Taurine protection of PC12 cells against endoplasmic reticulum stress induced by oxidative stress

Background

Taurine is a free amino acid present in high concentrations in a variety of organs of mammalians. As an antioxidant, taurine has been found to protect cells against oxidative stress, but the underlying mechanism is still unclear.

Methods

In this report, we present evidence to support the conclusion that taurine exerts a protective function against endoplasmic reticulum (ER) stress induced by H₂O₂ in PC 12 cells. Oxidative stress was introduced by exposure of PC 12 cells to 250 uM H₂O₂ for 4 hours.

Results

It was found that the cell viability of PC 12 cells decreased with an increase of H₂O₂ concentration ranging from approximately 76% cell viability at 100 uM H₂O₂ down to 18% at 500 uM H₂O₂. At 250 uM H₂O₂, cell viability was restored to 80% by taurine at 25 mM. Furthermore, H₂O₂ treatment also caused a marked reduction in the expression of Bcl-2 while no significant change of Bax was observed. Treatment with taurine restored the reduced expression of Bcl-2 close to the control level without any obvious effect on Bax. Furthermore, taurine was also found to suppress up-regulation of GRP78, GADD153/CHOP and Bim induced by H₂O₂, suggesting that taurine may also exert a protective function against oxidative stress by reducing the ER stress.

Conclusion

In summary, taurine was shown to protect PC12 cells against oxidative stress induced by H₂O₂. ER stress was induced by oxidative stress and can be suppressed by taurine.

     

Stress influenced the aerotolerance of <Emphasis Type="Italic">Lactobacillus rhamnosus</Emphasis> hsryfm 1301

Objective

To investigate the aerotolerance of Lactobacillus rhamnosus hsryfm 1301 and its influencing factors.

Results

The growth rate of L. rhamnosus hsryfm 1301 weakened noticeably when the concentration of supplemented H₂O₂ reached 1 mM, and only 2% of all L. rhamnosus hsryfm 1301 cells survived in MRS broth supplemented with 2 mM H₂O₂ for 1 h. After pretreatment with 0.5 mM H₂O₂, the surviving cells of L. rhamnosus hsryfm 1301 in the presence of 5 mM H₂O₂ for 1 h increased from 3.7 to 7.8 log CFU. Acid stress, osmotic stress, and heat stress at 46 °C also enhanced its aerotolerance, while heat stress at 50 °C reduced the tolerance of L. rhamnosus hsryfm 1301 to oxidative stress. Moreover, treatment with 0.5 mM H₂O₂ increased the heat stress tolerance of L. rhamnosus hsryfm 1301 by approximately 150-fold.

Conclusions

Lactobacillus rhamnosus hsryfm 1301 possesses a stress-inducible defense system against oxidative stress, and the cross-adaptation to different stresses is a promising target to increase the stress tolerance of L. rhamnosus hsryfm 1301 during probiotic food and starter culture production.

     

Asymmetric effects of litter removal and litter addition on the structure and function of soil microbial communities in a managed pine forest

Aims

The effect of different MeJA doses applied prior to or simultaneously with toxic Al on biochemical and physiological properties of Vaccinium corymbosum cultivars with contrasting Al resistance was studied.

Methods

Legacy (Al-resistant) and Bluegold (Al-sensitive) plants were treated with and without toxic Al under controlled conditions: a) without Al and MeJA, b) 100 μM Al, c) 100 μM Al + 5 μM MeJA, d) 100 μM Al + 10 μM MeJA and e) 100 μM Al + 50 μM MeJA. MeJA was applied to leaves 24 h prior to or simultaneously with Al in nutrient solution. After 48 h, Al-concentration, lipid peroxidation (LP), H₂O₂, antioxidant activity, total phenols, total flavonoids, phenolic compounds and superoxide dismutase activity (SOD) of plant organs were analyzed.

Results

Al-concentrations increased with Al-treatment in both cultivars, being Al, LP and H₂O₂ concentrations reduced with low simultaneous MeJA application. Higher MeJA doses induced more oxidative damage than the lowest. Legacy increased mainly non-enzymatic compounds, whereas Bluegold increased SOD activity to counteract Al³⁺.

Conclusions

Low MeJA doses applied simultaneously with Al³⁺ increased Al-resistance in Legacy by increasing phenolic compounds, while Bluegold reduced oxidative damage through increment of SOD activity, suggesting a diminution of its Al-sensitivity. Higher MeJA doses could be potentially toxic. Studies are needed to determine the molecular mechanisms involved in the protective MeJA effect against Al-toxicity.

     

Tat-DJ-1 enhances cell survival by inhibition of oxidative stress,NF-κB and MAPK activation in HepG2 cells

Objectives

To identify the protective effect of DJ-1 protein against oxidative stress-induced HepG2 cell death, we used cell-permeable wild type (WT) and a mutant (C106A Tat-DJ-1) protein.

Results

By using western blotting and fluorescence microscopy, we observed WT and C106A Tat-DJ-1 proteins were efficiently transduced into HepG2 cells. Transduced WT Tat-DJ-1 proteins increased cell survival and protected against DNA fragmentation and intracellular ROS generation levels in H₂O₂-exposed HepG2 cells. At the same time, transduced WT Tat-DJ-1 protein significantly inhibited NF-κB and MAPK (JNK and p38) activation as well as regulated the Bcl-2 and Bax expression levels. However, C106A Tat-DJ-1 protein did not show any protective effect against cell death responses in H₂O₂-exposed HepG2 cells.

Conclusions

Oxidative stress-induced HepG2 cell death was significantly reduced by transduced WT Tat-DJ-1 protein, not by C106A Tat-DJ-1 protein. Thus, transduction of WT Tat-DJ-1 protein could be a novel strategy for promoting cell survival in situations of oxidative stress-induced HepG2 cell death.

     

Matrix association region/scaffold attachment region (MAR/SAR) sequence: its vital role in mediating chromosome breakages in nasopharyngeal epithelial cells via oxidative stress-induced apoptosis

Background

Oxidative stress is known to be involved in most of the aetiological factors of nasopharyngeal carcinoma (NPC). Cells that are under oxidative stress may undergo apoptosis. We have previously demonstrated that oxidative stress-induced apoptosis could be a potential mechanism mediating chromosome breakages in nasopharyngeal epithelial cells. Additionally, caspase-activated DNase (CAD) may be the vital player in mediating the chromosomal breakages during oxidative stress-induced apoptosis. Chromosomal breakage occurs during apoptosis and chromosome rearrangement. Chromosomal breakages tend to cluster in certain regions, such as matrix association region/scaffold attachment region (MAR/SAR). We hypothesised that oxidative stress-induced apoptosis may result in chromosome breaks preferentially at the MAR/SAR sites. The AF9 gene at 9p22 was targeted in this study because 9p22 is a deletion site commonly found in NPC.

Results

By using MAR/SAR recognition signature (MRS), potential MAR/SAR sites were predicted in the AF9 gene. The predicted MAR/SAR sites precisely match to the experimentally determined MAR/SARs. Hydrogen peroxide (H₂O₂) was used to induce apoptosis in normal nasopharyngeal epithelial cells (NP69) and NPC cells (HK1). Nested inverse polymerase chain reaction was employed to identify the AF9 gene cleavages. In the SAR region, the gene cleavage frequency of H₂O₂-treated cells was significantly higher than that of the non-treated cells. A few chromosomal breakages were detected within the AF9 region which was previously found to be involved in the mixed lineage leukaemia (MLL)-AF9 translocation in an acute lymphoblastic leukaemia patient. As for the non-SAR region, no significant difference in the gene cleavage frequency was found between the untreated control and H₂O₂-treated cells. Furthermore, H₂O₂-induced cleavages within the SAR region were reduced by caspase-3 inhibitor, which indirectly inhibits CAD.

Conclusions

These results reaffirm our previous findings that oxidative stress-induced apoptosis could be one of the potential mechanisms underlying chromosome breakages in nasopharyngeal epithelial cells. MAR/SAR may play a vital role in defining the location of chromosomal breakages mediated by oxidative stress-induced apoptosis, where CAD is the major nuclease.

     

Sublethal concentration of H<Subscript>2</Subscript>O<Subscript>2</Subscript> enhances the protective effect of mesenchymal stem cells in rat model of spinal cord injury

Objective

To investigate the effect of H₂O₂ on the migration and antioxidant defense of mesenchymal stem cells (MSCs) and the neurotrophic effects of H₂O₂-treated MSCs on spinal cord injury (SCI).

Results

Sublethal concentrations of H₂O₂ decreased cell migration and expression of CXCR4 and CCR2 as well as Nrf2 expression in MSCs. In the second phase, transplantation of treated and untreated MSCs to SCI caused minor changes in locomotor dysfunction. There was a significantly difference between cell-treated and spinal cord injury groups in expression of BDNF (brain-derived neurotrophic factor). Transplantation of H₂O₂-treated cells caused an increase in BDNF expression compared to non-treated cells.

Conclusion

Transplantation of H₂O₂-treated stem cells may have protective effects against SCI through by increasing neurotrophic factors.

     

Identification of suitable reference genes for real-time quantitative PCR analysis of hydrogen peroxide-treated human umbilical vein endothelial cells

Background

Oxidative stress can induce cell injury in vascular endothelial cells, which is the initial event in the development of atherosclerosis. Although quantitative real-time polymerase chain reaction (qRT-PCR) has been widely used in gene expression studies in oxidative stress injuries, using carefully validated reference genes has not received sufficient attention in related studies. The objective of this study, therefore, was to select a set of stably expressed reference genes for use in qRT-PCR normalization in oxidative stress injuries in human umbilical vein endothelial cells (HUVECs) induced by hydrogen peroxide (H₂O₂).

Results

Using geNorm analysis, we found that five stably expressed reference genes were sufficient for normalization in qRT-PCR analysis in HUVECs treated with H₂O₂. Genes with the most stable expression according to geNorm were U6, TFRC, RPLP0, GAPDH, and ACTB, and according to NormFinder were ALAS1, TFRC, U6, GAPDH, and ACTB.

Conclusion

Taken together, our study demonstrated that the expression stability of reference genes may differ according to the statistical program used. U6, TFRC, RPLP0, GAPDH, and ACTB was the optimal set of reference genes for studies on gene expression performed by qRT-PCR assays in HUVECs under oxidative stress study.

     

Co-cultivation of <Emphasis Type="Italic">Chlamydomonas reinhardtii</Emphasis> with <Emphasis Type="Italic">Azotobacter chroococcum</Emphasis> improved H<Subscript>2</Subscript> production

Objectives

To improve H₂ production, the green algae Chlamydomonas reinhardtii cc849 was co-cultured with Azotobacter chroococcum.

Results

The maximum H₂ production of the co-culture was 350% greater than that of the pure algal cultures under optimal H₂ production conditions. The maximum growth and the respiratory rate of the co-cultures were about 320 and 300% of the controls, and the dissolved O₂ of co-cultures was decreased 74%. Furthermore, the in vitro maximum hydrogenase activity of the co-culture was 250% greater than that of the control, and the in vivo maximum hydrogenase activity of the co-culture was 1.4-fold greater than that of the control. In addition, the maximum starch content of co-culture was 1400% that of the control.

Conclusions

Azotobacter chroococcum improved the H₂ production of the co-cultures by decreasing the O₂ content and increasing the growth and starch content of the algae and the hydrogenase activity of the co-cultures relative to those of pure algal cultures.

     

Characterization of H<Subscript>2</Subscript> photoproduction by marine green alga <Emphasis Type="Italic">Tetraselmis subcordiformis</Emphasis> integrated with an alkaline fuel cell

Objectives

To investigate the feasibility of coupling carbonyl cyanide m-chlorophenylhydrazone-regulated photohydrogen production by Tetraselmis subcordiformis in a photobioreactor to an alkaline fuel cell (AFC).

Results

H₂ evolution kinetics in the AFC integrated process was characterized. The duration of H₂ evolution was prolonged and its yield was improved about 1.5-fold (to 78 ± 5 ml l^?1) compared with that of the process without AFC. Improved H₂ yield was possibly caused by removal of H₂ feedback inhibition by H₂ consumption in situ. Decreases in the H₂ production rate correlated with the gradual deactivation of PSII and hydrogenase activities. The H₂ yield was closely associated with catabolism of starch and protein.

Conclusion

A marine green algal CO₂-supplemented culture integrated with in situ H₂-consumption by an AFC system was developed as a viable protocol for the H₂ production.

     

Mitochondrial H<Subscript>2</Subscript>O<Subscript>2</Subscript> as an enable signal for triggering autophosphorylation of insulin receptor in neurons

Background

Insulin receptors are widely distributed in the brain, where they play roles in synaptic function, memory formation, and neuroprotection. Autophosphorylation of the receptor in response to insulin stimulation is a critical step in receptor activation. In neurons, insulin stimulation leads to a rise in mitochondrial H₂O₂ production, which plays a role in receptor autophosphorylation. However, the kinetic characteristics of the H₂O₂ signal and its functional relationships with the insulin receptor during the autophosphorylation process in neurons remain unexplored to date.

Results

Experiments were carried out in culture of rat cerebellar granule neurons. Kinetic study showed that the insulin-induced H₂O₂ signal precedes receptor autophosphorylation and represents a single spike with a peak at 5–10 s and duration of less than 30 s. Mitochondrial complexes II and, to a lesser extent, I are involved in generation of the H₂O₂ signal. The mechanism by which insulin triggers the H₂O₂ signal involves modulation of succinate dehydrogenase activity. Insulin dose–response for receptor autophosphorylation is well described by hyperbolic function (Hill coefficient, n_H, of 1.1±0.1; R²=0.99). N-acetylcysteine (NAC), a scavenger of H₂O₂, dose-dependently inhibited receptor autophosphorylation. The observed dose response is highly sigmoidal (Hill coefficient, n_H, of 8.0±2.3; R²=0.97), signifying that insulin receptor autophosphorylation is highly ultrasensitive to the H₂O₂ signal. These results suggest that autophosphorylation occurred as a gradual response to increasing insulin concentrations, only if the H₂O₂ signal exceeded a certain threshold. Both insulin-stimulated receptor autophosphorylation and H₂O₂ generation were inhibited by pertussis toxin, suggesting that a pertussis toxin-sensitive G protein may link the insulin receptor to the H₂O₂-generating system in neurons during the autophosphorylation process.

Conclusions

In this study, we demonstrated for the first time that the receptor autophosphorylation occurs only if mitochondrial H₂O₂ signal exceeds a certain threshold. This finding provides novel insights into the mechanisms underlying neuronal response to insulin. The neuronal insulin receptor is activated if two conditions are met: 1) insulin binds to the receptor, and 2) the H₂O₂ signal surpasses a certain threshold, thus, enabling receptor autophosphorylation in all-or-nothing manner. Although the physiological rationale for this control remains to be determined, we propose that malfunction of mitochondrial H₂O₂ signaling may lead to the development of cerebral insulin resistance.

     

Heat shock protein 27 plays a protective role in thoracic aortic dissection by promoting cell proliferation and inhibiting apoptosis

Background

Thoracic aortic dissection (TAD) is one of the most severe aortic diseases. The study aimed to explore the potential role of heat shock protein 27 (HSP27) in the pathogenesis of TAD using an in vitro model of oxidative stress in vascular smooth muscle cells (VSMCs).

Methods

HSP27 was analyzed in aortic surgical specimens from 12 patients with TAD and 8 healthy controls. A lentiviral vector was used to overexpress HSP27 in rat aortic VSMCs. Cell proliferation and apoptosis were measured under oxidative stress induced by H₂O₂.

Results

HSP27 expression was significantly higher in aortic tissue from patients with TAD and VSMCs in the aortic media were the main cell type producing HSP27. Elevated oxidative stress was also detected in the TAD samples. Overexpression of HSP27 significantly attenuated H₂O₂-induced inhibition of cell proliferation. Furthermore, HSP27 was found to decrease H₂O₂-induced cell apoptosis and oxidative stress.

Conclusions

These results suggest that HSP27 expression promotes VSMC viability, suppresses cell apoptosis, and confers protection against oxidative stress in TAD.

     

Rapid and efficient degradation of bisphenol A by chloroperoxidase from <Emphasis Type="Italic">Caldariomyces fumago</Emphasis>: product analysis and ecotoxicity evaluation of the degraded solution

Objectives

To degrade enzymatically bisphenol A (BPA) that causes serious environmental concerns and is difficult to be degraded by chemical or physical methods.

Results

BPA (150 mg l^?1) was completely degraded by chloroperoxidase (CPO)/H₂O₂ within 7 min at room temperature, atmospheric pressure with the enzyme at 6 μg CPO ml^?1. The degradation products were identified by HPLC–MS, which suggested involvement of multiple steps. Enzymatic treatment followed by existing bioremediation technologies (activated sludge) enhanced removal of COD from 9 to 54 %. Using an ecotoxicity evaluation with Chlorella pyrenoidosa, the degradation products had a lower toxicity than BPA.

Conclusion

BPA can be degraded rapidly and efficiently under mild conditions with chloroperoxidase at 6 μg ml^?1. The degradation products had a lower toxicity than BPA.

     

Protection effect of taurine on nitrosative stress in the mice brain with chronic exposure to arsenic

Background

Arsenic exposure induces overproduction of reactive nitrogen species (RNS) in brain tissue and results in nucleic acid damage to the nerve cells. The 8-nitroguanine is one of the major products formed by the reaction of guanine, and ONOO^-, and has been used as a popular biomarker of nucleic acid damage due to RNS attacking. In the present study, we examined whether the administration of taurine can protect against nucleic acid damage of brain neurons by arsenic-induced RNS.

Materials and methods

Sixty mice (30 male and 30 female) weighing 19.5 ± 1.5 g were divided into 3 groups: (1) control group, (2) experimental group that received arsenic (As₂O₃), and (3) antagonistic group that received taurine with arsenic. Arsenic was administered for 60 days. 8-Nitroguanine expressions in brain neurons of mice were examined by the immunohistochemical method. Histopathological changes in brain tissues of mice were observed under light microscope and the immunohistochemistry method was used to investigate 8-nitroguanine expressions in cerebrum and cerebellum of mice.

Results

In the control group, no abnormal histopathological changes were observed in brain tissue of the mice. In brain tissue of the mice exposed to arsenic, histopathological results showed swells, evident vacuolar degeneration in cytoplasm, karyorrhexis and karyolysis. Relatively light pathological changes were observed in brain of the mice co-administered arsenic and taurine. Little or no expression of 8-nitroguanine in brain tissue was observed in controls. However, intensive expression of 8-nitroguanine was found in brain tissue of mice exposed to arsenic and it was mainly distributed in nucleus neighbouring the nuclear membrane, but a little in cytoplasm. A weak expression of 8-nitroguanine was observed in brain cells of mice co-administered arsenic and taurine.

Conclusions

The brain neurons may be the major target cells of arsenic neurotoxicity. Co-administration of arsenic and taurine can alleviate DNA damage of brain neurons caused by arsenic through the RNS signal pathway.

     

Protective effects of mangafodipir against chemotherapy-induced ovarian damage in mice

Background

Given the seriousness of chemotherapy-induced ovarian injury in female cancer patients, the preservation of fertility, including through the use of cryopreservation technology and pharmaceuticals, requires investigation. Previous studies have shown that damage to the ovaries is related to oxidative stress caused by anticancer drugs. Therefore, superoxide dismutase (SOD) may represent a key factor in the pharmacological protection of the ovaries. The aim of our study was to identify the effects of mangafodipir, a manganese chelate and SOD-mimetic, on suppression of apoptosis in granulosa cells and primordial follicle activation induced by anticancer drugs.

Methods

Cell viability assays using methyltrichlorosilane solutions and immunoblotting for cleaved caspase-3 were performed in in vitro experiments with the simultaneous addition of mangafodipir to human non-luteinized granulosa cell line (HGrC) cultures treated with hydrogen peroxide (H₂O₂), cisplatin, or paclitaxel. Count and morphological analyses of follicles at each developing stage in the ovaries and immunohistochemistry for cleaved caspase-3, Ki67 and 4-hydroxynonenal, a marker for oxidative stress, were also performed using mangafodipir-injected 6-week-old female ICR mice treated with cisplatin or paclitaxel. Further, mangafodipir was injected into 6-week-old female BALB/c mice inoculated with ES-2 to analyze whether mangafodipir inhibits the anti-tumor effects of cisplatin or paclitaxel treatment.

Results

Mangafodipir attenuated apoptosis induced by H₂O₂ and anticancer drugs in vitro. Mangafodipir also decreased the expression of 4-hydroxynonenal and reduced cisplatin- and paclitaxel-induced apoptosis in granulosa cells in vivo. In addition, mangafodipir inhibited the loss of primordial follicles. Tumor xenograft studies in mice showed that mangafodipir did not affect anticancer drug antitumor effects.

Conclusions

Oxidative stress might be one of the mechanisms of cisplatin- and paclitaxel-induced the loss of primordial follicles. Mangafodipir can reduce cisplatin- and paclitaxel-induced apoptosis in granulosa cells and primordial follicle activation partially via its SOD activity. At the same time, mangafodipir might have other potential mechanisms to inhibit the activation of primordial follicles. Further, mangafodipir attenuated the ovarian damage caused by cisplatin and paclitaxel without affecting their antitumor activities. Mangafodipir, therefore, though its efficacy might be limited, may be a new option for the preservation of fertility during anticancer treatment.

     

Monitoring of pre-frontal oxygen status in helicopter pilots using near-infrared spectrophotometers

Background

There are few in-flight studies of cognition-related cerebral oxygen status in helicopter pilots.

Methods

Four male helicopter pilots volunteered for nine sorties during visual flight in a BK117 and UH-60J. The pilots' pre-frontal oxy-hemoglobin (O₂Hb) and deoxy-hemoglobin (HHb) concentration were continuously monitored from the right/left sections of the forehead using near-infrared spectrophotometers with a consideration of motion artifacts.

Results

The concentration of O₂Hb progressively increased (13.98 μmol?L^-1 as a maximum increased concentration) in both the right/left sections of the forehead from the basal level during the heightened cognitive demand of helicopter flight. There was comparatively little change (4.32 μmol?L^-1 as a maximum increased concentration) in HHb concentration during measurement of helicopter flight. HHb changes were apparently not affected by a heightened cognitive demand of helicopter pilots.

Conclusion

These results demonstrate that near-infrared spectroscopy, especially O₂Hb measurements, provides a sensitive method for the monitoring of cognitive demand (maneuvers) in helicopter pilots.

     

The negative effect of ANGPTL8 on HDL-mediated cholesterol efflux capacity

Background

It is well known that angiopoietin-like protein 8 (ANGPTL8) exerts its effects on lipid metabolism through the inhibition of lipoprotein lipase and subsequent elevation of plasma triglyceride. However, it is not clear whether ANGPTL8 could affect lipid metabolism via other pathways. The study was aimed to investigate the effects of ANGPTL8 on the function of high-density lipoprotein (HDL), which plays a protective role in atherosclerosis progression.

Methods

Two hundred and ten subjects were recruited. Plasma ANGPTL8 was measured by enzyme-linked immunosorbent assays. Cholesterol efflux capacity was chosen as the biomarker of HDL function and measured via H³-cholesterol loading THP-1 cell models.

Results

ANGPTL8 exhibited no significant difference between CAD group and nonCAD group, but ANGPTL8 in DM group was significantly higher than that in the nonDM group [568.3 (406.2–836.8) vs 458.2 (356.8–755.6), P?=?0.023]. Compared to controls, subjects in CAD group and DM group exhibited significantly lower cholesterol efflux capacity [CAD: 14.58?±?2.06 vs 12.51?±?2.83%, P?<?0.0001; DM: 13.62?±?2.57 vs 12.34?±?3.16%, P?=?0.0099]. ANGPTL8 was inversely correlated with cholesterol efflux capacity (r?=???0.188, P?<?0.01). Regression analysis revealed that plasma ANGPTL8 was an independent contributor to cholesterol efflux capacity (standardized β?=???0.143, P?=?0.023).

Conclusion

ANGPTL8 presents a negative effect on HDL-mediated cholesterol efflux capacity.

     

Do green wooden composites using lignin-based binder have environmentally benign alternatives? A preliminary LCA case study in China

Purpose

Nowadays, formaldehyde emissions from petroleum-based adhesives contribute considerably to environmental problems and are a constraint to the development of forest-based industries. Although many efforts are being made to develop new lignin-based adhesives for panels, very few studies were carried out via life cycle assessment (LCA). This study aims to assess the life cycle of green wooden composites by using hybrid-modified ammonium lignosulfonate (HMAL) as the binder and investigate the possibility of lignin-based binder to be a good alternative.

Methods

This study is a step further of the previous work conducted on HMAL as an alternative binder for medium-density fiberboard (MDF) or, in other words, the wooden composite made from HMAL and wood fiber (WF). LCA was carried out to assess the environmental impacts during the life cycle of the new manufacturing process of HMAL/WF production using ReCiPe 1.08 Endpoint and IPCC global warming potential (GWP) method built into the GaBi version 6.0 software. The production system involved two subsystems: raw material supply and board manufacture. Meanwhile, a comparative LCA of conventional MDF, with three main damage categories and GWP, was also carried out.

Results and discussion

The hydrogen peroxide (H₂O₂) production, electricity, and the HMAL/WF manufacturing stages had the greatest environmental impact. The comparative results pointed out that HMAL/WF production is environmentally superior to conventional MDF in general. Due to the environmental impacts associated with the HMAL binder, a sensitivity analysis was carried out. Suggestions were made for a cleaner production, in which the H₂O₂ dose was reduced to 24 wt%.

Conclusions

H₂O₂ use, energy, and electricity consumption are main contributors to most impact categories, which help us to find the potential improvements of sustainability, choose the appropriate HMAL technology, and optimize the HMAL/WF system. Feasible production processes and life cycle costs are factors that still need to be studied.

     

Taurine regulation of short term synaptic plasticity in fragile X mice

Background

Fragile X Syndrome is the most common known genetic cause of autism. The Fmr1-KO mouse, lacks the fragile X mental retardation protein (FMRP), and is used as a model of the syndrome. The core behavioral deficits of autism may be conceptualized either as excessive adherence to patterns as seen in repetitive actions and aberrant language, or as insensitivity to subtle but socially important changes in patterns. The hippocampus receives information from the entorhinal cortex and plays a crucial role in the processing of patterned information. To gain more insight into the physiological function of FMRP and the neuronal mechanisms underlying fragile X syndrome, we examined the electrophysiological response of the hippocampus to pair pulse stimulation as a measure of patterned information processing and how it is affected in the Fmr1-KO mouse.

Methods

In this study, we used paired-pulse stimulation of the afferent perforant path and recorded from the CA1 region of the hippocampus. Two-month-old FVB/NJ male mice and age-matched Fmr1-KO mice were used in this study. Hippocampal slices were prepared, equilibrated in artificial cerebrospinal fluid (aCSF), and excitatory post synaptic potentials (EPSPs) measured by stimulating the perforant path of the dentate gyrus (DG) while recording from the molecular layer of CA1. Stimulation occurred by setting current and pulse width to evoke a fixed percentage of maximal EPSP amplitude. This stimulation paradigm allowed us to examine the processing capabilities of the hippocampus as a function of increasing interstimulus intervals (ISI) and how taurine, a GABA_A receptor agonist, affects such information processing.

Results

We found that hippocampal slices from wild type (WT) showed pair-pulse facilitation at ISI of 100-300 ms whereas slices from Fmr1-KO brains showed a consistent pair-pulse depression at a comparable ISI. Addition of 10 μM taurine to WT slices resulted in a drastic decrease of the peak response to the second stimulus, resulting in an initial depression at 100 ms ISI followed by potentiation at higher ISI (150 ms and above). In the presence of taurine, the amplitude of the second response remained significantly lower than in its absence. Fmr1-KO mice however, were completely insensitive to taurine application and pair-pulse stimulation always resulted in a depression of the response to the second stimulus.

Conclusions

Previously we reported that Fmr1-KO mice have reduced beta subunits of the GABA_A receptors. We also showed as well as others that taurine acts as an agonist or a modulator for GABA_A receptors. Therefore, the insensitivity of Fmr1-KO slices to taurine application could be due to the reduced binding sites on the GABA_A receptors in the Fmr1-KO mice.