoma-derived (RD) cell line that exhibits strong blebbing dynamics and myoblast fusion defects, PIP3 was constitutively abundant on the membrane during myogenesis. Targeting phosphatase and tensin homolog (PTEN) to the plasma membrane reduced PIP3 levels, inhibited bubbling blebs and rescued myoblast fusion defects in RD cells. These findings highlight the differential distribution and crucial role of PIP3 during myoblast fusion and reveal a novel mechanism underlying myogenesis defects in human rhabdomyosarcoma.

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