Miracle-dz/UniFAR-FTUs huggingface dataset:
La métamémoire : théorie et clinique Metamemory: theory and clinical point of view

In everyday life, we are facing situations where cognitive faculties are challenged, evaluated, and regulated. This monitoring faculty of our cognitive processes refers, in cognitive psychology, to the concept of metacognition. It is the cognition on the cognition which, applied to the memory domain, corresponds to the multidimensional theoretical concept of metamemory. Indeed, this concept comprises knowledge one has about memory processing in general and about one's own memory functioning, in particular. Metamemory is also made up of the control and regulation strategies necessary to solve a memory task. As its various aspects interact, metamemory contributes to the adaptation, on the memory level, of each subject in every- day life. This rich theoretical context transpired through the development of different measu- res of metamemory. Moreover, a wide variety of clinical cases is described. Studies on neurological populations (amnesia, traumatic brain injury and focal frontal lesions, Alzhei- mer's disease) suggest that a joint decline of episodic memory and executive functions may cause disorders of metamemory, which in turn can cause memory difficulties. Beyond a bet- ter understanding of neuropsychological metamemory foundations, it appears necessary to take into account its alteration given its direct implications in patient care like cognitive rehabilitation for patients with severe head injury or in neurodegenerative diseases.
Stimulation of autophagy reduces neurodegeneration in a mouse model of human tauopathy

The accumulation of insoluble proteins is a pathological hallmark of several neurodegenerative disorders. Tauopathies are caused by the dysfunction and aggregation of tau protein and an impairment of cellular protein degradation pathways may contribute to their pathogenesis. Thus, a deficiency in autophagy can cause neurodegeneration, while activation of autophagy is protective against some proteinopathies. Little is known about the role of autophagy in animal models of human tauopathy. In the present report, we assessed the effects of autophagy stimulation by trehalose in a transgenic mouse model of tauopathy, the human mutant P301S tau mouse, using biochemical and immunohistochemical analyses. Neuronal survival was evaluated by stereology. Autophagy was activated in the brain, where the number of neurons containing tau inclusions was significantly reduced, as was the amount of insoluble tau protein. This reduction in tau aggregates was associated with improved neuronal survival in the cerebral cortex and the brainstem. We also observed a decrease of p62 protein, suggesting that it may contribute to the removal of tau inclusions. Trehalose failed to activate autophagy in the spinal cord, where it had no impact on the level of sarkosyl-insoluble tau. Accordingly, trehalose had no effect on the motor impairment of human mutant P301S tau transgenic mice. Our findings provide direct evidence in favour of the degradation of tau aggregates by autophagy. Activation of autophagy may be worth investigating in the context of therapies for human tauopathies.
Etiopathogenetic mechanisms of fibromyalgia syndrome Meccanismi eziopatogenetici della sindrome fibromialgica

SUMMARY Fibromyalgia syndrome (FMS) is a common chronic condition of widespread pain with causal mechanisms that are large-ly unknown. It is characterized by moderate to severe musculoskeletal pain and allodynia, but its pathogenesis appearsconﬁned to the nociceptive structures of the central nervous system. FMS is often triggered by negative environmentalinﬂuences, especially if they occur in childhood. In a fetus, these environmental triggers may inﬂuence the developmentof the autonomic nervous system (ANS) and the hypothalamic-pituitary-adrenal axis (HPA). Increasing evidence sup-ports the comorbidity of psychological conditions including depression, panic disorders, anxiety, and post-traumaticstress disorder (PTSD). Recent evidence suggests that genetic factors may play a role in the pathogenesis of FMS. Cen-tral sensitization has long been associated with FMS pain. It describes enhanced excitability of dorsal horn neurons, whichleads to transmission of altered nociceptive information to the brain. Understanding of pathogenetic pathways in FMShas advanced beyond observing patient responses to neurophysiologically targeted therapies and basic research.
Asymptomatic severe carotid stenosis

Objective: To analyze, for patients with asymptomatic severe carotid stenosis, the risks and benefits of two strategies: (1) immediate prophylactic carotid endarterectomy (CEA), and (2) medical management followed by CEA only after a transient ischemic attack (TIA) or a minor stroke has occurred. Design: A Markov-based decision analysis model that simulates and counts the possible clinical outcomes (deaths, TIAs, and major strokes) of the two strategies. Data were drawn from the current literature. Subjects: A hypothetical cohort of asymptomatic patients with severe (more than 75% diameter reduction) carotid stenosis identified by noninvasive diagnostic tests. Main results: Given the immediate surgery-related risks, patients with a stroke incidence without preceding TIA of 3% per year will benefit from prophylactic CEA only if they survive more than 4 years after the procedure, whereas those with a higher stroke incidence (5% per year) will benefit from prophylactic CEA after just 2 years. However, the gain yielded by prophylactic CEA remains small. As age- or cardiovascular-related mortality increases, the maximum tolerated combined surgical mortality and morbidity rate below which prophylactic CEA yields an improved 5-year stroke- and surgery-related-event-free survival decreases--from 5% for patients aged 55 years to 2% for patients aged 85 years with a stroke incidence of 3% per year, and from 8.5% for patients aged 55 years to 4% for patients aged 85 years with a stroke incidence of 5% per year. On the other hand, for risk-intolerant patients who value the 2-year stroke- and surgery-related-event-free survival more than life in the distant future, the combined surgical morbidity and mortality rate below which prophylactic CEA remains the preferred strategy is below 3% at any age. Conclusion: Risk-intolerant patients should not undergo prophylactic CEA. On the other hand, for risk-tolerant patients willing to accept an immediate and dangerous procedure to decrease the future risk of death or chronic disability due to stroke, assessment of both perioperative risk and the risk of premature death from coexistent coronary artery disease should guide individual therapeutic decision-making. NEUROLOGY 1995;45: 2147-2153
Bio-digital device impact on a constant load cognitive test of children with physical and neurological impairments

In this paper we extend on our earlier work utilizing maximum consecutive success as a measure used in the context of testing motor skills, for children with physical and neurological impairment. Here we verify a change in the "ceiling" of performance that takes place as the cognitive load is increased. In the results we see two groups establish themselves in terms of the ones capable of achieving the test objectives and the ones that engage but are not successful. In this study, we compare results for two different tests, one of motor skills and the second of categorization assessment and find agreement between the two using our approach. Working on our main hypothesis that it is possible to provide better fit of devices to PNI children, the results provide initial suggestions that cognitive test success depend on a combination of motor skill and cognitive ability which is not completely separable. Ranking of bio-digital devices ideally need to be done using the target application or the use of direct communication which is some form of Signing. It is the intention in a future project to further show that for some children their cognitive capacity can deal with just the motor skill for a physical device or the cognitive load for a test but not both. The ideal fit of a physical device for the child depend on both the demands of the application and device and it is not possible to draw conclusions on a fit without considering a triad which involves the user, the device and the test. The role of novel non- hand held devices in complex working environments are a potential market but fatigue is a serious problem in critical environments. This study provides a start to examining the fatigue levels imposed by in a user-device-application triad as a result of different levels of cognitive loads.
Processing of the major autolysin of E. faecalis, AtlA, by the zinc-metalloprotease, GelE, impacts AtlA septal localization and cell separation

AtlA is the major peptidoglycan hydrolase of Enterococcus faecalis involved in cell division and cellular autolysis. The secreted zinc metalloprotease, gelatinase (GelE), has been identified as an important regulator of cellular function through post-translational modification of protein substrates. AtlA is a known target of GelE, and their interplay has been proposed to regulate AtlA function. To study the protease-mediated post-translational modification of AtlA, monoclonal antibodies were developed as research tools. Flow cytometry and Western blot analysis suggests that in the presence of GelE, surface-bound AtlA exists primarily as a N-terminally truncated form whereas in the absence of GelE, the N-terminal domain of AtlA is retained. We identified the primary GelE cleavage site occurring near the transition between the T/E rich Domain I and catalytic region, Domain II via N-terminal sequencing. Truncation of AtlA had no effect on the peptidoglycan hydrolysis activity of AtlA. However, we observed that N-terminal cleavage was required for efficient AtlA-mediated cell division while unprocessed AtlA was unable to resolve dividing cells into individual units. Furthermore, we observed that the processed AtlA has the propensity to localize to the cell septum on wild-type cells whereas unprocessed AtlA in the ΔgelE strain were dispersed over the cell surface. Combined, these results suggest that AtlA septum localization and subsequent cell separation can be modulated by a single GelE-mediated N-terminal cleavage event, providing new insights into the post-translation modification of AtlA and the mechanisms governing chaining and cell separation.
Nkrp1 Family, from Lectins to Protein Interacting Molecules

The C-type lectin-like receptors include the Nkrp1 protein family that regulates the activity of natural killer (NK) cells. Rat Nkrp1a was reported to bind monosaccharide moieties in a Ca2+-dependent manner in preference order of GalNac > GlcNAc >> Fuc >> Gal > Man. These findings established for rat Nkrp1a have been extrapolated to all additional Nkrp1 receptors and have been supported by numerous studies over the past two decades. However, since 1996 there has been controversy and another article showed lack of interactions with saccharides in 1999. Nevertheless, several high affinity saccharide ligands were synthesized in order to utilize their potential in antitumor therapy. Subsequently, protein ligands were introduced as specific binders for Nkrp1 proteins and three dimensional models of receptor/protein ligand interaction were derived from crystallographic data. Finally, for at least some members of the NK cell C-type lectin-like proteins, the “sweet story” was impaired by two reports in recent years. It has been shown that the rat Nkrp1a and CD69 do not bind saccharide ligands such as GlcNAc, GalNAc, chitotetraose and saccharide derivatives (GlcNAc-PAMAM) do not directly and specifically influence cytotoxic activity of NK cells as it was previously described.
Spine ultrasounds should not be routinely performed for patients with simple sacral dimples

Primary care providers commonly obtain spine ultrasounds for neonates with simple sacral dimples due to perceived concerns about underlying spinal dysraphism, despite a lack of scientific evidence. Nine papers addressing routine spine ultrasounds for children with sacral dimples showed that 3.4% of the 5166 patients had abnormal spine ultrasounds, compared with the 4.8% reported by another study for children without sacral dimples. Most of the abnormal findings in patients with sacral dimples were of no clinical significance.
Rapid Perceptual Switching of a Reversible Biological Figure

Certain visual stimuli can give rise to contradictory perceptions. In this paper we examine the temporal dynamics of perceptual reversals experienced with biological motion, comparing these dynamics to those observed with other ambiguous structure from motion (SFM) stimuli. In our first experiment, naïve observers monitored perceptual alternations with an ambiguous rotating walker, a figure that randomly alternates between walking in clockwise (CW) and counter-clockwise (CCW) directions. While the number of reported reversals varied between observers, the observed dynamics (distribution of dominance durations, CW/CCW proportions) were comparable to those experienced with an ambiguous kinetic depth cylinder. In a second experiment, we compared reversal profiles with rotating and standard point-light walkers (i.e. non-rotating). Over multiple test repetitions, three out of four observers experienced consistently shorter mean percept durations with the rotating walker, suggesting that the added rotational component may speed up reversal rates with biomotion. For both stimuli, the drift in alternation rate across trial and across repetition was minimal. In our final experiment, we investigated whether reversals with the rotating walker and a non-biological object with similar global dimensions (rotating cuboid) occur at random phases of the rotation cycle. We found evidence that some observers experience peaks in the distribution of response locations that are relatively stable across sessions. Using control data, we discuss the role of eye movements in the development of these reversal patterns, and the related role of exogenous stimulus characteristics. In summary, we have demonstrated that the temporal dynamics of reversal with biological motion are similar to other forms of ambiguous SFM. We conclude that perceptual switching with biological motion is a robust bistable phenomenon.
Sleep problems in children with attention-deficit/hyperactivity disorder: impact of subtype, comorbidity, and stimulant medication.

OBJECTIVE To determine the relationship of sleep problems to attention-deficit/hyperactivity disorder (ADHD), diagnostic subtype, comorbid disorders, and the effects of stimulant treatment. METHOD On the basis of clinical diagnostic interviews, children aged 6 to 12 years were assigned to 4 groups: unmedicated ADHD (n = 79), medicated ADHD (n = 22), clinical comparison (n = 35), and healthy nonclinical comparison (n = 36). These groups were compared on 2 sleep questionnaires completed by the parents that assessed current sleep problems and factors associated with sleep difficulties (i.e., sleep routines, sleep practices, child and family sleep history). RESULTS Factor analysis revealed 3 sleep problem categories: dyssomnias, parasomnias, and sleep-related involuntary movements. Linear regression analyses showed that (1) dyssomnias were related to confounding factors (i.e., comorbid oppositional defiant disorder and stimulant medication) rather than ADHD; (2) parasomnias were similar in clinical and nonclinical children; and (3) the DSM-IV combined subtype of ADHD was associated with sleep-related involuntary movements. However, sleep-related involuntary movements were more highly associated with separation anxiety. CONCLUSIONS The results suggest that the relationship between sleep problems and ADHD is complex and depends on the type of sleep problem assessed as well as confounding factors such as comorbid clinical disorders and treatment with stimulant medication.
Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a highly prevalent breathing disorder in sleep that is an independent risk factor for cardiovascular morbidity and mortality. A large body of evidence, including clinical studies and cell culture and animal models utilising intermittent hypoxia, delineates the central role of oxidative stress in OSAHS as well as in conditions and comorbidities that aggregate with it. Intermittent hypoxia, the hallmark of OSAHS, is implicated in promoting the formation of reactive oxygen species (ROS) and inducing oxidative stress. The ramifications of increased ROS formation are pivotal. ROS can damage biomolecules, alter cellular functions and function as signalling molecules in physiological as well as in pathophysiological conditions. Consequently, they promote inflammation, endothelial dysfunction and cardiovascular morbidity. Oxidative stress is also a crucial component in obesity, sympathetic activation and metabolic disorders such as hypertension, dyslipidaemia and type 2 diabetes/insulin resistance, which aggregate with OSAHS. These conditions and comorbidities could result directly from the oxidative stress that is characteristic of OSAHS or could develop independently. Hence, oxidative stress represents the common underlying link in OSAHS and the conditions and comorbidities that aggregate with it.
Correcting erasure bursts with minimum decoding delay

Erasure correcting codes are widely used in upper layers of packet-switched networks, where the packet erasures often exhibit bursty patterns. The conventional wisdom to deal with bursty erasures is to apply block interleaving to break down the bursty patterns prior to error correcting coding, or use long-block Reed-Solomon codes. We show that they unnecessarily lead to sub-optimal decoding delay. In this work, with the problem model of multiple erasure bursts present in a coding block, we study the fundamental tradeoff among the rate, decoding delay and burst correction performance of erasure correcting codes. Focusing on a class of codes achieving the Singleton bound, we show that the lowest delay to recover any individual symbol not only depends on the erasure burst patterns correctable by a code, but also on whether the source symbols are encoded causally or non-causally. We also describe a few practical linear code constructions that achieve the performance limit discussed.
Kalman prediction based VFH of dynamic obstacle avoidance for intelligent vehicles

a mixed obstacle avoidance algorithm for intelligent vehicles to avoid dynamic obstacles is presented in uncertain environments. Traditional Vector Field Histogram method is combined with kalman prediction algorithm in this algorithm. The kalman predictor forecasts the optimal position estimation of dynamic obstacles at the next moment, then the intelligent vehicle calls VFH algorithm to avoid obstacles according the current position and the next position predicted by the predictor. This method solves the problem that intelligent vehicle can not choose optimal path for the reason that the intelligent vehicle has no priori knowledge about the local environment. It is more suitable for dynamic obstacles avoidance of the intelligent vehicle. The simulation results show that the method has a good real-time performance, and the intelligent vehicle can avoid the dynamic obstacles accurately and reach the target point.
Folate, colorectal carcinogenesis, and DNA methylation: Lessons from animal studies

Folate, a water‐soluble B vitamin and cofactor in one‐carbon transfer, is an important nutritional factor that may modulate the development of colorectal cancer (CRC). Epidemiologic and clinical studies indicate that dietary folate intake and blood folate levels are inversely associated with CRC risk. Collectively, these studies suggest an ∼ 40% reduction in the risk of CRC in individuals with the highest dietary folate intake compared with those with the lowest intake. Animal studies using chemical and genetically predisposed rodent models have provided considerable support for a causal relationship between folate depletion and colorectal carcinogenesis as well as a dose‐dependent protective effect of folate supplementation. However, animal studies also have shown that the dose and timing of folate intervention are critical in providing safe and effective chemoprevention; exceptionally high supplemental folate levels and folate intervention after microscopic neoplastic foci are established in the colorectal mucosa promote, rather than suppress, colorectal carcinogenesis. These animal studies, in conjunction with clinical observations, suggest that folate possesses dual modulatory effects on carcinogenesis depending on the timing and dose of folate intervention. Folate deficiency has an inhibitory effect, whereas folate supplementation has a promoting effect on the progression of established neoplasms. In contrast, folate deficiency in normal epithelial tissues appears to predispose them to neoplastic transformation, and modest levels of folate supplementation suppress the development of tumors in normal tissues. Notwithstanding the limitations associated with animal models, these studies suggest that the optimal timing and dose of folate intervention must be established for safe and effective chemoprevention in humans. Folate is an important factor in DNA synthesis, stability, and integrity, the repair aberrations of which have been implicated in colorectal carcinogenesis. Folate may also modulate DNA methylation, which is an important epigenetic determinant in gene expression (an inverse relationship), in the maintenance of DNA integrity and stability, in chromosomal modifications, and in the development of mutations. A mechanistic understanding of how folate status modulates colorectal carcinogenesis further strengthens the case for a causal relationship and provides insight into a possible chemopreventive role of folate. Environ. Mol. Mutagen. 44:10–25, 2004. © 2004 Wiley‐Liss, Inc.