EEG subject-dependent neurofeedback training selectively impairs declarative memories consolidation process.

The process of stabilization and storage of memories, known as consolidation, can be modulated by different interventions. Research has shown that self-regulation of brain activity through Neurofeedback (NFB) during the consolidation phase significantly impacts memory stabilization. While some studies have successfully modulated the consolidation phase using traditional EEG-based Neurofeedback (NFB) that focuses on general parameters, such as training a specific frequency band at particular electrodes, they often overlook the unique and complex neurodynamics that underlie each memory content in different individuals, potentially limiting the selective modulation of memories. The main objective of this study is to investigate the effects of a Subject-Dependent NFB (SD-NFB), based on individual models created from the brain activity of each participant, on long-term declarative memories. Participants underwent an experimental protocol involving three sessions. In the first session, they learned images of faces and houses while their brain activity was recorded. This EEG data was used to create individualized models to identify brain patterns related to learning these images. Participants were then divided into three groups, with one group receiving SD-NFB to enhance brain activity linked to faces, another to houses, and a CONTROL SHAM group that did not receive SD-NFB. Memory performance was evaluated 24 h and seven days later using an 'old-new' recognition task, where participants distinguished between 'old' and 'new' images. The results showed that memory contents (faces or houses) whose brain patterns were trained via SD-NFB scored lower in recognition compared to untrained contents, as evidenced 24 h and seven days post-training. In summary, this study demonstrates that SD-NFB can selectively impact the consolidation of specific declarative memories. This technique could hold significant implications for clinical applications, potentially aiding in the modulation of declarative memory strength in neuropsychiatric disorders where memories are pathologically exacerbated.

Classifying brain states and pupillary responses associated with the processing of old and new information.

Memory retrieval of consolidated memories has been extensively studied using "old-new tasks", meaning tasks in which participants are instructed to discriminate between stimuli they have experienced before and new ones. Significant differences in the neural processing of old and new elements have been demonstrated using different techniques, such as electroencephalography and pupillometry. In this work, using the data from a previously published study (Campos-Arteaga, Forcato et al. 2020), we investigated whether machine learning methods can classify, based on single trials, the brain activity and pupil responses associated with the processing of old and new information. Specifically, we used the EEG and pupillary information of 39 participants who completed an associative recall old-new task in which they had to discriminate between previously seen or new pictures and, for the old ones, to recall an associated word. Our analyses corroborated the differences in neural processing of old and new items reported in previous studies. Based on these results, we hypothesized that the application of machine learning methods would allow an optimal classification of old and new conditions. Using a Windowed Means approach (WM) and two different machine learning algorithms - Logistic Regression (WM-LR) and Linear Discriminant Analysis (WM-LDA) - mean classification performances of 0.75 and 0.74 (AUC) were achieved when EEG and pupillary signals were combined to train the models, respectively. In both cases, when the EEG and pupillary data were merged, the performance was significantly better than when they were used separately. In addition, our results showed similar classification performances when fused classification models (i.e., models created with the concatenated information of 38 participants) were applied to individuals whose EEG and pupillary information was not considered for the model training. Similar results were found when alternative preprocessing methods were used. Taken together, these findings show that it is possible to classify the neurophysiological activity associated with the processing of experienced and new stimuli using machine learning techniques. Future research is needed to determine how this knowledge might have potential implications for memory research and clinical practice.

Differential neurophysiological correlates of retrieval of consolidated and reconsolidated memories in humans: An ERP and pupillometry study.

Consolidated memories can return to a labile state if they are reactivated by unpredictable reminders. To persist, active memories must be re-stabilized through a process known as reconsolidation. Although there is consistent behavioral evidence about this process in humans, the retrieval process of reconsolidated memories remains poorly understood. In this context, one fundamental question is whether the same or different neurophysiological mechanisms are involved in retrieval of consolidated and reconsolidated memories. Because it has been demonstrated that the exposure to the reconsolidation process may restructure and strengthen memories, we hypothesized distinct neurophysiological patterns during retrieval of reconsolidated memories. In addition, we hypothesized that interfering with the reconsolidation process using a new learning can prevent these neurophysiological changes. To test it, consolidated, reconsolidated and declarative memories whose reconsolidation process was interfered (i.e., picture-word pairs) were evaluated in humans in an old/new associative recall task while the brain activity and the pupillary response were recorded using electroencephalography and eyetracking. Our results showed that retrieval of reconsolidated memories elicits specific patterns of brain activation, characterized by an earlier peak latency and a smaller magnitude of the left parietal ERP old/new effect compared to memories that were only consolidated or whose reconsolidation process was interfered by a new learning. Moreover, our results demonstrated that only retrieval of reconsolidated memories is associated with a late reversed mid-frontal effect in a 600-690 time window. Complementarily, memories that were reactivated showed an earlier peak latency of the pupil old/new effect compared to non-reactivated memories. These findings support the idea that reconsolidation has an important impact in how memories are retrieved in the future, showing that retrieval of reconsolidated memories is partially supported by specific brain mechanisms.

Von Economo neurons are present in the dorsolateral (dysgranular) prefrontal cortex of humans.

Von Economo neurons (VENs), also known as spindle cells, have been described in layer V of the anterior cingulate (BA 24) and frontoinsular cortex (FI) of humans and other great apes. In the present study we used immunohistochemistry against two specific neuronal markers (NeuN and MAP2) in order to establish the presence of these cell types in Brodmann area 9 (BA 9) of the human prefrontal cortex. We evaluated tissue samples of eight human postmortem brains (age range 26-50) from BAs 9, 24, 4, 46, 45, 10 and 17. We identified a group of cells with similar morphology to that previously described for VENs in all specimens of BA 9 examined, albeit less frequently than in BA 24. This is the first description of this cell type in a human brain area with well developed granular layers (BA 9).

Expression of slow skeletal troponin I in adult transgenic mouse heart muscle reduces the force decline observed during acidic conditions.

1. Acidosis in cardiac muscle is associated with a decrease in developed force. We hypothesized that slow skeletal troponin I (ssTnI), which is expressed in neonatal hearts, is responsible for the observed decreased response to acidic conditions. To test this hypothesis directly, we used adult transgenic (TG) mice that express ssTnI in the heart. Cardiac TnI (cTnI) was completely replaced by ssTnI either with a FLAG epitope introduced into the N-terminus (TG-ssTnI) or without the epitope (TG-ssTnI) in these mice. TG mice that express cTnI were also generated as a control TG line (TG-cTnI). Non-transgenic (NTG) littermates were used as controls. 2. We measured the force-calcium relationship in all four groups at pH 7.0 and pH 6.5 in detergent-extracted fibre bundles prepared from left ventricular papillary muscles. The force-calcium relationship was identical in fibre bundles from NTG and TG-cTnI mouse hearts, therefore NTG mice served as controls for TG-ssTnIand TG-ssTnI mice. Compared to NTG controls, the force generated by fibre bundles from TG mice expressing ssTnI was more sensitive to Ca(2+). The shift in EC(50) (the concentration of Ca(2+) at which half-maximal force is generated) caused by acidic pH was significantly smaller in fibre bundles isolated from TG hearts compared to those from NTG hearts. However, there was no difference in the force-calcium relationship between hearts from the TG-ssTnIand TG-ssTnI groups. 3. We also isolated papillary muscles from the right ventricle of NTG and TG mouse hearts expressing ssTnI and measured isometric force at extracellular pH 7.33 and pH 6.75. At acidic pH, after an initial decline, twitch force recovered to 60 +/- 3 % (n = 7) in NTG papillary muscles, 98 +/- 2 % (n = 5) in muscles from TG-ssTnIand 96 +/- 3 % (n = 7) in muscles from TG-ssTnI hearts. Our results indicate that TnI isoform composition plays a crucial role in the determination of myocardial force sensitivity to acidosis.

A familial hypertrophic cardiomyopathy alpha-tropomyosin mutation causes severe cardiac hypertrophy and death in mice.

Tropomyosin, an essential component of the sarcomere, regulates muscle contraction through Ca(2+)-mediated activation. Familial hypertrophic cardiomyopathy (FHC) is caused by mutations in numerous cardiac sarcomeric proteins, including myosin heavy and light chains, actin, troponin T and I, myosin binding protein C, and alpha-tropomyosin. This study developed transgenic mouse lines that encode an FHC mutation in alpha-tropomyosin; this mutation is an amino acid substitution at codon 180 (Glu180Gly) which occurs in a troponin T binding region. Non-transgenic and control mice expressing wild-type alpha-tropomyosin demonstrate no morphological or physiological changes. Expression of exogenous mutant tropomyosin leads to a concomitant decrease in endogenous alpha-tropomyosin without altering the expression of other contractile proteins. Histological analysis shows that initial pathological changes, which include ventricular concentric hypertrophy, fibrosis and atrial enlargement, are detected within 1 month. The disease-associated changes progressively increase and result in death between 4 and 5 months. Physiological analyses of the FHC mice using echocardiography, work-performing heart analyses, and force measurements of cardiac myofibers, demonstrate dramatic functional differences in diastolic performance and increased sensitivity to calcium. This report demonstrates that mutations in alpha-tropomyosin can be severely disruptive of sarcomeric function, which consequently triggers a dramatic hypertrophic response that culminates in lethality.

Attenuation of length dependence of calcium activation in myofilaments of transgenic mouse hearts expressing slow skeletal troponin I.

We compared sarcomere length (SL) dependence of the Ca2+-force relation of detergent-extracted bundles of fibres dissected from the left ventricle of wild-type (WT) and transgenic mouse hearts expressing slow skeletal troponin I (ssTnI-TG). Fibre bundles from the hearts of the ssTnI-TG demonstrated a complete replacement of the cardiac troponin I (cTnI) by ssTnI. Compared to WT controls, ssTnI-TG fibre bundles were more sensitive to Ca2+ at both short SL (1.9 +/- 0.1 micrometer) and long SL (2.3 +/- 0.1 micrometer). However, compared to WT controls, the increase in Ca2+ sensitivity (change in half-maximally activating free Ca2+; DeltaEC50) associated with the increase in SL was significantly blunted in the ssTnI-TG myofilaments. Agents that sensitize the myofilaments to Ca2+ by promoting the actin-myosin reaction (EMD 57033 and CGP-48506) significantly reduced the length-dependent DeltaEC50 for Ca2+ activation, when SL in WT myofilaments was increased from 1.9 to 2.3 micrometer. Exposure of myofilaments to calmidazolium (CDZ), which binds to cTnC and increases its affinity for Ca2+, sensitized force developed by WT myofilaments to Ca2+ at SL 1.9 micrometer and desensitized the WT myofilaments at SL 2.3 micrometer. There were no significant effects of CDZ on ssTnI-TG myofilaments at either SL. Our results indicate that length-dependent Ca2+ activation is modified by specific changes in thin filament proteins and by agents that promote the actin-myosin interaction. Thus, these in vitro results provide a basis for using these models to test the relative significance of the length dependence of activation in situ.

Increased cardiomyocyte intracellular calcium during endotoxin-induced cardiac dysfunction in guinea pigs.

Septic shock is a complex pathophysiologic state characterized by circulatory insufficiency, multiple system organ dysfunction, and frequent mortality. Although profound cardiac dysfunction occurs during sepsis, the pathogenesis of this dysfunction remains poorly understood. To determine whether abnormalities in intramyocyte calcium accumulation might contribute to the development of cardiac dysfunction, we measured myocyte intracellular calcium during peak cardiac dysfunction after an endotoxin challenge. Intraperitoneal administration of Escherichia coli lipopolysaccharide 4 mg/kg to adult guinea pigs resulted in significantly impaired cardiac performance (Langendorff preparation) 18 h after challenge compared with control. This included diminished left ventricular pressure development (56 +/- 7 versus 95 +/- 4 mm Hg, p < 0.05), maximal rate of left ventricular pressure rise (998 +/- 171 versus 1784 +/- 94 mm Hg/s, p < 0.05) and left ventricular pressure fall (1014 +/- 189 versus 1621 +/- 138 mm Hg/s, p < 0.05). Assay of intracellular calcium in fura-2AM-loaded cardiac myocytes demonstrated increased intracellular calcium concentration in myocytes obtained from lipopolysaccharide-challenged animals compared with controls (234 +/- 18 versus 151 +/- 6 nM, p < 0.05). Inhibition of calcium-release channel (ryanodine receptor) opening by administration of dantrolene prevented the increase in intracytoplasmic calcium (159 +/- 8 versus 234 +/- 18 nM, p < 0.05) and partially ameliorated systolic and diastolic ventricular dysfunction. These data indicate that abnormalities of intracellular calcium contribute to the development of endotoxin-induced myocardial dysfunction.

Raman spectral analysis in the C-H stretching region of proteins and amino acids for investigation of hydrophobic interactions.

Raman spectra of amino acids showed complexity in the C-H stretching region (2800-3100 cm(-)(1)) attributed to diversity of CH, CH(2), and CH(3) groups in the side chains, ionization state, and microenvironment. The involvement of specific amino acids in the C-H stretching region of selected proteins, namely, lysozyme, alpha-lactalbumin, beta-lactoglobulin, and their binary mixtures, was investigated by deconvolution using maximum likelihood techniques. The main protein band near 2940 cm(-)(1) was attributed not only to aromatic and aliphatic amino acids but also to many other amino acids. A band near 3065 cm(-)(1) was assigned to aromatic residues, whereas bands near 2880 and 2900 cm(-)(1) corresponded primarily to aliphatic amino acids. Heating at 90 degrees C increased relative intensity near 2940 cm(-)(1) and decreased relative intensity at 2895-2902 cm(-)(1) for lysozyme and its mixtures with alpha-lactalbumin or beta-lactoglobulin. Additional bands at 2812 or 2838 and 3003 cm(-)(1) were observed after heating or in 8 M deuterated urea, reflecting changes upon denaturation.

[Experiences in community participation to promote nutritional education]. / Experiencias en participación comunitaria para promover la educación en nutrición.

This paper presents several experiences obtained in the Rural Research Center of the Solís Valley in relation to community participation programs. The main objective of these projects was to improve the nutritional practices of children in the rural areas of highland Mexico. As first experience, small groups were formed with mothers, fathers, married couples and teenagers. Each of these groups started a project oriented to promote nutritional self-sufficiency. One group of mothers was successful in assuring the provision of government subsidized milk in their community. A second group of mothers started a chicken-raising farm, but the project failed because all the chicken died in an epidemic. The group of fathers started a sheep-raising project as the first step to get a milk-producing cow. The sheep-raising was successful, but when the sheep were sold each man in the group kept the revenue to himself and the group disappeared. The married couples were successful both in a home-gardening project and in a chicken-raising farm. The teenagers were also successful with their home-gardening project and acted as "injection groups" to spread the project in other communities. As a second experience in community participation, community health workers taught mothers how to use locally available food to improve their diets, preparing culturally acceptable food recipes. This intervention was successful in increasing mother's awareness of a balanced diet. A second intervention combined the presentation of a drama ("peasant's theater") in order to increase mother's participation in these projects.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermal denaturation of Turkey breast myosin under different conditions: Effect of temperature and pH, and reversibility of the denaturation.

The thermal denaturation and renaturation of turkey breast myosin (TBM) under different conditions of pH and temperature was evaluated by circular dichroism. TBM unfolds upon heating, and the degree of unfolding was dependent on the pH and temperature. The transition temperature (T(m)) of TBM at pH values of 6 and 12 was found to be 40°C, suggesting that TBM is more temperature sensitive than other myosins. Full reversibility of the thermal denaturation of TBM was usually present when TBM was heated for 5-30 min at 40°C for 5 min at 50°C and incubated for 24 h at 4°C.