Analysis of pelletizing from corn cob waste.

In recent years, biomass market has constantly increased. Pellet industry has started looking for new products with the potential to be used as biofuels. Among them are agricultural wastes, such as corn cob waste, which presents some characteristics that make its direct use in industrial facilities possible. However, these properties are not enough for its use in domestic stoves and boilers, where higher quality of fuel is needed. For this reason, densification is used. In the present research work a technical and energy analysis of corn cob waste pelletizing was carried out in a semi-industrial pelletizer. Some relationships between variables, such as moisture, bulk density and mechanical durability, were analyzed, as well as their influence on energy use and final productivity. The results were satisfactory, as the pellets manufactured fulfilled with most specifications that were consulted, with higher values than those recorded for similar kinds of pellets. Concerning the energy study, the increase in production justified a higher energy consumption of the process in order to get a higher productivity ratio.

Role of membrane GM1 on early neuronal membrane actions of Aß during onset of Alzheimer's disease.

The ability of beta-amyloid peptide (Aß) to disrupt the plasma membrane through formation of pores and membrane breakage has been previously described. However, the molecular determinants for these effects are largely unknown. In this study, we examined if the association and subsequent membrane perforation induced by Aß was dependent on GM1 levels. Pretreatment of hippocampal neurons with D-PDMP decreased GM1 and Aß clustering at the membrane (Aß fluorescent-punctas/20µm, control=16.2±1.1 vs. D-PDMP=6.4±0.4, p<0.001). Interestingly, membrane perforation with Aß occurred with a slower time course when the GM1 content was diminished (time to establish perforated configuration (TEPC) (min): control=7.8±2 vs. low GM1=12.1±0.5, p<0.01), suggesting that the presence of GM1 in the membrane can modulate the distribution and the membrane perforation by Aß. On the other hand, increasing GM1 facilitated the membrane perforation (TEPC: control=7.8±2 vs. GM1=6.2±1min, p<0.05). Additionally, using Cholera Toxin Subunit-B (CTB) to block the interaction of Aß with GM1 attenuated membrane perforation significantly. Furthermore, pretreatment with CTB decreased the membrane association of Aß (fluorescent-punctas/20µm, Aß: control=14.8±2.5 vs. CTB=8±1.4, p<0.05), suggesting that GM1 also plays a role in both association of Aß with the membrane and in perforation. In addition, blockade of the Aß association with CTB inhibited synaptotoxicity. Taken together, our results strongly suggest that membrane lipid composition can affect the ability of Aß to associate and subsequently perforate the plasma membrane thereby modulating its neurotoxicity in hippocampal neurons.

[Distal pancreatectomy with splenic preservation in pediatric patient with blunt abdominal trauma]. / Pancreatectomía distal con preservación esplénica en paciente pediátrico con traumatismo cerrado de abdomen.

INTRODUCTION: Traumatic injuries of the pancreas occur in 3 to 12% of cases of blunt abdominal trauma in children and these are associated with a mortality of 30%. CASE REPORT: A four-year-old girl was brought to the emergency room after an automobile accident. On physical examination, she was stable with abdominal pain and signs of peritoneal irritation. An abdominal CT scan showed a grade II liver lesion, a grade II splenic lesion, and a grade III pancreatic lesion. Laparotomy was performed with the patient stable, finding the same lesions as those on the CT scan. Distal pancreatectomy was performed preserving the splenic vessels. The liver and splenic lesions were conservatively treated. The patient was discharged on the seventh day after surgery and at four month follow-up no surgical complications have been observed. DISCUSSION: Surgery should be considered first-line therapy for grade III or greater pancreatic lesions; conservative medical management should be used for Grade I and II lesions.

INTRODUCCION: Las lesiones traumáticas del páncreas se presentan en 3% -12% de los traumatismos abdominales cerrados pediátricos y está asociada con una mortalidad del 30%. CASO CLINICO: Mujer de 4 años de edad que acudió a Urgencias por accidente en automóvil. Al ingreso se encontraba estable, con dolor abdominal e irritación peritoneal. La TAC abdominal evidenció lesión hepática grado II, esplénica grado II y pancreática grado III a nivel del cuerpo. Permaneciendo el paciente estable, se realiza laparotomía y se evidencian las mismas lesiones encontradas en la TAC. Se procede a pancreatectomía distal, preservándose vasos esplénicos; las lesiones hepática y esplénica se manejaron de forma conservadora. Alta hospitalaria al séptimo día y tras el seguimiento a los 4 meses de la cirugía continúa sin presentar complicaciones. DISCUSION: Cuando existe una lesión pancreática grado III o mayor se debe de considerar el tratamiento quirúrgico como el de primera línea, pudiendo emplear el tratamiento conservador para las lesiones grado I y II.

Aß oligomers induce glutamate release from hippocampal neurons.

Soluble oligomers of the amyloid-ß peptide (AßOs) accumulate in Alzheimer's disease (AD) brain and have been implicated in mechanisms of pathogenesis. The neurotoxicity of AßOs appears to be, at least in part, due to dysregulation of glutamate signaling. Here, we show that AßOs promote extracellular accumulation of glutamate and d-serine, a co-agonist at glutamate receptors of the N-methyl-d-aspartate subtype (NMDARs), in hippocampal neuronal cultures. The increase in extracellular glutamate levels induced by AßOs was blocked by the sodium channel blocker tetrodotoxin (TTX), by the NMDAR blocker (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) and by removal of Ca(2+) from the extracellular medium, indicating dependence on excitatory neuronal activity. AßOs enhanced both the release of pre-synaptic vesicles labeled by FM1-43 and spontaneous post-synaptic activity measured by whole-cell patch-clamp. Activation of inhibitory GABA(A) receptors by taurine blocked the increase in extracellular glutamate levels, suggesting that selective pharmacological inhibition of neuronal activity can counteract the impact of AbOs on glutamate dyshomeostasis. Results reveal a novel mechanism by which Ab oligomers promote abnormal release of glutamate in hippocampal neurons, which may contribute to dysregulation of excitatory signaling in the brain.

Regulation of glycinergic and GABAergic synaptogenesis by brain-derived neurotrophic factor in developing spinal neurons.

Brain-derived neurotrophic factor (BDNF) effects on the establishment of glycinergic and GABAergic transmissions in mouse spinal neurons were examined using combined electrophysiological and calcium imaging techniques. BDNF (10 ng/ml) caused a significant acceleration in the onset of synaptogenesis without large effects on the survival of these neurons. Amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) associated to activation of glycine and GABA(A) receptors were augmented in neurons cultured with BDNF. The neurotrophin effect was blocked by long term tetrodotoxin (TTX) addition suggesting a dependence on neuronal activity. In addition, BDNF caused a significant increase in glycine- and GABA-evoked current densities that partly explains the increase in synaptic transmission. Presynaptic mechanisms were also involved in BDNF effects since triethylammonium(propyl)-4-(2-(4-dibutylamino-phenyl)vinyl)pyridinium (FM1-43) destaining with high K(+) was augmented in neurons incubated with the neurotrophin. The effects of BDNF were mediated by receptor tyrosine kinase B (TrkB) and mitogen-activated protein kinase kinase (MEK) activation since culturing neurons with either (9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'- kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester (K252a) or 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) blocked the augmentation in synaptic activity induced by the neurotrophin.

Anti-homeostatic synaptic plasticity of glycine receptor function after chronic strychnine in developing cultured mouse spinal neurons.

In this study, we describe a novel form of anti-homeostatic plasticity produced after culturing spinal neurons with strychnine, but not bicuculline or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Strychnine caused a large increase in network excitability, detected as spontaneous synaptic currents and calcium transients. The calcium transients were associated with action potential firing and activation of gamma-aminobutyric acid (GABA(A)) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors as they were blocked by tetrodotoxin (TTX), bicuculline, and CNQX. After chronic blockade of glycine receptors (GlyRs), the frequency of synaptic transmission showed a significant enhancement demonstrating the phenomenon of anti-homeostatic plasticity. Spontaneous inhibitory glycinergic currents in treated cells showed a fourfold increase in frequency (from 0.55 to 2.4 Hz) and a 184% increase in average peak amplitude compared with control. Furthermore, the augmentation in excitability accelerated the decay time constant of miniature inhibitory post-synaptic currents. Strychnine caused an increase in GlyR current density, without changes in the apparent affinity. These findings support the idea of a post-synaptic action that partly explains the increase in synaptic transmission. This phenomenon of synaptic plasticity was blocked by TTX, an antibody against brain-derived neurotrophic factor (BDNF) and K252a suggesting the involvement of the neuronal activity-dependent BDNF-TrkB signaling pathway. These results show that the properties of GlyRs are regulated by the degree of neuronal activity in the developing network.