Simulation of carbon dioxide concentrator

Includes vita."Recycling of most of the consumables in manned spacecraft becomes essential in extended missions. The most urgent task is to supply a continuous stream of breathable oxygen to the cabin to balance the consumption. This can be derived from the metabolically produced carbon dioxide. In recent years several systems have been developed for that purpose. They consist essentially of some device to remove the CO2 so as to keep its concentration in the cabin atmosphere below a prescribed level, followed by a reactor to decompose the CO2 eventually into O2 which is recycled to the cabin. One particular method has been adopted by NASA as the most practical and reliable method for missions lasting six months or more. The recovery of O2 from CO2 is achieved in three steps. First, CO2 is concentrated and mixed with H2 in an electrochemical cell (sometimes called a hydrogen depolarized cell or HDC); the mixture is then transferred to a catalytic reactor where it is converted into water and CH4, the methane is then dumped into space; and finally the water vapor is electrolysed in a special electrolysis cell (called water vapor electrolysis cell or WVE) to O2 which is recycled to the cabin and H2 which is transferred to the concentrator. Electrochemical CO2 concentration provides several advantages. The process is continuous and the equivalent weight of the system needed to maintain the atmospheric level of C02 concentration (0.25 nw Hg) is considerably lower than the adsorption systems which do the same duty. C02 compressors which are frequently needed in other systems, e.g., in the vacuum desorption from molecular sieves, are totally eliminated. In addition, the concentration of C02 protects the catalyst in the Sabatier reactor from contamination by the cabin air and supplies the CO2/H2 mixture in proper ratio to the reactor. The development of the device was undertaken in the past five years by two private contractors, Life Systems, Inc., and Hamilton Standard Division of United Technologies. The designs agree in principle but differ in detailed mechanical design and operating conditions. One of the major problems encountered in designing the C02 concentrator is the need to use a concentrated carbonate solution as a cell electrolyte. The air temperature and humidity determine the electrolyte concentration at steady-state. At a high air relative humidity the electrolyte becomes more dilute and increases in volume. This may lead to electrolyte run-off in the gas cavities and is avoided in the Hamilton Standard design by providing a reservoir to absorb the excess electrolyte at humid conditions. At a low air relative humidity the concentration of the electrolyte increases and may exceed the solubility limit. In that case precipitation would commence which may lead to the crossover of the H2 to the air stream causing a hazardous condition. This should be avoided by proper selection of the carbonate electrolyte and air humidity. K2CO3 was first used but was replaced by CS2CO3 which has a higher solubility. Still, this did not allow for cell operation at air relative humidities below about 60%. Below this limit the cell performance decreased because of the loss of electrolyte and precipitation of CsHC03 at the anode. It was necessary to use extensive humidity controllers at the air inlet which added to the total system weight and power requirements. Through its efforts to overcome this problem, Hamilton Standard introduced aqueous solutions of a new electrolyte, TMAC or tetramethyl ammonium carbonate, which have such low water vapor pressures that they can be used safely for air relative humidities as low as 35% without significant change in performance. Very recently, Hamilton Standard completed the design and fabrication of a full-scale device for use in one-man air revitalization systems and finished a 90-day test program to demonstrate the maintainability and durability of the device with a predicted life of two years (Huddleston and Aylward, 1975 a,b,c). The HDC and WVE cells are connected electrically in series so that the energy produced by the fuel cell reactions in the HDC cell is utilized in the water vapor electrolysis. The cost of air revitalization in a spacecraft is measured in millions of dollars and the final design and operation of the system should lead to the minimum cost for a certain duty. The economy of the system is based on two factors: minimum system equivalent weight and minimum power requirements. The weight appears in cost of propellant needed to accelerate the spacecraft and it includes the weight of the HDC cells, WVE cells, Sabatier reactor and other auxiliary equipment. The power requirements are functions of the current densities used and the electrical efficiency of the cells. The total system cost depends greatly on the performance of the HDC cell. For example, a low CO2 transfer efficiency would result in additional cost of the power needed to make Hg and O2 from the H2O produced in the HDC cell. A poor H2/CO2 flow to the Sabatier reactor would lead to a low conversion efficiency which requires additional amounts of the expensive catalyst and would add to the weight of the system. The decrease in cell performance if precipitation occurs would require extra cells adding to the system weight. It is clear that an optimum design of the system is unattainable without a mathematical model that describes the performance of the HDC cell under all possible conditions. Lin and Winnick (1974) developed a fundamental model of the early versions of the device which used CS2CO3 electrolyte. The model was based on the steady-state transport equations and kinetics of the reactions which take place in the cell. Since then, several changes have taken place in the Hamilton Standard design; new electrodes and matrix materials were used and a new electrolyte was employed. It was necessary to develop a new model for the units which use TMAC electrolyte. The model should be able to simulate the new test data and predict the cell performance under all practical conditions. In that way a clear basis for design evaluation can be obtained and optimization studies can be started. This work describes the development of this mathematical model. The starting point will be to review all information pertaining to the electrochemical CO2 concentration. This is followed by a brief description of the cell design, test data and their accuracy, and all useful information concerning the new electrolyte and modifications of the cell design. Chapter IV summarizes the equations which form the basis of the steady-state mathematical model. The important model parameters are then evaluated and used to predict the cell performance over a wide range of operating conditions. Conclusions and recommendations of areas of possible improvements are finally presented."--Introduction.Includes bibliographical references

Cytokines and growth factors in Duchene muscular dystrophy patients

Introduction: Dystrophin deficiency associated with Duchene muscular dystrophy (DMD) results in chronic inflammation and severe skeletal muscle degeneration, where the extent of muscle fibrosis contributes to disease severity. The microenvironment of dystrophic muscles is associated with variation in levels of cytokine and growth factors. Most of the current researches test for such cytokines and growth factors in tissue biopsies, which is an invasive technique. The Aim: Of the present study is to investigate whether cytokines and growth factors, as indicators of inflammatory response, can be detected in blood of DMD patients as non-invasive technique. Patient and Methods: Accordingly the cytokine tumor necrosis factor alfa (TNF TNF-α), as well as the growth factors basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) were measured in blood of 24 boys with DMD diagnosed clinically and at the molecular level versus 20 age matching healthy boys. Results: Showed a significant increases in TNF-ά (30.2 ± 9.5 vs. 3.6 ± 0.9 pg/ ml) and bFGF (21.7 ± 10.3 vs. 4.75 ± 2.2 pg/ml.), while VEGF was significantly decreased (190 ± 115 vs. 210 ± 142 pg/ml) in blood of DMD patients compared to controls. Conclusion: Results provide further proof that inflammatory response is associated with DMD pathogenesis and favours the use of biomarkers in blood of such patients as a non invasive technique. Keywords:(basic fibroblast growth factor (bFGF), duchene muscular dystrophy, necrosis factor alfa (TNF TNF-α), vascular endothelial growth factor (VEGF)).Egyptian Journal of Medical Human Genetics Vol. 9 (2) 2008: pp. 181-18

Assessment of immune function in Down syndrome patients

In Down syndrome (DS), trisomy 21 leads to overexpression of gene coding for specific enzymes. This overexpression translates directly into biochemical aberrations that affect multiple interacting metabolic pathways which culminates in cellular dysfunction and contributes to the unique pathogenesis of DS. The aim of this study is to evaluate parameters of immune response in terms of cytokines [tumor necrosis factor-a (TNF-a) and interlukin-2 (IL-2)] together with the quantitative expression of cystathionine beta synthase (CBS), whose transsulfuration pathway generates cysteine and hydrogen sulfide (H2S). H2S is known to boost host defense at physiological concentrations and to display cytotoxic activity at higher concentrations. Calcineurin activity (CAN) was also measured as its dysregulation has been shown to cause immune  suppression. Subjects were 60 DS patients vs. 30 age and socioeconomic matching healthy controls. In their blood, the cytokines: TNF-a and IL-2, together with CBS and its by product H2S as well as CAN activity, were measured. Results showed that CBSmRNA relative expression (0.56± .06 vs. 0.32 ± .02), plasma H2S (72 ±8.5 vs. 50.8 ± 4.1) and TNF-a (8.11 ± .01 vs. 3.6± 0.9) were significantly higher among DS patients compared to controls, while CAN (0.27 ± 0.1 vs. 0.45 ±0.2 units), was significantly decreased in blood of DS patients compared to controls. IL-2 (36.4 ± 2.6 vs. 37.4 ±0.9) showed no significant difference between DS patients and controls. Accordingly it can be concluded that excessive synthesis of multiple gene products derived from overexpression of the genes present on chromosome 21 may be the cause for decreased immunity in DS patients compared to controls

Caveolin 3 gene and mitochondrial tRNA methionin gene in Duchenne muscular dystrophy

Background: It was recently reported that Duchene muscular dystrophy(DMD) patients and mdx mice have elevated levels of caveolin-3 expression in their skeletal muscles. However, it remains unknown whether this increased caveolin-3 levels contribute to the pathogenesis of DMD. Also mitochondrial DNA mutation in the tRNA methionin (tRNA Met) gene has been shown to be associated with muscle weakness, severe exercise intolerance, lactic acidosis and growth retardation. Since DMD is X-linked maternally inherited disease, mitochondrial mutation in tRNA (Met) gene can be suspected to be the cause for the inefficient splicing of dystrophin gene during its expression and can be implicated as the cause of dystrophin inactive protein. Aim of the Work: The aim of the present study is to investigate whether mutations in caveolin gene leads to its increased expression and/or mutation in the tRNA (Met) gene can be associated with DMD pathogenesis. Patients and Methods: Expression of caveolin mRNA by RT-PCR and mutations in caveolin gene and tRNA (Met) gene were measured in 28 patients presented with DMD symptoms using the single strand conformation polymorphism assay (SSCP). Results: Results gave further proof to decreased expression of inducible nitric oxide synthase (iNOS) mRNA, which leads to increased expression in caveolin3 mRNA in lymphocytes of DMD patients compared to controls. However using SSCP, there was no evidence for tRNA (Met) gene mutation among DMD patients and only one patient presented a mutation in the caveolin gene compared to controls. Conclusion: There is an inverse relation between iNOS and Caveolin 3 in lymphocytes of DMD patients compared to controls. However, Caveolin 3 gene mutation is excluded as the main cause of increased caveolin gene expression. Also, there was no evidence for tRNA (Met) gene mutation among DMD patients.Keywords: mRNA, duchene muscular dystrophy (DMD), inducible nitric oxide synthase (iNOS) mRNA, mitochondrial DNA

Indicators of Apoptosis in Duchenne Muscular Dystrophy Patients

Background: Tissue sections of dystrophic muscle demonstrate apoptotic myonuclei in degenerating muscle fibers of Duchene muscle dystrophy (DMD) patients. The apoptosis cascade can be triggered by 2 main pathways, via an intrinsic, endogenous system such as the mitochondrial Bax/Bcl-2 or via an extrinsic system involving transmembrane receptors of the death receptor family Fas and Fas Ligand (FasL). Aim of the Work: The present study is an attempt to demonstrate the levels of Fas and FasL and Bax/Bcl-2 in DMD pathogenesis. Patient and Methods: Subjects were 16 boys with DMD diagnosed clinically and at the molecular level versus 20 age and socioeconomic matching healthy boys. Results: Plasma DNA fragmentation (0.38%±0.12 vs. 0.2%±.0.1.5) and Fas (9.9±2.8 vs. 2±0.1,

Citric acid strongly inhibits visceral pain response in mice

Citric acid introduced into the stomach of mice at increasing concentrations of 0.1, 1 or 10 % (4.8 µM-0.48 mM; 95 µmol/kg-9.5 mmol/kg, 0.5 ml) caused dose-dependent inhibition of abdominal constrictions induced 1 h later by i. p. acetic acid injection by -51 % to -69.5 %. When administered at 10 % (0.48 mM, 0.5 ml) 15 min before nociceptive challenge, citric acid inhibited the nociceptive response by 96.8 %. Inhibition of the acetic acid-induced abdominal constrictions was also observed when lower doses of citric acid were introduced into the stomach (0.2 ml of 0.1-1 %; 38.1 µmol/kg-0.38 mmol/kg). The effect was evident as early as 5 min after administration of citric acid into the stomach and with the maximal effect being at 15-30 min after dosing. Lidocaine given orally 5 min prior to citric acid (1 %, 48 µM; 0.38 mmol/kg, 0.2 ml) prevented antinociception by citric acid, but lidocaine given 15 min before oral introduction of citric acid enhanced the citric acid-induced inhibition of the nociceptive response to acetic acid. The antinociceptive effect of orally administered citric acid (1 %, 48 µM; 0.38 mmol/kg, 0.2 ml) was increased by pre-treatment with propranolol (4 mg/kg, s. c.), yohimbine (4 mg/kg, s. c.), guanethidine (32 mg/kg, s. c.), but reduced after treatment with atropine (3 mg/kg, s. c.), which itself increased the nociceptive behavior. Similar inhibition of the acetic acid-induced nociceptive behavior was also observed when sodium citrate (pH 7.21) or 0.1 N HCl (pH 3) or 1 % sucrose solution (0.2 ml) was intragastrically given. It is suggested that citric acid might act to stimulate sensory afferents and that transmission of nociceptive information centrally leads to the activation of descending antinociceptive mechanism to a noxious stimulus

Markers of neural degeneration and regeneration in Down syndrome patients

On the trisomy Down syndrome Critical Region (DSCR1) is located the APP gene, which accelerates amyloid peptide protein (APP) expression leading to cerebral accumulation of APP-derived amyloid-beta peptides (Ab) and age-dependent cognitive sequelae. Also DSCR1 attenuates endothelial cell proliferation and angiogenesis required for tissue repair. The aim of the present work is to determine markers of neural degeneration and regeneration in the blood of young and adolescent Down syndrome (DS) patients as well as controls. Markers of regeneration were measured in terms of circulating mononuclear cells expressing Nestin and CD34, while markers of degeneration were measured in terms of plasma Ab42 and advanced glycation end products receptors (RAGES). Results showed a significant increase in plasma Ab42 (20 ± 5.1 vs. 11.9 ± 3.4) and RAGES leucocytes mRNA relative expression (1.9 ±0.2 vs. 1.1 ±0.6) in adolescentDS patients compared to young DS. Both parameters were also significantly increased in DS compared to controls: Ab42 (15.4 ± 5.9 vs. 12. 3± 4.5); RAGES (1.4 ± 0.5 vs. 0.7± 0.2). Nestin (5.2 ± 1.4 vs. 6.3± 0.6) and CD34 (52 ± 2.5 vs. 53± 4.7) were non-significantly lower in adolescent DS patients compared to young DS, but significantly lower in DS patients compared to controls: Nestin (6.3 ± 1.5 vs. 9±4.4); CD34 (54 ± 3.4 vs. 60± 4.8). The significant decrease in the number of mononuclear cells bearing Nestin and CD34 markers accompanied by a significantincrease in Ab42 and RAGES indicate that degeneration in DS is an ongoing process, which is not counterbalanced by the regenerative mechanism

Assessment of plasma and urinary transforming growth factor beta 1 (TGF-β1) in children with lupus nephritis

Background: Kidney disease is one of the most serious manifestations of systemic lupus erythematosus (SLE). Despite the improvement in the medical care of SLE in the past two decades, the prognosis of lupus nephritis remains unsatisfactory. Transforming growth factor- β1 (TGF-β1) is an immunosuppressive cytokine, as it inhibits T and B cell proliferation and NK cell cytotoxic activity . Objective: The aim of this study was to assess serum and urinary TGF- β1 levels in children with SLE and their possible role in the renal involvement and activity of the disease. Study design: This cross sectional study was conducted in Nephrology Unit of Pediatric Department, plus Outpatient Clinic of Rheumatology Department, Zagazig University Hospital during the year of 2010. Methods: Twenty-five pediatric patients with SLE were randomly selected and classified according to into 2 groups: Group (Ι): included 13 patients presented with urinary abnormalities and/or disturbed renal function(active nephritis): 5 males, 8 females. Their mean age was 9.7±2.53 years and the mean disease duration was 2.46±1.4 years. Group (ΙΙ): included 12 patients presented by lupus without nephritis : 5 males,7 females. Their mean age was 9.9±2.1 years and the mean disease duration was 2.41±0.9 years. Control group(group ΙΙΙ): Twenty healthy children of matched age and sex served as a control group included 8 males ,12 females. Their mean age was 10.0±2.3 years. Results: There was no significant difference among studied patients groups regarding age, sex , disease duration and lupus therapy (p>0.05). There was a significant difference between both groups regarding urinary albumin and serum creatinine (2.76±0.97 and 1.96±0.84 mg/dl respectively), while there was a high significant difference between them regarding C3 (47.3±12.5 and 76.6±6.6 mg/ml respectively) and anti double stranded DNA (anti-dsDNA) (80.7±32.8 and 26.8±4.5 IU/ml respectively). Plasma TGF- β1 showed significantly lower levels in patients with active nephritis relative to other groups, while urinary TGF- β1 levels were significantly high in SLE patients either with active or silent nephritis when compared with the control group. Plasma TGF- β1 showed a highly significant positive correlation with C3 and a highly significant negative correlation with serum creatinine, urinary albumin, anti dsDNA and SLE disease activity index (SLEDAI) score. While, urinary TGF- β1 had a significant negative correlation with C3 and a high significant positive correlation with anti-dsDNA and SLEDAI score. Conclusion: Low plasma TGF β1 level and increased urinary TGF β1 excretion denotes active renal affection in children with SLE.Keywords: SLE , nephritis , TGF- β1Egypt J Pediatr Allergy Immunol 2011;9(1):21-2