Low-Cost and High-Reduction Approaches for Power Droop during Launch-On-Shift Scan-Based Logic BIST

During at-speed test of high performance sequential ICs using scan-based Logic BIST, the IC activity factor (AF) induced by the applied test vectors is significantly higher than that experienced during its in field operation. Consequently, power droop (PD) may take place during both shift and capture phases, which will slow down the circuit under test (CUT) signal transitions. At capture, this phenomenon is likely to be erroneously recognized as due to delay faults. As a result, a false test fail may be generated, with consequent increase in yield loss. In this paper, we propose two approaches to reduce the PD generated at capture during at-speed test of sequential circuits with scan-based Logic BIST using the Launch-On-Shift scheme. Both approaches increase the correlation between adjacent bits of the scan chains with respect to conventional scan-based LBIST. This way, the AF of the scan chains at capture is reduced. Consequently, the AF of the CUT at capture, thus the PD at capture, is also reduced compared to conventional scan-based LBIST. The former approach, hereinafter referred to as Low-Cost Approach (LCA), enables a 50% reduction in the worst case magnitude of PD during conventional logic BIST. It requires a small cost in terms of area overhead (of approximately 1.5% on average), and it does not increase the number of test vectors over the conventional scan-based LBIST to achieve the same Fault Coverage (FC). Moreover, compared to three recent alternative solutions, LCA features a comparable AF in the scan chains at capture, while requiring lower test time and area overhead. The second approach, hereinafter referred to as High-Reduction Approach (HRA), enables scalable PD reductions at capture of up to 87%, with limited additional costs in terms of area overhead and number of required test vectors for a given target FC, over our LCA approach. Particularly, compared to two of the three recent alternative solutions mentioned above, HRA enables a significantly lower AF in the scan chains during the application of test vectors, while requiring either a comparable area overhead or a significantly lower test time. Compared to the remaining alternative solutions mentioned above, HRA enables a similar AF in the scan chains at capture (approximately 90% lower than conventional scan-based LBIST), while requiring a significantly lower test time (approximately 4.87 times on average lower number of test vectors) and comparable area overhead (of approximately 1.9% on average)

Scalable Approach for Power Droop Reduction During Scan-Based Logic BIST

The generation of significant power droop (PD) during at-speed test performed by Logic Built-In Self Test (LBIST) is a serious concern for modern ICs. In fact, the PD originated during test may delay signal transitions of the circuit under test (CUT): an effect that may be erroneously recognized as delay faults, with consequent erroneous generation of test fails and increase in yield loss. In this paper, we propose a novel scalable approach to reduce the PD during at-speed test of sequential circuits with scan-based LBIST using the launch-on-capture scheme. This is achieved by reducing the activity factor of the CUT, by proper modification of the test vectors generated by the LBIST of sequential ICs. Our scalable solution allows us to reduce PD to a value similar to that occurring during the CUT in field operation, without increasing the number of test vectors required to achieve a target fault coverage (FC). We present a hardware implementation of our approach that requires limited area overhead. Finally, we show that, compared with recent alternative solutions providing a similar PD reduction, our approach enables a significant reduction of the number of test vectors (by more than 50%), thus the test time, to achieve a target FC

Faults Affecting Energy-Harvesting Circuits of Self-Powered Wireless Sensors and Their Possible Concurrent Detection

We analyze the effects of faults on an energy-harvesting circuit (EHC) providing power to a wireless biomedical multisensor node. We show that such faults may prevent the EHC from producing the power supply voltage level required by the multisensor node. Then, we propose a low-cost (in terms of power consumption and area overhead) additional circuit monitoring the voltage level produced by the EHC continuously, and concurrently with the normal operation of the device. Such a monitor gives an error indication if the generated voltage falls below the minimum value required by the sensor node to operate correctly, thus allowing the activation of proper recovery actions to guarantee system fault tolerance. The proposed monitor is self-checking with regard to the internal faults that can occur during its in-field operation, thus providing an error signal when affected by faults itself

A CD11d monoclonal antibody treatment reduces tissue injury and improves neurological outcome after fluid percussion brain injury in rats

Traumatic brain injury (TBI) is an international health concern often resulting in chronic neurological abnormalities, including cognitive deficits, emotional disturbances, and motor impairments. An anti-CD11d monoclonal antibody that blocks the CD11d/CD18 integrin and vascular cell adhesion molecule (VCAM)-1 interaction following experimental spinal cord injury improves functional recovery, while reducing the intraspinal number of neutrophils and macrophages, oxidative activity, and tissue damage. Since the mechanisms of secondary injury in the brain and spinal cord are similar, we designed a study to evaluate fully the effects of anti-CD11d treatment after a moderate lateral fluid percussion TBI in the rat. Rats were treated at 2 h after TBI with either the anti-CD11d antibody or an isotype-matched control antibody 1B7, and both short (24-to 72-h) and long (4-week) recovery periods were examined. The anti-CD11d integrin treatment reduced neutrophil and macrophage levels in the injured brain, with concomitant reductions in lipid peroxidation, astrocyte activation, amyloid precursor protein accumulation, and neuronal loss. The reduced neuroinflammation seen in anti-CD11d-treated rats correlated with improved performance on a number of behavioral tests. At 24 h, the anti-CD11d group performed significantly better than the 1B7 controls on several water maze measures of spatial cognition. At 4 weeks post-injury the anti-CD11d-treated rats had better sensorimotor function as assessed by the beam task, and reduced anxiety-like behaviors, as evidenced by elevated-plus maze testing, compared to 1B7 controls. These findings suggest that neuroinflammation is associated with behavioral deficits after TBI, and that anti-CD11d antibody treatment is a viable strategy to improve neurological outcomes after TBI. © 2012, Mary Ann Liebert, Inc

The Telomerase Database

Telomerase is a ribonucleoprotein enzyme that extends DNA at the chromosome ends in most eukaryotes. Since 1985, telomerase has been studied intensively and components of the telomerase complex have been identified from over 160 eukaryotic species. In the last two decades, there has been a growing interest in studying telomerase owing to its vital role in chromosome stability and cellular immortality. To keep up with the remarkable explosion of knowledge about telomerase, we compiled information related to telomerase in an exhaustive database called the Telomerase Database (http://telomerase.asu.edu/). The Telomerase Database provides comprehensive information about (i) sequences of the RNA and protein subunits of telomerase, (ii) sequence alignments based on the phylogenetic relationship and structure, (iii) secondary structures of the RNA component and tertiary structures of various subunits of telomerase, (iv) mutations of telomerase components found in human patients and (v) active researchers who contributed to the wealth of current knowledge on telomerase. The information is hierarchically organized by the components, i.e. the telomerase reverse transcriptase (TERT), telomerase RNA (TR) and other telomerase-associated proteins. The Telomerase Database is a useful resource especially for researchers who are interested in investigating the structure, function, evolution and medical relevance of the telomerase enzyme

First wave of COVID-19 in Venezuela:Epidemiological, clinical, and paraclinical characteristics of first cases

The coronavirus disease 2019 (COVID-19) pandemic has particularly affected countries with weakened health services in Latin America, where proper patient management could be a critical step to address the epidemic. In this study, we aimed to characterize and identify which epidemiological, clinical, and paraclinical risk factors defined COVID-19 infection from the first confirmed cases through the first epidemic wave in Venezuela. A retrospective analysis of consecutive suspected cases of COVID-19 admitted to a sentinel hospital was carried out, including 576 patient cases subsequently confirmed for severe acute respiratory syndrome coronavirus 2 infection. Of these, 162 (28.1%) patients met the definition criteria for severe/critical disease, and 414 (71.2%) were classified as mild/moderate disease. The mean age was 47 (SD 16) years, the majority of which were men (59.5%), and the most frequent comorbidity was arterial hypertension (23.3%). The most common symptoms included fever (88.7%), headache (65.6%), and dry cough (63.9%). Severe/critical disease affected mostly older males with low schooling (p < 0.001). Similarly, higher levels of glycemia, urea, aminotransferases, total bilirubin, lactate dehydrogenase, and erythrocyte sedimentation rate were observed in severe/critical disease patients compared to those with mild/moderate disease. Overall mortality was 7.6% (44/576), with 41.7% (28/68) dying in hospital. We identified risk factors related to COVID-19 infection, which could help healthcare providers take appropriate measures and prevent severe clinical outcomes. Our results suggest that the mortality registered by this disease in Venezuela during the first epidemic wave was underestimated. An increase in fatalities is expected to occur in the coming months unless measures that are more effective are implemented to mitigate the epidemic while the vaccination process is ongoing

Salmonella enterica Serovar Typhimurium Lacking hfq Gene Confers Protective Immunity against Murine Typhoid

Salmonella enterica is an important enteric pathogen and its various serovars are involved in causing both systemic and intestinal diseases in humans and domestic animals. The emergence of multidrug-resistant strains of Salmonella leading to increased morbidity and mortality has further complicated its management. Live attenuated vaccines have been proven superior over killed or subunit vaccines due to their ability to induce protective immunity. Of the various strategies used for the generation of live attenuated vaccine strains, focus has gradually shifted towards manipulation of virulence regulator genes. Hfq is a RNA chaperon which mediates the binding of small RNAs to the mRNA and assists in post-transcriptional gene regulation in bacteria. In this study, we evaluated the efficacy of the Salmonella Typhimurium Δhfq strain as a candidate for live oral vaccine in murine model of typhoid fever. Salmonella hfq deletion mutant is highly attenuated in cell culture and animal model implying a significant role of Hfq in bacterial virulence. Oral immunization with the Salmonella hfq deletion mutant efficiently protects mice against subsequent oral challenge with virulent strain of Salmonella Typhimurium. Moreover, protection was induced upon both multiple as well as single dose of immunizations. The vaccine strain appears to be safe for use in pregnant mice and the protection is mediated by the increase in the number of CD4+ T lymphocytes upon vaccination. The levels of serum IgG and secretory-IgA in intestinal washes specific to lipopolysaccharide and outer membrane protein were significantly increased upon vaccination. Furthermore, hfq deletion mutant showed enhanced antigen presentation by dendritic cells compared to the wild type strain. Taken together, the studies in murine immunization model suggest that the Salmonella hfq deletion mutant can be a novel live oral vaccine candidate

Excitability of Aβ sensory neurons is altered in an animal model of peripheral neuropathy

<p>Abstract</p> <p>Background</p> <p>Causes of neuropathic pain following nerve injury remain unclear, limiting the development of mechanism-based therapeutic approaches. Animal models have provided some directions, but little is known about the specific sensory neurons that undergo changes in such a way as to induce and maintain activation of sensory pain pathways. Our previous studies implicated changes in the Aβ, normally non-nociceptive neurons in activating spinal nociceptive neurons in a cuff-induced animal model of neuropathic pain and the present study was directed specifically at determining any change in excitability of these neurons. Thus, the present study aimed at recording intracellularly from Aβ-fiber dorsal root ganglion (DRG) neurons and determining excitability of the peripheral receptive field, of the cell body and of the dorsal roots.</p> <p>Methods</p> <p>A peripheral neuropathy was induced in Sprague Dawley rats by inserting two thin polyethylene cuffs around the right sciatic nerve. All animals were confirmed to exhibit tactile hypersensitivity to von Frey filaments three weeks later, before the acute electrophysiological experiments. Under stable intracellular recording conditions neurons were classified functionally on the basis of their response to natural activation of their peripheral receptive field. In addition, conduction velocity of the dorsal roots, configuration of the action potential and rate of adaptation to stimulation were also criteria for classification. Excitability was measured as the threshold to activation of the peripheral receptive field, the response to intracellular injection of depolarizing current into the soma and the response to electrical stimulation of the dorsal roots.</p> <p>Results</p> <p>In control animals mechanical thresholds of all neurons were within normal ranges. Aβ DRG neurons in neuropathic rats demonstrated a mean mechanical threshold to receptive field stimulation that were significantly lower than in control rats, a prolonged discharge following this stimulation, a decreased activation threshold and a greater response to depolarizing current injection into the soma, as well as a longer refractory interval and delayed response to paired pulse electrical stimulation of the dorsal roots.</p> <p>Conclusions</p> <p>The present study has demonstrated changes in functionally classified Aβ low threshold and high threshold DRG neurons in a nerve intact animal model of peripheral neuropathy that demonstrates nociceptive responses to normally innocuous cutaneous stimuli, much the same as is observed in humans with neuropathic pain. We demonstrate further that the peripheral receptive fields of these neurons are more excitable, as are the somata. However, the dorsal roots exhibit a decrease in excitability. Thus, if these neurons participate in neuropathic pain this differential change in excitability may have implications in the peripheral drive that induces central sensitization, at least in animal models of peripheral neuropathic pain, and Aβ sensory neurons may thus contribute to allodynia and spontaneous pain following peripheral nerve injury in humans.</p