bluuebunny/crossref_metadata_2025_split huggingface dataset:
Organic polymer monoliths as stationary phases for capillary HPLC
Authors: Svec Frantisek 
Published: September 2004

AbstractModern rigid porous polymer monoliths were conceived as a new class of stationary phases in classical columns in the early 1990s and later extended to the capillary format. These monolithic materials are typically prepared using a simple molding process carried out within the confines of the capillary. Polymerization of a mixture comprising monomers, initiator, and porogenic solvent affords macroporous materials with large through‐pores that enable applications in a rapid flow‐through mode. Since all the mobile phase must flow through the monolith, convection considerably accelerates mass transport within the monolithic separation medium and improves the separations. As a result, monolithic columns perform well even at very high flow rates. Various mechanisms including thermally and UV initiated free radical polymerization as well as ring opening metathesis copolymerizations were demonstrated for the preparation of monolithic capillary columns. The versatility of these preparation techniques was demonstrated by their use with hydrophobic (styrene, divinylbenzene, butyl methacrylate, ethylene dimethacrylate), hydrophilic (2‐hydroxyethyl methacrylate, methacrylamide, methylenebisacrylamide), ionizable (vinylsulfonic acid, 2‐acrylamido‐2‐methyl‐propanesulfonic acid), and tailor‐made (norborn‐2‐ene, 1,4,4a,5,8,8a‐hexahydro‐1,4,5,8‐exo,endo‐dimethanonaphthalene) monomers. Variation of polymerization conditions enables control of the porous properties of the monolith over a broad range and mediates the hydrodynamic properties of the monolithic columns. The applications of polymer‐based monolithic capillary columns are demonstrated for numerous separations in the μHPLC mode.
Separation, pre‐concentration, and HPLC analysis of methylxanthines in urine samples
Authors: Zydroń Mirosława , Baranowski Jacek , Baranowska Irena 
Published: September 2004

AbstractAn SPE method, using RP18 phases, for the simultaneous extraction of caffeine, theobromine, theophylline, paraxanthine, 1‐methylxanthine, 3‐methylxanthine, 7‐methylxanthine, 1‐methyluric acid, 1,3‐dimethyluric acid, 1,7‐dimethyluric acid, and 1,3,7‐trimethyluric acid from urine has been developed. Besides a gradient HPLC system for the analysis of the compounds of interest on a LiChrosorb RP‐18 (7 μm) column with mobile phase containing 0.05% aq. solution of trifluoroacetic acid and acetonitrile has been elaborated. The procedure has been successfully applied to the analysis of methylxanthines and methyluric acids in urine of patients with chronic asthma treated with theophylline and in urine of healthy subjects.
Split-liver transplantation: Coming of age
Authors: Cronin David C. , Millis Michael J. 
Published: September 2004

Objective
To identify predictors of graft and recipient survival from a single-institution series of in situ split-liver transplantations and compare outcomes to living donor and whole organs for adults and children.

Summary Background Data
Split-liver transplantation is a surgical technique that creates 2 allografts from a single cadaver donor. We have applied split-liver transplantation to all indications and categories of medical urgency for initial as well as retransplantation to expand the current donor pool and decrease reliance upon living donation.

Methods
A retrospective analysis was conducted of 100 consecutive in situ split-liver transplantations yielding a left lateral segment and right trisegment graft that were performed at the University of California Los Angeles between 9/91 and 02/03. These 100 transplantations generated 190 allografts for transplantation into 105 children and 60 adults, with the sharing of 25 allografts among transplant centers across the United States. Outcomes and incidence of complications were compared with living donor and whole organ recipients receiving liver transplantation during the same time period with independent predictors of split-liver graft and recipient survival identified by multivariate analysis.

Results
The incidence of biliary and vascular complications observed in recipients of left lateral segment grafts created by split-liver transplantation was not statistically different from recipients of left lateral segment grafts created from living donation or children receiving whole-organ grafts from pediatric donors. Kaplan-Meier survival estimations of left lateral segment graft and recipient survival also demonstrated no statistical difference among split-liver, living donor, and whole-organ recipients. Right trisegment grafts from split-liver transplantation demonstrated a 10% incidence of biliary and 7% incidence of vascular complications. Long-term graft function was excellent with patient and graft survival equal to 1086 recipients of cadaver whole-organ grafts from donors ages 10-40 years who underwent transplant operations during the same time period. Predictors of split-liver transplantation graft and recipient survival included United Network for Organ Sharing status at transplantation, indication, occurrence of a complication, donor creatinine, and donor length of hospitalization.

Conclusions
Split-liver transplantation is an effective mechanism for immediate expansion of the cadaver donor pool that can reduce dependence upon living donation in adults and children. (Ann Surg 2003;238:496-507).
Prospective highlights of functional skin proteomics
Authors: Huang Chun‐Ming , Elmets Craig A. , van Kampen Kent R. , DeSilva Tivanka S. , Barnes Stephen , Kim Helen , Tang De‐chu C. 
Published: September 2004

AbstractAlthough a wide variety of protein profiles have been extensively constructed via proteomic analysis, the comprehensive proteomic profiling of the skin, which is considered to be the largest organ of the human body, is still far from complete. Our efforts to establish the functional skin proteome, a protein database describing the protein networks that underlie biological processes, has set in motion the identification and characterization of proteins expressed in the epidermis and dermis of the BALB/c mice. In this review, we will highlight various cutaneous proteins we have characterized and discuss their biological functions associated with skin distress, immunity, and cancer. This type of research into functional skin proteomics will provide a critical step toward understanding disease and developing successful therapeutic strategies. © 2004 Wiley Periodicals, Inc., Mass Spec Rev 24:647–660, 2005
Gas chromatographic–mass spectrometric urinary metabolome analysis to study mutations of inborn errors of metabolism
Authors: Kuhara Tomiko 
Published: September 2004

AbstractUrine contains numerous metabolites, and can provide evidence for the screening or molecular diagnosis of many inborn errors of metabolism (IEMs). The metabolomic analysis of urine by the combined use of urease pretreatment, stable‐isotope dilution, and capillary gas chromatography/mass spectrometry offers reliable and quantitative data for the simultaneous screening or molecular diagnosis of more than 130 IEMs. Those IEMs include hyperammonemias and lactic acidemias, and the IEMs of amino acids, pyrimidines, purines, carbohydrates, and others including primary hyperoxalurias, hereditary fructose intolerance, propionic acidemia, and methylmalonic acidemia. Metabolite analysis is comprehensive for mutant genotypes. Enzyme dysfunction—either by the abnormal structure of an enzyme/apoenzyme, the reduced quantity of a normal enzyme/apoenzyme, or the lack of a coenzyme—is involved. Enzyme dysfunction—either by an abnormal regulatory gene, abnormal sub‐cellular localization, or by abnormal post‐transcriptional or post‐translational modification—is included. Mutations—either known or unknown, common or uncommon—are involved. If the urine metabolome approach can accurately observe quantitative abnormality for hundreds of metabolites, reflecting 100 different disease‐causing reactions in a body, then it is possible to simultaneously detect different mutant genotypes of far more than tens of thousands. © 2004 Wiley Periodicals, Inc., Mass Spec Rev 24:814–827, 2005
The chemokines CCL11, CCL20, CCL21, and CCL24 are preferentially expressed in polarized human secondary lymphoid follicles
Authors: Buri Caroline , Gutersohn Andreas , Hauser Chantal , Kappeler Andreas , Mueller Christoph 
Published: September 2004

AbstractChemokines regulate cellular trafficking to and from lymphoid follicles. Here, the distribution pattern of four CCL chemokines is defined by in situ hybridization in human lymphoid follicles from tonsils and lymph nodes (LNs) of newborns and adults. Cells expressing CCL11 (eotaxin) and CCL20 (Exodus) were preferentially located within follicles, while cells expressing CCL21 (secondary lymphoid‐tissue chemokine) and CCL24 (eotaxin‐2) mRNA were almost exclusively found in the perifollicular areas. Hence, the two CCR3‐binding chemokines, CCL11 and CCL24, showed a mutually exclusive expression pattern in the intra‐ and extra‐follicular areas, respectively. Chemokine gene expression paralleled follicular maturation: in tonsils, where approximately 80% of follicles are polarized, CCL11 and CCL20 mRNA‐positive cells were detected more frequently than in lymph nodes from adults, where about half of follicles are non‐polarized. No intrafollicular chemokine expression was detectable in the primary follicles from newborns. Extrafollicular cells expressing CCL21 and CCL24 were again more frequent in tonsils than in LNs from adults. The observed preferential presence of cells expressing CC chemokines in polarized human lymphoid follicles indicates that chemokines are not only instrumental in the induction of follicle formation, but may also be involved in their further differentiation. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Chromosomal instability and APC gene mutations in human sporadic colorectal adenomas
Authors: Giaretti Walter , Venesio Tiziana , Prevosto Claudia , Lombardo Federica , Ceccarelli Jenny , Molinu Silvia , Risio Mauro 
Published: September 2004

AbstractThe mechanisms by which adenomatous polyposis coli (APC) gene mutations contribute to colorectal tumourigenesis and progression are still not fully understood. Using in vitro mouse embryonic stem cells, APC mutations have been proposed to dysregulate the interactions between kinetochores and microtubules during mitosis, leading to chromosomal instability (CIN) and aneuploidy. A link between APC mutations and aneuploidy in vivo among human sporadic colorectal adenomas has not been reported previously and was therefore investigated in the present series of 61 adenomas. Multi‐parameter flow cytometry, based on scattering and fluorescence from the DNA‐specific 4,6‐diamidino‐2‐phenylindole‐2‐hydrochloride (DAPI) dye, which separates epithelial from stromal lymphocyte nuclei, was used to evaluate the DNA index (DI) and to sort epithelial nuclei. Additionally, DNA extracted from these sorted nuclei was used to analyse APC mutations by DNA sequencing. Aneuploidy was present in 20 of 61 adenomas (33%), with 15 of these 20 cases (75%) having a near‐diploid DI (DI different from 1 and less than 1.3). APC mutations were detected in 19 adenomas (31%): 12 were within or downstream of the mutation cluster region (MCR), roughly defined by codons 1200–1500, and seven were upstream of the MCR. Overall, the prevalence of aneuploidy in APC wild‐type and mutated adenomas was 26% and 47%, respectively, and no statistically significant association was found between APC status and DI (p = 0.142). However, when APC mutations were subdivided into two groups, ie occurring within/downstream of the MCR and upstream of the MCR, the association of APC mutations within and downstream of the MCR with aneuploidy was statistically significant (p = 0.017). In conclusion, the present data suggest that the type of APC mutation may play a role in the origin of CIN in vivo in human sporadic colorectal adenomas and that APC mutations within and downstream of the MCR, and large‐scale chromosomal alterations, may co‐operate in the progression of a subgroup of adenomas. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
p53 overexpression and mutation in metaplastic carcinoma of the breast: genetic evidence for a monoclonal origin of both the carcinomatous and the heterogeneous sarcomatous components
Authors: Lien Huang‐Chun , Lin Chung‐Wu , Mao Tsui‐Lien , Kuo Sung‐Hsin , Hsiao Cheng‐Hsiang , Huang Chiun‐Sheng 
Published: September 2004

AbstractMetaplastic carcinoma of the breast (MCB) is characterized by the biphasic presence of both a carcinomatous component (CC) and heterogeneous sarcomatous components (HSCs). Although an epithelial or myoepithelial origin of the HSCs has been suggested, molecular evidence for a common origin for the CC and HSCs is limited and the mechanism underlying the sarcomatous or metaplastic change is unknown. The present study investigated the frequency and nature of p53 expression and mutation in 11 biphasic and three monophasic MCBs by immunohistochemistry and either needle‐assisted or laser‐capture microdissection, followed by PCR and direct sequencing. In all 11 biphasic MBCs, staining for p53 was concordant in the CC and HSCs (8/11 positive and 3/11 negative), consistent with a monoclonal origin of both components. Significantly, whenever a component of carcinoma in situ was present (5/11), the p53 staining was always concordant with that in the CC and HSCs. Screening of the 14 cases for p53 mutation identified four mutants, each in a single case of biphasic MCB with concordant p53 overexpression. Both the CC and each of the HSCs revealed identical p53 mutation in all four cases; in addition, one of the four cases also had an in situ component and the same mutant was found simultaneously in the in situ, invasive, and sarcomatous components. The concordant pattern of p53 alteration (overexpression or mutation) implies that early p53 mutation, occurring prior to invasion, was maintained throughout tumour progression and metaplastic change. The findings therefore support a monoclonal histogenesis of the various components, but are neutral regarding the role of p53 alteration in the development of metaplastic change in MCBs. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Geminin predicts adverse clinical outcome in breast cancer by reflecting cell‐cycle progression
Authors: Gonzalez Michael A , Tachibana Kiku‐e K , Chin Suet‐Feung , Callagy Grace , Madine Mark A , Vowler Sarah L , Pinder Sarah E , Laskey Ronald A , Coleman Nicholas 
Published: September 2004

AbstractGeminin inhibits DNA replication by preventing Cdt1 from loading minichromosome maintenance (MCM) proteins onto DNA. The present study has investigated whether the frequency of geminin expression predicts clinical outcome in breast cancer. Immunohistochemistry was used first to examine geminin expression in normal and malignant breast tissue (n = 67). Correlations with cell‐cycle parameters, pathological features, and clinical outcome were then determined using an invasive breast carcinoma tissue microarray (n = 165). Breast carcinomas were scanned for mutations (n = 61) and copy number imbalances (n = 241) of the geminin gene. Finally, the cell cycle distribution of geminin in breast cancer cells was investigated in vivo and in vitro. Despite a putative tumour suppressor function, it was found that increased geminin expression is a powerful independent indicator of adverse prognosis in invasive breast cancer. Both poor overall survival (p = 0.0002) and the development of distant metastases (p = 0.005) are predicted by high geminin expression, which performs better in this patient cohort than traditional factors currently used to determine prognosis and appropriate therapy. No mutations or deletions of the geminin gene and no evidence that a high frequency of protein expression is related to gene amplification were found. It is shown that geminin is expressed from S to M phase in breast carcinoma tissue and cell lines, disappearing at the metaphase–anaphase transition. While MCM proteins identify all non‐quiescent cells, geminin identifies the sub‐fraction that have entered S phase, but not exited mitosis, thereby indicating the rate of cell‐cycle progression. It is suggested that this explains its unexpected value as a prognostic marker in breast cancer. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Angiogenesis and VEGF expression in pre‐invasive lesions of the human breast
Authors: Viacava Paolo , Naccarato Antonio Giuseppe , Bocci Guido , Fanelli Giovanni , Aretini Paolo , Lonobile Antonino , Evangelista Giuseppe , Montruccoli Giancarlo , Bevilacqua Generoso 
Published: September 2004

AbstractAngiogenesis (as microvascular density—MVD) and vascular endothelial growth factor (VEGF) expression were evaluated by immunohistochemistry in all types of human pre‐invasive breast lesion, un‐associated with invasive carcinoma, including florid ductal hyperplasia of usual type (FDHUT, 40 cases), atypical ductal hyperplasia (ADH, 10), well‐differentiated intraductal carcinoma (WDIC, 16), intermediately differentiated intraductal carcinoma (IDIC, 25), poorly differentiated intraductal carcinoma (PDIC, 20), atypical lobular hyperplasia (ALH, 13), and lobular carcinoma in situ (LCIS, 12). Both parameters were also studied in normal glandular structures obtained from normal breasts or from breasts containing pre‐invasive lesions. Increased vascularization was present in all lesion types (MVD mean values (expressed as vessel number/mm2): 115 ± 8 in normal lobules, 146 ± 26 in lesions; p < 0.05) and increased with lesion severity. In ductal lesions, MVDs were significantly higher in PDIC (190 ± 65) and IDIC (167 ± 61) than in FDHUT (123 ± 40) and ADH (122 ± 47); MVD was much higher in PDIC than in WDIC (p < 0.001). WDIC showed peculiar features, with a degree of vascularization closer to hyperplasia than to the other histological types of in situ ductal cancer; this observation is in line with the hypothesis that IDIC and PDIC may originate ‘de novo’, without a mandatory transition through WDIC. LCIS was more vascularized than ALH (168 ± 50 and 125 ± 40, respectively; p < 0.05), showing MVD values similar to those of PDIC and IDIC. The vascularization of normal lobules was constant, regardless of their association with lesions. VEGF expression in normal glandular structures was lower than in lesions, with the highest levels found in ductal lesions when compared with lobular lesions. No correlation was found between VEGF expression and the degree and/or type of vascularization. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Analysis of microsatellite alterations in gastric carcinoma using the crypt isolation technique
Authors: Jiao Yu‐Fei , Sugai Tamotsu , Habano Wataru , Suzuki Masamichi , Takagane Akinori , Nakamura Shin‐ichi 
Published: September 2004

AbstractThe crypt isolation technique was used to analyse loss of heterozygosity (LOH) and microsatellite instability (MSI) in gastric carcinomas (36 intestinal type, 17 solid type, and 23 diffuse type) using a polymerase chain reaction assay. Increased LOH frequencies and fractional allelic losses (FAL) were observed in samples prepared using the crypt isolation technique compared with those isolated by the conventional method. A significant increase in LOH was found at several chromosomal loci, and significant differences in FAL were found in patients with intestinal‐ and solid‐type tumours. There was no difference in the frequency of MSI using either technique. In samples prepared by the crypt isolation technique, significant allelic losses (≥50%) were observed at most loci tested in intestinal‐ and solid‐type tumours, but not in diffuse‐type tumours. Significant losses of some of these loci are novel findings for gastric cancer. FAL values were significantly higher in intestinal‐ and solid‐type tumours than in diffuse‐type tumours. MSI‐high was observed in intestinal‐ (17%) and solid‐type (12%) tumours. The results suggest that the crypt isolation technique is useful for accurate allelic loss analysis in gastric carcinoma and that LOH and MSI are more common in intestinal‐ and solid‐type tumours than in diffuse‐type tumors. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Caspase‐3 expression is reduced, in the absence of cleavage, in terminally differentiated normal oral epithelium but is increased in oral squamous cell carcinomas and correlates with tumour stage
Authors: Hague Angela , Eveson John W , MacFarlane Marion , Huntley Suzanne , Janghra Nari , Thavaraj Selvam 
Published: September 2004

AbstractOral carcinomas are known to have a greater apoptotic index than normal oral epithelium, evident as shrinking cells with condensed chromatin. In this study, these morphologically apoptotic cells stained positively for cleaved (active) caspase‐3. In normal oral epithelium, cleaved caspase‐3 positive‐cells were only rarely detected. The terminally differentiated surface epithelial layers did not express cleaved caspase‐3. The caspase‐3 pro‐enzyme showed a gradient of expression in normal oral epithelium, decreasing with differentiation. No expression was detectable in surface epithelial layers. Lack of expression of the major ‘executioner’ caspase‐3 may, at least in part, explain differences in morphology between terminally differentiated and apoptotic cells. In cancers of different tissue origins, caspase‐3 pro‐enzyme expression can be either increased or decreased compared with normal tissue counterparts. To determine how caspase‐3 expression alters during oral carcinogenesis, caspase‐3 expression was compared in 39 samples of normal oral epithelium and 54 oral squamous cell carcinomas. Squamous cell carcinomas had more intense caspase‐3 staining than normal epithelium (p < 0.001). Moreover, within the oral squamous cell carcinoma series, there was significantly more intense nuclear and cytoplasmic staining with increasing STNMP stage (p = 0.017 and 0.03, respectively). This was a reflection of significant associations with site (S), palpable lymph nodes (N), and differentiation (P). Both caspase‐3 staining intensity and the percentage of cells positive for caspase‐3 were inversely associated with differentiation. Studies of the mechanisms by which high levels of caspase‐3 expression are tolerated in oral carcinoma cells may identify targets that can be used to harness caspase‐3 overexpression for therapeutic benefit. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.