bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimization of microbiological assay of folic acid and determination of folate content in spinach
Authors: Pandrangi Srilatha , LaBorde Luke F. 
Published: April 2004

SummaryThe microbiological method for the determination of folate in plant foods uses the growth response of folate‐dependent Lactobacillus rhamnosus in extracts that have been enzymatically treated to release the bound vitamin. However, the use of cryoprotected cultures is hampered by low recovery of the microorganism after extended frozen storage times. In this study, growth of L. rhamnosus was enhanced using a microaerophilic enrichment procedure and optimal pH conditions and enzyme reaction times were determined for the release of bound folate in spinach. Optimum pH values for the release of bound folate in spinach samples treated with α‐amylase or protease were 3.0 and 4.0, respectively. Although treatment with α‐amylase had no significant (P > 0.05) effect on measured folate, addition of protease at pH 4.0 significantly (P  0.05) increased the release of folate at an optimum incubation time of 8 h. Therefore, a dual‐enzyme treatment (protease and conjugase) is sufficient to determine folate content in spinach.
Survival of Escherichia coli O157:H7 in the processing and post‐processing stages of acidophilus yogurt
Authors: Kasımoğlu Aylin , Akgün Sadi 
Published: April 2004

SummaryIn this study the survival of Escherichia coli O157:H7 in the production process of acidophilus yogurt was examined and compared with traditional yogurt. Milk was inoculated with different doses of E. coli O157:H7 (102, 104 and 106 CFU mL−1) and two kinds of yogurt were produced. Samples were taken for pH measurements and bacterial enumeration at 0, 3, 24, 48, and 72 h after inoculation. Escherichia coli O157:H7 was analysed by using a Most Probable Number technique and yogurt starter culture and Lactobacillus acidophilus were counted by using classical culture methods. Elimination times of E. coli O157:H7 were determined for 102 CFU mL−1 as 3 h, and for 104 and 106 CFU mL−1 as 48 h in acidophilus yogurt. Elimination times in traditional yogurt were 48 h for 102 and 104 CFU mL−1 and 72 h for 106 CFU mL−1E. coli O157:H7. In conclusion, the elimination time of E. coli O157:H7 in acidophilus yogurt was shorter than in traditional yogurt during the processing and post‐processing stages.
Ownership Structure and Technological Upgrading in International Joint Ventures
Authors: Lin Ping , Saggi Kamal 
Published: April 2004

AbstractIn a model of a joint venture between a local and a foreign firm who provide complementary inputs, this paper derives optimal ownership structures under different sharing rules. The local firm's profits may be maximized by assigning a majority share to the foreign firm. Efficiency (i.e., the minimization of double moral hazard) requires that the firm with the more productive input should get majority ownership. When only the foreign firm can upgrade its input, it should receive a larger share than what it receives in the absence of upgrading. The analysis implies that a blanket policy of prohibiting majority foreign ownership is theoretically unfounded.
p73α is a candidate effector in the p53 independent apoptosis pathway of cisplatin damaged primary murine colonocytes
Authors: Oniscu A , Sphyris N , Morris R G , Bader S , Harrison D J 
Published: April 2004

Aims:Colonocytes were derived from wild-type (wt) and p53 deficient mice to investigate p53 dependent and independent death pathways after cisplatin treatment, and the role of p53 in growth regulation of primary, untransformed epithelial cells.Methods:Wt and p53 null colonocytes were exposed to cisplatin and DNA synthesis, apoptosis, and p53, p21, and p73 expression were investigated after six, 12, and 24 hours. Major p73 isoforms were identified by reverse transcription polymerase chain reaction (RT-PCR).Results:Cisplatin treated wt cells exhibited cell cycle arrest, whereas p53 null cells continued to synthesise DNA, although both cell types died. Apoptosis was significantly higher in cisplatin treated wt and p53 null colonocytes than in controls at all timepoints, although apoptosis was lower in cisplatin treated p53 null colonocytes than in wt cells. p53 expression was upregulated in cisplatin treated wt colonocytes. p21 expression was high and remained unchanged in cisplatin treated wt cells, although it was reduced in the absence of p53. p73 was investigated because it could account for p53 independent p21 expression and p53 independent death. RT-PCR detected full length p73α. p73 transcript levels remained unchanged, whereas p73 protein accumulated in the nucleus of cisplatin treated cells, irrespective of genotype.Conclusions:p53 is essential for cell cycle arrest, but not apoptosis in primary murine colonocytes. Apoptosis is reduced in cisplatin treated p53 null cells. Nuclear accumulation of endogenous p73 after cisplatin treatment suggests a proapoptotic role for p73α in the absence of p53 and collaboration with p53 in wt colonocytes.
COX-2 dependent PGE2downregulates αvintegrin expression via the EP3receptor in cultured mesangial cells
Authors: Waldner C , Schrör K , Heering P 
Published: April 2004

Background:In experimental glomerulonephritis, inhibition of cyclooxygenase 2 (COX-2) enhances the renocortical expression of pathogenic αvintegrins.Aims:To study whether this effect is mediated by prostaglandin E2(PGE2) acting through its EP3receptor in cultured rat mesangial cells (MCs).Methods:MCs were incubated with lipopolysaccharide (LPS), celecoxib, PGE2, or the selective EP3agonist, MB28767. The expression of COX-2, EP3, and αvintegrin mRNA was measured by reverse transcriptase polymerase chain reaction.Results:LPS upregulated COX-2 expression 2.8-fold and αvintegrin expression twofold. The COX-2 inhibitor celecoxib increased αvintegrin mRNA expression twofold. Both exogenous PGE2and the specific EP3receptor agonist, MB28767, reduced constitutive αvintegrin mRNA expression to half normal values. COX-2 dependent PGE2suppressed the expression of αvintegrin mRNA mediated by the EP3receptor in MCs.Conclusions:These results suggest that COX-2 suppresses the expression of αvintegrins by an increased production of PGE2activating its EP3receptor in glomerulonephritis.
Distinct activities of suppressor of cytokine signaling (SOCS) proteins and involvement of the SOCS box in controlling G-CSF signaling
Authors: van de Geijn Gert-Jan M , Gits Judith , Touw Ivo P 
Published: April 2004

AbstractGranulocyte-colony stimulating factor (G-CSF) induces proliferation of myeloid progenitor cells and controls their differentiation into mature neutrophils. Signal transducer and activator of transcription (STAT) proteins STAT3 and STAT5 are activated by G-CSF and play distinct roles in neutrophil development. Suppressor of cytokine signaling (SOCS) proteins are induced by STATs and inhibit signaling through various negative-feedback mechanisms. SOCS proteins can compete with docking of signaling substrates to receptors, interfere with Janus tyrosine kinase activity, and target proteins for proteasomal degradation. The latter process is mediated through the conserved C-terminal SOCS box. We determined the role of various SOCS proteins in controlling G-CSF responses and investigated the involvement of the SOCS box therein. We show that SOCS1 and SOCS3, but not CIS and SOCS2, inhibited G-CSF-induced STAT activation in human embryo kidney 293 cells. In myeloid 32D cells, SOCS1 and SOCS3 are induced by G-CSF. However, relative to interleukin-3-containing cultures, during G-CSF-induced neutrophilic differentiation, SOCS3 expression was further elevated, while SOCS1 levels remained constant. SOCS box deletion mutants of SOCS1 and SOCS3 were severely hampered in their abilities to inhibit STAT activation and to efficiently suppress colony formation by primary myeloid progenitors in response to G-CSF. These data demonstrate the importance of the SOCS box for the inhibitory effects of SOCS proteins on G-CSF signaling and show that among the different SOCS family members, SOCS3 is the major negative regulator of G-CSF responses during neutrophilic differentiation.
A putative osmoreceptor system that controls neutrophil function through the release of ATP, its conversion to adenosine, and activation of A2 adenosine and P2 receptors
Authors: Chen Yu , Shukla Alok , Namiki Sachiko , Insel Paul A , Junger Wolfgang G 
Published: April 2004

AbstractWe have previously shown that hypertonic stress (HS) can suppress chemoattractant-induced neutrophil responses via cyclic adenosine monophosphate and enhance these responses through p38 mitogen-activated protein kinase (MAPK) activation. The underlying mechanisms are unknown. Here, we report that HS dose-dependently releases adenosine 5′-triphosphate (ATP) from neutrophils and that extracellular ATP is rapidly converted to adenosine or activates p38 MAPK and enhances N-formyl-methionyl-leucyl-phenylalanine-induced superoxide formation. In contrast, adenosine suppresses superoxide formation. Adenosine deaminase treatment abolished the suppressive effect of HS, indicating that HS inhibits neutrophils through adenosine generation. Neutrophils express mRNA, encoding all known P1 adenosine receptors (A1, A2a, A2b, and A3) and the nucleotide receptors P2Y2, P2Y4, P2Y6, P2Y11, and P2X7. A2 receptor agonists mimicked the suppressive effects of HS; the A2 receptor antagonists 8-(p-sulfophenyl)theophylline, 3,7-dimethyl-1-(2-propynyl)xanthine, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine, and 3-propylxanthine, but not A1 and A3 receptor antagonists, decreased the suppressive effect of HS, indicating that HS suppresses neutrophils via A2 receptor activation. Antagonists of P2 receptors counteracted the enhancing effects of ATP, suggesting that HS costimulates neutrophils by means of P2 receptor activation. We conclude that hypertonic stress regulates neutrophil function via a single molecule (ATP) and its metabolite (adenosine), using positive- and negative-feedback mechanisms through the activation of P2 and A2 receptors, respectively.
Effects of endothelin ETA receptor antagonism on granulocyte and lymphocyte accumulation in LPS-induced inflammation
Authors: Sampaio André L F , Rae Giles A , Henriques Maria das Graças M O 
Published: April 2004

AbstractEndothelin peptides play active roles in different aspects of inflammation. This study investigates the contribution of endogenous endothelins to lipopolysaccharide (LPS) pulmonary inflammation by assessing the influence of ETA receptor antagonism on leukocyte accumulation, granulocyte adhesion molecule expression, and chemokine/cytokine modulation. Local pretreatment with BQ-123 or A-127722 (150 pmol), two selective and chemically unrelated endothelin ETA receptor antagonists, inhibits neutrophil and eosinophil accumulation in LPS-induced pleurisy at 24 h but not neutrophil migration at 4 h. The effect of endothelin antagonism on neutrophil accumulation at 24 h was concomitant with inhibition of eosinophil and CD4 and CD8 T lymphocyte influx. It is surprising that the ETA receptor blockade did not inhibit the accumulation of γδ T lymphocytes, cells that are important for granulocyte recruitment in this model. Blockade of ETA receptors did not influence the expression of adhesion molecules (CD11b, CD49d) on granulocytes but abrogated the increase in tumor necrosis factor α levels 4 h after LPS stimulation and also markedly inhibited increases in levels of interleukin-6 and keratinocyte-derived chemokine/CXC chemokine ligand 1 but not eotaxin/chemokine ligand 11. Thus, acting via ETA receptors, endogenous endothelins play an important role in early cytokine/chemokine production and on granulocyte and lymphocyte mobilization in LPS-induced pleurisy.
Sex and Age Differences in Lipoprotein Subclasses Measured by Nuclear Magnetic Resonance Spectroscopy: The Framingham Study
Authors: Freedman David S , Otvos James D , Jeyarajah Elias J , Shalaurova Irina , Cupples L Adrienne , Parise Helen , D’Agostino Ralph B , Wilson Peter W F , Schaefer Ernst J 
Published: April 2004

AbstractBackground: The sex differential in coronary heart disease (CHD) risk, which is not explained by male/female differences in lipid and lipoprotein concentrations, narrows with age. We examined whether this differential CHD risk might, in part, be attributable to the sizes of lipoprotein particles or concentrations of lipoprotein subclasses.Methods: We analyzed frozen plasma samples from 1574 men and 1692 women from exam cycle 4 (1988–1990) of the Framingham Offspring Study. Nuclear magnetic resonance (NMR) spectroscopy was used to determine the subclass concentrations and mean sizes of VLDL, LDL, and HDL particles. Concentrations of lipids and apolipoproteins were measured by standard chemical methods.Results: In addition to the expected sex differences in concentrations of triglycerides, LDL-cholesterol, and HDL-cholesterol, women also had a lower-risk subclass profile consisting of larger LDL (0.4 nm) and HDL (0.5 nm) particles. The sex difference was most pronounced for HDL, with women having a twofold higher (8 vs 4 μmol/L) concentration of large HDL particles than men. Furthermore, similar to the narrowing of the sex difference in CHD risk with age, the observed male/female difference in HDL particle size also decreased with age. Although lipoprotein particle sizes were highly correlated with lipid and lipoprotein concentrations, the sex differences in the mean sizes of lipoprotein particles persisted (P &lt;0.001) even after adjustment for lipid and lipoprotein concentrations.Conclusions: Women have a less atherogenic subclass profile than men, even after accounting for differences in lipid concentrations.
Effect of Recombinant Human Growth Hormone and Insulin‐Like Growth Factor‐1 Administration on IGF‐1 and IGF‐Binding Protein‐3 Levels in Brain Injury
Authors: Rockich Kevin T. , Hatton Jimmi C. , Kryscio Richard J. , Young Byron A. , Blouin Robert A. 
Published: April 2004

Study Objective. To assess the effect of recombinant human growth hormone (rhGH) on the insulin‐like growth factor‐1 (IGF‐1) plasma concentration versus time profile during continuous infusion of recombinant human (rh)IGF‐1 to patients with traumatic brain injury (TBI).Setting. University of Kentucky Chandler Medical Center.Patients. Twenty‐three patients with TBI (aged 18–59 yrs) with Glascow Coma Scale scores of 4–10.Intervention. Patients were randomized to receive rhIGF‐1 0.01 mg/kg/hour and daily subcutaneous doses of rhGH 0.05 mg/kg/day or saline for 14 days.Measurements and Main Results. Plasma concentrations of IGF‐1 and IGF‐binding protein (BP)‐3 were quantified by radioimmunoassay. Patients receiving rhIGF‐1/rhGH reached a peak IGF‐1 concentration (1199.3 ± 84.0 μg/L) at 72 hours and maintained it throughout the study. Levels of IGF‐1 in the control group did not change significantly above baseline throughout the study. Concentrations of IGFBP‐3 were significantly higher after 48 hours in the treated group (5.1 ± 0.4 mg/L) than in controls (2.9 ± 0.5 mg/L) and continued until the end of the study (p<0.05).Conclusion. Infusion of rhIGF‐l in conjunction with rhGH effectively achieved and maintained supraphysiologic IGF‐1 plasma concentrations throughout the dosing period in patients with TBI. It appears that rhGH alters the IGF‐1 plasma concentration versus time profile during continuous administration. Although speculative, changes in protein binding of IGF‐1 are the most likely mechanism.
Indole Synthesis by
Pd
‐Catalyzed Annulation Of Ketones With o‐Iodoaniline: 1,2,3,4‐Tetrahydrocarbazole
Authors: Chen Cheng‐yi , Larsen Robert D. 
Published: April 2004

Abstract

1, 2, 3, 4‐Tetrahydrocarbazole

R Cyclohexanone

o‐Iodoaniline

P 1, 2, 3, 4‐Tetrahydrocarbozole
(Phenyl)[2‐(Trimethylsilyl)Phenyl]Iodonium Triflate. An Efficient And Mild Benzyne Precursor
Authors: Kitamura Tsugio , Todaka Mitsuru , Fujiwara Yuzo 
Published: April 2004

Abstract

(Phenyl)[2‐(trimethylsilyl)phenyl] iodonium triflate

R 1,2‐Dichlorobenzene

I 1, 2‐Bis(trimethylsilyl) benzene 1

R (Diacetoxyiodo) benzene

I (phenyl)[2‐(trimethylsilyl) phenyl] iodonium triflate 2

Furan

P 1, 4‐Dihydronaphthalene 1,4‐oxide 3
4‐Hydroxy[1‐13C]Benzoic Acid
Authors: Lang Martin , Lang‐Fugmann Susanne , Steglich Wolfgang 
Published: April 2004

Abstract4‐Hydroxy[1‐13C] benzoic acidR Ethyl [2‐13C] acetateI Diethyl [2‐13C] malonate4H, Pyran‐4‐oneEthyl‐4‐hydroxy[1‐13C]benzoateP 4‐Hydroxy[1‐13C] benzoic acid
[4 + 2] Cycloaddition of 1‐Dimethylamino‐3‐tert‐Butyldimethylsiloxy‐1,3‐Butadiene with Methyl Acrylate: 4‐Hydroxymethyl‐2‐Cyclohexen‐1‐One
Authors: Kozmin Sergey A. , He Shuwen , Rawal Viresh H. 
Published: April 2004

Abstract

4‐Hydroxymethyl‐2‐cyclohexen‐1‐one

R 1‐Dimethylamino‐3‐tert‐butyldimethylsiloxy‐1,3‐butadiene 1

Methyl acrylate

I 4‐Carbomethoxy‐3‐dimethylamino‐1‐tert‐butyldimethylsiloxy‐1‐cyclohexene 2

4‐Hydroxymethyl‐3‐dimethylamino‐1‐tert‐butyldimethylsiloxy‐1‐cyclohexene 3

P 4‐Hydromethyl‐2‐cyclohexen‐1‐one 4
(+)‐(1R,2S,3R)‐Tetracarbonyl[(1–3η)‐1‐(Phenylsulfonyl)‐ But‐2‐en‐1‐yl]Iron(1+) Tetrafluoroborate
Authors: Enders D. , Jandeleit B. , von Berg S. 
Published: April 2004

Abstract

(+)‐(1R,2S,3R)‐Tetracarbonyl[(1‐3n)‐1‐(phenylsulfonyl)‐but‐2‐en‐1‐yl]iron (1+)tetrafluoroborate

R (−)‐(E,S)‐3‐(benzyloxy)‐1‐butenyl phenyl sulfone

I (+)‐(E,1R,3S)‐Tetracarbonyl[(3‐(benzyloxy)‐1‐(phenylsulfonyl)‐n
2
‐but‐1‐ene]‐iron (0)

P (+)‐(1R,2S,3R)‐Tetracarbonyl[(1‐3n)‐1‐(phenylsulfonyl)‐but‐2‐en‐1‐yl]iron (1+)tetrafluoroborate (1)
Tributylstannane (
Bu
3
Sn
H
)‐Catalyzed
B
arton‐
M
c
C
ombie Deoxygenation of Alcohols: 3‐Deoxy‐1,2:5,6‐Bis‐O‐(1‐Methylethylidene)‐α‐
D
‐Ribo‐Hexofuranose
Authors: Tormo Jordi , Fu Gregory C. 
Published: April 2004

Abstract

3‐Deoxy‐1,2:5,6‐bis‐O‐(1‐methylethylidene)‐α‐D‐ribo‐hexanose

R 1,2:5,6‐Di‐O‐isopropylidene‐D‐glucose; Phenylchlorothionoformate

I 1,2:5,6‐Bis‐O‐(1‐methylethylidene)‐O‐phenyl carbonothioate‐α‐D‐glucofuranose 1

P B‐Deoxy‐1,2:5,6‐bis‐O‐(1‐methylethylidene)‐α‐D‐ribo‐hexofuranose 2
Ethyl 3‐(p‐Cyanophenyl)Propionate from Ethyl 3‐Iodopropionate and p‐Cyanophenylzinc Bromide
Authors: Jensen Anne Eeg , Kneisel Florian , Knochel Paul 
Published: April 2004

Abstract

Ethyl 3‐(p‐cyanophenyl)prolonate

R Ethyl 3‐iodopropionate

4‐Cyanophenylzinc bromide

P Ethyl 3‐(p‐cyanophenyl)propionate
Anti‐Selective Boron‐Mediated Asymmetric
A
ldol Reaction of Carboxylic Esters: Synthesis of (2S, 3R)‐2,4‐Dimethyl‐1,3‐Pentanediol
Authors: Abiko Atsushi 
Published: April 2004

Abstract

(2S,3R)‐2,4‐Dimethyl‐1,3‐pentanediol

R 2(N‐Benzyl‐N‐mesitylenesulfonyl)amino‐1‐phenyl‐1‐propyl propionate Is this (+)‐1

I (1′R)‐Phenyl‐(2′S)‐[(phenylmethyl)[(2,4,6‐trimethylphenyl)sulfonyl]amino‐propyl(3R)‐hydroxy‐(2R),4‐dimethylpentanoate 2

R (2S,3R)‐2,4‐Dimethyl‐1,3‐pentanediol 3

2‐(N‐Benzyl‐N‐mesitylenesulfonyl)amino‐1‐phenyl‐propanol
2‐Amino‐3‐Fluorobenzoic Acid
Authors: Kollmar Martin , Parlitz Richard , Oevers Stephan R. , Helmchen Günter 
Published: April 2004

Abstract

2‐Amino‐3fluorobenzoic acid

R 2‐Fluoroaminobenzene 1

I N‐(2‐Fluorophenyl)‐2‐(hydroxyimino)acetamide 2

7‐Fluoroisatin 3

P 2‐Amino‐3‐fluorobenzoic acid 4
Nucleophilic Aromatic Substitution of Aryl Fluorides by Secondary Nitriles: Preparation of 2‐(2‐Methoxyphenyl)‐2‐Methylpropionitrile
Authors: Caron Stéphane , Wojcik Jill M. , Vazquez Enrique 
Published: April 2004

Abstract

2‐(2‐Methoxyphenyl)‐2‐methylpropionitrile

R 2‐Fluoroanisole

P 2‐(2‐Methoxyphenyl)‐2‐methylpropionitrile
(5
S
)‐(
d
‐Menthyloxy)‐2(5
H
)‐Furanone
Authors: Moradei Oscar M. , Paquette Leo A. 
Published: April 2004

Abstract

(5S)‐(d‐Menthyloxy)‐2(5H)‐furanone

5‐Hydroxy‐2(5H)‐furanone

Camphorsulfonic acid

Furfural

Rose Bengal
Synthesis of Indoles by Palladium‐Catalyzed Reductive
N
‐Heteroannulation of 2‐Nitrostyrenes: Methyl Indole‐4‐Carboxylate
Authors: Söderberg Björn C. , Shriver James A. , Wallace Jeffery M. 
Published: April 2004

Abstract

Methyl indole‐4‐carboxylate

Methyl 2‐methyl‐3‐nitrobenzoate

Methyl 2‐bromomethyl‐3‐nitrobenzoate

Methyl 2‐ethenyl‐3‐nitrobenzoate

Palladium acetate
Ring‐Closing Metathesis Synthesis of
N
‐Boc‐3‐Pyrroline
Authors: Ferguson Marcelle L. , O'Leary Daniel J. , Grubbs Robert H. 
Published: April 2004

Abstract

N‐Boc‐3‐pyrroline

Boc‐diallyamine

1H‐Pyrrole‐1‐carboxylic acid, 2,5‐dihydro‐, 1,1‐dimethylethyl ester

Triethylamine

Ruthenium chloride

Tris(hydroxymethyl)phosphine
Ruthenium‐Catalyzed Alkylation of Aromatic Ketones with Olefins: 8‐[2‐(Triethoxysilyl)Ethyl]‐1‐Tetralone
Authors: Kakiuchi Fumitoshi , Murai Shinji 
Published: April 2004

Abstract

8‐[2(Triethoxysilyl)ethyl]‐1‐tetralone

Ruthenium carbonyldihydridotris(triphenylphosphine)

Triethoxyvinylsilane

1‐Tetralone
Transformation of Primary Amines to
N
‐Monoalkylhydroxylamines:
N
‐Hydroxy‐(
S
)‐1‐Phenylethylamine Oxalate
Authors: Tokuyama Hidetoshi , Kuboyama Takeshi , Fukuyama Tohru 
Published: April 2004

Abstract

(S)‐1‐Phenylethylamine

Diisopropylethylamine

Bromoacetonitrile

(S)‐[1‐Phenylethyl]imino]acetonitrile N‐oxide

Hydroxylamine hydrochloride

Oxalic acid

N‐Hydroxy‐(S)‐1‐phenylethylamine oxalate
Tetrabenzyl Pyrophosphate
Authors: Nelson Todd D. , Rosen Jonathan D. , Bhupathy M. , McNamara James , Sowa Michael J. , Rush Chad , Crocker Louis S. 
Published: April 2004

AbstractTetrabenzyl pyrophosphateDibenzyl phosphateIsopropyl acetate1, 3‐Dicyclohexylcarbodiimide1, 3‐ Dicyclohexylurea
Aluminum Compounds, Organic
Authors: Krause Michael J. , Orlandi Frank , Saurage Alfred T. , Zietz Joseph R. 
Published: April 2004

AbstractThe article contains sections titled:1.Introduction2.Alkylaluminums and Derivatives2.1.Physical Properties2.2.Chemical Properties2.2.1.Reactions with Olefins2.2.2.Reactions with Oxygen2.2.3.Reactions with Metal Compounds2.2.4.Reactions with Proton‐Donating Materials2.2.5.Alkylaluminums in Organic Synthesis2.3.Production of Trialkylaluminums and Alkylaluminum Chlorides2.3.1.Hydroalumination to Produce Trialkylaluminums2.3.2.Reaction of Aluminum With Alkyl Halides to Make Alkylaluminum Sesquichlorides2.3.3.Reduction of Alkylaluminum Sesquichlorides to Make Trialkylaluminums2.3.4.Reaction of Acids With Trialkylaluminums to Produce Alkylaluminum Chlorides2.3.5.Reproportionation Reactions2.3.6.Olefin Elimination and Displacement Reactions2.3.7.Other Organoaluminum Conversions2.4.Uses of Alkylaluminum Compounds2.4.1.Stoichiometric Applications2.4.2.Catalytic Applications2.5.Quality Specifications3.Aluminoxanes3.1.Production3.2.Physical and Chemical Properties3.3.Uses3.3.1.Mechanism of Polymerization Using Aluminoxanes3.3.2.Production of Stereoregular Polymers using Aluminoxanes3.3.3.Polymers Produced by Aluminoxanes3.4.Analysis and Quality Specifications4.Handling, Storage, and Transportation5.Waste Disposal and Environmental Protection6.Economic Aspects7.Toxicology and Occupational Health8.Acknowledgments
Aluminum Oxide
Authors: Hudson L. Keith , Misra Chanakya , Perrotta Anthony J. , Wefers Karl , Williams F. S. 
Published: April 2004

AbstractThe article contains sections titled:1.General Aspects1.1.Aluminum Hydroxides1.2.Aluminum Oxide Hydroxides1.3.Aluminum Oxide, Corundum1.4.The Al2O3‐ H2O System1.5.Thermal Decomposition of Aluminum Hydroxides1.6.Aluminates and Related Compounds2.Bauxite, the Principal Raw Material2.1.Definition and Geology2.2.Composition and Properties2.3.Genesis of Bauxites2.4.Major Bauxite Deposits2.5.Economic Aspects3.Bayer Process3.1.History and Procedure3.1.1.Bauxite Preparation3.1.2.Digestion3.1.3.Equipment3.1.4.Residue Separation3.1.5.Precipitation3.1.6.Impurities3.1.7.Calcination3.1.8.Evaporation3.1.9.Residue Disposal3.1.10.Energy in the Process3.2.Economic Aspects4.Other Processes for Alumina Production4.1.Raw Materials4.2.Alkaline Processes4.3.Acid Processes5.Metallurgical Alumina5.1.Alumina Properties Required for Smelting5.2.Typical Specifications for Metallurgical Alumina6.Industrial Alumina Chemicals6.1.Aluminum Hydroxides6.2.Adsorbent and Catalytic Aluminas6.2.1.Preparation of Activated Aluminas6.2.2.Adsorbent Applications6.2.3.Catalytic Applications7.Ceramic Uses of Alumina7.1.Calcined Alumina7.2.Fused Alumina8.Toxicology and Industrial Hygiene