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At least 1,099 records · Page 61Linked to original sources
PubMed2004

Nucleophosmin sets a threshold for p53 response to UV radiation.

Because activation of p53 can trigger cell cycle arrest and apoptosis, it is necessary for a cell to suppress this activation until it is absolutely required for survival. The mechanisms underlying this important regulatory event are poorly understood. Here we show that nucleophosmin (NPM) acts as a natural repressor of p53 by setting a threshold for p53 activation in response to UV radiation. NPM binds to the p53 N terminus and inhibits p53 transcriptional activity by more than 70%. Our data indicate that the levels of NPM in a cell determine the UV dose at which the tumor suppressor p53 can be phosphorylated on Ser15. Moreover, we show that NPM is a substrate for the UV-activated protein kinase ATR and inhibits the UV-induced p53 phosphorylation at Ser15. In addition, NPM forms a complex with p53 and ATR in vivo. These data suggest that NPM is an early responder to DNA damage that prevents premature activation of p53. In normal cells, NPM could contribute to suppressing p53 activation until its functions are absolutely required while in cancer cells overexpression of NPM could contribute to p53 inactivation and tumor progression.

Cell Line, Tumor↗
PubMed1991

X linked alpha thalassaemia/mental retardation: spectrum of clinical features in three related males.

We describe three males (two brothers and a cousin) who have the X linked alpha thalassaemia/mental retardation (ATR-X) syndrome. The diagnosis, originally suspected in the brothers because of similarity in dysmorphic features to previous cases, was confirmed haematologically in the surviving brother. The cousin has less typical dysmorphism and a virtually normal routine blood count, but haemoglobin H inclusions were found in his red blood cells showing that he has the same condition. This report expands the clinical phenotype of the ATR-X syndrome and emphasises that a normal blood count does not exclude the diagnosis.

Adolescent↗
PubMed2006

Caspase-mediated cleavage of ATM during cisplatin-induced tubular cell apoptosis: inactivation of its kinase activity toward p53.

Cisplatin induces renal cell injury and death, resulting in nephrotoxicity that limits its use in cancer therapy. Using cell culture models, recent work has suggested the involvement of p53 in renal cell apoptosis during cisplatin treatment. However, the signals upstream of p53 remain elusive. ATM and ATR are critical regulators of p53 under various conditions of DNA damage. Here, we show that ATM, and not ATR, was proteolytically cleaved into specific fragments of approximately 210 and 150 kDa during cisplatin-induced tubular cell apoptosis. ATM cleavage was paralleled by the development of apoptosis. VAD, a broad-spectrum inhibitor of caspases, attenuated the cleavage of ATM, whereas the inhibitors of specific caspases were less effective. In caspase-3-deficient MCF-7 cells, ATM was cleaved, releasing the 210- but not the 150-kDa fragment. Recombinant caspase-3 was much more effective than caspase-7 in cleaving ATM that was immunoprecipitated from cell lysates. During cisplatin incubation, VAD protected ATM and enhanced p53 phosphorylation. In vitro assay of protein kinase activity further showed that ATM immunoprecipitated from cisplatin-treated cells had significantly lower kinase activity toward p53 than that from control cells. Importantly, the protein kinase activity was restored in ATM that was protected by VAD during cisplatin incubation. ATM deficiency sensitized the cells to cisplatin-induced apoptosis, suggesting a cytoprotective role of ATM in this experimental model. Thus proteolysis of ATM by caspases may inactivate this regulatory molecule to facilitate the progression of apoptosis.

Animals↗
PubMed1986

An intracellular study of myenteric neurons in the mouse colon.

Intracellular recordings have been made in vitro from the myenteric neurons of the distal colon of normal littermates of the piebald-lethal mouse. Out of a total of 90 neurons, 82 were classified as S/type 1 cells and 8 as AH/type 2 cells. Seventy-eight out of 82 S cells showed spontaneous fast excitatory postsynaptic potentials (EPSPs) sensitive to d-tubocurarine (dTC, 280 microM), and 22 S cells showed spontaneous action potentials (APs). Six S cells and 1 AH cell showed spontaneous nonnicotinic slow depolarizations associated with an increase in the input resistance of the cells; during the spontaneous slow depolarization in the S cells there was an increase in the frequency of nicotinic fast EPSPs and APs. Three S cells showed spontaneously occurring regular oscillations of the membrane potential (approximately mV in amplitude and approximately 4/min). Transmural nerve stimulation produced fast EPSPs with a wide range of latencies (3 ms to 20 s) in S cells; the fast EPSPs were blocked by dTC (280 microM) or solutions containing low Ca2+ (0.25 mM) and high Mg2+ (12 mM) but not by atropine (ATR, 14 microM). Single or repetitive transmural stimulation produced slow EPSPs in 24 S cells and 3 AH cells; these were not blocked by dTC (280 microM) nor ATR (14 microM). During the slow EPSPs there was an increase in the input resistance of the cells. In those S cells that showed slow EPSPs there were many long-latency fast EPSPs; long-latency fast EPSPs were also observed in 11 other S cells that did not show a slow EPSP following repetitive transmural nerve stimulation. Long-latency fast EPSPs may be related to the firing of other neurons during their slow EPSPs. The myenteric neurons in the mouse colon have similar properties to the myenteric neurons in the guinea pig small intestine. However, the colonic myenteric neurons show more ongoing synaptic activity and more prolonged activity after nerve stimulation than myenteric neurons in the guinea pig small intestine. This activity may be due to regional differences, species differences, or preparation differences (in this study the myenteric plexus was adherent to the underlying circular muscle layer).

Action Potentials↗
PubMed1992

Catecholamine and acetylcholine sensitivity of rat lateral hypothalamic neurons related to learning.

1. Unit activity in the rat lateral hypothalamus (LHA) was recorded during discrimination learning of cue tone (CTS) or cue light (CL) stimulation that predicted reward by glucose or intracranial self stimulation (ICSS), or aversion by weak electric shock or tail pinch. Roles of the catecholaminergic and cholinergic systems in the LHA were investigated by electrophoretic application of dopamine (DA), norepinephrine (NE), acetylcholine (ACh), and their antagonists [spiperone (SPP), phenoxybenzamine (PBZ), phentolamine, propranolol, and atropine (Atr)]. 2. Activity of 264 LHA neurons was recorded. Of these, 234 (89%) responded during CTS learning in one or more phases. Of 121 neurons tested by both rewarding and aversive stimuli, 86 (71%) discriminated reward and aversion and their respective CTSs. 3. Effects of DA on 138, NE on 134, and ACh on 73 neurons were tested. Among these, 67 were tested with all three. DA inhibited 40 and excited 14. NE inhibited 74 and excited 10. ACh excited 35 and inhibited 3. DA-sensitive neurons responded to both NE (P less than 0.001) and ACh (P less than 0.05) more often than DA-insensitive neurons. In most cases, the effect of DA was similar to the effect of NE, and opposite to the effect of ACh. The inhibitory effect of DA was blocked by SPP, a D2 antagonist, and the excitatory effect of ACh was blocked by Atr. The inhibitory effect of NE was blocked by the beta-antagonist, propranolol, and enhanced by the alpha-antagonist, phentolamine. 4. DA-sensitive neurons responded to both rewarding and aversive stimuli and respective CTS+ and CTS- more often than DA-insensitive neurons (P less than 0.01). The effect of DA was usually similar to the effect of rewarding stimuli and their predicting CTS+ and was opposite to the effect of aversive stimuli and their predicting CTS-. 5. The proportion of NE-sensitive neurons that responded to rewarding and aversive stimuli was the same as the proportion of NE-insensitive neurons that responded to the same stimuli. NE-sensitive neurons responded to CTS+ and CTS- more often than NE-insensitive neurons (P less than 0.01). The effect of NE was usually similar to the effect of rewarding stimuli and predicting CTS+, and opposite to the effect of aversive stimuli and predicting CTS-. 6. ACh-sensitive neurons responded to aversive stimuli and predicting CTS- more often than ACh-insensitive neurons (P less than 0.01), but the response ratio of ACh-sensitive neurons to rewarding stimuli was similar to that of ACh-sensitive neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed2005

Valosin-containing protein phosphorylation at Ser784 in response to DNA damage.

The response of eukaryotic cells to DNA damage includes the activation of phosphatidylinositol-3 kinase-related kinases (PIKK), such as ATM, ATR, and DNA-dependent protein kinase (DNA-PK). These three kinases have very similar substrate specificities in vitro, but in vivo, their substrates overlap only partially. Several in vivo substrates of ATM and ATR have been identified and almost all of them are involved in DNA damage-induced cell cycle arrest and/or apoptosis. In contrast, few in vivo substrates of DNA-PK have been identified. These include histone H2AX and DNA-PK itself. We identify here valosin-containing protein (VCP) as a novel substrate of DNA-PK and other PIKK family members. VCP is phosphorylated at Ser784 within its COOH terminus, a region previously shown to target VCP to specific intracellular compartments. Furthermore, VCP phosphorylated at Ser784 accumulated at sites of DNA double-strand breaks (DSBs). VCP is a protein chaperone that unfolds and translocates proteins. Its phosphorylation in response to DNA damage and its recruitment to sites of DNA DSBs could indicate a role of VCP in DNA repair.

Adenosine Triphosphatases↗
PubMed2006

The dispersal of replication proteins after Etoposide treatment requires the cooperation of Nbs1 with the ataxia telangiectasia Rad3-related/Chk1 pathway.

In mammalian cells, DNA replication takes place in functional subnuclear compartments, called replication factories, where replicative factors accumulate. The distribution pattern of replication factories is diagnostic of the different moments (early, mid, and late) of the S phase. This dynamic organization is affected by different agents that induce cell cycle checkpoint activation via DNA damage or stalling of replication forks. Here, we explore the cell response to etoposide, an anticancer drug belonging to the topoisomerase II poisons. Etoposide does not induce an immediate block of DNA synthesis and progressively affects the distribution of replication proteins in S phase. First, it triggers the formation of large nuclear foci that contain the single-strand DNA binding protein replication protein A (RPA), suggesting that lesions produced by the drug are processed into extended single-stranded regions. These RPA foci colocalize with DNA replicated at the beginning of the treatment. Etoposide also triggers the dispersal of replicative proteins, proliferating cell nuclear antigen and DNA ligase I, from replication factories. This event requires the activity of the ataxia telangiectasia Rad3-related (ATR) checkpoint kinase. By comparing the effect of the drug in cell lines defective in different DNA repair and checkpoint pathways, we show that, along with the downstream kinase Chk1, the Nbs1 protein, mutated in the Nijmegen breakage syndrome, is also relevant for this response and for ATR-dependent phosphorylation. Finally, our analysis evidences a critical role of Nbs1 in the etoposide-induced inhibition of DNA replication in early S phase.

Antineoplastic Agents, Phytogenic↗
PubMed2006

Chk1- and claspin-dependent but ATR/ATM- and Rad17-independent DNA replication checkpoint response in HeLa cells.

When DNA synthesis is inhibited, DNA replication checkpoint is activated to prevent mitosis entry without fully replicated DNA. In Xenopus, caffeine-sensitive kinases [ataxia telangiectasia mutated (ATM) and ATM-related protein (ATR)] are essential in this checkpoint response, but in mammal cells an ATR/ATM-independent checkpoint response to DNA synthesis inhibition exists. Using HeLa cells, which have a caffeine-insensitive checkpoint response, we have analyzed here which molecules known to be involved in the DNA replication checkpoint participate in the caffeine-insensitive response. When DNA synthesis was inhibited in the presence of UCN01 or after knocking down Chk1 expression [Chk1 small interfering RNA (siRNA)], HeLa cells entered into aberrant mitosis. Consequently, Chk1 is essential for both the ATR/ATM-dependent and ATR/ATM-independent checkpoint response in HeLa cells. Neither wortmannin, Ly294002, nor SB202190 abrogated the caffeine-insensitive checkpoint response, indicating that DNA-PK and p38 alpha,beta are not involved in the ATR/ATM-independent Chk1 activation upon DNA synthesis inhibition. Using siRNA to knock down Rad17 and claspin, two molecules involved in sensing stalled replication forks, we also showed that claspin but not Rad17 is essential for the ATR/ATM-independent checkpoint response. Inhibition of DNA synthesis in HeLa cells led to a decrease in cyclin B1 protein accumulation that was abrogated when UCN01 was added or when claspin was knocked down. We conclude that upon DNA synthesis inhibition, Chk1 can be activated in a claspin-dependent manner independently of ATR and ATM, leading to cyclin B1 down-regulation and providing the cells of an additional mechanism to inhibit mitosis entry.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Ras induces chromosome instability and abrogation of the DNA damage response.

Ras mutations are frequent in thyroid tumors, the most common endocrine malignancy. The ability of Ras to transform thyroid cells is thought to rely on its mitogenic activity. Unexpectedly, acute expression of activated Ras in normal rat thyroid cells induced a DNA damage response, followed by apoptosis. Notably, a subpopulation of cells evaded apoptosis and emerged with features of transformation, including the loss of epithelial morphology, dedifferentiation, and the acquisition of hormone- and anchorage-independent proliferation. Strikingly, the surviving cells showed marked chromosomal instability. Acutely, Ras stimulated replication stress as evidenced by the induction of ataxia telangiectasia mutated and Rad3-related protein kinase (ATR) activity (Chk1 phosphorylation) and of gammaH2A.X, a marker of DNA damage. Despite the activation of a checkpoint, cells continued through mitosis in the face of DNA damage, resulting in an increase in cells harboring micronuclei, an indication of defects in chromosome segregation and other forms of chromosome damage. Cells that survived exposure to Ras continued to exhibit replication stress (ATR activation) but no longer exhibited gammaH2A.X or full activation of p53. When rechallenged with Ras or DNA-damaging agents, the surviving cells were more resistant to apoptosis than parental cells. These data show that acute expression of activated Ras is sufficient to induce chromosomal instability in the absence of other signals, and suggest that Ras-induced chromosomal instability arises as a consequence of defects in the processing of DNA damage. Hence, abrogation of the DNA damage response may constitute a novel mechanism for Ras transformation.

Animals↗
PubMed2006

Fanconi anemia D2 protein confers chemoresistance in response to the anticancer agent, irofulven.

The Fanconi anemia-BRCA pathway of genes are frequently mutated or epigenetically repressed in human cancer. The proteins of this pathway play pivotal roles in DNA damage signaling and repair. Irofulven is one of a new class of anticancer agents that are analogues of mushroom-derived illudin toxins. Preclinical studies and clinical trials have shown that irofulven is effective against several tumor cell types. The exact nature of irofulven-induced DNA damage is not completely understood. Previously, we have shown that irofulven activates ATM and its targets, NBS1, SMC1, CHK2, and p53. In this study, we hypothesize that irofulven induces DNA double-strand breaks and FANCD2 may play an important role in modulating cellular responses and chemosensitivity in response to irofulven treatment. By using cells that are proficient or deficient for FANCD2, ATR, or ATM, we showed that irofulven induces FANCD2 monoubiquitination and nuclear foci formation. ATR is important in mediating irofulven-induced FANCD2 monoubiquitination. Furthermore, we showed that FANCD2 plays a critical role in maintaining chromosome integrity and modulating chemosensitivity in response to irofulven-induced DNA damage. Therefore, this study suggests that it might be clinically significant to target irofulven therapy to cancers defective for proteins of the Fanconi anemia-BRCA pathway.

Antineoplastic Agents, Alkylating↗
PubMedDate not supplied

Use of infrared attenuated total reflectance spectroscopy for the in vivo measurement of hydration level and silicone distribution in the stratum corneum following skin coverage by polymeric dressings.

The ability of wound dressings to hydrate the stratum corneum has been tested experimentally using attenuated total reflectance (ATR) infrared spectroscopy. A silicone gel dressing was able to hydrate the stratum corneum to the extent that its water content within the sampled volume was >60% after 5 h of contact compared with about 15% of normal exposed skin and about 30% for a highly permeable hydrophilic polyurethane dressing. An ATR method was devised to determine the presence and depth of penetration of silicone in the stratum corneum as a result of skin coverage by the polymeric dressing.

Algorithms↗
PubMedDate not supplied

The effect of liposomes on skin barrier structure.

The present work deals with the 'in vivo' stripping technique to evaluate the percutaneous absorption of sodium fluorescein (NaFl) vehiculized in two different liposome preparations formed by phosphatidylcholine (PC) and lipids mimicking the stratum corneum (SC; ceramides, cholesterol, palmitic acid and cholesteryl sulphate), respectively. Furthermore, the possible effect of these vesicles on the SC lipid alkyl chain conformational order were evaluated at different depths of SC by non-invasive biophysical techniques: Corneometer, Tewameter and especially ATR-FTIR. The results of NaFl percutaneous absorption indicate the highest penetration in the case of incorporation in PC liposomes, which could be related to the increase in SC lipid disorder detected by ATR-FTIR, i.e. a decrease in skin barrier function. On the other hand, SC lipid liposomes have been shown to have a higher affinity for SC owing to the high amount of NaFl found in this layer, suggesting a greater reservoir capacity of SC when similar lipid composition formulation is applied. A lipid order increase is observed by infrared spectroscopy, when these types of liposomes are topically applied, resulting in a strong barrier effect. These results could be useful in designing specific liposomal topical applications.

Adult↗
PubMed2006

Analysis of an approach to astigmatism correction during cataract surgery.

PURPOSE: To determine if a system of astigmatic keratomy at the time of cataract surgery is safe and effective. SETTING: Academic Ophthalmology Center. METHODS: One hundred and ten consecutive patients with greater than 0.50 diopters (d) of cylinder with the rule (WTR) and 0.75 d against the rule (ATR) were enrolled. Those with an axis between 16 and 74 degrees and 106 and 164 degrees were defined as oblique axis. Peripheral clear corneal relaxing incisions 600 mum deep were used with a nomogram of 60 degrees length per 1.0 d of attempted correction. Keratometry was taken from IOL Master biometry and refractive results at 4-12 weeks were compared. RESULTS: 60.5% of ATR, 62% of WTR and 23% of oblique attempted correction was achieved. Splitting the patients to under and over 70 years of age had no impact on the results. Of the 14 overcorrected, 7 had oblique cylinder (p = 0.009) and 10 had less than 1 d of preoperative cylinder (p = 0.00015). CONCLUSIONS: Using the IOL Master topography with this nomogram was quite effective in reducing preoperative cylinder. Oblique axis results were unpredictable, however, and much more likely to lead to an overcorrection.

Aged↗
PubMed1999

Genetic polymorphisms of the renin-angiotensin system and atheromatous renal artery stenosis.

Genes that influence the renin-angiotensin system have been investigated in recent years as potential etiologic candidates of cardiovascular and renal diseases. In atheromatous renal artery stenosis (RAS), a condition characterized by persistent activation of the renin-angiotensin system, the study of these genes may be of particular relevance. We evaluated angiotensin-converting enzyme (ACE) insertion/deletion, angiotensinogen (AGT) M235T, and angiotensin II receptor (ATR) A1166C polymorphisms in relation to the occurrence of RAS. We studied 58 patients with angiographically documented RAS; 102 normotensive subjects with normal coronary arteries and no history or clinical or instrumental evidence of atherosclerosis in other vascular districts were considered the control group. Patients had a significantly higher D allele frequency (0.70 versus 0.55; chi(2) 6.88, P=0.01; odds ratio [OR] 1. 9, 95% CI 1.17 to 3.07) than did the control population; 48.3% of patients were homozygous for DD (chi(2) 6.62, P<0.05; OR 2.04, 95% CI 1.05 to 3.95); and only 8.6% carried the II genotype (OR 0.34, 95% CI 0.19 to 1.47). No significant association was found for AGT M235T and ATR A1166C. Our results suggest a predisposing role for ACE genetic polymorphism in the development and progression of atheromatous RAS.

Adult↗
PubMed2002

Grafting sulfobetaine monomer onto the segmented poly(ether-urethane) surface to improve hemocompatibility.

Polyurethanes are widely used as blood-contacting biomaterials, due to their good biocompatibility and mechanical properties. Nevertheless, their blood compatibility is still not adequate for more demanding applications. Surface modification is an effective way to improve the hemocompatibility for biomaterials. The purpose of the present study was to synthesize a novel nonthrombogenic biomaterial by modifying the surface of polyurethane. Ozonization was used to introduce active peroxide groups onto the segmented poly(ether-urethane) (SPEU) film surface and graft polymerization of N,N'-dimethyl (methacryloyloxyethyl) ammonium propanesulfonate (DMAPS), a sulfobetaine structure, onto the ozone-activated SPEU surface was conducted. The SPEU-g-PDMAPS film was characterized by ATR-FTIR, XPS, and contact angle measurements. ATR-FTIR and XPS confirmed the graft polymerization. The grafted film possessed a relatively hydrophilic surface, as revealed by contact angle measurement. The blood compatibility of the grafted films was evaluated by a platelet-rich plasma (PRP) adhesion study and scanning electron microscopy, using SPEU film as the reference. No platelet adhesion was observed for the grafted films incubated with PRP at 37 degrees C for 60 and 180 min. This new sulfobetaine structure grafted biomaterial might have potential for biomedical applications.

Betaine↗
PubMed2003

Platelet adhesion onto segmented polyurethane surfaces modified by carboxybetaine.

Polyurethanes are widely used as blood-contacting biomaterials due to their good biocompatibility and mechanical properties. Nevertheless, their blood compatibility is still not adequate for more demanding applications. Surface modification is an effective way to improve the hemocompatibility for biomaterials. The purpose of present study was to synthesize a novel nonthrombogenic biomaterial by modifying the surface of polyurethane with Zwitterions of carboxybetaine monomer. The films of polyurethane were grafted with two kinds of carboxybetaine by a three-step procedure. In the first step, the film surfaces were treated with hexamethylene diisocyanate (HDI) in toluene at 50 degrees C in the presence of di-n-butyl tin dilaurate (DBTDL) as a catalyst. The extent of the reaction was measured by ATR-FT-IR spectra: a maximum number of free NCO group was obtained after a reaction time of 90 min. In the second step, the hydroxyl group of N,N-dimethylethylethanolamine (DMEA) or 4-dimethylamino-1-butanol (DMBA) was allowed to react in toluene with isocyanate groups bound on surface. In the third step, carboxybetaines were formed in the surface through the ring-opening reaction between tertiary amine of DMEA or DMBA and beta-propiolactone (PL). It was characterized by ATR-FT-IR and XPS that the grafted surfaces were composed of carboxybetaine. The results of the contact angle measurements showed that they were strongly hydrophilic. Platelet adhesion tests showed that films grafted carboxybetaine have good blood compatibility, as featured by the low platelet adhesion.

Betaine↗
PubMed2003

Compression-induced changes on physical structures and calcification of the aromatic polyether polyurethane composite.

It is generally accepted that stress causes calcification in both bio-prosthetic and polyurethane heart valves. However, simple uni-axially- and bi-axially-stretched samples did not yield a feasible model for the elaboration of the stress-induced calcification. In this study, heat compaction combined with the incorporation of polyethylene has been explored. Specimens of polyurethane were solution cast onto a porous bi-axially-drawn ultra-high-molecular-weight polyethylene film and then heat compacted under a pressure of 18 MPa at a chosen temperature for 1.5 h. The heat-compaction-induced calcification and physical changes of the polyurethane composite were evaluated using a 28-day in vitro calcification model and Attenuated Total Reflection-Fourier Transform-Infrared (ATR-FT-IR) spectroscopy. The calcification results indicated that heat-compaction-induced calcification was double that achieved without heat compaction. Heat-compacted polyurethane composite showed higher affinity to calcium ions than the non-heat compacted sample. The ATR-FT-IR results showed that the heat-compaction-induced physical changes include distortions of polymeric molecules and permanent changes of microstructures. The distortions of polymeric molecules could be deteriorated in contact with different media. The relaxation of the stressed structures of the polyether moiety might serve as a calcium trap and a heterogeneous nucleation site for calcification. The permanent changes of microstructures resulted from high distortions also served as affinity sites attracting calcification.

Biocompatible Materials↗
PubMed2005

Chemical modification of chitosan by phosphorylation: an XPS, FT-IR and SEM study.

In the present work, the surface of chitosan membranes was modified using a phosphorylation method carried out at room temperature. Phosphorylation may be of particular interest in materials for orthopaedic applications, due to the cation-exchange properties of phosphate functionalities. Phosphate groups chelate calcium ions, thus inducing the deposition of an apatite-like layer known to improve the osteoconduction of polymer-based implants. Additionally, the negatively charged phosphate functionalities, together with the positively charged amine groups from chitosan, are expected to provide chitosan with an amphoteric character, which may be useful as a combinatorial therapeutic strategy, by simultaneously allowing the immobilization of signalling molecules like growth factors. Phosphorylation was carried out at room temperature using the H3PO4/Et3PO4/P2O5/butanol method. Surface characterization was performed by XPS, ATR-FT-IR, and SEM. Cross-sections were analyzed by SEM fitted with EDS. The phosphate content increased with the reaction time, as shown by XPS and ATR-FT-IR, a P/N atomic ratio of 0.73 being obtained after 48 h of treatment. High-resolution XPS spectra regarding C1s, O1s, N1s and P2p are discussed. The introduction of a neutralization step led to a reduction of P content, which pointed out to the presence of phosphates ionically bound to protonated amines, in addition to phosphate esters. EDS analysis of cross-sections revealed a gradual P reduction up to 50% towards the inner part of the membrane.

Acetylation↗