Multi-cell battery protection system

A multi-cell battery protection system is described wherein each cell has its own individual protective circuit. The protective circuits consist of a solid state comparator unit and a high current switching device such as a relay. The comparator units each continuously monitor the associated cell and when the cell voltage either exceeds a predetermined high level or falls below a predetermined low level, the relay is actuated whereby a bypass circuit is completed across the cell thereby effectively removing the cell from the series of cells

Load cell protection device Patent

Load cell protection device using spring-loaded breakaway mechanis

Revisiting interval protection, a.k.a. partial cell suppression, for tabular data

The final publication is available at link.springer.comInterval protection or partial cell suppression was introduced in “M. Fischetti, J.-J. Salazar, Partial cell suppression: A new methodology for statistical disclosure control, Statistics and Computing, 13, 13–21, 2003” as a “linearization” of the difficult cell suppression problem. Interval protection replaces some cells by intervals containing the original cell value, unlike in cell suppression where the values are suppressed. Although the resulting optimization problem is still huge—as in cell suppression, it is linear, thus allowing the application of efficient procedures. In this work we present preliminary results with a prototype implementation of Benders decomposition for interval protection. Although the above seminal publication about partial cell suppression applied a similar methodology, our approach differs in two aspects: (i) the boundaries of the intervals are completely independent in our implementation, whereas the one of 2003 solved a simpler variant where boundaries must satisfy a certain ratio; (ii) our prototype is applied to a set of seven general and hierarchical tables, whereas only three two-dimensional tables were solved with the implementation of 2003.Peer ReviewedPostprint (author's final draft

Protection and mechanism of action of a novel human respiratory syncytial virus vaccine candidate based on the extracellular domain of small hydrophobic protein

Infections with human respiratory syncytial virus (HRSV) occur globally in all age groups and can have devastating consequences in young infants. We demonstrate that a vaccine based on the extracellular domain (SHe) of the small hydrophobic (SH) protein of HRSV, reduced viral replication in challenged laboratory mice and in cotton rats. We show that this suppression of viral replication can be transferred by serum and depends on a functional IgG receptor compartment with a major contribution of FcRI and FcRIII. Using a conditional cell depletion method, we provide evidence that alveolar macrophages are involved in the protection by SHe-specific antibodies. HRSV-infected cells abundantly express SH on the cell surface and are likely the prime target of the humoral immune response elicited by SHe-based vaccination. Finally, natural infection of humans and experimental infection of mice or cotton rats does not induce a strong immune response against HRSV SHe. Using SHe as a vaccine antigen induces immune protection against HRSV by a mechanism that differs from the natural immune response and from other HRSV vaccination strategies explored to date. Hence, HRSV vaccine candidates that aim at inducing protective neutralizing antibodies or T-cell responses could be complemented with a SHe-based antigen to further improve immune protection

Development of single cell protectors for sealed silver-zinc cells, phase 1

A single cell protector (SCP) assembly capable of protecting a single silver-zinc (Ag Zn) battery cell was designed, fabricated, and tested. The SCP provides cell-level protection against overcharge and overdischarge by a bypass circuit. The bypass circuit consists of a magnetic-latching relay that is controlled by the high and low-voltage limit comparators. Although designed specifically for secondary Ag-Zn cells, the SCP is flexible enough to be adapted to other rechargeable cells. Eighteen SCPs were used in life testing of an 18-cell battery. The cells were sealed Ag-Zn system with inorganic separators. For comparison, another 18-cell battery was subjected to identical life test conditions, but with battery-level protection rather than cell-level. An alternative approach to the SCP design in the form of a microprocessor-based system was conceptually designed. The comparison of SCP and microprocessor approaches is also presented and a preferred approach for Ag-Zn battery protection is discussed

Long-lasting cross-protection against influenza A by neuraminidase and M2e-based immunization strategies

There is mounting evidence that in the absence of neutralizing antibodies cross-reactive T cells provide protection against pandemic influenza viruses. Here, we compared protection and CD8+ T cell responses following challenge with H1N1 2009 pandemic and H3N2 viruses of mice that had been immunized with hemagglutinin (HA), neuraminidase (NA) and the extracellular domain of matrix protein 2 (M2e) fused to a virus-like particle (VLP). Mice were challenged a first time with a sublethal dose of H1N1 2009 pandemic virus and, four weeks later, challenged again with an H3N2 virus. Mice that had been vaccinated with HA, NA, NA + M2e-VLP and HA + NA + M2e-VLP were protected against homologous H1N1 virus challenge. Challenged NA and NA + M2e-VLP vaccinated mice mounted CD8+ T cell responses that correlated with protection against secondary H3N2 challenge. HA-vaccinated mice were fully protected against challenge with homologous H1N1 2009 virus, failed to mount cross-reactive CD8+ T cells and succumbed to the second challenge with heterologous H3N2 virus. In summary, NA- and M2e-based immunity can protect against challenge with (homologous) virus without compromising the induction of robust cross-reactive CD8+ T cell responses upon exposure to virus

Analysis and hardware testing of cell capacitor discharge currents during DC faults in half-bridge modular multilevel converters

This paper focuses on the behaviour of the cell capacitor discharge currents during DC faults in half-bridge modular multilevel converters. Active switches, not designed for fault conditions, are tripped to minimize discharge currents effect on the semiconductor switches. Two levels of device protection are commonly in place; driver level protection monitoring collector-emitter voltage and overcurrent protection with feedback measurement and control. However, unavoidable tripping delay times, arising from factors such as sensor lags, controller sampling delays and hardware propagation delays, impact transient current shape and hence affect the selection of semiconductor device ratings as well as arm inductance. Analytical expressions are obtained for current slew rate, peak transient current and resultant I2t for the cell capacitor discharge current taking into account such delays. The study is backed by experimental testing on discharge of a 900V MMC capacitor

Development of single-cell protectors for sealed silver-zinc cells

Three design approaches to cell-level protection were developed, fabricated, and tested. These systems are referred to as the single-cell protector (SCP), multiplexed-cell protector(MCP). To evaluate the systems 18-cell battery packs without cell level control were subjected to cycle life test. A total of five batteries were subjected to simulate synchronous orbit cycling at 40% depth of discharge at 22C. Batteries without cell-level protection failed between 345 and 255 cycles. Cell failure in the cell level protected batteries occurred between 412 and 540. It was determined that the cell-level monitoring and protection is necessary to attain the long cycle life of a AgZn battery. The best method of providing control and protection of the AgZn cells depends on the specific application and capability of the user

Elongation factor 2-diphthamide is critical for translation of two IRES-dependent protein targets, XIAP and FGF2, under oxidative stress conditions

Elongation factor-2 (eEF2) catalyzes the movement of the ribosome along the mRNA. A single histidine residue in eEF2 (H715) is modified to form diphthamide. A role for eEF2 in cellular stress responses is highlighted by the fact that eEF2 is sensitive to oxidative stress and that it must be active in order to drive the synthesis of proteins that help cells to mitigate the adverse effects of oxidative stress. Many of the latter proteins are encoded by mRNAs containing a sequence called an “internal ribosomal entry site” (IRES). Under high oxidative stress conditions diphthamide-deficient cells were significantly more sensitive to cell death. These results suggest that diphthamide may play a role in protection against the degradation of eEF2. Its protection is especially important under those situations where it is necessary for the re-programming of translation from global to IRES synthesis. Indeed, we found that the expression of X-linked inhibitor of apoptosis (XIAP) and fibroblast growth factor 2 (FGF2), two proteins synthesized from mRNAs with IRES that promote cell survival are deregulated in diphthamide-deficient cells. Our findings therefore suggest that eEF2/diphthamide controls the selective translation of IRES-dependent protein targets XIAP and FGF2, critical for cell survival under conditions of oxidative stress.España, Ministerio de Ciencia e Innovación BFU 2010-20882

Protease-activated receptor 1 mediates thrombin-dependent, cell-mediated renal inflammation in crescentic glomerulonephritis.

Protease-activated receptor (PAR)-1 is a cellular receptor for thrombin that is activated after proteolytic cleavage. The contribution of PAR-1 to inflammatory cell-mediated renal injury was assessed in murine crescentic glomerulonephritis (GN). A pivotal role for thrombin in this model was demonstrated by the capacity of hirudin, a selective thrombin antagonist, to attenuate renal injury. Compared with control treatment, hirudin significantly reduced glomerular crescent formation, T cell and macrophage infiltration, fibrin deposition, and elevated serum creatinine, which are prominent features of GN. PAR-1-deficient (PAR-1(-/-)) mice, which have normal coagulation, also showed significant protection from crescentic GN compared with wild-type mice. The reductions in crescent formation, inflammatory cell infiltration, and serum creatinine were similar in PAR-1(-/-) and hirudin-treated mice, but hirudin afforded significantly greater protection from fibrin deposition. Treatment of wild-type mice with a selective PAR-1-activating peptide (TRAP) augmented histological and functional indices of GN, but TRAP treatment did not alter the severity of GN in PAR(-/-) mice. These results indicate that activation of PAR-1 by thrombin or TRAP amplifies crescentic GN. Thus, in addition to its procoagulant role, thrombin has proinflammatory, PAR-1-dependent effects that augment inflammatory renal injury