Miracle-dz/UniFAR-FTUs huggingface dataset:
Rapid Critical Period Induction by Tonic Inhibition in Visual Cortex

Mice lacking a synaptic isoform of glutamic acid decarboxylase (GAD65) do not exhibit ocular dominance plasticity unless an appropriate level of GABAergic transmission is restored by direct infusion of benzodiazepines into the brain. To better understand how intracortical inhibition triggers experience-dependent changes, we dissected the precise timing requirement for GABA function in the monocular deprivation (MD) paradigm. Diazepam (DZ) or vehicle solution was infused daily before and/or during 4 d of MD in GAD65 knock-out mice. Extracellular single-unit recordings from the binocular zone of visual cortex were performed at the end of deprivation. We found that a minimum treatment of 2 d near the beginning of MD was sufficient to fully activate plasticity but did not need to overlap the deprivation per se. Extended delay after DZ infusion eventually led to loss of plasticity accompanied by improved intrinsic inhibitory circuit function. Two day DZ treatment just after eye opening similarly closed the critical period prematurely in wild-type mice. Raising wild-type mice in complete darkness from birth delayed the peak sensitivity to MD as in other mammals. Interestingly, 2 d DZ infusion in the dark also closed the critical period, whereas equally brief light exposure during dark-rearing had no such effect. Thus, enhanced tonic signaling through GABAA receptors rapidly creates a milieu for plasticity within neocortex capable of triggering a critical period for ocular dominance independent of visual experience itself.
Minimum intervention dentistry approach to managing early childhood caries: a randomized control trial.

OBJECTIVES A pragmatic randomized control trial was undertaken to compare the minimum intervention dentistry (MID) approach, based on the atraumatic restorative treatment procedures (MID-ART: Test), against the standard care approach (Control) to treat early childhood caries in a primary care setting. METHODS Consenting parent/child dyads were allocated to the Test or Control group using stratified block randomization. Inclusion and exclusion criteria were applied. Participants were examined at baseline and at follow-up by two calibrated examiners blind to group allocation status (κ = 0.77), and parents completed a questionnaire at baseline and follow-up. Dental therapists trained in MID-ART provided treatment to the Test group and dentists treated the Control group using standard approaches. The primary outcome of interest was the number of children who were referred for specialist pediatric care. Secondary outcomes were the number of teeth treated, changes in child oral health-related quality of life and dental anxiety and parental perceptions of care received. Data were analyzed on an intention to treat basis; risk ratio for referral for specialist care, test of proportions, Wilcoxon rank test and logistic regression were used. RESULTS Three hundred and seventy parents/carers were initially screened; 273 children were examined at baseline and 254 were randomized (Test = 127; Control = 127): mean age = 3.8 years, SD 0.90; 59% male, mean dmft = 4.9, SD 4.0. There was no statistically significant difference in age, sex, baseline caries experience or child oral health-related quality of life between the Test and Control group. At follow-up (mean interval 11.4 months, SD 3.1 months), 220 children were examined: Test = 115, Control = 105. Case-notes review of 231 children showed Test = 6 (5%) and Control = 53 (49%) were referred for specialist care, P < 0.0001. More teeth were filled in the Test group (mean = 2.93, SD 2.48) than in the Control group (mean = 1.54, SD 2.20), Wilcoxon's test, P < 0.0001. Logistic regression, after controlling for age and baseline caries experience, showed a higher risk of referral by allocation to control group, OR 32.6, 95% CI 10.8-98.4, P < 0.0001. CONCLUSION The MID-ART approach reduced significantly the likelihood of referral for specialist care, and more children and teeth were provided with treatment.
The effect of oral propranolol plus oxytocin versus oxytocin only on the process and outcome of labor: A double-blind randomized trial

Background: Prolonged labor can lead to maternal and neonatal complications. The purpose of this study was to investigate the effect of oral propranolol plus oxytocin versus oxytocin only on the process and outcome of labor. Materials and Methods: In a randomized, double-blind, controlled trial performed in Ilam Mustafa hospital, a total of 146 nulliparous pregnant women at gestational age of 40-42 weeks were randomly allocated to receive 20 mg oral dose of propranolol or placebo plus oxytocin infusion (73 participants in each group). The outcome measures were the mean duration of labor stages, type of delivery, and neonatal outcome. Results: The mean duration of active phase and the second stage of labor were significantly shorter in the propranolol group than in the placebo group on both the first and the second days of induction. The mean duration of third stage of labor was shorter in the propranolol group than in the placebo group, but the difference was not significant statistically on the first (P = 0.159) and second (P = 0.065) days. Frequency of cesarean section deliveries significantly decreased in the propranolol plus oxytocin group compared to the placebo plus oxytocin group (P = 0.005, P = 0.015) on the first and the second days, respectively. No significant difference in the neonatal outcome measures, such as Apgar scores at 1 and 5 min and the need for neonatal intensive care unit (NICU) admission, was found between the groups. Conclusions: This study showed that oral propranolol is an effective agent in both shortening the labor duration and reducing the frequency of cesarean section.
Early angiography in patients with chronic kidney disease: a collaborative systematic review.

BACKGROUND AND OBJECTIVES In the general population, an early invasive strategy of routine coronary angiography is superior to a conservative strategy of selective angiography in patients who are admitted with unstable angina or non-ST segment elevation myocardial infarction (MI), but the effectiveness of this strategy in individuals with chronic kidney disease (CKD) is uncertain. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS We conducted a collaborative meta-analysis with data provided by the main authors of identified trials to estimate the effectiveness of early angiography in patients with CKD. The Cochrane, Medline, and EMBASE databases were searched to identify randomized trials that compared invasive and conservative strategies in patients with unstable angina or non-ST MI. Pooled risks ratios were estimated using data from enrolled patients with estimated GFR <60 ml/min per 1.73 m(2). RESULTS Five randomized trials that enrolled 1453 patients with CKD were included. An early invasive strategy was associated with nonsignificant reductions in all-cause mortality, nonfatal MI, and a composite of death or nonfatal MI. The invasive strategy significantly reduced rehospitalization. CONCLUSIONS This collaborative study suggests that the benefits of an early invasive strategy are preserved in patients with CKD and that an early invasive approach reduces the risk for rehospitalization and is associated with trends of reduction in the risk for death and nonfatal re-infarction in patients with CKD. Coronary angiography should be considered for patients who have CKD and are admitted with non-ST elevation acute coronary syndromes.
A hardware pipelined architecture of a scalable Montgomery modular multiplier over GF(2m)

Computing modular multiplication over GF(2m) is often a performance critical operation in cryptographic applications. This paper describes the architecture of a scalable and configurable Montgomery modular multiplier over binary fields. This architecture, implemented on a FPGA platform, aims to reduce the computation time thanks to the pipelining of the datapath. Scalability is achieved by allowing to change field parameters while keeping the same design. A timing area tradeoff allows to get a significant speedup at a reasonable cost.
Speaking and Instructed Foreign Language Acquisition

PrefacePart I: Theoretical perspectives on instructed acquisition of speaking 1.Miros? aw Pawlak: Instructed acquisition of speaking: Reconciling theory and practice 2.Agnieszka Nowicka and Weronika Wilczy? ska: Authenticity in oral communication of instructed l 2 learners 3.Piotr Bia? as: Formulaic sequences in the output of instructed l 2 learners 4.Agnieszka Wrobel: Formulaicity vs. fluency and accuracy in using English as a foreign language. 5.Jan Majer: Talking the same language: Sociocultural aspects of code-switching in l 2 classroom discourse 6.Anna Ni? egorodcew: Speaking in English for Academic Purposes in the light of Lingua Franca English Part II: Speaking and individual variables 7.Adriana Biedro? : Near-nativeness as a function of cognitive and personality factors. Three case studies of highly able foreign language learners 8.Ewa Waniek-Klimczak: 'I am good at speaking, but I failed my phonetics class' - pronunciation and speaking in advanced learners of English 9.Krystyna Dro? dzia? -Szelest: Oral skills awareness of advanced ESL learners 10.Aneta Ca? ka: Pronunciation learning strategies - identification and classification 11.Magdalena Wrembel: Metaphonetic awareness in the production of speech 12.Krzysztof Nerlicki: Foreign language speaking anxiety from the perspective of Polish students of German studies 13.Ewa Piechurska-Kuciel: The relationship between language anxiety and the development of the speaking skill. Results of a longitudinal studyPart III: Research into instructed acquisition of speaking 14.Sebastian Piotrowski: On the authenticity of communication in the foreign language classroom 15.Irena Czwenar: Ways to proficiency in spoken English as a foreign language - tracing individual development 16.Anna Mystkowska-Wiertelak: Task repetition as a way of enhancing oral communication in a foreign language 17.Mariusz Kruk: The use of the Internet and Instant Messengers in assisting the acquisition of speaking skills in English lessons 18.Dorota Werbi? ska: Investigating the perception of speaking skills with metaphor-based methods 19.Jolanta Szpyra-Koz? owska: Phonetically difficult words in intermediate learners' English 20.Przemys? aw Krakowian: Transcultural interference, communities of practice and collaborative assessment of oral performance
Metformin limits the adipocyte tumor-promoting effect on ovarian cancer

Omental adipocytes promote ovarian cancer by secretion of adipokines, cytokines and growth factors, and acting as fuel depots. We investigated if metformin modulates the ovarian cancer promoting effects of adipocytes. Effect of conditioned media obtained from differentiated mouse 3T3L1 preadipoctes on the proliferation and migration of a mouse ovarian surface epithelium cancer cell line (ID8) was estimated. Conditioned media from differentiated adipocytes increased the proliferation and migration of ID8 cells, which was attenuated by metformin. Metformin inhibited adipogenesis by inhibition of key adipogenesis regulating transcription factors (CEBPα, CEBPß, and SREBP1), and induced AMPK. A targeted Cancer Pathway Finder RT-PCR (real-time polymerase chain reaction) based gene array revealed 20 up-regulated and 2 down-regulated genes in ID8 cells exposed to adipocyte conditioned media, which were altered by metformin. Adipocyte conditioned media also induced bio-energetic changes in the ID8 cells by pushing them into a highly metabolically active state; these effects were reversed by metformin. Collectively, metformin treatment inhibited the adipocyte mediated ovarian cancer cell proliferation, migration, expression of cancer associated genes and bio-energetic changes. Suggesting, that metformin could be a therapeutic option for ovarian cancer at an early stage, as it not only targets ovarian cancer, but also modulates the environmental milieu.
Enhancement of Peripheral Nerve Regrowth by the Purine Nucleoside Analog and Cell Cycle Inhibitor, Roscovitine

Peripheral nerve regeneration is a slow process that can be associated with limited outcomes and thus a search for novel and effective therapy for peripheral nerve injury and disease is crucial. Here, we found that roscovitine, a synthetic purine nucleoside analog, enhances neurite outgrowth in neuronal-like PC12 cells. Furthermore, ex vivo analysis of pre-injured adult rat dorsal root ganglion (DRG) neurons showed that roscovitine enhances neurite regrowth in these cells. Likewise, in vivo transected sciatic nerves in rats locally perfused with roscovitine had augmented repopulation of new myelinated axons beyond the transection zone. By mass spectrometry, we found that roscovitine interacts with tubulin and actin. It interacts directly with tubulin and causes a dose-dependent induction of tubulin polymerization as well as enhances Guanosine-5′-triphosphate (GTP)-dependent tubulin polymerization. Conversely, roscovitine interacts indirectly with actin and counteracts the inhibitory effect of cyclin-dependent kinases 5 (Cdk5) on Actin-Related Proteins 2/3 (Arp2/3)-dependent actin polymerization, and thus, causes actin polymerization. Moreover, in the presence of neurotrophic factors such as nerve growth factor (NGF), roscovitine-enhanced neurite outgrowth is mediated by increased activation of the extracellular signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) pathways. Since microtubule and F-actin dynamics are critical for axonal regrowth, the ability of roscovitine to activate the ERK1/2 and p38 MAPK pathways and support polymerization of tubulin and actin indicate a major role for this purine nucleoside analog in the promotion of axonal regeneration. Together, our findings demonstrate a therapeutic potential for the purine nucleoside analog, roscovitine, in peripheral nerve injury.
Elimination of Epidemic Methicillin-Resistant Staphylococcus aureus from a University Hospital and District Institutions, Finland

From August 1991 to October 1992, two successive outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) occurred at a hospital in Finland. During and after these outbreaks, MRSA was diagnosed in 202 persons in our medical district; >100 cases involved epidemic MRSA. When control policies failed to stop the epidemic, more aggressive measures were taken, including continuous staff education, contact isolation for MRSA-positive patients, systematic screening for persons exposed to MRSA, cohort nursing of MRSA-positive and MRSA-exposed patients in epidemic situations, and perception of the 30 medical institutions in that district as one epidemiologic entity brought under surveillance and control of the infection control team of Turku University Hospital. Two major epidemic strains, as well as eight additional strains, were eliminated; we were also able to prevent nosocomial spread of other MRSA strains. Our data show that controlling MRSA is possible if strict measures are taken before the organism becomes endemic. Similar control policies may be successful for dealing with new strains of multiresistant bacteria, such as vancomycin-resistant strains of S. aureus.
A fast parallel matrix multiplication reconfigurable unit utilized in face recognitions systems

In this paper we present a reconfigurable device which significantly improves the execution time of the most computational intensive functions of three of the most widely used face recognition algorithms; those tasks multiply very large dense matrices. The presented architecture utilizes numerous digital signal processing units (DSPs) organized in a parallel manner within a state-of-the-art FPGA device. In order to accelerate those functions we have implemented a ldquoblockedrdquo matrix multiplication algorithm which multiplies certain sub-matrices of fixed-point 32-bit numbers; the size of the sub-matrices has been selected so as to fully exploit the resources of the underlying reconfigurable device. Our system is up to 550 times faster than a conventional general purpose processor when implementing the most CPU intensive parts of a number of very widely used face identification schemes, whereas it is more than 40 times faster than the similar schemes implemented in reconfigurable devices. Moreover, our system is general enough so as to be efficiently utilized in any application incorporating fixed-point matrix multiplications.
Maternal and Fetal Mechanisms of B Cell Regulation during Pregnancy: Human Chorionic Gonadotropin Stimulates B Cells to Produce IL-10 While Alpha-Fetoprotein Drives Them into Apoptosis

Maternal immune tolerance toward the fetus is an essential requisite for pregnancy. While T cell functions are well documented, little is known about the participation of B cells. We have previously suggested that IL-10-producing B cells are involved in pregnancy tolerance in mice and humans. By employing murine and human systems, we report now that fetal trophoblasts positively regulate the generation of IL-10-producing B cells. We next studied the participation of hormones produced by the placenta as well as the fetal protein alpha-fetoprotein (AFP) in B cell modulation. Human chorionic gonadotropin (hCG), but not progesterone, estrogen, or a combination of both, was able to promote changes in B cell phenotype and boost their IL-10 production, which was abolished after blocking hCG. The hCG-induced B cell phenotype was not associated with augmented galactosylation, sialylation, or fucosylation of IgG subclasses in their Fc. In vitro, hCG induced the synthesis of asymmetrically glycosylated antibodies in their Fab region. Interestingly, AFP had dual effects depending on the concentration. At concentrations corresponding to maternal serum levels, it did not modify the phenotype or IL-10 secretion of B cells. At fetal concentrations, however, AFP was able to drive B cells into apoptosis, which may indicate a protective mechanism to avoid maternal B cells to reach the fetus. Our data suggest that the fetus secrete factors that promote a pregnancy-friendly B cell phenotype, unraveling interesting aspects of B cell function, and modulation by pregnancy hormones and fetal proteins.
Response to Comments on "Saturation of the Southern Ocean CO2 Sink Due to Recent Climate Change"

We estimated a weakening of the Southern Ocean carbon dioxide (CO2) sink since 1981 relative to the trend expected from the large increase in atmospheric CO2. We agree with Law et al. that network choice increases the uncertainty of trend estimates but argue that their network of five locations is too small to be reliable. A future reversal of Southern Ocean CO2 saturation as suggested by Zickfeld et al. is possible, but only at high atmospheric CO2 concentrations, and the effect would be temporary.
Corticotropin‐releasing hormone neurons in hypertensive patients are activated in the hypothalamus but not in the brainstem

The corticotrophin‐releasing hormone (CRH)‐expressing neurons were studied in the hypothalamus and brainstem of individuals who suffered from essential hypertension and had died due to acute myocardial infarction or brain hemorrhage. Healthy normotensive individuals who died in accidents made up the control group. In hypertensive patients we found extremely high expression of CRH in all parts of the hypothalamic paraventricular nucleus (Pa). In addition, CRH neuronal profiles were observed in the caudal hypothalamic area and dorsal parts of the extended amygdala. In the control group, CRH neurons were found only in the Pa and in much smaller numbers than in hypertensive patients. Also, in contrast to the controls, we found in hypertensives a very high number of CRH fibers running from the most rostral part of the Pa to the median eminence and innervating the caudal part of the suprachiasmatic nucleus (SCh). A quantitative evaluation showed that the area covered by CRH fibers in the SCh of hypertensives was about three times larger than that in the control SCh. Linear regression analysis demonstrated a negative correlation between the area of CRH fibers and the number of vasopressin (VP) or neurotensin (NT) neurons within the SCh. This relationship occurred particularly in hypertensive patients in whose SCh a larger CRH fiber area and a smaller number of VP or NT neurons were observed. We found a few CRH neuronal profiles and fibers in brainstem nuclei that are involved in cardiovascular regulation, but no apparent difference was observed between the control and hypertensive group. J. Comp. Neurol. 503:148–168, 2007. © 2007 Wiley‐Liss, Inc.
Overexpression of IFN-Induced Protein 10 and Its Receptor CXCR3 in Myasthenia Gravis1

Myasthenia gravis (MG) and its animal model, experimental autoimmune MG (EAMG), are autoimmune disorders in which the acetylcholine receptor (AChR) is the major autoantigen. Microarray technology was used to identify new potential drug targets for treatment of myasthenia that would reduce the need for the currently used nonspecific immunosuppression. The chemokine IFN-γ-inducible protein 10 (IP-10; CXCL10), a CXC chemokine, and its receptor, CXCR3, were found to be overexpressed in lymph node cells of EAMG rats. Quantitative real-time PCR confirmed these findings and revealed up-regulated mRNA levels of another chemoattractant that activates CXCR3, monokine induced by IFN-γ (Mig; CXCL9). TNF-α and IL-1β, which act synergistically with IFN-γ to induce IP-10, were also up-regulated. These up-regulations were observed in immune response effector cells, namely, lymph node cells, and in the target organ of the autoimmune attack, the muscle of myasthenic rats, and were significantly reduced after suppression of EAMG by mucosal tolerance induction with an AChR fragment. The relevance of IP-10/CXCR3 signaling in myasthenia was validated by similar observations in MG patients. A significant increase in IP-10 and CXCR3 mRNA levels in both thymus and muscle was observed in myasthenic patients compared with age-matched controls. CXCR3 expression in PBMC of MG patients was markedly increased in CD4+, but not in CD8+, T cells or in CD19+ B cells. Our results demonstrate a positive association of IP-10/CXCR3 signaling with the pathogenesis of EAMG in rats as well as in human MG patients.
Musical Instrument Sound Multi-Excitation Model for Non-Negative Spectrogram Factorization

This paper presents theoretical and experimental results about constrained non-negative matrix factorization (NMF) to model the excitation of the musical instruments. These excitations represent vibrating objects, while the filter represents the resonance structure of the instrument, which colors the produced sound. We propose to model the excitations as the weighted sum of harmonically constrained basis functions, whose parameters are tied across different pitches of an instrument. An NMF-based framework is used to learn the model parameters. We assume that the excitations of a well-tempered instrument should possess an identifiable characteristic structure whereas the conditions of the music scene might produce variations in the filter. In order to test the reliability of our proposal, we evaluate our method for a music transcription task in two scenarios. On the first one, comparison with state-of-the-art methods has been performed over a dataset of piano recordings obtaining more accurate results than other NMF-based algorithms. On the second one, two woodwind instrument databases have been used to demonstrate the benefits of our model in comparison with previous excitation-filter model approaches.