Thermal-electromagnetic susceptibility behaviors of PWM patterns used in control electronic circuit

with constraints for high-level integration of electronics, new EMC behaviors have to be considered to prevent real electromagnetic compliance. Especially, in embedded and on-board device's context, environmental temperature has an influence on the circuit behavior and EMC figures. This paper deals with susceptibility studies combined with temperature effects on electronic devices used to control power and transmissions. Specific dual thermal-electromagnetic test set-up developed for this are presented. Main results of an experimental campaign on digital PCB dedicated for generation of Pulse Width Modulation (PWM) patterns are presented. Temperature dependant susceptibility and sensitivity of the PWM parameters are compared and analyzed

Field coupled electrostatic discharge sensitivity database

Electrostatic Discharge (ESD) can disrupt the performance of an electronic system, like an MP3 player either by injected currents or by transient fields. It is possible to predict at least the approximate transient field levels inside a system, but it is difficult to determine the response of ICs subjected to these fields, as no IC specific data is available, and as it is often too involved to measure the sensitivity of every IC possibly used in a product. As deterministic solutions are difficult to achieve, a statistical approach has been selected in this research. The goal of this database for field coupled ESD (Electrostatic Discharge) sensitivity is to give guidance on estimating if soft-error (e.g., resets) problems are likely to occur, for a given ESD scenario. Electric field probes, magnetic field probes, and the ΣΔ probe, which can inject either electrical fields or magnetic fields as desired, are designed as field injection devices for the project. A TEM cell and an IC-stripline, which are designed for high voltage immunity testing, are also developed as injection methods for the purpose of the IC measurements for this database. The measurement setups for the off-shelf electronic products using the probes are shown. Further detailing parameter dependence, a 1.2 mm spacer and a 100 MHz low pass were inserted into the test setups. Observing the crash levels of the ICs under varying conditions allows better insight into the mechanism and the robustness of the database with respect to uncertainties introduced by the field injection methods and their calibrations. In the end, the data from 37 real ICs are analyzed and discussed, and the examples of applications for the database are also discussed --Abstract, page iii

Effects of thermal aggressions on susceptibility responses and immunity figures of PWM patterns

In embedded and on-board electronics context, environmental temperature has an influence on the real electromagnetic compliance and EMC figures. We present studies and results of temperature impacts on susceptibility and immunity figures. Specific dual thermal-electromagnetic set-up have been developed for this. A campaign of EMC-Thermal-parametric measurements has been realized on PWM patterns of digital PCBs dedicated for electronic drive and command. Temperature dependent susceptibility behaviors are presented, in the range of 3GHz for harmonic aggressions, that leads to discuss of new cases of EM sensitivity, couplings and immunity approach on electronic devices

Design and Implementation of Closed TEM Cells: Simulation-Based Approach

In the paper, a simulation-based design procedure for the implementation of a TEM cell (the Crawford cell) is presented. The empirical approach uses computer simulations carried out in the CST Microwave Studio to design the cell that operates in the frequency range from 100 kHz to 400 MHz. Following the developed procedure, the TEM cell was implemented, and the cell was tested experimentally. The TEM cell can be used for electromagnetic susceptibility (EMS) measurements, where the DUT is irradiated by the field in a wide frequency band. The DUT is tested to operate without the performance degradation under the influence of electromagnetic disturbances. In addition, the cell can be used for electromagnetic interference (EMI) measurements focused on interference emissions generated by the DUT

Trypanosoma brucei brucei invasion and T-cell infiltration of the brain parenchyma in experimental sleeping sickness: timing and correlation with functional changes

Background: The timing of Trypanosoma brucei entry into the brain parenchyma to initiate the second, meningoencephalitic stage of human African trypanosomiasis or sleeping sickness is currently debated and even parasite invasion of the neuropil has been recently questioned. Furthermore, the relationship between neurological features and disease stage are unclear, despite the important diagnostic and therapeutic implications. Methodology: Using a rat model of chronic Trypanosoma brucei brucei infection we determined the timing of parasite and T-cell neuropil infiltration and its correlation with functional changes. Parasite DNA was detected using trypanosome-specific PCR. Body weight and sleep structure alterations represented by sleep-onset rapid eye movement (SOREM) periods, reported in human and experimental African trypanosomiasis, were monitored. The presence of parasites, as well as CD4+ and CD8+ T-cells in the neuropil was assessed over time in the brain of the same animals by immunocytochemistry and quantitative analyses. Principal findings: Trypanosome DNA was present in the brain at day 6 post-infection and increased more than 15-fold by day 21. Parasites and T-cells were observed in the parenchyma from day 9 onwards. Parasites traversing blood vessel walls were observed in the hypothalamus and other brain regions. Body weight gain was reduced from day 7 onwards. SOREM episodes started in most cases early after infection, with an increase in number and duration after parasite neuroinvasion. Conclusion: These findings demonstrate invasion of the neuropil over time, after an initial interval, by parasites and lymphocytes crossing the blood-brain barrier, and show that neurological features can precede this event. The data thus challenge the current clinical and cerebrospinal fluid criteria of disease staging

The orphan receptor GPR35 contributes to angiotensin II–induced hypertension and cardiac dysfunction in mice

BACKGROUND: The orphan receptor G protein–coupled receptor 35 (GPR35) has been associated with a range of diseases, including cancer, inflammatory bowel disease, diabetes, hypertension, and heart failure. To assess the potential for GPR35 as a therapeutic target in cardiovascular disease, this study investigated the cardiovascular phenotype of a GPR35 knockout mouse under both basal conditions and following pathophysiological stimulation. METHODS: Blood pressure was monitored in male wild-type and GPR35 knockout mice over 7–14 days using implantable telemetry. Cardiac function and dimensions were assessed using echocardiography, and cardiomyocyte morphology evaluated histologically. Two weeks of angiotensin II (Ang II) infusion was used to investigate the effects of GPR35 deficiency under pathophysiological conditions. Gpr35 messenger RNA expression in cardiovascular tissues was assessed using quantitative polymerase chain reaction. RESULTS: There were no significant differences in blood pressure, cardiac function, or cardiomyocyte morphology in GPR35 knockout mice compared with wild-type mice. Following Ang II infusion, GPR35 knockout mice were protected from significant increases in systolic, diastolic, and mean arterial blood pressure or impaired left ventricular systolic function, in contrast to wild-type mice. There were no significant differences in Gpr35 messenger RNA expression in heart, kidney, and aorta following Ang II infusion in wild-type mice. CONCLUSIONS: Although GPR35 does not appear to influence basal cardiovascular regulation, these findings demonstrate that it plays an important pathological role in the development of Ang II–induced hypertension and impaired cardiac function. This suggests that GPR35 is a potential novel drug target for therapeutic intervention in hypertension

The Fungal Cell Wall : Structure, Biosynthesis, and Function

N.G. is funded by the Wellcome Trust via a senior investigator award and a strategic award and by the MRC Centre for Medical Mycology. C.M. acknowledges the support of the Wellcome Trust and the MRC. N.G. and C.M. are part of the MRC Centre for Medical Mycology. J.P.L. acknowledges support from ANR, Aviesan, and FRM.Peer reviewedPublisher PD

Isotropic Broadband E-Field Probe

An E-field probe has been developed for EMC immunity tests performed in closed space. The leads are flexible resistive transmission lines. Their influence on the field distribution is negligible. The probe has an isotropic reception from 100 MHz to 18 GHz; the sensitivity is in the 3 V/m–10 V/m range. The device is an accessory of the EMC test chamber. The readout of the field magnitude is carried out by personal computer, which fulfils also the required corrections of the raw data

Branched polyethylenimine re-sensitizes methicillin-resistant Staphylococcus aureus to beta-lactam antibioitics through a novel mechanism of action

Methicillin-resistant Staphylococcus aureus (MRSA) is a growing concern in the medical industry due to high morbidity and difficulty of treatment in infected patients. Conventional β-lactam antibiotics kill Staphylococcus aureus bacteria by inhibiting the function of cell-wall penicillin binding proteins (PBPs). However, β-lactams are ineffective against MRSA due to an extra PBP (PBP2a) that has a low binding affinity for β-lactam antibiotics. Branched polyethylenimine (BPEI), a non-toxic, cationic polymer, restores MRSA’s susceptibility to β-lactam antibiotics including oxacillin, ampicillin, imipenem, ceftizoxime, and piperacillin. Checkerboard assays with MRSA demonstrated synergy between BPEI and β-lactam antibiotics. BPEI and oxacillin were effective against MRSA USA300, MRSA MW2, MRSA 700787, and clinical isolates of MRSA. A time-killing curve showed BPEI in combination with oxacillin to be bactericidal. BPEI did not potentiate vancomycin, chloramphenicol, or linezolid against MRSA. Additionally, the BPEI:β-lactam efficacy was specific to MRSA and was not observed against methicillin-susceptible Staphylococcus aureus (MSSA), Gram-negative Escherichia coli, or Bacillus subtilis. When exposed to BPEI, MRSA cells increased in size and had difficulty forming septa. Nuclear magnetic resonance (NMR) data show that BPEI alters the teichoic acid chemical environment, an anionic polymer found in the cell wall of Gram-positive bacteria. Laser scanning confocal microscopy (LSCM) images depict BPEI residing on the MRSA cell wall, where teichoic acids and PBPs are located. BPEI electrostatically binds to wall teichoic acid (WTA), a polymer that is important for localization of certain cell wall proteins. BPEI does not potentiate ampicillin or oxacillin when WTA is removed from the cell by genetic mutation or chemical inhibition of WTA synthesis. Using LSCM, we found that BPEI also prevents proper localization of PBP4, another PBP that aids in β-lactam resistance. Since PBP4 and PBP2a require WTA to properly localize in MRSA, in situ disabling of WTA using BPEI inhibits proper orientation and functioning of the enzymes. PBP2a requires teichoic acid to properly locate and orient the enzyme, and thus MRSA is susceptible to antibiotics that prevent teichoic acid synthesis in the bacterial cytoplasm. These data suggest that BPEI may prevent proper localization of cell wall machinery by binding to WTA and leading to cell death when administered in combination with β-lactam antibiotics. By creating steric hindrance through WTA binding, BPEI in combination with β-lactam antibiotics could be used as a viable treatment option for MRSA infections