Miracle-dz/UniFAR-FTUs huggingface dataset:
Low-VDD Operation of SRAM Synaptic Array for Implementing Ternary Neural Network

For Internet of Things (IoT) edge devices, it is very attractive to have the local sensemaking capability instead of sending all the data back to the cloud for information processing. For image pattern recognition, neuro-inspired machine learning algorithms have demonstrated enormous powerfulness. To effectively implement learning algorithms on-chip for IoT edge devices, on-chip synaptic memory architectures have been proposed to implement the key operations such as weighted-sum or matrix-vector multiplication. In this paper, we proposed a low-power design of static random access memory (SRAM) synaptic array for implementing a low-precision ternary neural network. We experimentally demonstrated that the supply voltage (VDD) of the SRAM array could be aggressively reduced to a level, where the SRAM cell is susceptible to bit failures. The testing results from 65-nm SRAM chips indicate that VDD could be reduced from the nominal 1–0.55 V (or 0.5 V) with a bit error rate ~0.23% (or ~1.56%), which only introduced ~0.08% (or ~1.68%) degradation in the classification accuracy. As a result, the power consumption could be reduced by more than <inline-formula> <tex-math notation="LaTeX">$8\times $ </tex-math></inline-formula> (or <inline-formula> <tex-math notation="LaTeX">$10\times $ </tex-math></inline-formula>).
The relationship between physicians’ and nurses’ personal physical activity habits and their health-promotion practice: A systematic review

Background: Sedentary lifestyles are rising in many countries which has implications for global health. Health professionals are well placed to promote increased physical activity levels to their patients. Objective: To examine the relationship between physicians’ and nurses’ personal physical activity and their physical activity promotion practices. Methods: Cochrane Library, PubMed, MEDLINE, EMBASE, CINAHL, PsychInfo, British Nursing Index and four Chinese databases were searched to March 2011. Extracted data were verified by a second researcher. Results: Thirteen studies met the inclusion criteria and were cross-sectional surveys employing a variety of self-report questionnaires. The majority of studies found that a higher personal physical activity level was associated with higher physical activity-promoting practices, and that health professionals with positive attitudes towards physical activity were more likely to promote physical activity to their clients. Conclusion: The findings of this review need to be confirmed by well-designed large studies which employ validated measures of physical activity and physical activity-promoting practices and involve multivariate analyses to identify the relative contribution of personal physical activity levels to physical activity-promoting practices.
An Association of Short Stature, Retarded Sexual Development and High Urinary Gonadotropin Titers in Women1

It has been a common and reasonable presumption that the association of unusual shortness of stature and retarded genital development bespeaks hypopituitarism, especially in the absence of cretinism, gross malnutrition or systemic disease. Even when roentgenological examination of the skull and studies of the visual fields are normal this presumption persists, fortified by a wealth of physiological data establishing the hypophysis as a controlling agent both for growth and for gonadal function and by our knowledge that demonstrable destructive pituitary disease produces similar physical consequences. Low titers of urinary gonadotropins would be expected in such people. However four short girls with deficient sexual development excreted 200 to 500 mouse units of gonadotropins per day, as judged by induced estrin production in the immature mouse, values corresponding to those of the castrate and usually taken to suggest primary ovarian insufficiency. Coincidentally, Albright, Smith and Fraser (1) have had a.
Bacteriophage P70: Unique Morphology and Unrelatedness to Other Listeria Bacteriophages

ABSTRACT Listeria monocytogenes is an important food-borne pathogen, and its bacteriophages find many uses in detection and biocontrol of its host. The novel broad-host-range virulent phage P70 has a unique morphology with an elongated capsid. Its genome sequence was determined by a hybrid sequencing strategy employing Sanger and PacBio techniques. The P70 genome contains 67,170 bp and 119 open reading frames (ORFs). Our analyses suggest that P70 represents an archetype of virus unrelated to other known Listeria bacteriophages.
Assessment of knowledge, attitudes and practices about adrenal insufficiency in the critically ill among endocrinologists and intensivists practicing in Chennai

Background: Adrenal insufficiency is a common occurrence in the critically ill and it is essential that intensivists and endocrinologists involved in the care of these patients have a good understanding of the concepts related to this condition. Objectives: To assess the knowledge, attitudes and practices about adrenal insufficiency in the critically ill among the endocrinologists and intensivists practicing in the city of Chennai. Materials and Methods: Questionnaires containing ten questions pertaining to adrenal insufficiency in the critically ill were sent to a total of six endocrinologists and 52 intensivists practicing in Chennai. Results: About 77% of all the respondents agreed to the fact that adrenal insufficiency is a frequent occurrence in critical illness. But 57% of them felt that there is no need for routine evaluation of critically ill patients for adrenal insufficiency. Random serum cortisol was selected by 62% of the responders as the method for evaluating adrenal function in the critically ill. There is clearly no agreement among the endocrinologists or the intensivists on the various cut off levels for diagnosis. Neither is there a clear consensus on the method followed for treatment of patients with adrenal insufficiency in the critical care unit. Conclusion: There is no concordance in the knowledge, attitudes or practices on adrenal insufficiency in the critically ill among the endocrinologists and intensivists in Chennai. There is a need for developing standard diagnostic and treatment guidelines and making it available for all the practicing endocrinologists and intensivists.
The influence of therapeutic blocking of Gp IIb/IIIa on platelet α‐granular fibrinogen

Recent evidence suggests that platelet a‐granule fibrinogen (fg) is derived from the plasma pool. Since platelets from patients with Type I Glanzmann's thrombasthenia (GT) are deficient in intracellular fibrinogen (fg) it was hypothesized that Gp IIb/IIIa could mediate the uptake of fg. To study the potential role of Gp IIb/IIIa in intracellular fg trafficking, the influence of therapeutic blocking of Gp IIb/IIIa on platelet fg was studied in 12 patients with stable ischaemic heart disease. Patients were either given a single intravenous dose of the monoclonal antibody 7E3 Fab (n= 4) or a combination of bolus and continuous infusion up to 24 (n= 3). 36 (n= 3) or 96 h (n= 2). All patients showed grossly prolonged bleeding times with a significant reduction of ex‐vivo ADP induced aggregation. Although, surface Gp IIb/IIIa binding sites were consistently reduced in all patients, there was a variable but delayed decrease in platelet fg relative to vWf: Ag in only six out of the 12 patients studied. The reduction in fg appeared dependent upon both dosage and duration of Gp IIb/IIIa blockade. The study provides further evidence for the novel role of Gp IIb/IIIa in the intracellular trafficking of fg to platelet and megakaryocytic alpha‐granules.
A Point Mutation in the N-Terminal Amphipathic Helix α0 in NS3 Promotes Hepatitis C Virus Assembly by Altering Core Localization to the Endoplasmic Reticulum and Facilitating Virus Budding

ABSTRACT The assembly of hepatitis C virus (HCV), a complicated process in which many viral and cellular factors are involved, has not been thoroughly deciphered. NS3 is a multifunctional protein that contains an N-terminal amphipathic α helix (designated helix α0), which is crucial for the membrane association and stability of NS3 protein, followed by a serine protease domain and a C-terminal helicase/NTPase domain. NS3 participates in HCV assembly likely through its C-terminal helicase domain, in which all reported adaptive mutations enhancing virion assembly reside. In this study, we determined that the N-terminal helix α0 of NS3 may contribute to HCV assembly. We identified a single mutation from methionine to threonine at amino acid position 21 (M21T) in helix α0, which significantly promoted viral production while having no apparent effect on the membrane association and protease activity of NS3. Subsequent analyses demonstrated that the M21T mutation did not affect HCV genome replication but rather promoted virion assembly. Further study revealed a shift in the subcellular localization of core protein from lipid droplets (LD) to the endoplasmic reticulum (ER). Finally, we showed that the M21T mutation increased the colocalization of core proteins and viral envelope proteins, leading to a more efficient envelopment of viral nucleocapsids. Collectively, the results of our study revealed a new function of NS3 helix α0 and aid understanding of the role of NS3 in HCV virion morphogenesis. IMPORTANCE HCV NS3 protein possesses the protease activity in its N-terminal domain and the helicase activity in its C-terminal domain. The role of NS3 in virus assembly has been mainly attributed to its helicase domain, because all adaptive mutations enhancing progeny virus production are found to be within this domain. Our study identified, for the first time to our knowledge, an adaptive mutation within the N-terminal helix α0 domain of NS3 that significantly enhanced virus assembly while having no effect on viral genome replication. The mechanistic studies suggested that this mutation promoted the relocation of core proteins from LD to the ER, leading to a more efficient envelopment of viral nucleocapsids. Our results revealed a possible new function of helix α0 in the HCV life cycle and provided new clues to understanding the molecular mechanisms for the action of NS3 in HCV assembly.
Persistent Simian Immunodeficiency Virus Infection Drives Differentiation, Aberrant Accumulation, and Latent Infection of Germinal Center Follicular T Helper Cells

ABSTRACT CD4+ follicular T helper (Tfh) cells play a prominent role in humoral immune responses, but the mechanisms of their accumulation and infection in AIDS remain unclear. Here we found that germinal center (GC) Tfh cells, defined here as CXCR5+ PD-1HIGH CD4+ T cells, do not express the HIV coreceptor CCR5 yet serve as a latent reservoir in GCs. With disease progression, an expansion of GC Tfh cells is accompanied by increases in dysfunctional CD8+ T cells. In contrast, Tfh precursor (CXCR5− CD4+ T) cells in lymph nodes do express CCR5 and differentiate into GC Tfh cells following interleukin-6 (IL-6) and IL-21 stimulation, and viral DNA is detectable in fully differentiated GC Tfh cells ex vivo. This suggests that SIV-infected GC Tfh cells may be derived from Tfh precursor cell subsets that become infected in marginal zones and then migrate into GCs as fully mature GC Tfh cells that serve as persistent virus reservoirs. These findings suggest that viral persistence in lymph nodes drives compensatory differentiation, aberrant accumulation, and latent infection of GC Tfh cells, resulting in marked impairment of humoral immune responses. IMPORTANCE Generation of antibodies that can effectively eliminate viruses requires interactions of B cells with highly specialized T cells in GCs of lymphoid tissues called follicular T helper cells. Here we show that in simian immunodeficiency virus infection, these cells are initially infected in a precursor stage that leads to alterations in their homing, accumulation, and function that may be responsible for the inability of human immunodeficiency virus-infected patients to generate effective antibody responses.
The Diversity of Torque Teno Viruses: In Vitro Replication Leads to the Formation of Additional Replication-Competent Subviral Molecules

ABSTRACT The family Anelloviridae comprises torque teno viruses (TTVs) diverse in genome structure and organization. The isolation of a large number of TTV genomes (TTV Heidelberg [TTV-HD]) of 26 TTV types is reported. Several isolates from the same type indicate sequence variation within open reading frame 1 (ORF1), resulting in considerably modified open reading frames. We demonstrate in vitro replication of 12 full-length genomes of TTV-HD in 293TT cells. Propagation of virus was achieved by several rounds of infections using supernatant and frozen whole cells of initially infected cells. Replication of virus was measured by PCR amplification and transcription analyses. Subgenomic molecules (μTTV), arising early during propagation and ranging in size from 401 to 913 bases, were cloned and characterized. Propagation of these μTTV in in vitro cultures was demonstrated in the absence of full-length genomes.
Experimental Evaluation of Location Methods Based on Signal-Strength Measurements

The accuracy of location methods based on received-signal-strength (RSS) measurements is highly variable, but the underlying causes are not well known. In this paper, narrowband measurements at five VHF frequencies are used to evaluate the accuracy of RSS-based location algorithms. The least squares algorithm is the most accurate if the propagation model is unbiased. Location error increases linearly with mean distance from transmitters and with RSS variation caused by shadow fading or varying antenna gain. Since shadow fading increases with frequency, location accuracy decreases with frequency. A satisfactory approximation of location accuracy in a given network is obtained by the error estimates that are based on linearization but modified when the receiver is close to one transmitter. Kalman filtering performed on the estimated coordinates removes the largest location errors, but it does not improve the median accuracy significantly due to the correlated shadowing process
Quantification of Entry Phenotypes of Macrophage-Tropic HIV-1 across a Wide Range of CD4 Densities

ABSTRACT Defining a macrophage-tropic phenotype for HIV-1 to assess a role in pathogenesis is complicated by the fact that HIV-1 isolates vary continuously in their ability to enter monocyte-derived macrophages (MDMs) in vitro, and MDMs vary in their ability to support HIV-1 entry. To overcome these limitations, we identified consistent differences in entry phenotypes between five paired blood-derived, T cell-tropic HIV-1 env genes, four of which are CCR5-using (R5) and one of which is CXCR4-using (X4), and cerebrospinal fluid (CSF)-derived, R5 macrophage-tropic env genes. We performed entry assays using the CD4- and CCR5-inducible Affinofile cell line, expressing a range of CD4 levels that approximates the range from MDMs to CD4+ T cells. The macrophage-tropic viruses were significantly better at infecting cells expressing low levels of CD4 than the T cell-tropic viruses from the same subjects, with the titration of CD4 providing a distinctive and quantitative phenotype. This difference in CD4 utilization was not due to macrophage-tropic viruses being CD4 independent. Furthermore, macrophage-tropic viruses did not differ from paired T cell-tropic viruses in their ability to use low levels of CCR5 (t paired = −1.39; P = 0.24) or their use of an alternative conformation of CCR5. We also infected MDMs with a panel of viruses and observed that infectivity of each virus differed across four donors and between three preparations from a single donor. We concluded that the evolutionary transition from replication in T cells to that in macrophages involves a phenotypic transition to acquire the ability to infect cells expressing low levels of CD4 and that this phenotype is more reliably measured in Affinofile cells than in macrophages. IMPORTANCE HIV-1 typically infects memory T cells by using CD4 and CCR5 to enter cells. The virus evolves to infect new cell types by changing the coreceptor from CCR5 to CXCR4 to infect naive T cells or adapting to the use of low levels of CD4 to infect macrophages. However, defining the phenotype of macrophage tropism has been difficult due to inherent variability in the use of macrophages generated in culture to support entry of HIV-1. We describe the use of Affinofile cells with inducible and variable levels of CD4 to identify a signature phenotype for macrophage-tropic HIV-1. The ability to define HIV-1 variants that have evolved an entry phenotype that allows more efficient entry into cells with low levels of CD4 sets the stage for a clearer placement of these variants in HIV-associated pathogenesis.
Adaptive MIMO Transmission for Exploiting the Capacity of Spatially Correlated Channels

We consider a novel low-complexity adaptive multiple-input multiple-output (MIMO) transmission technique. The approach is based on switching between low-complexity transmission schemes, including statistical beamforming, double space-time transmit diversity, and spatial multiplexing, depending on the changing channel statistics, as a practical means of approaching the spatially correlated MIMO channel capacity. We first derive new ergodic capacity expressions for each MIMO transmission scheme in spatially correlated channels. Based on these results, we demonstrate that adaptive switching between MIMO schemes yields significant capacity gains over fixed transmission schemes. We also derive accurate analytical approximations for the optimal signal-to-noise-ratio switching thresholds, which correspond to the crossing-points of the capacity curves. These thresholds are shown to vary, depending on the spatial correlation, and are used to identify key switching parameters. Finally, we propose a practical switching algorithm that is shown to yield significant spectral efficiency improvements over nonadaptive schemes for typical channel scenarios
Suppressor of Cytokine Signaling 3 Suppresses Hepatitis C Virus Replication in an mTOR-Dependent Manner

ABSTRACT We and others have observed that hepatic levels of suppressor of cytokine signaling 3 (SOCS3) are significantly higher in persons with chronic hepatitis C, particularly those who are nonresponders to interferon (IFN) treatment, than in healthy individuals. However, the relationship between SOCS3 and hepatitis C virus (HCV) replication remains unclear. Given its putative role, we hypothesized that SOCS3 is permissive for viral replication. We therefore used the OR6 cell line, which harbors a genotype 1b full-length HCV replicon, and the genotype 2a full-length HCV strain JFH1 infection system to analyze the effects of SOCS3 overexpression and short hairpin RNA (shRNA)-mediated knockdown on HCV replication. We further analyzed the role of mTOR in the effects of SOCS3 by treating selected cells with rapamycin. OR6 cells and JFH1-infected Huh7.5. 1 cells expressed significantly less SOCS3 than control cells. Furthermore, inhibition of HCV replication with the HCV protease inhibitor BILN 2061 restored SOCS3 protein levels. SOCS3 overexpression in OR6 cells and JFH1-infected Huh7.5. 1 cells resulted in significantly lower HCV replication than that in the control cells, despite SOCS3-related inhibition of STAT1 phosphorylation and type I IFN signaling. In contrast, JFH1-infected cells with stable SOCS3 knockdown expressed higher levels of HCV proteins and RNA than did control cells. SOCS3-targeting shRNA also knocked down mTOR and phospho-mTOR. The mTOR inhibitor rapamycin reversed the inhibitory effects of SOCS3. In independent investigations, SOCS3 unexpectedly suppressed HCV replication in an mTOR-dependent manner. These findings suggest that increased SOCS3 levels consistently observed in chronic IFN nonresponders may reflect a compensatory host antiviral response to persistent infection and that manipulation of SOCS3/mTOR may offer benefit against HCV infection.
Profiling and Characterization of Influenza Virus N1 Strains Potentially Resistant to Multiple Neuraminidase Inhibitors

ABSTRACT Neuraminidase inhibitors (NAIs) have been widely used to control influenza virus infection, but their increased use could promote the global emergence of resistant variants. Although various mutations associated with NAI resistance have been identified, the amino acid substitutions that confer multidrug resistance with undiminished viral fitness remain poorly understood. We therefore screened a known mutation(s) that could confer multidrug resistance to the currently approved NAIs oseltamivir, zanamivir, and peramivir by assessing recombinant viruses with mutant NA-encoding genes (catalytic residues R152K and R292K, framework residues E119A/D/G, D198N, H274Y, and N294S) in the backbones of the 2009 pandemic H1N1 (pH1N1) and highly pathogenic avian influenza (HPAI) H5N1 viruses. Of the 14 single and double mutant viruses recovered in the backbone of pH1N1, four variants (E119D, E119A/D/G-H274Y) exhibited reduced inhibition by all of the NAIs and two variants (E119D and E119D-H274Y) retained the overall properties of gene stability, replicative efficiency, pathogenicity, and transmissibility in vitro and in vivo. Of the nine recombinant H5N1 viruses, four variants (E119D, E119A/D/G-H274Y) also showed reduced inhibition by all of the NAIs, though their overall viral fitness was impaired in vitro and/or in vivo. Thus, single mutations or certain combination of the established mutations could confer potential multidrug resistance on pH1N1 or HPAI H5N1 viruses. Our findings emphasize the urgency of developing alternative drugs against influenza virus infection. IMPORTANCE There has been a widespread emergence of influenza virus strains with reduced susceptibility to neuraminidase inhibitors (NAIs). We screened multidrug-resistant viruses by studying the viral fitness of neuraminidase mutants in vitro and in vivo. We found that recombinant E119D and E119A/D/G/-H274Y mutant viruses demonstrated reduced inhibition by all of the NAIs tested in both the backbone of the 2009 H1N1 pandemic (pH1N1) and highly pathogenic avian influenza H5N1 viruses. Furthermore, E119D and E119D-H274Y mutants in the pH1N1 background maintained overall fitness properties in vitro and in vivo. Our study highlights the importance of vigilance and continued surveillance of potential NAI multidrug-resistant influenza virus variants, as well as the development of alternative therapeutics.