Association of Health and Psychological Factors with Academic Achievement and Non-Verbal Intelligence in University Students with Low Academic Performance: The Influence of Sex.

Academic achievement, measured with the grade point average (GPA), is a stable characteristic that has been associated with many sociodemographic and psychological variables; however, the relation of these variables with GPA has not been totally elucidated. The objective of this study was to perform an association of health, psychological and personal variables with GPA and non-verbal intelligence in low-academic performance population according to sex. We invited health sciences university students who had failed the same subject twice to complete a set of sociodemographic and psychological variables and a non-verbal intelligence test. The GPA, admission exam test and preparatory GPA were obtained. We included 124 students, and found that GPA was associated with non-verbal intelligence in women but not in men; in whom, having a job and having a romantic partner, were more correlated. In women, positive relations with others, emotion perception and weekly physical activity hours were marginally correlated with GPA; while in men, emotion regulation and self-motivation had a tendency of correlation with GPA. In addition, we found that non-verbal intelligence was associated somatization and the number of diseases in women. Academic achievement is regulated by different variables in each sex; therefore, intervention programs addressed by sex are needed to increase it.

Effect of supercritical incorporation of cinnamaldehyde on physical-chemical properties, disintegration and toxicity studies of PLA/lignin nanocomposites.

Poly (lactic acid)/lignin nanocomposites (PLA/Lig-Np) containing cinnamaldehyde (Ci) were obtained by a combination of melt extrusion and supercritical impregnation process. In this work, Ci impregnation tests were carried out in a high-pressure cell at 40 °C for 3 h using 12 MPa and 1 MPa min-1 of depressurization rate, obtaining impregnation yields ranging from 5.7 to 10.8% w/w. Thermal, mechanical and colorimetric properties of the developed films were affected by the incorporation of lignin nanoparticles and the active compound, obtaining biodegradable plastic materials with a strong UV-light barrier property compared to PLA films. In addition, disintegrability tests under composting conditions confirmed the biodegradable character of nanocomposites developed. On day 23, a disintegration percentage greater than 90% was determined for all bionanocomposites. Finally, to establish the possible toxicity effect of the nanocomposites obtained, studies in vivo were performed in normal rats. Toxicity studies showed normal blood parameters after a single dose of nanocomposites. PLA/Ci/Lig-Np bionanocomposite films could be potentially applied to design biodegradable UV-light barrier materials for food packaging and biomedical applications.

Antinociceptive antibiotics-loaded into solid lipid nanoparticles of prolonged release: Measuring pharmacological efficiency and time span on chronic monoarthritis rats.

Pain is a sensory experience of a complex physiological nature in which is not only involved the nervous system. Among its many features is the development of chronic pain that is more complicated to treat because of the central somatization processes involved, becoming inefficient treatments used in other forms of pain. Among them is the role of glial cells, whose participation is such that some authors have proposed to chronic pain as a gliopathy. Because of this, the drug target of possible treatments focuses on modulating nociceptive response affecting transduction into the central nervous system through affecting synapses in the dorsal horn of the spinal cord. Solid lipid nanoparticles enter the central nervous system, protecting the drug, and in addition to the advantage of having greater absorption surface, all factors that improve drug activity. This work is based on the development and characterization of lipid nanoparticles of solid phase incorporating two antibiotics, minocycline, and ciprofloxacin with antinociceptive properties and challenged them with a rat monoarthritis model using Sprague-Dawley adult male rats. The solid lipid nanoparticles were prepared to modify the lipid, and surfactant amounts to obtain the best encapsulation capacity of the antibiotics, size and z potential. By using the Randall-Selitto test, we measured its pharmacological efficiency as an anti-inflammatory and measuring the time span the antibiotics are active. The encapsulated antibiotics were at least 50% more efficient than the antibiotic alone, and that is possible to measure anti-inflammatory activity up to seven days after the antibiotic application. The former is important for example, in the veterinary field, since a single application of the antibiotic will be necessary for the complete treatment, avoiding excessive stress for the animals. We can conclude that antinociceptive antibiotics encapsulation is a very effective, environmentally safe and inexpensive method for improving the pharmacological efficiency and time span the antibiotics are acting. Since these antibiotics are both anti-microbial and antinociceptive, his use in the field of veterinary presents the advantage of being adequate in single doses, with the saving of time and stress to the animals under treatment.

"How and when Chilean Pharmacology started to be experimental and became a science".

Pharmacology in Chile has about 75 years of history and from its beginning until today has grown exponentially. Today, pharmacology is taught in the biomedical careers of the main Chilean universities and research centers in pharmacology are in the north, central and south of Chile. This editorial offers an overview of the main milestones that have led to the consolidation of Chilean pharmacology in Latin America and the world.

An NR2B-Dependent Decrease in the Expression of trkB Receptors Precedes the Disappearance of Dopaminergic Cells in Substantia Nigra in a Rat Model of Presymptomatic Parkinson's Disease.

Compensatory changes occurring during presymptomatic stages of Parkinson's disease (PD) would explain that the clinical symptoms of the disease appear late, when the degenerative process is quite advanced. Several data support the proposition that brain-derived neurotrophic factor (BDNF) could play a role in these plastic changes. In the present study, we evaluated the expression of the specific BDNF receptor, trkB, in a rat model of presymptomatic PD generated by intrastriatal injection of the neurotoxin 6-OHDA. Immunohistochemical studies revealed a decrease in trkB expression in SN pars compacta (SNc) seven days after 6-OHDA injection. At this time point, no change in the number of tyrosine hydroxylase (TH) immunoreactive (TH-IR) cells is detected, although a decrease is evident 14 days after neurotoxin injection. The decrease in TH-positive cells and trkB expression in SNc was significantly prevented by systemic administration of Ifenprodil, a specific antagonist of NR2B-containing NMDA receptors. Therefore, an NR2B-NMDA receptor-dependent decrease in trkB expression precedes the disappearance of TH-IR cells in SNc in response to 6-OHDA injection. These results support the idea that a functional coupling between NMDA receptors and BDNF/trkB signalling may be important for the maintenance of the dopaminergic phenotype in SNc during presymptomatic stages of PD.

Programa piloto para pacientes beneficiarios de Fonasa, que padecen esclerosis multiple: tratamiento con inmunomoduladores en el sistema público de salud de Chile: Informe del primer año, 10 de julio 2008-30 de Junio 2009 / Pilot national treatment program for multiple sclerosis patients belonging to the public health care system of Chile (FONASA) with immunomodulating disease-modifying therapies: first year report from July 2008 to June 2009

Multiple Sclerosis (MS) is a chronic disease of the central nervous system. It is manifested in the young adult who presents at the beginning alternation between transient neurological dysfunction and normality, followed by a progressive level of disability. MS affects the quality of life in the young adults in their full productive and creative age limiting not only in their personal lives but also affects to the whole society in terms of "dreams and life projects". Besides, this illness also influences the family group who has to assume progressively the help and care for the patient. In healthcare aspect MS implies intensive and progressive resources. In Chile, although we don't have epidemiological studies that indicate which is the MS prevalence it exist a projection that states 14 per 100.000 inhabitants. Considering a population of 16.5 million of inhabitants our expectative of patients with MS is of 2310 cases in our country. The MS immunomodulating injectable disease-modifying therapies are of high cost and were not available in a regular way in the state health care system of Chile (FONASA) that attends the 70 percent of the population; the other 30 percent has different private health insurances. In 2008 the ministry of health decided to initiate and pilot (exploratory) program which had a great meaning and impact concerning to start offering immunomodulating therapies to relapsing remitting MS, for patients belonging to FONASA system. The pilot program was thought with a double mission, on the one hand to achieve that a very limited group of MS patients belonging to FONASA system (80 cases) from all over the country had access to immunomodulating injectable disease-modifying therapies of high cost in a regular way. The second objective was to obtain clinical and epidemiological information which let us to evaluate the clinical and administrative obstacles generated by the incorporation of this treatment in the public health...

Introducción El presente documento corresponde al informe del primer año de trabajo operativo del "Programa piloto de tratamiento con inmunomoduladores, para pacientes beneficiarios de Fonasa1, que padecen esclerosis múltiple (EM)", elaborado por el equipo del centro de referencia nacional, para este programa, con sede en el Servicio de Neurología del Complejo Asistencial Barros Luco (CABL) del SSMS2. Dado su origen no incluye antecedentes del proceso de gestión ni toma de decisiones del nivel Minsal3 o Fonasa. Este trabajo, no es ni aspira ser: un ensayo clínico, una guía de práctica clínica, una revisión bibliográfica, ni una puesta al día sobre el tratamiento de la Esclerosis Múltiple (EM), es simplemente el informe anual de un centro de referencia, para una tarea específica, a la autoridad ministerial competente. El informe incluye algunos antecedentes generales y referencias presentadas como "notas al pie", sólo para contextualizar la información presentada4. La EM es una enfermedad crónica del SNC, de origen incierto, inmunológicamente mediada, bien definida en sus características inmunopatogénicas, patológicas, imagenológicas y clínicas. Se expresa en el adulto joven, quien presenta inicialmente alternancia entre disfunción neurológica transitoria y normalidad y cuya progresión determina múltiples efectos discapacitantes. La EM afecta la calidad de vida de adultos jóvenes en plena edad productiva y creativa limitando tanto los "sueños y proyectos de vida" como el desarrollo laboral, social y afectivo. Además trasciende al grupo familiar, cuando deben asumir la asistencia del paciente. En lo sanitario, la EM, genera uso intensivo y progresivo de recursos. Las terapias inmunomoduladores para la EM, que tienen la posibilidad de detener o reducir la evolución de la modalidad recurrente remitente de la EM, no se encontraban disponibles en forma regular en el sector público de salud de nuestro país, por esto el presente programa piloto...

NMDA receptors mediate an early up-regulation of brain-derived neurotrophic factor expression in substantia nigra in a rat model of presymptomatic Parkinson's disease.

The clinical symptoms of Parkinson's disease (PD) appear late and only when the degenerative process at the level of the nigrostriatal dopamine (DA) pathway is quite advanced. An increase in brain-derived neurotrophic factor (BDNF) expression may be one of the molecular signals associated to compensatory and plastic responses occurring in basal ganglia during presymptomatic PD. In the present study, we used in vivo microdialysis, semiquantitative reverse transcriptase-polymerase chain reaction, and immunohistochemistry to study N-methyl-D-aspartic acid (NMDA) receptor regulation of BDNF expression in substantia nigra (SN) of adult rats after partial lesioning of the nigrostriatal DA pathway with unilateral striatal injections of 6-hydroxydopamine (6-OHDA). A time-dependent partial decrease of striatal DA tissue content as well as parallel and gradual increases in extracellular glutamate and aspartate levels in SN were found 1 to 7 days after unilateral 6-OHDA intrastriatal injection. Instead, the number of tyrosine hydroxylase-immunoreactive (IR) cells in the ipsilateral SN pars compacta remained statistically unchanged after neurotoxin injection. Intrastriatal administration of 6-OHDA also produced an early and transient augmentation of pan-BDNF, exon II-BDNF, and exon III-BDNF transcripts in the ipsilateral SN. The pan-BDNF and exon II-BDNF transcript increases were completely abolished by the prior systemic administration of MK-801, a selective antagonist of NMDA receptors. MK-801 also blocked the increase in BDNF-IR cells in SN observed 7 days after unilateral 6-OHDA intrastriatal injections. Our findings suggest that a coupling between glutamate release, NMDA receptor activation, and BDNF expression may exist in the adult SN and represent an important signal in this midbrain nucleus triggered in response to partial DA loss occurring in striatal nerve endings during presymptomatic PD.

Functional interactions between somatodendritic dopamine release, glutamate receptors and brain-derived neurotrophic factor expression in mesencephalic structures of the brain.

Dopaminergic nigrostriatal neurons may be considered as bipolar functional entities since they are endowed with the ability to synthesize, store and release the transmitter dopamine (DA) at the somatodendritic level in the substantia nigra (SN). Such dendritic DA release seems to be distinct from the transmitter release occurring at the axon terminal and seems to rely preferentially on volume transmission to exert its physiological effects. An increased glutamatergic (Gluergic) transmission into the SN facilitates such dendritic DA release via activation of NMDA-receptors (NMDA-Rs) and to a lesser extent through group II metabotropic glutamate receptors (mGluRs). In addition, nigral mGluRs functionally interact with NMDA-Rs in the SN, further modulating the NMDA-R-mediated increase of DA release from dendrites in the SN. In turn, dendritically released DA may exert, via D1 receptors, a tonic inhibitory control upon nigral glutamate (Glu). Furthermore, released DA, via D2/D3 autoreceptors, produces an autoinhibitory effect upon DA cell firing and its own release process. An increased Gluergic transmission into the SN may also induce, via activation of NMDA-Rs, an augmented expression of different brain-derived neurotrophic factor (BDNF) gene transcripts in this brain area. Pharmacological evidence suggests that non-NMDA-Rs could also participate in the regulation of BDNF gene expression in the SN. Glu-mediated changes of nigral BDNF expression could regulate, in turn, the expression of important transmitter-related proteins in the SN, such as different NMDA-R subunits, mGluRs and DA-D3 receptors. In conclusion, Glu-DA-BDNF interactions in the SN may play an important role in modulating the flow of neuronal information in this brain structure under normal conditions, as well as during adaptive and plastic responses associated with various neurological and psychiatric disorders.

Expression of amphetamine-induced behavioral sensitization after short- and long-term withdrawal periods: participation of mu- and delta-opioid receptors.

Repeated amphetamine administration results in behavioral sensitization, an enduring behavioral transformation expressed after short and long periods of withdrawal. To investigate the participation of the opioid system in amphetamine-induced behavioral sensitization, we studied the effect of naloxone, an opioid receptor antagonist, on the expression of behavioral sensitization tested after short- (2 days) and long-term (14 days) withdrawal periods. In addition, using quantitative competitive RT-PCR, we examined the levels of mu-opioid receptor (MOR) and delta-opioid receptor (DOR) mRNA in the nucleus accumbens shell (NAcSh) and ventral tegmental area (VTA) of behaviorally sensitized rats, at these two withdrawal times. This study showed that whereas naloxone did not modify the expression of behavioral sensitization tested after 2 days of withdrawal, it completely blocked the expression when tested after 14 days of withdrawal. DOR and MOR mRNA levels were not modified in the NAcSh of rats expressing behavioral sensitization after 2 or 14 days of withdrawal. Conversely, DOR and MOR mRNA levels were elevated in the VTA of animals expressing behavioral sensitization after 2 days of withdrawal. However, whereas DOR mRNA returned to control levels, MOR mRNA levels remained elevated in animals expressing behavioral sensitization after 14 days of withdrawal. These results indicate a striking difference between the role played by opioid receptors in the expression of amphetamine-induced behavioral sensitization, when tested after short- or long-term withdrawal periods. In addition, our results support the notion that repeated amphetamine-induced changes in opioid receptor expression may contribute to the perpetuation of psychostimulant abuse and/or relapse.

Modulation of dendritic release of dopamine by metabotropic glutamate receptors in rat substantia nigra.

A superfusion system was used to study the effects of metabotropic glutamate receptor (mGluR) ligands upon the release of [(3)H]dopamine ([(3)H]DA) previously taken up by rat substantia nigra (SN) slices. trans-(+/-)-1-Amino-(1S,3R)-cyclopentane dicarboxylic acid (trans-ACPD; 100 and 600 microM), a group I and II mGluR agonist, evoked the release of [(3)H]DA from nigral slices. This last effect was reduced significantly by (2S,3S,4S)-2-methyl-2-(carboxycyclopropyl)-glycine (MCCG; 300 microM), an antagonist of group II mGluR, or by the addition of tetrodotoxin (D-APV; 1 microM) to the superfusion medium. D-(-)-2-Amino-5-phosphono-valeric acid (100 microM), an N-methyl-D-aspartate receptor antagonist, or the presence of Mg(2+) (1.2mM) in the superfusion medium did not modify trans-ACPD-induced [(3)H]DA release. In addition, a group II mGluR agonist such as (2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)-glycine (DCG-IV; 100 microM) significantly induced the release of [(3)H]DA from nigral slices, whereas a group I mGluR agonist such as (RS)-3,5-dihydroxyphenylglycine (DHPG; 50 and 100 microM) did not modify the release of the [(3)H]-amine. Further experiments showed that the NMDA (100 microM)-evoked release of [(3)H]DA was decreased significantly by prior exposure of SN slices to trans-ACPD. Finally, partial denervation of the DA nigro-striatal pathway with 6-hydroxydopamine (6-OH-DA) increased trans-ACPD-induced release of [(3)H]DA, whereas it decreased trans-ACPD inhibitory effects on NMDA-evoked release of [(3)H]DA from nigral slices. The present results suggest that the dendritic release of DA in the SN is regulated by mGluR activation. Such nigral mGluR activation may produce opposite effects upon basal and NMDA-evoked release of DA in the SN. In addition, such mGluR-induced effects in the SN are modified in response to partial denervation of the DA nigro-striatal pathway.

Liberación estriatal de un análogo de aminoácidos excitatorios en un modelo experimental de hipoxia cerebral in vitro / Striatal release of a tritiated analog of excitatory amino acid in a in vitro experimental model of brain hypoxia

Este trabajo presenta la metodología experimental de un modelo de hipoxia cerebral in vitro. El modelo fue empleado para evaluar la liberación de un análogo no metabolizable de glutamato en condiciones de hipoxia, como un reflejo del estado funcional de los terminales nerviosos glutamatérgicos en condiciones de hipoxia, observándose una significativa liberación del marcador tritiado en relación a la hipoxia, lo cual concuerda con hallazgos previos tanto en animales de experimentación como en seres humanos. La metodología presentada es simple y permite manejar a voluntad del investigador una serie de parámetros relevantes desde el punto de vista fisiopatológico de la injuria neuronal por hipoxia, de un modo que es imposible de lograr en los estudios in vivo

Evaluación del efecto neuroprotector de lidocaína y ketamina en un modelo de hipoxia-isquemia cerebral en la rata: estudio histopatológico en estriado, hipocampo y corteza cerebral / Evaluation of the neuroprotective effect of lidocaine and ketamine on a cerebral hypoxia-ischemia model in the rat: histopathological analysis of the striatum, hippocampus and cerebral cortex

Los fectos de la lidocaína como droga protectora del Sistema Nervioso central por isquemia y traume han sido extensamente investigados sin conclusiones definitivas. Algunos experimentos que mostraban un efecto neuroprotector promisorio de la lidocaína utilizan como agente anestésico la ketamina sin considerar su posible contribución neuroprotectora en los resultados comunicados. Esto también se observa en otros experimentos que evalúan los efectos de varias drogas: bloqueadores orgánicos de los canales de calcio, recolectores de radicales libres, esteroides y ganglioosidos. La ketamina anestésico disociativo, es un análogo de feniciclidina, que actúa como un análogo de fenciclidina, que actúa como un antagonista no competitivo en le sitio del N-metil-D-aspartato, receptor subtipo glutamato, dela fenciclidina, y su acción neuroprotectora ha sido comunicada en varios modelos experimentales. El presente trabajo evalúa los efectos de la lidocaína y ketamina en el modelo de hipoxia-isquemia incompleta cerebral de la rata neonata (modelo Levine). Los resultados muestran un efcto neuroprotector significativo de la lidocaína y ketamina, evaluados por análisis hitopatológico del estriado, hipocampo y corteza cerebral-estriado en el modelo de la hipoxia-isquemia en modelo roedor vivo