Miracle-dz/UniFAR-FTUs huggingface dataset:
Bimorph pMUT with dual electrodes

The concept of “bimorph” piezoelectric micromachined ultrasonic transducers (pMUTs) has been demonstrated by utilizing a two active AlN layers structure constructed in a CMOS-compatible process. The prototype device has two 0. 95μm-thick AlN layers sandwiched by three 0. 15μm-thick Mo electrodes. In a prototype, both an inner circular and an outer annular electrode are designed on a 230 μm in radius, circular-shape diaphragm. When actuated with the inner electrode of 160μm in radius, the pMUT has a resonant frequency of 198.8 kHz and central displacement of 407.4 nm/V. Under the differential drive scheme using the dual-electrodes for large acoustic outputs at a low frequency, the measured central displacement is 13.0 nm/V, which is about 400% higher than that of a unimorph AlN-pMUT under similar actuation conditions. As such, the dual-electrode bimorph pMUT presents the improved operation as compared with the state-of-the-art flat pMUT design to achieve enhanced acoustic outputs.
In vitro analysis of a primary, major histocompatibility complex (MHC)-restricted, cytotoxic T-lymphocyte response to avian leukosis virus (ALV), using target cells expressing MHC class I cDNA inserted into a recombinant ALV vector

The interaction between the major histocompatibility complex (MHC) and cytotoxic T lymphocytes (CTLs) is an important component of the host's resistance to viral infections and tumor formation. In this study, an avian leukosis virus (ALV) vector system, RCASBP, expressing MHC chicken class I (B-F) cDNA was used to develop target cells expressing the chicken class I glycoproteins complexed with ALV antigens on the cell surface. Peripheral blood from chickens inoculated with ALV was shown to contain antigen-specific, MHC-restricted, CD8+ effector CTLs, using a 51Cr release assay utilizing the RCASBP B-F target cells. The stimulated effector cells were also predominantly alpha beta T-cell receptor-positive (TCR2) T cells. The CTL response varied between two haplotypes of chickens which differed in their response to Rous sarcoma virus (RSV)-induced tumors. Chickens with the B21 haplotype which regress RSV-induced tumors showed maximal cytolytic activity, while chickens with the B13 haplotype which do not regress RSV-induced tumors had minimal to no cytolytic activity. In addition to assessing the CTL response to ALV, the creation of MHC-specific immortal target cell lines will be extremely useful in evaluating CTL responses to other viral disease in chickens.
Arabidopsis hot Mutants Define Multiple Functions Required for Acclimation to High Temperatures1

Plants acquire thermotolerance to lethal high temperatures if first exposed to moderately high temperature or if temperature is increased gradually to an otherwise lethal temperature. We have taken a genetic approach to dissecting acquired thermotolerance by characterizing loss-of-function thermotolerance mutants in Arabidopsis. In previous work, we identified single recessive alleles of four loci required for thermotolerance of hypocotyl elongation, hot1-1, hot2-1, hot3-1, and hot4-1. Completed screening of M2 progeny from approximately 2500 M1 plants has now identified new alleles of three of these original loci, along with three new loci. The low mutant frequency suggests that a relatively small number of genes make a major contribution to this phenotype or that other thermotolerance genes encode essential or redundant functions. Further analysis of the original four loci was performed to define the nature of their thermotolerance defects. Although the HOT1 locus was shown previously to encode a major heat shock protein (Hsp), Hsp101, chromosomal map positions indicate that HOT2, 3, and 4 do not correspond to major Hsp or heat shock transcription factor genes. Measurement of thermotolerance at different growth stages reveals that the mutants have growth stage-specific heat sensitivity. Analysis of Hsp accumulation shows that hot2 and hot4 produce normal levels of Hsps, whereas hot3 shows reduced accumulation. Thermotolerance of luciferase activity and of ion leakage also varies in the mutants. These data provide the first direct genetic evidence, to our knowledge, that distinct functions, independent of Hsp synthesis, are required for thermotolerance, including protection of membrane integrity and recovery of protein activity/synthesis.
Aspirin Inhibits Secretagogue‐Stimulated and Postprandial Pancreatic Exocrine Secretion in Conscious Rats

The effect of salicylate and nonsalicylate antiinflammatory drugs and prostaglandins (PGs) on pancreatic exocrine secretion are controversial. We studied the effect of aspirin (ASA) on secretin- and cholecystokinin (CCK)- or meal-stimulated pancreatic secretion. The interrelation between ASA, PG, and pancreatic exocrine secretion was also investigated. Conscious rats with chronic duodenal, pancreatic, and biliary cannulas received secretin (5 pmol/kg/h, i.v.) and CCK (56 pmol/kg/h) or a meal with administration of cimetidine (20 mg/kg/h, i.v.), ASA (1.2, 12, or 60 μmol/h, i.v.), Salicylic acid (SA) (1.2, 12, or 60 μmol/h, i.v.), prostaglandin E2 (PGE2) (10 μg/kg/h), or indomethacin (2 mg/kg) was given, respectively. Pancreatic flow volume, bicarbonate, and protein were determined every 15 min. An inhibitor, 1-(5 isoquinolinylsulfonyl)-2-methylpiperazine (H-7) (36 μg/kg/h) and an activator, phorbol ester (12-O-tetradecanoylphorbol 13-acetate, TPA) (100 ng/kg/h) were used for evaluation of the role of protein kinase C on basal and secretagogue-stimulated pancreatic secretion. ASA, but not SA inhibited the secretin- and CCK-stimulated pancreatic secretion including volume, bicarbonate, and protein in a dose-dependent manner without affecting basal pancreatic secretion. ASA and indomethacin suppressed meal-stimulated pancreatic secretion up to 83.8%. PGE2 significantly inhibited the secretin- and CCK-stimulated pancreatic secretion which was further suppressed by the concomitant ASA infusion. Modulation of protein kinase C failed to affect pancreatic secretion. The data indicate that ASA inhibits both secretin- and CCK-stimulated pancreatic secretion by a mechanism independent of prostaglandin biosynthesis inhibition.
Oxidative Stress and Pancreatic β-Cell Dysfunction

Oxidative stress is induced under diabetic conditions through various pathways, including the electron transport chain in mitochondria and the nonenzymatic glycosylation reaction, and is likely involved in progression of pancreatic β-cell dysfunction developing in diabetes. β-Cells are vulnerable to oxidative stress, possibly due to low levels of antioxidant enzyme expression. When oxidative stress was induced in vitro in β cells, the insulin gene promoter activity and mRNA levels were suppressed, accompanied by the reduced activity of pancreatic and duodenal homeobox factor-1 (PDX-1) (also known as IDX-1/STF-1/IPF1), an important transcription factor for the insulin gene. The suppression of oxidative stress by a potent antioxidant, N-acetyl-l-cysteine or probucol, led to the recovery of insulin biosynthesis and PDX-1 expression in nuclei and improved glucose tolerance in animal models for type 2 diabetes. As a possible cause of this, we recently found that PDX-1 was translocated from the nucleus to the cytoplasm in response to oxidative stress. Furthermore, the addition of a dominant-negative form of c-Jun N-terminal kinase (JNK) inhibited the oxidative stress-induced PDX-1 translocation, suggesting an essential role of JNK in mediating the phenomenon. Taken together, the oxidative stress-mediated activation of the JNK pathway leads to nucleocytoplasmic translocation of PDX-1 and thus is likely involved in the progression of β-cell dysfunction found in diabetes.
Lack of antibodies to human heart tissue in sera of rhesus monkeys immunized with Streptococcus mutans antigens and comparative study with rabbit antisera

Immunization of rabbits and rhesus monkeys with Streptococcus mutans whole cells, cell walls, and defined streptococcal antigens (SAs) SA I/II, SA I, and SA II resulted in high antibody titers to SA I/II (10(-4) to 10(-6)) when tested by the solid-phase radioimmunoassay. Cross-reactive antibodies to heart homogenates (HH) were not elicited in rhesus monkeys. A few rabbits immunized with cell wall or SA II preparation in Freund complete adjuvant followed by the incomplete adjuvant yielded low antibody titers (up to 10(-2)) to the HH. The specificity of the putative heart cross-reactive antibodies was tested by immunoadsorption with related and unrelated antigens. Whereas antibody to SA I/II showed specific adsorption with SA I/II but not with HH, immunoglobulin G, or the unrelated antigens, antibody to HH seemed to have been adsorbed with all of the related and unrelated antigens. There was no evidence for the development of heart cross-reactive antibodies on immunization of rhesus monkeys or rabbits with SA I/II and aluminium hydroxide or Freund incomplete adjuvant, administered by the subcutaneous or intramuscular route in doses of up to 13 mg of the immunogen.
Delayed-Onset Ulnar Neuritis After Release of Elbow Contractures

Background: Little information exists regarding delayed-onset ulnar neuritis (DOUN) after arthroscopic release of elbow contractures. Purpose: To describe, in a large cohort of patients, the clinical presentation of and risk factors for developing DOUN after arthroscopic release of elbow contractures. Study Design: Case-control study; Level of evidence, 3. Methods: A retrospective study of 565 consecutive arthroscopic releases of elbow contractures was conducted. Essentially, DOUN was defined as ulnar neuritis or neuropathy, or worsening of pre-existing ulnar nerve symptoms, that developed postoperatively in patients with normal neurological examination findings immediately after surgery. After inclusion and exclusion criteria were met, 235 contracture releases in patients who had not undergone any ulnar nerve surgery remained and were used for the analysis of risk factors with a multivariate logistic regression analysis. Results: Twenty-six patients (11%) developed DOUN. The patients fell into 1 of 3 distinct groups. Fifteen (58%) presented with rapidly progressive DOUN, characterized by rapidly progressive sensorimotor ulnar neuropathy, increasing pain at the cubital tunnel during end-range flexion and/or extension, and rapidly deteriorating range of motion within the first week after surgery. Urgent ulnar subcutaneous nerve transposition was performed within 1 or 2 days of diagnosis. Eight (31%) presented with nonprogressive DOUN, characterized by mild sensory ulnar neuropathy, neither motor weakness nor substantial pain at the cubital tunnel, or loss of motion. Three (12%) presented with slowly progressive DOUN, characterized by the insidious onset of mild ulnar neuropathy. Significant risk factors for DOUN included a diagnosis of heterotopic ossification (odds ratio, 31; 95% CI, 5-191; P < .001), preoperative neurological symptoms (odds ratio, 6; 95% CI, 2-19; P = .001), and preoperative arc of motion (odds ratio, 0.97 per degree of motion; 95% CI, 0.96-0.99; P = .02). Conclusion: Delayed-onset ulnar neuritis is an important complication of arthroscopic release of elbow contractures. We recommend a high index of suspicion and monitoring patients with progressive loss of elbow motion and end-range pain for evidence of subclinical ulnar neuritis.
Link State Update Algorithm considering Traffic Variation

Routers determine a routing path considering network topology and link state information for guaranteeing quality of service (QoS). Therefore, it is important that routers should know link state information so as to calculate a routing path. However, if routers generate link state update messages inordinately, their router performance may be reduced due to the processing burden of link state update messages. On the other side, in case that link state information is not updated appropriately, route setup requests can be rejected even though there are available routes. In this paper, we propose an algorithm to improve router performance and evaluate the proposed algorithm performance as compared with conventional algorithm by simulations.
Age-related differences in the automatic processing of single letters: implications for selective attention

Older adults exhibit diminished ability to inhibit the processing of visual stimuli that are supposed to be ignored. The extent to which age-related changes in early visual processing contribute to impairments in selective attention remains to be determined. Here, 103 adults, 18–85 years of age, completed a color selective attention task in which they were asked to attend to a specified color and respond to designated target letters. An optimal approach would be to initially filter according to color and then process letter forms in the attend color to identify targets. An asymmetric N170 ERP component (larger amplitude over left posterior hemisphere sites) was used as a marker of the early automatic processing of letter forms. Young and middle-aged adults did not generate an asymmetric N170 component. In contrast, young–old and old–old adults produced a larger N170 over the left hemisphere. Furthermore, older adults generated a larger N170 to letter than nonletter stimuli over the left, but not right hemisphere. More asymmetric N170 responses predicted greater allocation of late selection resources to target letters in the ignore color, as indexed by P3b amplitude. These results suggest that unlike their younger counterparts, older adults automatically process stimuli as letters early in the selection process, when it would be more efficient to attend to color only. The inability to ignore letters early in the processing stream helps explain the age-related increase in subsequent processing of target letter forms presented in the ignore color.
Comparison of a Commercial Real-Time PCR Assay for tcdB Detection to a Cell Culture Cytotoxicity Assay and Toxigenic Culture for Direct Detection of Toxin-Producing Clostridium difficile in Clinical Samples

ABSTRACT Rapid detection of toxin-producing strains of Clostridium difficile is essential for optimal management of patients with C. difficile infection. The BD GeneOhm (San Diego, CA) Cdiff assay, a real-time PCR assay that amplifies tcdB, was compared to a cell culture neutralization assay (Wampole C. difficile Toxin B [TOX-B] test; TechLab, Blacksburg, VA) and to toxigenic culture. Using liquid (n = 273) and soft (n = 131) stool specimens from 377 symptomatic patients, all testing was performed on the same day by independent laboratory staff according to the manufacturers' protocols. Toxigenic bacterial culture was performed as follows. A 0.5-ml aliquot of stool was heated to 80°C for 10 min, followed by inoculation onto modified cycloserine cefoxitin fructose agar with and without horse blood (Remel, Lenexa, KS) and into prereduced chopped-meat broth. Of the 404 stool specimens tested, 340 were negative and 40 were positive (10.0% prevalence) both by PCR for tcdB and by cytotoxin production. The overall agreement between the BD GeneOhm Cdiff assay and the TOX-B test was 94.8% (380/401). When the TOX-B test was used as the reference method, the initial sensitivity, specificity, and positive and negative predictive values of the BD GeneOhm Cdiff assay were 90.9% (40/44), 95.2% (340/357), 70.2% (40/57), and 98.8% (340/344), respectively. When toxigenic culture was used as the “gold standard,” the sensitivity, specificity, and positive and negative predictive values of the BD GeneOhm Cdiff assay were 83.6%, 98.2%, 89.5%, and 97.1%, respectively, and those of the TOX-B test were 67.2%, 99.1%, 93.2%, and 94.4%, respectively. PCRs for three samples were inhibited upon initial testing; one sample was resolved upon retesting. One sample produced nonspecific cytotoxin results. The BD GeneOhm Cdiff assay performed well compared to a standard cell culture neutralization assay and to toxigenic culture for the detection of toxigenic C. difficile directly from fecal specimens.
A review of progress in single particle tracking: from methods to biophysical insights

Optical microscopy has for centuries been a key tool to study living cells with minimum invasiveness. The advent of single molecule techniques over the past two decades has revolutionized the field of cell biology by providing a more quantitative picture of the complex and highly dynamic organization of living systems. Amongst these techniques, single particle tracking (SPT) has emerged as a powerful approach to study a variety of dynamic processes in life sciences. SPT provides access to single molecule behavior in the natural context of living cells, thereby allowing a complete statistical characterization of the system under study. In this review we describe the foundations of SPT together with novel optical implementations that nowadays allow the investigation of single molecule dynamic events with increasingly high spatiotemporal resolution using molecular densities closer to physiological expression levels. We outline some of the algorithms for the faithful reconstruction of SPT trajectories as well as data analysis, and highlight biological examples where the technique has provided novel insights into the role of diffusion regulating cellular function. The last part of the review concentrates on different theoretical models that describe anomalous transport behavior and ergodicity breaking observed from SPT studies in living cells.
Prednisone Withdrawal Followed by Interferon Alpha for Treatment of Chronic Hepatitis C Infection: Results of a Randomized Controlled Trial

Immunosuppressive therapy increases levels of hepatitis C virus (HCV) RNA, and when combined with interferon, corticosteroids have been reported to variably improve or have no effect on sustained response rates. We conducted a randomized double-blind placebo-controlled trial in 39 patients with biopsy-proven chronic HCV infection and elevated alanine aminotransferase levels. Patients received either 6 weeks of a tapering dose of prednisone (60 mg, 40 mg, and 20 mg in 2-week intervals) or an identical placebo. All patients then received recombinant interferon alpha-2b, 3 million units three times a week for 24 weeks. Patients were then followed for a further 24 weeks. At the end of the study there was no significant difference in the sustained biochemical response rates between the two groups (4/20 vs. 3/19, p value was not significant). Prednisone-treated patients had a significant increase in HCV RNA from baseline during steroid treatment (400 ± 60% increase vs. −280 ± 140% decrease;p = 0.005). Two prednisone-treated patients were withdrawn from the study secondary to serious complications related to therapy. Prednisone priming before interferon alpha therapy in patients with chronic HCV infection does not improve the sustained response rate. This therapy was associated with an increase in viral burden and significant morbidity.
Ca2+/Calmodulin-Dependent Facilitation and Inactivation of P/Q-Type Ca2+ Channels

Trains of action potentials cause Ca2+-dependent facilitation and inactivation of presynaptic P/Q-type Ca2+ channels that can alter synaptic efficacy. A potential mechanism for these effects involves calmodulin, which associates in a Ca2+-dependent manner with the pore-forming α1A subunit. Here, we report that Ca2+ and calmodulin dramatically enhance inactivation and facilitation of P/Q-type Ca2+channels containing the auxiliary β2a subunit compared with their relatively small effects on channels with β1b. Tetanic stimulation causes an initial enhancement followed by a gradual decline in P/Q-type Ca2+ currents over time. Recovery of Ca2+ currents from facilitation and inactivation is relatively slow (30 sec to 1 min). These effects are strongly inhibited by high intracellular BAPTA, replacement of extracellular Ca2+ with Ba2+, and a calmodulin inhibitor peptide. The Ca2+/calmodulin-dependent facilitation and inactivation of P/Q-type Ca2+ channels observed here are consistent with the behavior of presynaptic Ca2+ channels in neurons, revealing how dual feedback regulation of P/Q-type channels by Ca2+ and calmodulin could contribute to activity-dependent synaptic plasticity.
Sparse coding reveals greater functional connectivity in female brains during naturalistic emotional experience

Functional neuroimaging is widely used to examine changes in brain function associated with age, gender or neuropsychiatric conditions. FMRI (functional magnetic resonance imaging) studies employ either laboratory-designed tasks that engage the brain with abstracted and repeated stimuli, or resting state paradigms with little behavioral constraint. Recently, novel neuroimaging paradigms using naturalistic stimuli are gaining increasing attraction, as they offer an ecologically-valid condition to approximate brain function in real life. Wider application of naturalistic paradigms in exploring individual differences in brain function, however, awaits further advances in statistical methods for modeling dynamic and complex dataset. Here, we developed a novel data-driven strategy that employs group sparse representation to assess gender differences in brain responses during naturalistic emotional experience. Comparing to independent component analysis (ICA), sparse coding algorithm considers the intrinsic sparsity of neural coding and thus could be more suitable in modeling dynamic whole-brain fMRI signals. An online dictionary learning and sparse coding algorithm was applied to the aggregated fMRI signals from both groups, which was subsequently factorized into a common time series signal dictionary matrix and the associated weight coefficient matrix. Our results demonstrate that group sparse representation can effectively identify gender differences in functional brain network during natural viewing, with improved sensitivity and reliability over ICA-based method. Group sparse representation hence offers a superior data-driven strategy for examining brain function during naturalistic conditions, with great potential for clinical application in neuropsychiatric disorders.