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Zero-pollution goals and the reduction in environmental pressures related to production and consumption have become a priority in recent environmental policies such as the 8th European Environment Action Program proposal. Adapting current industrial processes is essential to this transition towards a regenerative economy. This work presents a redesign plan for an industrial system that includes mechanical workshops and a hazardous waste intermediate management plant, covering all management activities (both off-site and on-site), such as collection, transport, and treatment. The waste management hierarchy is modified/amplified considering the original definition and the circular economy focus. This includes the improvement of existing processes and/or the design of new sustainable processes from waste to energy and useful materials, with different foci (integrated pollution prevention and control, industrial ecology, the circular economy, system dynamics, and life-cycle thinking (LCT)) and different tools employed (Best Available Techniques inventory (BAT), process simulation, BAT analysis, industrial symbiosis, dynamic material and energy flow analysis, and LCT tools). These tools help us to improve the sustainability of waste to energy and useful materials processes and improve symbiotic behaviour in the industrial system. This study shows the real possibility of achieving the circularity of products, transforming the waste sector into a productive one. Meanwhile, it contributes to the extinction of the traditional concept of waste. [ABSTRACT FROM AUTHOR]

Abstract: We introduce the notion of radical parametrization of a surface, and we provide algorithms to compute such type of parametrizations for families of surfaces, like: Fermat surfaces, surfaces with a high multiplicity (at least the degree minus 4) singularity, all irreducible surfaces of degree at most 5, all irreducible singular surfaces of degree 6, and surfaces containing a pencil of low-genus curves. In addition, we prove that radical parametrizations are preserved under certain type of geometric constructions that include offset and conchoids. [Copyright &y& Elsevier]

Abstract: We present algorithms for parametrizing by radicals an irreducible curve, not necessarily plane, when the genus is less than or equal to 4 and the curve is defined over an algebraically closed field of characteristic zero. In addition, we also present an algorithm for parametrizing by radicals any irreducible plane curve of degree having at least a point of multiplicity , with and, as a consequence, every irreducible plane curve of degree and every irreducible singular plane curve of degree 6. [Copyright &y& Elsevier]

We had described a muscarinic-mediated long-term synaptic enhancement at Schaffer collateral synapses caused by the insertion of AMPARs in spines of rat hippocampal CA1 pyramidal neurons that requires Ca2+ release from IP3-sensitive stores (Fernández de Sevilla et al., 2008). We now show that this AMPA-mediated LTPIP3 is precisely matched by an amplification of NMDAR-mediated transmission. The enhanced AMPAR transmission involves SNARE protein activity and CaMKII activation. The amplification of NMDA transmission requires combined CaMKII, PKC, and SRC kinase activity without detectable surface incorporation of NMDARs, suggesting that changes in receptor properties mediate this process. The enhanced AMPAR- and NMDAR-mediated transmission markedly reduce the induction threshold of "Hebbian" LTP. We conclude that both modes of glutamatergic synaptic potentiation may play a critical functional role in the regulation of the learning machinery of the brain by adding flexibility to the demands of the hippocampal network. [ABSTRACT FROM AUTHOR]

Cholinergic--glutamatergic interactions influence forms of synaptic plasticity that are thought to mediate memory and learning. We tested in vitro the induction of long-lasting synaptic enhancement at Schaffer collaterals by acetylcholine (ACh) at the apical dendrite of CA1 pyramidal neurons and in vivo by stimulation of cholinergic afferents. In vitro ACh induced a Ca2+ wave and synaptic enhancement mediated by insertion of AMPA receptors in spines. Activation of muscarinic ACh receptors (mAChRs) and Ca2+ release from inositol 1,4,5-trisphosphate (IP3 )-sensitive stores were required for this synaptic enhancement that was insensitive to blockade of NMDA receptors and also triggered by IP3 uncaging. Activation of cholinergic afferents in vivo induced an analogous atropine-sensitive synaptic enhancement. We describe a novel form of synaptic enhancement (LTPIP3) that is induced in vitro and in vivo by activation of mAChRs. Weconclude that Ca2+released from postsynaptic endoplasmic reticulum stores is the critical event in the induction of this unique form of long-lasting synaptic enhancement. [ABSTRACT FROM AUTHOR]

Somatosensory information, conveyed through the gracilis nucleus (GN), is regulated by descending corticofugal (CF) glutamatergic fibers. In addition, the GN receives cholinergic inputs with still unclear source and functional significance. Using both the in vitro slice and intracellular recording with sharp and patch electrodes and in vivo extracellular single-unit recordings, we analyzed the effects of activation of cholinergic receptors on synaptic, intrinsic, and functional properties of rat GN neurons. The cholinergic agonist carbamilcholine-chloride [carbachol (CCh); 1-10 µM] in vitro (1) induced presynaptic inhibition of EPSPs evoked by both dorsal column and CF stimulation, (2) increased postsynaptic excitability, and (3) amplified the spike output of GN neurons. The inhibition by atropine (1 µM) and pirenzepine (10 µM) of all presynaptic and postsynaptic effects of CCh suggests actions through muscarinic M1 receptors. The above effects were insensitive to nicotinic antagonists. We searched the anatomical origin of the cholinergic projection to the GN throughout the hindbrain and forebrain, and we found that the cholinergic fibers originated mainly in the pontine reticular nucleus (PRN). Electrical stimulation of the PRN amplified sensory responses in the GN in vivo, an effect prevented by topical application of atropine. Our results demonstrate for the first time that cholinergic agonists induce both presynaptic and postsynaptic effects on GN neurons and suggest an important regulatory action of inputs from cholinergic neuronal groups in the pontine reticular formation in the functional control of somatosensory information flow in the GN. [ABSTRACT FROM AUTHOR]

We present an algorithm that transforms, if possible, a given ODE or PDE with radical function coefficients into one with rational coefficients by means of a rational change of variables so that solutions correspond one-to-one. Our method also applies to systems of linear ODEs. It is based on previous work on reparametrization of radical algebraic varieties. [ABSTRACT FROM AUTHOR]

Using spike-timing-dependent plasticity (STDP) protocols that consist of pairing an EPSP and a postsynaptic backpropagating action potential (BAP), we investigated the contribution of the changes in EPSP waveform induced by the slow Ca2+-dependent K+-mediated after hyperpolarization (sAHP) in the regulation of long-term potentiation (LTP). The "temporal window" between Schaffer collateral EPSPs and BAPs in CA1 pyramidal neurons required to induce LTP was narrowed by a reduction of the amplitude and decay time constant of the EPSP, which could be reversed with cyclothiazide. The EPSP changes were caused by the increased conductance induced by activation of the sAHP. Therefore, the EPSP waveform and its regulation by the sAHP are central in determining the duration of the temporal window for STDP, thus providing a possible dynamic regulatory mechanism for the encoding of cognitive processes. [ABSTRACT FROM AUTHOR]

Parametric representations do not cover, in general, the whole geometric object that they parametrize. This can be a problem in practical applications. In this paper we analyze the question for surfaces of revolution generated by real rational profile curves, and we describe a simple small superset of the real zone of the surface not covered by the parametrization. This superset consists, in the worst case, of the union of a circle and the mirror curve of the profile curve. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor-I (IGF-I) signaling plays a key role in learning and memory. IGF-I increases the spiking and induces synaptic plasticity in the mice barrel cortex (Noriega-Prieto et al., 2021), favoring the induction of the long-term potentiation (LTP) by Spike Timing-Dependent Protocols (STDP) (Noriega-Prieto et al., 2021). Here, we studied whether these IGF-I effects depend on endocannabinoids (eCBs) and nitric oxide (NO). We recorded both excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) evoked by stimulation of the basal dendrites of layer II/III pyramidal neurons of the Barrel Cortex and analyzed the effect of IGF-I in the presence of a CB1R antagonist, AM251, and inhibitor of the NO synthesis, L-NAME, to prevent the eCBs and the NO-mediated signaling. Interestingly, L-NAME abolished any modulatory effect of the IGF-I-induced excitatory and inhibitory transmission changes, suggesting the essential role of NO. Surprisingly, the inhibition of CB1Rs did not only block the potentiation of EPSCs but reversed to a depression, highlighting the remarkable functions of the eCB system. In conclusion, eCBs and NO play a vital role in deciding the sign of the effects induced by IGF-I in the neocortex, suggesting a neuromodulatory interplay among IGF-I, NO, and eCBs. [ABSTRACT FROM AUTHOR]

A recent approach to promote central nervous system (CNS) regeneration after injury or disease is direct conversion of somatic cells to neurons. This is achieved by transduction of viral vectors that express neurogenic transcription factors. In this work we propose adult human mucosal olfactory ensheathing glia (hmOEG) as a candidate for direct reprogramming to neurons due to its accessibility and to its well-characterized neuroregenerative capacity. After induction of hmOEG with the single neurogenic transcription factor NEUROD1, the cells under study exhibited morphological and immunolabeling neuronal features, fired action potentials and expressed glutamatergic and GABAergic markers. In addition, after engraftment of transduced hmOEG cells in the mouse hippocampus, these cells showed specific neuronal labeling. Thereby, if we add to the neuroregenerative capacity of hmOEG cultures the conversion to neurons of a fraction of their population through reprogramming techniques, the engraftment of hmOEG and hmOEG-induced neurons could be a procedure to enhance neural repair after central nervous system injury., (© 2024. The Author(s).)

Insulin-like growth factor-I (IGF-I) plays a key role in the modulation of synaptic plasticity and is an essential factor in learning and memory processes. However, during aging, IGF-I levels are decreased, and the effect of this decrease in the induction of synaptic plasticity remains unknown. Here we show that the induction of N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) at layer 2/3 pyramidal neurons (PNs) of the mouse barrel cortex is favored or prevented by IGF-I (10 nM) or IGF-I (7 nM), respectively, when IGF-I is applied 1 h before the induction of Hebbian LTP. Analyzing the cellular basis of this bidirectional control of synaptic plasticity, we observed that while 10 nM IGF-I generates LTP (LTP IGF-I ) of the post-synaptic potentials (PSPs) by inducing long-term depression (LTD) of the inhibitory post-synaptic currents (IPSCs), 7 nM IGF-I generates LTD of the PSPs (LTD IGF-I ) by inducing LTD of the excitatory post-synaptic currents (EPSCs). This bidirectional effect of IGF-I is supported by the observation of IGF-IR immunoreactivity at both excitatory and inhibitory synapses. Therefore, IGF-I controls the induction of Hebbian NMDAR-dependent plasticity depending on its concentration, revealing novel cellular mechanisms of IGF-I on synaptic plasticity and in the learning and memory machinery of the brain., Competing Interests: IT-A was employed by Ikerbasque Science Foundation. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Noriega-Prieto, Maglio, Perez-Domper, Dávila, Gutiérrez, Torres-Alemán and Fernández de Sevilla.)

The type-1 cannabinoid receptor (CB 1 R) is widely expressed in excitatory and inhibitory nerve terminals, and by suppressing neurotransmitter release, its activation modulates neural circuits and brain function. While the interaction of CB 1 R with various intracellular proteins is thought to alter receptor signaling, the identity and role of these proteins are poorly understood. Using a high-throughput proteomic analysis complemented with an array of in vitro and in vivo approaches in the mouse brain, we report that the C-terminal, intracellular domain of CB 1 R interacts specifically with growth-associated protein of 43 kDa (GAP43). The CB 1 R-GAP43 interaction occurs selectively at mossy cell axon boutons, which establish excitatory synapses with dentate granule cells in the hippocampus. This interaction impairs CB 1 R-mediated suppression of mossy cell to granule cell transmission, thereby inhibiting cannabinoid-mediated anti-convulsant activity in mice. Thus, GAP43 acts as a synapse type-specific regulatory partner of CB 1 R that hampers CB 1 R-mediated effects on hippocampal circuit function., (© 2023. The Author(s).)

An approach to generate new neurons after central nervous system injury or disease is direct reprogramming of the individual's own somatic cells into differentiated neurons. This can be achieved either by transduction of viral vectors that express neurogenic transcription factors and/or through induction with small molecules, avoiding introducing foreign genetic material in target cells. In this work, we propose olfactory ensheathing glia (OEG) as a candidate for direct reprogramming to neurons with small molecules due to its well-characterized neuro-regenerative capacity. After screening different combinations of small molecules in different culture conditions, only partial reprogramming was achieved: induced cells expressed neuronal markers but lacked the ability of firing action potentials. Our work demonstrates that direct conversion of adult olfactory ensheathing glia to mature, functional neurons cannot be induced only with pharmacological tools., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Portela-Lomba, Simón, Fernández de Sevilla, Moreno-Flores and Sierra.)

Objective: In order to know the social and health consequences of hip fractures (HF)., Design: A retrospective cohort study of an entire health area was carried out in patients aged 75 or more, over a period of 5 years. SITE: Segovia Health Area., Participants: All patients older than 75 years with a diagnosis of HF, excluding displaced and passerby., Interventions: The socio-sanitary changes that occur after the HF in respect to their baseline situation (family situation, comorbidities, dependence and mental situation) and the variables which most influence mortality and institutionalization after the HF were analyzed., Main Measurements: One thousand one hundred fifty-nine HF were recorded, with a constant annual incidence of 10.7‰. The prevalence was higher in women: 7.4% versus 3.7%., Results: The baseline profile is a pluripatological, non-institutionalized, 87-year-old woman, who retains her independent in her daily life and suffers from a HF due to an accidental fall in her home. At the end of the study period 51% were permanently institutionalized, negatively influencing having worse mental deterioration, worse dependence and subsequent readmissions and in addition, 45.5% died, 25.5% during the first year. The most unfavorable conditions were being previously dependent, having severe mental deterioration, male and within the comorbidities the most influential was previously having an anemia., Conclusions: Our data confirms the deterioration of the autonomy-functional capacity after a HF, in line with what has been published, and has allowed to identify which elderly people are at the greatest risk of complications in the short and medium term (institutionalization and death)., (Copyright © 2021 The Authors. Publicado por Elsevier España, S.L.U. All rights reserved.)

Cholinergic mechanisms in the hippocampus regulate forms of synaptic plasticity linked with cognition and spatial navigation, but the underlying mechanisms remain largely unknown. Here, in rat hippocampal CA1 pyramidal cells under blockade of ionotropic glutamate receptors, we report that a single acetylcholine pulse and repeated depolarization activated a robust and enduring postsynaptic depolarization-induced enhancement of inhibition (DEI) that masked a presynaptic depolarization-induced suppression of inhibition (DSI). Increased cytosolic Ca2+ and M1-muscarinic receptor activation caused the rise in voltage-sensitive α5βγ2-containing γ-aminobutyric acid type-A receptors that generated DEI. In summary, this muscarinic-mediated activity-dependent plasticity rapidly transfers depolarization effects on inhibition from presynaptic suppression or DSI to postsynaptic enhancement or DEI, a change potentially relevant in behavior., (© The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Acetylcholine (ACh) regulates network operation in the hippocampus by controlling excitation and inhibition in rat CA1 pyramidal neurons (PCs), the latter through gamma-aminobutyric acid type-A receptors (GABA A Rs). Although, the enhancing effects of ACh on GABA A Rs have been reported (Dominguez et al., 2014, 2015), its role in regulating tonic GABA A inhibition has not been explored in depth. Therefore, we aimed at determining the effects of the activation of ACh receptors on responses mediated by synaptic and extrasynaptic GABA A Rs. Here, we show that under blockade of ionotropic glutamate receptors ACh, acting through muscarinic type 1 receptors, paired with post-synaptic depolarization induced a long-term enhancement of tonic GABA A currents ( t GABA A ) and puff-evoked GABA A currents ( p GABA A ). ACh combined with depolarization also potentiated IPSCs (i.e., phasic inhibition) in the same PCs, without signs of interactions of synaptic responses with p GABA A and t GABA A , suggesting the contribution of two different GABA A receptor pools. The long-term enhancement of GABA A currents and IPSCs reduced the excitability of PCs, possibly regulating plasticity and learning in behaving animals.