The effect of chemical treatment of stainless steel wire surfaces on Zymomonas mobilis cell attachment and product synthesis

The attachment, growth and product synthesis of non-flocculating Zymomonas mobilis cell, fixed in stainless steel wire spheres (WS), were investigated. The carrier surface was activated by treatment with titanium (IV) chloride (TiCl₄) and γ-aminopropyltriethoxysilane (AS) in an attempt to raise the efficiency in the immobilization of the cells. System productivity for ethanol and levan production, using cells immobilized on a modified stainless steel in the batch fermentation of a sucrose medium, rose as a result of increased biomass compared to the productivity of cells fixed on untreated (control) metal surfaces. Stabilized ethanol synthesis was demonstrated in the course of four cycles (each cycle 48 h) of repeated fermentations with a stainless steel carrier treated with AS, and three cycles when TiCl₄ was used. Levan synthesis decreased after three cycles with cells immobilized on a silanized surface. System productivity for ethanol and levan production after the fourth cycle in experiments with TiCl₄-activated, silanized and unmodified carriers were Q_eth = 1.01, 1.06 and 0.27 g/l × h; Q_lev = 0.32, 0.29 and 0.12 g/l × h, respectively. However, the specific productivity of biomass for product synthesis was higher in fermentation systems with untreated stainless steel surfaces, probably due to some loss of physiological activity of cells attached to a modified carrier. Investigations of throughly washed activated stainless steel wire surfaces, by scanning electron microscopy after immobilization, showed significant attachment of cells to the carriers. A polymer layer covered the wire surface treated with TiCl₄ after fermentations. This may be explained as the binding of extracellular polysaccharide, such as the fructose-polymer levan and yeast extract components, to the modified support via chelation. After four fermentations, craters and holes in the polymer layer were evident, probably as a result of CO₂ formation. A small number of cells appeared on this layer. In view of the good ethanol formation during all fermentation cycles, it is probably that active Z. mobilis cells remained under the polymer layer. Wire treatment with AS resulted in the formation of long filamentous cells during fermentation and some disturbance of cellular fission. This may be partly explained by strong electrostatic interactions between the positively charged carrier surface and the predominately negatively charged surface of Z mobilis cells. However, this did not significantly affect other cellular functions. The surface of the wire treated with AG was practically without a polymer layer.     

Exercise causes blood glutathione oxidation in chronic obstructive pulmonary disease: prevention by O2 therapy

Viña, José, Emilio Servera, Miguel Asensi, JuanSastre, Federico V. Pallardó, José A. Ferrero, JoséGarcía-de-la-Asunción, Vicente Antón, and JulioMarín. Exercise causes blood glutathione oxidation inchronic obstructive pulmonary disease: prevention by O₂therapy. J. Appl. Physiol. 81(5):2199-2202, 1996.The aim of the present study was to determinewhether glutathione oxidation occurs in chronic obstructive pulmonarydisease (COPD) patients who perform exercise and whether this could beprevented. Blood glutathione red-ox ratio [oxidized-to-reducedglutathione (GSSG/GSH)] was significantly increased when patientsperformed exercise for a short period of time until exhaustion. Theirresting blood GSSG/GSH was 0.039 ± 0.008 (SD)(n = 5), whereas after exercise itincreased to 0.085 ± 0.019, P < 0.01. Glutathione oxidation associated with exercise was partiallyprevented by oxygen therapy (resting value: 0.037 ± 0.014, n = 5; after exercise: 0.047 ± 0.016, n = 5, P < 0.01). We conclude that lightexercise causes an oxidation of glutathione in COPD patients, which canbe partially prevented by oxygen therapy.

     

Glutamine transport by the blood-brain barrier: a possible mechanism for nitrogen removal

Glutamine and glutamate transport activities were measuredin isolated luminal and abluminal plasma membrane vesiclesderived from bovine brain endothelial cells. Facilitativesystems for glutamine and glutamate were almost exclusivelylocated in luminal-enriched membranes. The facilitativeglutamine carrier was neither sensitive to2-aminobicyclo(2,2,1)heptane-2-carboxylic acid inhibition nor did itparticipate in accelerated amino acid exchange; it therefore appearedto be distinct from the neutral amino acid transport system L1. TwoNa-dependent glutamine transporters were found in abluminal-enrichedmembranes: systems A and N. System N accounted for ~80% ofNa-dependent glutamine transport at 100 µM. Abluminal-enriched membranes showed Na-dependent glutamate transport activity. The presence of 1) Na-dependent carrierscapable of pumping glutamine and glutamate from brain into endothelialcells, 2) glutaminase withinendothelial cells to hydrolyze glutamine to glutamate and ammonia, and3) facilitative carriers forglutamine and glutamate at the luminal membrane may provide a mechanismfor removing nitrogen and nitrogen-rich amino acids from brain.

     

The effect of aspirin and two nitric oxide donors on the infarcted heart in situ

Nitric oxide (NO) donors are heterogeneous substances which release NO, a biologically active compound. NO released by nitric oxide donors has important effects on the circulation by causing vasodilation, diminishing myocardial contractile force, inhibiting platelet aggregation, and counteracting the effects of thromboxane A2. In the infarcted heart, activation of the inducible form of nitric oxide synthase (iNOS) and the formation of prostacyclin and thromboxane A2 by cyclooxygenase (COX) were increased. Myocardial infarction also resulted in increased myocardial NO production. Aspirin (acetylsalicylic acid. ASA) at low concentration (35 mg/kg/day) fails to change iNOS production, in contrast to higher dose (150 mg/kg/day) which, as previously shown, inhibits iNOS activity. ASA at all doses also suppresses myocardial prostanoid formation because of inhibition of COX. Recently, two NO donors have been synthesized: NCX 4016 and Diethylenetriamine/NO (DETA/NO). NCX 4016 combines an NO-releasing moiety with a carboxylic residue via an esteric bond. We describe here that NCX 4016 (65 mg/kg/day) increased prostacyclin and thromboxane A2 production in the infarcted heart muscle, overcoming the inhibitory effects of ASA. As a result of nitric oxide release, oxidation products of NO (NO2- and NO3-; NOx) in arterial blood rose following administration of NCX 4016. On oral administration, NCX 4016 did not change systemic arterial pressure. The effects of a single NO donor, DETA/NO (1.0 mg/kg/day) on the infarcted heart were also investigated On intravenous administration, the compound increased NO concentration in arterial blood slightly but to a lesser degree than NCX 4016. Like NCX 4016, it raised myocardial production of prostacyclin and thromboxane A2 in the infarcted heart. However, it caused a severe fall in blood pressure. These findings demonstrate that newly-synthesized NO donors release nitric oxide in situ and increase myocardial production of prostanoids. NCX 4016 has therapeutic potential because it can be orally administered, lacks hypotensive effects, increases blood levels of nitric oxide and myocardial prostacyclin production.     

Oxidative damage to mitochondrial DNA and glutathione oxidation in apoptosis: studies in vivo and in vitro.

Free radicals may be involved in apoptosis although this is the subject of some controversy. Furthermore, the source of free radicals in apoptotic cells is not certain. The aim of this study was to elucidate the role of oxidative stress in the induction of apoptosis in serum-deprived fibroblast cultures and in weaned lactating mammary glands as in vitro and in vivo experimental models, respectively. Oxidative damage to mtDNA is higher in apoptotic cells than in controls. Oxidized glutathione (GSSG) levels in mitochondria from lactating mammary gland are also higher in apoptosis. There is a direct relationship between mtDNA damage and the GSSG/reduced glutathione (GSH) ratio. Furthermore, whole cell GSH is decreased and GSSG is increased in both models of apoptosis. Glutathione oxidation precedes nuclear DNA fragmentation. These signs of oxidative stress are caused, at least in part, by an increase in peroxide production by mitochondria from apoptotic cells. We report a direct relationship between glutathione oxidation and mtDNA damage in apoptosis. Our results support the role of mitochondrial oxidative stress in the induction of apoptosis.     

Dual N-Back Working Memory Training in Healthy Adults: A Randomized Comparison to Processing Speed Training

Enhancing cognitive ability is an attractive concept, particularly for middle-aged adults interested in maintaining cognitive functioning and preventing age-related declines. Computerized working memory training has been investigated as a safe method of cognitive enhancement in younger and older adults, although few studies have considered the potential impact of working memory training on middle-aged adults. This study investigated dual n-back working memory training in healthy adults aged 30–60. Fifty-seven adults completed measures of working memory, processing speed, and fluid intelligence before and after a 5-week web-based dual n-back or active control (processing speed) training program. Results: Repeated measures multivariate analysis of variance failed to identify improvements across the three cognitive composites, working memory, processing speed, and fluid intelligence, after training. Follow-up Bayesian analyses supported null findings for training effects for each individual composite. Findings suggest that dual n-back working memory training may not benefit working memory or fluid intelligence in healthy adults. Further investigation is necessary to clarify if other forms of working memory training may be beneficial, and what factors impact training-related benefits, should they occur, in this population.     

C-3 Amido-indole cannabinoid receptor modulators

C-3 Amido-indoles were found to selectively bind to the CB2 receptor. SAR studies led to optimized compounds with excellent in vivo potency against LPS induced TNF-alpha release in murine models of cytokine production.