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The aim of this paper is to investigate the possibility to recover lactic acid (LA) from the whey of yoghurt by easy and effective solvent extraction technique using tri-n-octylamine, tri-n-butyl phosphate, and their mixtures as extractant. All parameters affecting the transfer of lactic acid to the organic phase were investigated including: time of stirring, tri-n-butyl phosphate and tri-n- octylamine concentrations, organic to aqueous phase ratio, temperature, NaCl concentration as a salting out agent, and number of contacts. The maximum yield of LA extraction can be obtained by using the following operation conditions: 0.8M TOA+11% TBP, Vorg/Vaq = 4/1, t = 30 oC, [NaCl] = 2M. Complete stripping of LA from loaded organic phase can be done in 2 stages using double distilled water at 60oC and Vaq/Vorg = 20/1.

High-quality three-dimensional (3D) seismic reflection and borehole data are used to characterize in detail the structural style and evolution of inversion structures in Horus oil field. This field lies in the central part of Alamein Basin, northern Western Desert of Egypt, in the hanging-wall of a major Jurassic-Early Cretaceous normal fault. This fault delineates the northwestern margin of the basin and extends in an ENE-WSW direction, bounding a half-graben trough in its hanging-wall. This trough had continued subsidence during Early Cretaceous time with depositional thickening of the Lower Cretaceous Alam el Bueib Formation. Fault displacement had ceased near the top of Barremian level. Aptian-Lower Senonian seismically traced levels show a major NE-plunging asymmetrical anticline overlying the Jurassic-Barremian half-graben. This anticline is sub-parallel to the inherited Jurassic rifting fault. At shallower Cretaceous levels, this fault is replaced by a set of WNW-ESE-trending en echelon faults of considerable displacements, which probably indicates a strike-slip component of deformation. These faults display normal separation on all displaced stratigraphic levels and tip upwards in the upper part of the Upper Cretaceous succession. This marks a considerable change in the tectonic mode of the area. NW-SE extensional faults were developed perpendicular to the fold axis, dissecting the anticline into several blocks entrapping hydrocarbons. Detailed seismic structural analysis of growth strata indicates that the fold initiated in Early Senonian time was associated with the inversion of the earlier Jurassic-Barremian half-graben. This basin inversion is attributed to the Syrian-Arc event that dominated North Africa during the Late Cretaceous time and continued through to the Early Miocene. Low fold amplitude coupled with normal displacements on the deep-seated ENE-WSW-trending Jurassic-Barremian fault indicate a mild phase of positive inversion. The Upper Senonian-Eocene stratigraphic sequences increased in thickness in the back-troughs that were associated with basin inversion.

Among the chemical factors that have been implicated in the etiology of dementia, recent concern has focused on both increased and decreased exposure to the metalloid selenium (Se). This report describes the molecular, behavioral, and electrophysiological analysis of rats that were fed with Se-free chow and Se-enriched tap water for 21 days. Three groups were produced, feeding them on a deficient diet with different Selenium content. Hippocampus-dependent spatial learning was measured using the water maze. Long-term potentiation (LTP) was recorded in the hippocampal dentate gyrus to assess how memory is formed at the cellular level. Hippocampal Se levels were measured in trained rats by using inductively coupled plasma mass spectrometry. Phosphorylated and total tau levels were measured in whole hippocampus by Western blot. An impairment of learning of rats feeding with Se-deficient diet was accompanied by attenuated LTP, and increased ratio of p231Tau-to- and decreased ratio of p416Tau-to-Tau in the non-stimulated hippocampus, despite no significant change was observed in Se levels of hippocampus and plasma. Se supplementation resulted in an increase in both tissues and an increase in the ratio of p231Tau-to-Tau in the non-stimulated hippocampus but did not change learning performance and LTP. Despite impaired learning and LTP, no group differed in probe trial and in the fraction of phosphorylated tau in LTP-induced hippocampus. Reduced level of selenium would probably result in reduced synaptic plasticity as well as impairment of learning ability, suggesting requirement of Se for normal synaptic function.

Metal Oxide Nanoparticles are of interest in modern research and applications. Fe3O4nanoparticles have interesting properties that can be manipulated in a various applications,some of these applications represent an advanced technology to biological and medical sciences [1-5], drugs and gene mapping [6-9], Detection of proteins moieties [10],Tumour removal [11,12] bioanalysis of pathogens [13], Tissue analysis [14],monitoring of DNA structure[15,16],and Magnetic Resonance Imaging resolution improvement [18-23] chromatographic separation and purification of molecules and biological cells [24].The purpose of this review is to summarize the different methods of preparations ofFe3O4 nanoparticlesand describes these methods of preparation allowing control of the size, morphology,and surface treatment. Thesenanoparticles can be preparedby different methods such as Gas , liquid, two-phase methods , Sol-gel methods , High pressure hydrothermal methods and Co-precipitation Method

It is well-known that some kinases which are involved in the induction of synaptic plasticity probably modulate tau phosphorylation. However, how depression of potentiated synaptic strength contributes to tau phosphorylation is unclear because of the lack of experiments in which depotentiation of LTP was induced. Field excitatory postsynaptic potential (fEPSP) and population spike (PS) were recorded from the dentate gyrus in response to the perforant pathway stimulation. To induce LTP, high-frequency stimulation (HFS) was used, while, for depotentiation of LTP, low-frequency stimulation (LFS) consisting of 900 pulses at 1 Hz was applied 5 min after tetanization. In some experiments, a neutral protocol at 0.033 Hz was applied throughout the experiment without any induction of synaptic plasticity. One-hertz depotentiation protocol was able to decrease fEPSP slope which was previously increased by HFS, whereas no significant change in fEPSP slope and PS amplitude was observed in neutral protocol experiments. Relative to saline infusion, LTP was lower in magnitude and was more reversed by subsequent LFS in the presence of ERK1/2 inhibitor. Western blot experiments indicated that tau protein was hyperphosphorylated at ser416 epitope but rather hypophosphorylated at thr231 epitope in the whole hippocampus upon depotentiation of LTP. These changes concomitantly occurred with a notable increase in the levels of total tau and in the levels of phosphorylated form of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). ERK1/2 inhibition resulted in a decrease in phosphorylation of tau at p416Tau when ERK1/2 was inhibited. These findings indicate that some forms of long-term plastic changes might be related with epitope-specific tau phosphorylation and ERK1/2 activation in the hippocampus. Therefore, we emphasize that tau may be crucial for physiological learning as well as Alzheimer's disease pathology.

Although the effects of long-term experimental dysthyroidism on long-term potentiation (LTP) and long-term depression (LTD) have been documented, the relationship between LTP/LTD and acute administration of L-thyroxine (T4) has not been described. Here, we investigated the effects of intra-hippocampal administration of T4 on synaptic plasticity in the dentate gyrus of the hippocampal formation. After a 15-minute baseline recording, LTP and LTD were induced by application of high- and low-frequency stimulation protocols, respectively. Infusions of saline or T4 and tetraiodothyroacetic acid (tetrac), a T4 analog that inhibits binding of iodothyronines to the integrin αvβ3 receptor, either alone or together, were made during the stimulation protocols. The averages of the excitatory postsynaptic potential (EPSP) slopes and population spike (PS) amplitudes, between 55 to 60 minutes, were used as a measure of the LTP/LTD magnitude and were analyzed by two-way univariate ANOVA with T4 and tetrac as between-subjects factors. The input-output curves of the infusion groups were comparable to each other, as shown by the non significant interaction observed between stimulus intensity and infused drug. The magnitude of the LTP in T4-infused rats was significantly lower as compared to saline-infused rats. Both the PS amplitude and the EPSP slope were depressed more markedly with T4 infusion than with saline, tetrac, and T4 + tetrac infusion. Data of this study provide in vivo evidence that T4 can promote LTD over LTP via the integrin αvβ3 receptor, and that the effect of endogenous T4 on this receptor can be suppressed by tetrac in the hippocampus. © 2016 Wiley Periodicals, Inc.

The expression of homosynaptic long-term depression (LTD) governs the subsequent induction of long-term potentiation (LTP) at hippocampal synapses. This process, called metaplasticity, is associated with a transient increase in the levels of several kinases, such as extracellular signal-regulated protein kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and Akt kinase. It has been increasingly realized that the chemical changes in the hippocampus caused by hypothyroidism may be the key underlying causes of the learning deficits, memory loss, and impaired LTP associated with this disease. However, the functional role of thyroid hormones in the “plasticity of synaptic plasticity” has only begun to be elucidated. To address this issue, we sought to determine whether the administration of 6-n-propyl-2-thiouracil (PTU) alters the relationship between priming and the induction of subsequent LTP and related signaling molecules. The activation of ERK1/2, JNK, and Akt was measured in the hippocampus at least 95 min after priming onset. We found that priming stimulation at 5 Hz for 3 s negatively impacted the induction of LTP by subsequent tetanic stimulation in hypothyroid animals, as manifested by a more rapid decrease in the fEPSP slope and population spike amplitude. This phenomenon was accompanied by lower levels of phosphorylated Akt in the surgically removed hippocampus of the hypothyroid rats compared to the euthyroid rats. The metaplastic response and the expression of these proteins in the 1-Hz-primed hippocampus were not different between the two groups. These observations suggest that decreased PI3K/Akt signaling may be involved in the compromised metaplastic regulation of LTP observed in hypothyroidism, which may account for the learning difficulties/cognitive impairments associated with this condition.

Objective Although, accumulating evidence is delineating a neuroprotective and neurotrophic role for lithium (Li), inconsistent findings have also been reported in human studies especially. Moreover, the effects of Li infusion into the hippocampus are still unknown. The aims of this work were (a) to assess whether basal synaptic activity and long-term potentiation (LTP) in the hippocampus are different in regard to intrahippocampal Li infusion; (b) to assess spatial learning and memory in rats chronically treated with LiCO3 in the Morris water maze. Methods Field potentials were recorded form the dentate gyrus, stimulating perforant pathways, in rats chronically (20 mg/kg for 40 days) or acutely treated with LiCO3 and their corresponding control rats. In addition, performance of rats in a Morris water maze was measured to link behaviour of rats to electrophysiological findings. Results LiCO3 infusion into the hippocampus resulted in enhanced LTP, especially in the late phases, but attenuated LTP was observed in rats chronically treated with Li as compared to controls. Li-treated rats equally performed a spatial learning task, but did spend less time in target quadrant than saline-treated rats in Morris water maze. Conclusion Despite most data suggest that Li always yields neuroprotective effects against neuropathological conditions; we concluded that a 40-day treatment of Li disrupts hippocampal synaptic plasticity underlying memory processes, and that these effects of prolonged treatment are not associated with its direct chemical effect, but are likely to be associated with the molecular actions of Li at genetic levels, because its short-term effect preserves synaptic plasticity.

Although the effects of long-term experimental dysthyroidism on long-term potentiation (LTP) and long-term depression (LTD) have been documented, the relationship between LTP/LTD and acute administration of L-thyroxine (T4) has not been described. Here, we investigated the effects of intra-hippocampal administration of T4 on synaptic plasticity in the dentate gyrus of the hippocampal formation. After a 15-minute baseline recording, LTP and LTD were induced by application of high- and low-frequency stimulation protocols, respectively. Infusions of saline or T4 and tetraiodothyroacetic acid (tetrac), a T4 analog that inhibits binding of iodothyronines to the integrin αvβ3 receptor, either alone or together, were made during the stimulation protocols. The averages of the excitatory postsynaptic potential (EPSP) slopes and population spike (PS) amplitudes, between 55 to 60 minutes, were used as a measure of the LTP/LTD magnitude and were analyzed by two-way univariate ANOVA with T4 and tetrac as between-subjects factors. The input-output curves of the infusion groups were comparable to each other, as shown by the non significant interaction observed between stimulus intensity and infused drug. The magnitude of the LTP in T4-infused rats was significantly lower as compared to saline-infused rats. Both the PS amplitude and the EPSP slope were depressed more markedly with T4 infusion than with saline, tetrac, and T4 + tetrac infusion. Data of this study provide in vivo evidence that T4 can promote LTD over LTP via the integrin αvβ3 receptor, and that the effect of endogenous T4 on this receptor can be suppressed by tetrac in the hippocampus. © 2016 Wiley Periodicals, Inc.