Effects of feed composition on the fouling on cation-exchange membranes desalinating polymer-flooding produced water.

HYPOTHESIS: Cation exchange membranes (CEMs) are subject to fouling when utilized to desalinate wastewater from the oil and gas industry, hampering their performance. The kind and extent of the fouling are most likely dependent on the composition of the stream, which in practical applications can vary significantly. EXPERIMENTS: Fouling experiments were performed on commercial cation exchange membranes, which were used in electrodialysis runs to desalinate solutions of varying composition. The variations included ionic strength, type of ions, amount of viscosifying polyelectrolyte (partially hydrolyzed polyacrylamide), presence of crude oil, and surfactants. Performance parameters, like electric potential and pH, were monitored during the runs, after which the membranes were recovered and analyzed. FINDINGS: Fouling was detected on most CEMs and occurred mainly in the presence of the viscosifying polyelectrolyte. Under normal pH conditions (pH ~ 8), the polyelectrolyte fouled the concentrate side of the CEMs, as expected due to electrophoresis. However, by applying a current in the opposite direction, the polyelectrolyte layer could be removed. Precipitation occurred mostly on the opposite side of the membrane, with different morphology depending on the feed composition.

Influence of solution composition on fouling of anion exchange membranes desalinating polymer-flooding produced water.

HYPOTHESIS: Anion exchange membranes (AEMS) are particularly prone to fouling when employed to desalinate polymer flooding produced water (PFPW), an abundant sub-product from the oil and gas industry. The formation of fouling on an AEM will be affected by the composition of the solution, which includes various dissolved salts, partially hydrolyzed polyacrylamide (HPAM), crude oil, and surfactants. EXPERIMENTS: Electrodialysis experiments were performed to desalinate feed solutions with different compositions, aiming to distinguish between their individual and combined effects. The solutions contained diverse mono- and divalent ions. The analysis included data collected during the desalination and characterization of the fouled AEMs by diverse analytical techniques. FINDINGS: HPAM produced the most severe effects in terms of visible fouling and increase of resistance. This polyelectrolyte fouls the AEM by adsorbing on its surface and by forming a viscous gel layer that hampers the replenishment of ions from the bulk solution. Ca and Mg have a large influence on the formation of thick HPAM gel layers, while the oily compounds have only a minimal influence acting mainly as a destabilizing agent. The membranes also presented scaling consisting of calcium precipitates. The effects of the gel layer were minimized by applying current reversal and foulant-free solution.

Synthesis and biological evaluation of novel pyrazoles and indazoles as activators of the nitric oxide receptor, soluble guanylate cyclase.

Database searching and compound screening identified 1-benzyl-3-(3-dimethylaminopropyloxy)indazole (benzydamine, 3) as a potent activator of the nitric oxide receptor, soluble guanylate cyclase. A comprehensive structure-activity relationship study surrounding 3 clearly showed that the indazole C-3 dimethylaminopropyloxy substituent was critical for enzyme activity. However replacement of the indazole ring of 3 by appropriately substituted pyrazoles maintained enzyme activity. Compounds were evaluated for inhibition of platelet aggregation and showed a general lipophilicity requirement. Aryl-substituted pyrazoles 32, 34, and 43 demonstrated potent activation of soluble guanylate cyclase and potent inhibition of platelet aggregation. Pharmacokinetic studies in rats showed that compound 32 exhibits modest oral bioavailability (12%). Furthermore 32 has an excellent selectivity profile notably showing no significant inhibition of phosphodiesterases or nitric oxide synthases.

Evidence that axon-derived neuregulin promotes oligodendrocyte survival in the developing rat optic nerve.

It was previously shown that newly formed oligodendrocytes depend on axons for their survival, but the nature of the axon-derived survival signal(s) remained unknown. We show here that neuregulin (NRG) supports the survival of purified oligodendrocytes and aged oligodendrocyte precursor cells (OPCs) but not of young OPCs. We demonstrate that axons promote the survival of purified oligodendrocytes and that this effect is inhibited if NRG is neutralized. In the developing rat optic nerve, we provide evidence that delivery of NRG decreases both normal oligodendrocyte death and the extra oligodendrocyte death induced by nerve transection, whereas neutralization of endogenous NRG increases the normal death. These results suggest that NRG is an axon-associated survival signal for developing oligodendrocytes.

Use of health services by the climacteric women in primary health care: the need for an integral approach.

During the climacteric, women experience multiple health problems. As their needs are not catered for in an integral fashion due to the lack of any specific programme or mechanism to provide for this, they show an increased use of the health services, and an increased rate of referrals to different specialists. This study, carried out in a Basic Health Zone in San Fernando (Cádiz, Andalusía, Spain) on a sample of climacteric women who attended the Health Centre during 1995, examines these points and shows a significantly higher use of the health services in relation to the rest of the female population (those who are not in the climacteric age group) as well as a high percentage of referrals (74.6%) to specialists. It was found that both the level of knowledge about the climacteric and the use of the health services were influenced by the educational level (p < 0.001) and age (p < 0.05). Women who felt that their families provided an understanding and supportive attitude were found to have less psychological problems and, consequently, less consultations and referrals for this reason (p < 0.00001). The authors hope that their findings will provide a basis for the setting up of a programme of integral health care for climacteric women at the level of primary health care. With careful planning and the drawing up of a strategic plan, it would be possible to provide for the needs of this population group in a more satisfactory way, and it would also permit a rationalization of the resources available.

Bax and Bak proteins require caspase activity to trigger apoptosis in sympathetic neurons.

We show that the pro-apoptotic proteins Bax and Bak trigger apoptosis when over-expressed in sympathetic neurons cultured in the presence of NGF. This effect can be blocked with z-VAD-fmk, a peptide inhibitor of caspases, but not with anti-apoptotic chemical compounds such as antioxidants or proteasome inhibitors. These results demonstrate that in sympathetic neurons Bax and Bak are sufficient to induce apoptosis in the absence of any other apparent cell death stimulus and that their effect is mediated by caspases but does not require reactive oxygen species nor activity of the proteasome.

Involvement of the proteasome in the programmed cell death of NGF-deprived sympathetic neurons.

Sympathetic neurons undergo programmed cell death (PCD) upon deprivation of nerve growth factor (NGF). PCD of neurons is blocked by inhibitors of the interleukin-1beta converting enzyme (ICE)/Ced-3-like cysteine protease, indicating involvement of this class of proteases in the cell death programme. Here we demonstrate that the proteolytic activities of the proteasome are also essential in PCD of neurons. Nanomolar concentrations of several proteasome inhibitors, including the highly selective inhibitor lactacystin, not only prolonged survival of NGF-deprived neurons but also prevented processing of poly(ADP-ribose) polymerase which is known to be cleaved by an ICE/Ced-3 family member during PCD. These results demonstrate that the proteasome is a key regulator of neuronal PCD and that, within this process, it is involved upstream of proteases of the ICE/Ced-3 family. This order of events was confirmed in macrophages where lactacystin inhibited the proteolytic activation of precursor ICE and the subsequent generation of active interleukin-1beta.

p53 protein in sympathetic neurons: cytoplasmic localization and no apparent function in apoptosis.

The p53 tumour suppressor gene plays a major role in controlling cell cycle and apoptosis in many different cell types. Here we have examined the status and the potential apoptosis inducing activity of p53 in sympathetic neurons. The p53 protein is expressed in rat sympathetic neurons cultured in the presence of NGF. The protein is not upregulated when these neurons are induced to die upon NGF deprivation. Over-expression of wild-type human p53 in neurons cultured in the presence of NGF does not trigger apoptosis nor does it accelerate apoptosis when the neurons are deprived of NGF. Finally endogenous p53 expression is not necessary for neuronal cell death triggered by NGF deprivation since neurons prepared from p53 knockout mice undergo normal cell death upon NGF deprivation. Our results suggest that p53 may have an unknown function in post-mitotic neurons which is distinct from its well described roles in apoptosis or cell cycle control.

Function and expression of the Bcl-x gene in the developing and adult nervous system.

We have shown that overexpression of Bcl-x can rescue sympathetic neurones from nerve growth factor deprivation in vitro. We have also examined the distribution and expression of Bcl-x mRNA in the developing and adult nervous system using Northern blot and in situ hybridization. Bcl-x mRNA is widespread during development of the nervous system. In embryonic spinal cord, mRNA levels increase at the beginning of the naturally occurring cell death period, suggesting that Bcl-x may be involved in the selection of neurones during this period. In the brain, Bcl-x expression increases after birth to reach a high level in the adult brain. Neurones from the cortex, olfactory bulb, and Purkinje cells are among those expressing the highest levels of Bcl-x mRNA. The widespread expression of Bcl-x during development and in adult brain suggests of a role for Bcl-x beyond simply protecting neurones from developmental cell death.

Expression of apogens and engulfens during programmed cell death in the nervous system of the chick embryo.

Two categories of cell death related to antigens, apogens and engulfens, have been reported to be expressed by apoptotic cells and the cells involved in their engulfment in the immune system, and in mesenchymal tissue in the limb of the chick embryo (ROTTELLO et al., 1994). To determine whether these antigens are also expressed during the process of neuronal death, the distribution of immunoreactivity to both anti-apogen and anti-engulfen antibodies was examined in the spinal cord and the dorsal root ganglia of the chick embryo. Anti-apogen antibodies labeled a sub-population of the profiles of dying cells in regions where cell death was occurring. The extent of labeling by anti-apogens varied from 3% to 70% of the total number of dying profiles depending on the specific antibody used and the neuronal region examined. Immunoreactive labeling by the anti-engulfen antibodies mainly involved large cells that contained debris of dead cells. These results indicate that at least some dying neuronal cells express common antigens that are shared by dying mesenchymal cells during programmed cell death, and that phagocytotic cells of the immune system are involved in the engulfment of neuronal cells that have undergone programmed cell death.

[Non-surgical extraction of intravascular foreign bodies in children. Experience with 8 cases]. / Extracción no quirúrgica de cuerpos extraños intravasculares en niños. Experiencia en 8 casos.

BACKGROUND AND OBJECTIVES: Foreign body retrieval in the catheter room is a useful procedure at any age, but, although its interest, few reports of such technique have been reported in children. METHODS: We review and present our experience in 8 children, aged 5 days to 11 years, five of them having congenital hearts defects. RESULTS: We retrieved 4 catheter fragments, 2 endocardial electrode catheter tips, 1 Rashkind 12 mm. PDA umbrella, and 1 detachable Jackson coil. All of them were placed in systemic veins, right heart chambers or pulmonary arteries. We used biplane fluoroscopy and percutaneous right femoral vein puncture in all cases. Goose-Neck (Microvena Corporation) snares were used in 5 patients, hand made snares in 2 and a Swan-Ganz catheter in one. In 4 cases, the snare was introduced trough a Mullins long sheath and the foreign body pulled into its distal end, in order to bring it out of the femoral vein. Six foreign bodies came off the femoral vein: 4 trough the puncture site and 2 needing a venous cut-down. The two remaining foreign bodies, stopped while pulling at the common iliac vein and a minor surgical procedure was needed for final extraction. CONCLUSIONS: Therapeutic catheterization is the technique of choice for intravascular foreign body retrieval in children.

Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.

To study molecular mechanisms underlying neuronal cell death, we have used sympathetic neurons from superior cervical ganglia which undergo programmed cell death when deprived of nerve growth factor. These neurons have been microinjected with expression vectors containing cDNAs encoding selected proteins to test their regulatory influence over cell death. Using this procedure, we have shown previously that sympathetic neurons can be protected from NGF deprivation by the protooncogene Bcl-2. We now report that the E1B19K protein from adenovirus and the p35 protein from baculovirus also rescue neurons. Other adenoviral proteins, E1A and E1B55K, have no effect on neuronal survival. E1B55K, known to block apoptosis mediated by p53 in proliferative cells, failed to rescue sympathetic neurons suggesting that p53 is not involved in neuronal death induced by NGF deprivation. E1B19K and p35 were also coinjected with Bcl-Xs which blocks Bcl-2 function in lymphoid cells. Although Bcl-Xs blocked the ability of Bcl-2 to rescue neurons, it had no effect on survival that was dependent upon expression of E1B19K or p35.

Expression of a specific marker of avian programmed cell death in both apoptosis and necrosis.

Apoptosis and necrosis are two types of cell death with different morphologic features. We report here the isolation of a monoclonal antibody, BV2, that specifically recognizes cells undergoing developmental programmed cell death in different tissues of the chicken and zebra-finch embryos. The antigen recognized by BV2 monoclonal antibody is detected in vitro in primary chicken embryonic fibroblasts induced to die by actinomycin D, as well as fibroblasts induced to die by chemical anoxia. The expression of this specific antigen during necrosis appears to require active protein synthesis. These findings provide evidence that cells from different embryonic tissues undergoing programmed cell death during vertebrate development express similar antigens and indicate that apoptosis and necrosis may share similar biochemical features.

Anti-apogens and anti-engulfens: monoclonal antibodies reveal specific antigens on apoptotic and engulfment cells during chicken embryonic development.

We have isolated a group of monoclonal antibodies that specifically recognize either apoptotic or engulfment cells in the interdigit areas of chicken hind limb foot plates, and throughout the embryo. Ten of these antibodies (anti-apogens) detect epitopes on dying cells that colocalize to areas of programmed cell death, characterized by the presence of apoptotic cells and bodies with typical cellular and nuclear morphology. Our results indicate that cells destined to die, or that are in the process of dying, express specific antigens that are not detectable in or on the surface of living cells. The detection of these apoptotic cell antigens in other areas of programmed cell death throughout the chick embryo indicates that different cell types, which form specific tissues and organs, may utilize similar cell death mechanisms. Six of the monoclonal antibodies (antiengulfens) define a class of engulfment cells which contain various numbers of apoptotic cells and/or apoptotic bodies in areas of programmed cell death. The immunostaining pattern of the anti-engulfen R15F is similar to that of an antibody against a common leukocyte antigen, suggesting the participation of cells from the immune system in the removal of apoptotic cell debris. These novel monoclonal antibody markers for apoptotic and engulfment cells will provide new tools to assist the further understanding of developmental programmed cell death in vertebrates.

Prevention of vertebrate neuronal death by the crmA gene.

Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.

Immunochemical studies of a murine polyreactive IgG2b autoantibody with rheumatoid factor activity.

The hybridoma, 62H3, which secretes a monoclonal IgG2b with anti-HLA-DR specificity, was expanded in pristane-primed BALB/c mice and the antibody was isolated from the ascitic fluid by affinity chromatography on Protein A-Sepharose. The purified IgG2b antibody was tested by an enzyme immunoassay for antibody activity against a panel of 40 self and non-self antigens. It was found to react strongly with beta-galactosidase, actin, glutamate dehydrogenase, rabbit and human IgG and di- and trinitrophenyl groups; and moderately with tubulin, insulin and phosphorylcholine; but it did not react with various other self and non-self antigens, such as DNA, albumin, keyhole limpet hemocyanin, hen lysozyme and horseradish peroxidase. Fab and Fc fragments were prepared from this IgG2b by papain proteolysis. The Fab fragment possessed the same spectrum of polyreactivities as the native IgG2b, whereas no activity was detected with the Fc fraction. In order to investigate the properties of the antigen binding site, the actin, TNP and rabbit IgG antibody activities were studied in more detail by enzyme immunoassay, Western blot and immunocytochemistry. The monomolecular nature of this multireactivity was confirmed by immunoabsorption analysis. Furthermore, 62H3 monoclonality was also verified by comparative isoelectric focusing and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis with other monospecific antibodies. The dissociation constants (Kd) of antigen-antibody equilibria in solution were measured. The Kd for actin was 1.11 +/- 0.24 x 10(-5) M and the Kd for TNP-BSA was 8.7 +/- 0.51 x 10(-7) M. No interaction with rabbit IgG could be detected in solution. These findings raise the question of the possible implication in autoimmune pathology or in normal physiology of IgG class polyspecific antibodies with solid-phase restricted cross-reactive rheumatoid factor activity.

[Fallot's tetralogy with severe symptomatology during the first year of life (author's transl)]. / Tetralogía de Fallot grave en el primer año de vida. Aspectos clínicos e implicaciones quirúrgicas

Seventeen cases of Fallot's Tetralogy with severe symptomatology during the first year of life are reviewed. In all of them, a cardiac catheterization and angiocardiography were performed. In 2 cases the pulmonary outflow tract was atretic. In general, the clinical, radiologic, electrocardiographic and hemodynamic findings were similar to those previously reported, although in 3 patients of the present series atypical electrocardiographic findings were found. Pronounced narrowing and horizontal orientation of the infundibular chamber, and accentuated hypoplasia of the pulmonary artery branches and of the left heart cavities and were all unfavourable findings for total correction frequently found in the present material. Minimal or non-existent aortic dextroposition was observed in association with cases of Fallot's Tetralogy with extreme severity. Surgery was indicated as an emergency measure in the majority of the cases. Palliatives procedures were performed in 10 patients, and corrective surgery in one. Surgical results agree with the extreme severity that this lesion has, when it gives rise to important symptomatology so early in the life.