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Biomedical subjects

H Sun

Publications and source records attributed to H Sun.

At least 19 recordsLinked to original sources

Characterization of 2-amino-4,5-dichlorophenol (2A45CP) in vitro toxicity in renal cortical slices from male Fischer 344 rats.

2-Amino-4,5-dichlorophenol (2A45CP) is a major, aromatic ring hydroxylated metabolite of the renal toxicant, 3,4-dichloroaniline. 3,4-Dichloroaniline is nephrotoxic with primary damage located to the proximal tubules. The purpose of this study was to first characterize the in vitro toxicity of 2A45CP in renal cortical slices. Second, the effect of antioxidants and sulfhydryl containing agents on the severity of 2A45CP toxicity was explored since part of the mechanism of toxicity for aminophenols may involve redox cycling. Renal tissue was isolated from male Fischer 344 rats (190--220 g). Renal slices were rinsed three times for 3 min each in 5-ml Krebs buffer. Tissues were then incubated for 90--120 min with varying concentrations of 2A45CP between 0 and 0.5 mM. In a separate series of experiments, the slices (50--100 mg) were preincubated for 30 min with 1 mM dithiothreitol (DTT), 1 mM glutathione (GSH) or 2 mM ascorbic acid prior to exposure to 0, 0.05, 0.1 or 0.25 mM 2A45CP. 2A45CP produced a concentration and time dependent increase in LDH leakage from renal cortical slices. Total glutathione levels were diminished by 0.5 mM 2A45CP within 30 min. Renal slices incubated for 60 and 120 min with 0.05 and 0.1 mM 2A45CP had lower malondialdehyde levels than control. Pretreatment with DTT did not alter 2A45CP toxicity. Pretreatment of renal cortical slices with GSH or ascorbic acid reduced 2A45CP toxicity. These findings indicate that 2A45CP is directly toxic to renal cortical slices and that cytotoxicity is at least partially mediated by a reactive intermediate.

Animals↗

Chronic neuropathic pain is accompanied by global changes in gene expression and shares pathobiology with neurodegenerative diseases.

Neuropathic pain is induced by injury or disease of the nervous system. Studies aimed at understanding the molecular pathophysiology of neuropathic pain have so far focused on a few known molecules and signaling pathways in neurons. However, the pathophysiology of neuropathic pain appears to be very complex and remains poorly understood. A global understanding of the molecular mechanisms involved in neuropathic pain is needed for a better understanding of the pathophysiology and treatment of neuropathic pain. Towards this end, we examined global gene expression changes as well as the pathobiology at the cellular level in a spinal nerve ligation neuropathic pain model using DNA microarray, quantitative real-time PCR and immunohistochemistry. We found that the behavioral hypersensitivity that is manifested in the persistent pain state is accompanied by previously undescribed changes in gene expression. In the DRG, we found regulation of: (1) immediate early genes; (2) genes such as ion channels and signaling molecules that contribute to the excitability of neurons; and (3) genes that are indicative of secondary events such as neuroinflammation. In addition, we studied gene regulation in both injured and uninjured DRG by quantitative PCR, and observed differential gene regulation in these two populations of DRGs. Furthermore, we demonstrated unexpected co-regulation of many genes, especially the activation of neuroinflammation markers in both the PNS and CNS. The results of our study provide a new picture of the molecular mechanisms that underlie the complexity of neuropathic pain and suggest that chronic pain shares common pathobiology with progressive neurodegenerative disease.

Animals↗

Identification of candidate lung cancer susceptibility genes in mouse using oligonucleotide arrays.

We applied microarray gene expression profiling to lungs from mouse strains having variable susceptibility to lung tumour development as a means to identify, within known quantitative trait loci (QTLs), candidate genes responsible for susceptibility or resistance to lung cancer. At least eight chromosomal regions of mice have been mapped and verified to be linked with lung tumour susceptibility or resistance. In this study, high density oligonucleotide arrays were used to measure the relative expression levels of >36 000 genes and ESTs in lung tissues of A/J, BALB/cJ, SM/J, C3H/HeJ, and C57BL/6J mice. A number of differentially expressed genes were found in each of the lung cancer susceptibility QTLs. Bioinformatic analysis of the differentially expressed genes located within QTLs produced 28 susceptibility candidates and 22 resistance candidates. These candidates may be extremely helpful in the ultimate identification of the precise genes responsible for lung tumour susceptibility or resistance in mice and, through follow up, humans. Complete data sets are available at http://thinker.med.ohio-state.edu.

Animals↗

Leptin mediates the parathyroid hormone-related protein paracrine stimulation of fetal lung maturation.

Developing rat lung lipofibroblasts express leptin beginning on embryonic day (E) 17, increasing 7- to 10-fold by E20. Leptin and its receptor are expressed mutually exclusively by fetal lung fibroblasts and type II cells, suggesting a paracrine signaling "loop." This hypothesized mechanism is supported by the following experimental data: 1) leptin stimulates the de novo synthesis of surfactant phospholipid by both fetal rat type II cells (400% x 100 ng(-1) x ml(-1) x 24 h(-1)) and adult human airway epithelial cells (85% x 100 ng(-1) x 24 h(-1)); 2) leptin is secreted by lipofibroblasts in amounts that stimulate type II cell surfactant phospholipid synthesis in vitro; 3) epithelial cell secretions such as parathyroid hormone-related protein (PTHrP), PGE(2), and dexamethasone stimulate leptin expression by fetal rat lung fibroblasts; 4) PTHrP or leptin stimulate the de novo synthesis of surfactant phospholipid (2- to 2.5-fold/24 h) and the expression of surfactant protein B (SP-B; >25-fold/24 h) by fetal rat lung explants, an effect that is blocked by a leptin antibody; and 5) a PTHrP receptor antagonist inhibits the expression of leptin mRNA by explants but does not inhibit leptin stimulation of surfactant phospholipid or SP-B expression, indicating that PTHrP paracrine stimulation of type II cell maturation requires leptin expression by lipofibroblasts. This is the first demonstration of a paracrine loop that functionally cooperates to induce alveolar acinar lung development.

Animals↗

Role of stereochemistry in N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA) nephrotoxicity.

The nephrotoxicity induced by the agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is mediated through oxidative metabolites of NDPS. Oxidation of the succinimide ring in NDPS yields the nephrotoxic metabolites N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and its hydrolysis product N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA). The oxidation of NDPS on the succinimide ring also introduces an asymmetric carbon atom into these NDPS metabolites, so that R- and S- enantiomers of NDHS and 2-NDHSA are possible. The purpose of this study was to begin to explore the importance of the stereochemical orientation at the asymmetric carbon atom for the nephrotoxicity induced by NDPS metabolites. Male Fischer 344 rats were administered a single intraperitoneal (ip) injection of R-(+)- or S-(-)-2-NDHSA (0.05, 0.1 or 2.0 mmol/kg) or vehicle, and renal function was monitored for 48 h. R-2-NDHSA (0.1 mmol/kg) administration had little effect on renal function. R-2-NDHSA (0.2 mmol/kg) treatment induced mild diuresis on day 1, increased proteinuria, and a small increase in blood urea nitrogen (BUN) concentration, but no change in kidney weight or glucosuria. S-2-NDHSA (0.1 mmol/kg) induced marked nephrotoxicity as evidenced by diuresis on both post-treatment days, increased proteinuria, glucosuria, and increased kidney weight and BUN concentration. No evidence of hepatotoxicity was obtained in any treated group. Thus, the S-isomer of 2-NDHSA is a more potent nephrotoxicant than the R-isomer, and stereochemistry may play a role in NDPS metabolite-induced nephrotoxicity.

Animals↗

Frequency of serum low-density lipoprotein cholesterol measurement and frequency of results < or=100 mg/dl among patients who had coronary events (Northwest VA Network Study).

This population-based, cross-sectional analysis targeted all veterans with coronary heart disease (CHD) who were active patients in primary care or cardiology clinics in the Veterans Health Administration Northwest Network from July 1998 to June 1999. We report guideline compliance rates, including whether low-density lipoprotein (LDL) was measured, and if measured, whether the LDL was < or=100 mg/dl. In addition, we utilized multivariate logistic regression to determine patient characteristics associated with LDL measurements and levels. Of 13,891 active patients with CHD, 5,552 (40.0%) did not have a current LDL measurement. Of those with LDL measurements, 39.1% were at the LDL goal of < or =100 mg/dl, whereas 26.5% had LDL > or =130 mg/dl. Male gender, younger age, history of angioplasty or coronary artery bypass grafting, current hypertension, diabetes mellitus, and angina pectoris were associated with increased likelihood of LDL measurement. Older age and current diabetes and angina were associated with increased likelihood of LDL being < or =100 mg/dl, if measured. Although these rates of guideline adherence in the CHD population compare well to previously published results, they continue to be unacceptably low for optimal clinical outcomes. Attention to both LDL measurement and treatment (if elevated) is warranted.

Aged↗

Interactions of bismuth with human lactoferrin and recognition of the Bi(III)-lactoferrin complex by intestinal cells.

Several bismuth compounds are currently used as antiulcer drugs, but the mechanism of action still remains unclear. The antimicrobial activity of Bi(III) complexes toward Gram-negative bacteria is reported to be dependent on the iron uptake system [Domenico, P., et al. (1996) J. Antimicrob. Chemother. 38, 1031-1040]. Electronic absorption and 13C NMR spectroscopic data show that Bi(III) binds to human lactoferrin at the specific Fe(III) sites along with either carbonate or oxalate as the synergistic anion. The uptake of Bi(III) by apo-hLF was rapid [minutes in 10 mM Hepes buffer and 5 mM bicarbonate (pH 7.4)], and almost equal in both lobes. The presence of ATP facilitates the release of Bi(III) from the Bi2-hLF complex when the pH is lowered. The Bi2-hLF complex blocked the uptake of the radiolabeled 59Fe-hLF complex into rat IEC-6 cells. Surprisingly, apo-hLF (but not apotransferrin) was almost as effective in blocking 59Fe uptake as bismuth-loaded lactoferrin. These results suggest that Bi(III)-loaded hLF might be recognized by the lactoferrin receptor and be taken up into cells.

Adenosine Triphosphate↗

Complete genome sequence of Salmonella enterica serovar Typhimurium LT2.

Salmonella enterica subspecies I, serovar Typhimurium (S. typhimurium), is a leading cause of human gastroenteritis, and is used as a mouse model of human typhoid fever. The incidence of non-typhoid salmonellosis is increasing worldwide, causing millions of infections and many deaths in the human population each year. Here we sequenced the 4,857-kilobase (kb) chromosome and 94-kb virulence plasmid of S. typhimurium strain LT2. The distribution of close homologues of S. typhimurium LT2 genes in eight related enterobacteria was determined using previously completed genomes of three related bacteria, sample sequencing of both S. enterica serovar Paratyphi A (S. paratyphi A) and Klebsiella pneumoniae, and hybridization of three unsequenced genomes to a microarray of S. typhimurium LT2 genes. Lateral transfer of genes is frequent, with 11% of the S. typhimurium LT2 genes missing from S. enterica serovar Typhi (S. typhi), and 29% missing from Escherichia coli K12. The 352 gene homologues of S. typhimurium LT2 confined to subspecies I of S. enterica-containing most mammalian and bird pathogens-are useful for studies of epidemiology, host specificity and pathogenesis. Most of these homologues were previously unknown, and 50 may be exported to the periplasm or outer membrane, rendering them accessible as therapeutic or vaccine targets.

Animals↗

An experimental and theoretical investigation of the chemical shielding tensors of (13)C(alpha) of alanine, valine, and leucine residues in solid peptides and in proteins in solution.

We have carried out a solid-state magic-angle sample-spinning (MAS) nuclear magnetic resonance (NMR) spectroscopic investigation of the (13)C(alpha) chemical shielding tensors of alanine, valine, and leucine residues in a series of crystalline peptides of known structure. For alanine and leucine, which are not branched at the beta-carbon, the experimental chemical shift anisotropy (CSA) spans (Omega) are large, about 30 ppm, independent of whether the residues adopt helical or sheet geometries, and are in generally good accord with Omega values calculated by using ab initio Hartree-Fock quantum chemical methods. The experimental Omegas for valine C(alpha) in two peptides (in sheet geometries) are also large and in good agreement with theoretical predictions. In contrast, the "CSAs" (Deltasigma) obtained from solution NMR data for alanine, valine, and leucine residues in proteins show major differences, with helical residues having Deltasigma values of approximately 6 ppm while sheet residues have Deltasigma approximately 27 ppm. The origins of these differences are shown to be due to the different definitions of the CSA. When defined in terms of the solution NMR CSA, the solid-state results also show small helical but large sheet CSA values. These results are of interest since they lead to the idea that only the beta-branched amino acids threonine, valine, and isoleucine can have small (static) tensor spans, Omega (in helical geometries), and that the small helical "CSAs" seen in solution NMR are overwhelmingly dominated by changes in tensor orientation, from sheet to helix. These results have important implications for solid-state NMR structural studies which utilize the CSA span, Omega, to differentiate between helical and sheet residues. Specifically, there will be only a small degree of spectral editing possible in solid proteins since the spans, Omega, for the dominant nonbranched amino acids are quite similar. Editing on the basis of Omega will, however, be very effective for many Thr, Val, and Ileu residues, which frequently have small ( approximately 15-20 ppm) helical CSA (Omega) spans.

Alanine↗

A human nuclease specific for G4 DNA.

We have identified a human nuclease that specifically cleaves four-stranded DNA stabilized by G quartets (G4 DNA). This nuclease, GQN1 (G quartet nuclease 1), cuts within the single-stranded region 5' of the barrel formed by stacked G quartets. GQN1 does not cleave duplex or single-stranded DNA, Holliday junctions, or G4 RNA. Cleavage depends on DNA structure and not on flanking sequence. Activity is elevated in but not restricted to B cells, making GQN1 a strong candidate for function in immunoglobulin heavy chain class switch recombination. Identification of a mammalian nuclease that specifically cleaves G4 DNA provides further support for the notion that DNA structures stabilized by G quartets form in vivo and function in regulated recombination and genomic evolution.

Base Sequence↗

Selective coactivation of estrogen-dependent transcription by CITED1 CBP/p300-binding protein.

CITED1, a CBP/p300-binding nuclear protein that does not bind directly to DNA, is a transcriptional coregulator. Here, we show evidence that CITED1 functions as a selective coactivator for estrogen-dependent transcription. When transfected, CITED1 enhanced transcriptional activation by the ligand-binding/AF2 domain of both estrogen receptor-alpha (ERalpha) and ERbeta in an estrogen-dependent manner, but it affected transcriptional activities of other nuclear receptors only marginally. CITED1 bound directly to ERalpha in an estrogen-dependent manner through its transactivating domain, and this binding activity was separable from its p300-binding activity. CITED1 was strongly expressed in nulliparous mouse mammary epithelial cells and, when expressed in ER-positive MCF-7 breast cancer cells by transduction, exogenous CITED1 enhanced sensitivity of MCF-7 cells to estrogen, stabilizing the estrogen-dependent interaction between p300 and ERalpha. The estrogen-induced expression of the transforming growth factor-alpha (TGF-alpha) mRNA transcript was enhanced in the CITED1-expressing MCF-7 cells, whereas estrogen-induced expression of the mRNA transcripts for progesterone receptor or pS2 was not affected. Chromatin immunoprecipitation assay revealed that endogenous CITED1 is recruited to the chromosomal TGF-alpha promoter in MCF-7 cells in an estrogen-dependent manner but not to the pS2 promoter. These results suggest that CITED1 may play roles in regulation of estrogen sensitivity in a gene-specific manner.

Animals↗

Mutation of Tyr138 disrupts the structural coupling between the opposing domains in vertebrate calmodulin.

We have used circular dichroism and frequency-domain fluorescence spectroscopy to determine how the site-specific substitution of Tyr138 with either Phe138 or Gln138 affects the structural coupling between the opposing domains of calmodulin (CaM). A double mutant was constructed involving conservative substitution of Tyr99 --> Trp99 and Leu69 --> Cys69 to assess the structural coupling between the opposing domains, as previously described [Sun, H., Yin, D., and Squier, T. C. (1999) Biochemistry 38, 12266-12279]. Trp99 acts as a fluorescence resonance energy transfer (FRET) donor in distance measurements to probe the conformation of the central helix. Cys69 provides a reactive group for the covalent attachment of 5-((((2-iodoacetyl)amino)ethyl)amino)naphthalene-1-sulfonic acid (IAEDANS), which functions as a FRET acceptor and permits the measurement of the rotational dynamics of the amino-terminal domain. These CaM mutants demonstrate normal calcium-dependent gel-mobility shifts and changes in their near-UV CD spectra, have similar secondary structures to wild-type CaM following calcium activation, and retain the ability to fully activate the plasma membrane Ca-ATPase. The global folds, therefore, of both the carboxyl- and amino-terminal domains in these CaM mutants are similar to that of wild-type CaM. However, in comparison to wild-type CaM, the substitution of Tyr138 with either Phe138 or Gln138 results in (i) alterations in the average spatial separation and increases in the conformational heterogeneity between the opposing globular domains and (ii) the independent rotational dynamics of the amino-terminal domain. These results indicate that alterations in either the hydrogen bond between Tyr138 and Glu82 or contact interactions between aromatic amino acid side chains have the potential to initiate the structural collapse of CaM normally associated with target protein binding and activation.

Animals↗

Overexpression of lipoprotein lipase in transgenic rabbits inhibits diet-induced hypercholesterolemia and atherosclerosis.

Lipoprotein lipase (LPL) is a key enzyme in the hydrolysis of TG-rich lipoproteins. To elucidate the physiological roles of LPL in lipid and lipoprotein metabolism, we generated transgenic rabbits expressing human LPL. In postheparinized plasma of transgenic rabbits, the human LPL protein levels were about 650 ng/ml, and LPL enzymatic activity was found at levels up to 4-fold greater than that in nontransgenic littermates. Increased LPL activity in transgenic rabbits was associated with as much as an 80% decrease in plasma triglycerides and a 59% decrease in high density lipoprotein-cholesterol. Analysis of the lipoprotein density fractions revealed that increased expression of the LPL transgene resulted in a remarkable reduction in the level of very low density lipoproteins as well as in the level of intermediate density lipoproteins. In addition, LDL cholesterol levels in transgenic rabbits were significantly increased. When transgenic rabbits were fed a cholesterol-rich diet, the development of hypercholesterolemia and aortic atherosclerosis was dramatically suppressed in transgenic rabbits. These results demonstrate that systemically increased LPL activity functions in the metabolism of all classes of lipoproteins, thereby playing a crucial role in plasma triglyceride hydrolysis and lipoprotein conversion, and that overexpression of LPL protects against diet-induced hypercholesterolemia and atherosclerosis.

Animals↗

C/EBP epsilon mediates myeloid differentiation and is regulated by the CCAAT displacement protein (CDP/cut).

Neutrophils from CCAAT enhancer binding protein epsilon (C/EBP epsilon) knockout mice have morphological and biochemical features similar to those observed in patients with an extremely rare congenital disorder called neutrophil-specific secondary granule deficiency (SGD). SGD is characterized by frequent bacterial infections attributed, in part, to the lack of neutrophil secondary granule proteins (SGP). A mutation that results in loss of functional C/EBP epsilon activity has recently been described in an SGD patient, and has been postulated to be the cause of the disease in this patient. We have previously demonstrated that overexpression of CCAAT displacement protein (CDP/cut), a highly conserved transcriptional repressor of developmentally regulated genes, suppresses expression of SGP genes in 32Dcl3 cells. This phenotype resembles that observed in both C/EBP epsilon(-/-) mice and in SGD patients. Based on these observations we investigated potential interactions between C/EBP epsilon and CDP/cut during neutrophil maturation. In this study, we demonstrate that inducible expression of C/EBP epsilon in 32Dcl3/tet cells results in granulocytic differentiation. Furthermore, Northern blot analysis of G-CSF-induced CDP/cut overexpressing 32Dcl3 cells revealed absence of C/EBP epsilon mRNA. We therefore hypothesize that C/EBP epsilon positively regulates SGP gene expression, and that C/EBP epsilon is itself negatively regulated by CDP/cut during neutrophil maturation. We further demonstrate that the C/EBP epsilon promoter is regulated by CDP/cut during myeloid differentiation.

Animals↗

First-principle approach to dielectric behavior of nonspherical cell suspensions.

We present a theoretical study of the dielectric behavior of cell suspensions by employing the Bergman-Milton spectral representation of the effective dielectric constant. By means of the spectral representation, we derive the dielectric dispersion spectrum in terms of the electrical and structure parameters of the cell models. Our results show that a better agreement with the experimental data can be obtained, provided that we introduce a conductivity contrast t=sigma(2)/(sigma(2)-sigma(1)). We find that the conductivity of the cell cytoplasm sigma(1) can be much larger than that of the suspending medium sigma(2), in contrast to the previous claim that sigma(1) approximately sigma(2).

Anisotropy↗

Transport of fluorescein in MDCKII-MRP1 transfected cells and mrp1-knockout mice.

The multidrug resistant-associated protein 1 (MRP1) is a membrane-bound transport protein that is involved in the efflux of organic anions and has been implicated in multidrug resistance in cancer. MRP1 has also been reported to be ubiquitously expressed in normal tissues, including the brain. The presence of functional organic anion transporters in the blood-brain and blood-CSF barriers that influence the distribution of various compounds to the brain has long been known. The purpose of this study was to examine the role of MRP1 in the brain distribution of a model organic anion, fluorescein. The substrate specificity of MRP1 for fluorescein was initially determined by examining the accumulation of fluorescein in MDCKII MRP1-transfected cells. The distribution of fluorescein in the brain was then examined in wild-type and mrp1 gene knockout mice. The results show that in MDCKII MRP1-transfected cells, the accumulation of fluorescein was significantly lower (about 40% lower) than that in wild-type MDCKII cells. MRP1 inhibitors such as probenecid, MK-571, and LY402913 enhanced fluorescein accumulation in MDCKII MRP1-transfected cells to a greater extent than in wild-type MDCKII cells. In an in vivo study, after intravenous injection of fluorescein, the fluorescein brain-to-plasma concentration ratio in mrp1 knockout mice was not significantly different than that in wild-type mice. However, when probenecid was co-administered with fluorescein in wild-type mice, the fluorescein brain-to-plasma ratio was significantly increased (1.5-fold). These findings suggest that fluorescein is a substrate for MRP1. Furthermore, the in vivo study also suggests that MRP1 has a limited role in the transport and distribution of fluorescein in the brain. Therefore, other organic anion transport proteins, including the various isoforms of the MRP family, may be responsible for the accumulation and transport of organic anions in the brain.

ATP-Binding Cassette Transporters↗

Incipient erosion of biostabilized sediments examined using particle-field optical holography.

Laser holography allows images of three-dimensional space at ultra-high resolution to be recorded onto photographic plates. Recorded scenes can be "replayed" with a second laser beam into free space and optically "interrogated" using either a microscope or a camera by sequentially focusing on increasing distances from the hologram in the field of view (optical sectioning). From these sections, information on the relative locations and orientation in space of suspended particles as well as the morphology of particles can be obtained. This paper examines the utility of "in-line" laser holography to discriminate the size and the morphology of sand particles eroded under turbulent shear flow during benthic sediment transport. The influence of a commercially available adhesive polymer (xanthan gum, derived from the bacterium Xanthomonas campestris) on sediment stability and resuspended particle morphology is described. The major implications for carbon and sediment cycling within estuaries are highlighted.

Environmental Monitoring↗

Mesoporous aluminosilicates with ordered hexagonal structure, strong acidity, and extraordinary hydrothermal stability at high temperatures.

Highly ordered hexagonal mesoporous aluminosilicates (MAS-5) with uniform pore sizes have been successfully synthesized from assembly of preformed aluminosilcate precursors with cetyltrimethylammonium bromide (CTAB) surfactant. The aluminosilicate precursors were obtained by heating, at 100--140 degrees C for 2--10 h, aluminasilica gels at the Al(2)O(3)/SiO(2)/TEAOH/H(2)O molar ratios of 1.0/7.0--350/10.0--33.0/500--2000. Mesoporous MAS-5 shows extraordinary stability both in boiling water (over 300 h) and in steam (800 degrees C for 2 h). Temperature-programmed desorption of ammonia shows that the acidic strength of MAS-5 is much higher than that of MCM-41 and is comparable to that of microporous Beta zeolite. In catalytic cracking of 1,3,5-triisopropylbenzene and alkylation of isobutane with butene, MAS-5 exhibits greater catalytic activity and selectivity, as compared with MCM-41 and HZSM-5. The MAS-5 samples were characterized with infrared, UV--Raman, and NMR spectroscopy and numerous other techniques. The results suggest that MAS-5 consists of both mesopores and micropores and that the pore walls of MAS-5 contain primary and secondary structural building units, similar to those of microporous zeolites. Such unique structural features might be responsible for the observed strong acidity and high thermal stability of the mesoporous aluminosilicates with well-ordered hexagonal symmetry.

Journal Article↗