TAUOLA the library for tau lepton decay, and KKMC/KORALB/KORALZ/... status report

The status of the Monte Carlo programs for the simulation of the $\tau$ lepton production in high energy accelerator experiments and decay is reviewed. In particular, the status of the following packages is discussed: (i) TAUOLA for tau-lepton decay, (ii) PHOTOS for radiative corrections in decays, (iii) KORALB, KORALZ, KKMC packages for tau-pair production in e+e- collisions and (iv) universal interface of TAUOLA for the decay of tau-leptons produced by``any'' generator. Special emphasis on requirements from new and future experiments is given. Some considerations about the software organization necessary to keep simultaneously distinct physics initializations for TAUOLA are also included.Comment: latex 7 pages, including 1 table and 5 figure files, all 6 in postscript format. Presented on 'Sixth international workshop on tau lepton physics', Victoria Canada, September 200

An audio FIR-DAC in a BCD process for high power Class-D amplifiers

A 322 coefficient semi-digital FIR-DAC using a 1-bit PWM input signal was designed and implemented in a high voltage, audio power bipolar CMOS DMOS (BCD) process. This facilitates digital input signals for an analog class-D amplifier in BCD. The FIR-DAC performance depends on the ISI-resistant nature of this PWM-signal. An impulse response with only positive coefficients was chosen, because of its resistance to deadzone and mismatch. With a DAC current of 0.5 mA, the dynamic range is 111 dB (A-weighted), with SINAD = 103 dB (A-weighted). The current consumption is 1mA for the analog part and 4.8 mA for the digital part. The power consumption is 29 mW at V/sub dd/ = 5 V and the chip area is 2 mm/sup 2/ including the reference diode that can be shared by more channels

Tet-On Systems For Doxycycline-inducible Gene Expression.

The tetracycline-controlled Tet-Off and Tet-On gene expression systems are used to regulate the activity of genes in eukaryotic cells in diverse settings, varying from basic biological research to biotechnology and gene therapy applications. These systems are based on regulatory elements that control the activity of the tetracycline-resistance operon in bacteria. The Tet-Off system allows silencing of gene expression by administration of tetracycline (Tc) or tetracycline-derivatives like doxycycline (dox), whereas the Tet-On system allows activation of gene expression by dox. Since the initial design and construction of the original Tet-system, these bacterium-derived systems have been significantly improved for their function in eukaryotic cells. We here review how a dox-controlled HIV-1 variant was designed and used to greatly improve the activity and dox-sensitivity of the rtTA transcriptional activator component of the Tet-On system. These optimized rtTA variants require less dox for activation, which will reduce side effects and allow gene control in tissues where a relatively low dox level can be reached, such as the brain

Integration of SARS-CoV-2 RNA in infected human cells by retrotransposons: an unlikely hypothesis and old viral relationships

Zhang et al. (Proc Natl Acad Sci 118:e2105968118, 2021) recently reported that SARS-CoV-2 RNA can be retrotranscribed and integrated into the DNA of human cells by the L1 retrotransposon machinery. This phenomenon could cause persistence of viral sequences in patients and may explain the prolonged PCR-positivity of SARS-CoV-2 infected patients, even long after the phase of active virus replication has ended. This commentary does critically review the available data on this topic and discusses them in the context of findings made for other exogenous viruses and ancestral endogenous retroviral elements

Destabilization of the TAR hairpin affects the structure and function of the HIV-1 leader RNA

The TAR hairpin of the human immunodeficiency virus type 1 (HIV-1) RNA genome is essential for virus replication. TAR forms the binding site for the transcriptional trans-activator protein Tat and multiple additional TAR functions have been proposed. We previously constructed an HIV-1 variant in which the TAR-Tat transcription control mechanism is replaced by the components of the Tet-ON regulatory system. In this context, the surprising finding was that TAR can be truncated or even deleted, but partial TAR deletions that destabilize the stem structure cause a severe replication defect. In this study, we demonstrate that the HIV-1 RNA genome requires a stable hairpin at its 5′-end because unpaired TAR sequences affect the proper folding of the untranslated leader RNA. Consequently, multiple leader-encoded functions are affected by partial TAR deletions. Upon evolution of such mutant viruses, the replication capacity was repaired through the acquisition of additional TAR mutations that restore the local RNA folding, thus preventing the detrimental effect on the leader conformation