bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surface modification of poly (D,L‐lactic acid) with chitosan and its effects on the culture of osteoblasts in vitro
Authors: Cai Kaiyong , Yao Kangde , Cui Yuanlu , Lin Songbai , Yang Zhiming , Li Xiuqiong , Xie Huiqi , Qing Tingwu , Luo Juan 
Published: August 2002

AbstractChitosan is a good biodegradable natural polymer, widely used in biomedical fields. In this study, chitosan was used to modify the surface of poly (D,L‐lactic acid) (PDLLA) in order to enhance its cell affinity. The properties of a modified PDLLA surface and control were investigated by contact angle and electron spectroscopy for chemical analysis (ESCA), which indicated the changes in surface energy and chemical structure. Scanning electron microscopy (SEM) observation displayed differences in surface morphology between the chitosan‐modified film and the control. These data reflected that PDLLA films could be modified with chitosan and in turn may affect the biocompatibility of the modified films. Therefore, adhesion and growth of osteoblasts on modified PDLLA films as well as control were studied. Cell morphologies on the films were examined by SEM and cell viability was evaluated using an MTT assay; the differentiated cell function was assessed by measuring alkaline phosphatase (ALP) activity. The ALP activity of modified PDLLA films was significantly higher than that found on the control (p < 0.01). The proliferation of osteoblasts on modified films was also found to be higher than that on the control (p < 0.05), suggesting that chitosan could be used to modify PDLLA and then enhance its cell biocompatibility. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 398–404, 2002; DOI 10.1002/jbm.10008
Cells, rather than extracellular matrix, nucleate apatite in glutaraldehyde‐treated vascular tissue
Authors: Kim Kookmin M. 
Published: August 2002

AbstractGlutaraldehyde (GA) causes a large increase in [Ca2+]i and [Pi]i and calcification of porcine aortic valve fibroblasts. Calcification in GA‐treated vascular tissue is likely to begin intracellularly, but the potential role of extracellular matrix has not been taken into account in earlier studies. To compare the role of cells and matrix in calcification, intestinal pouches made of a lipid‐extracted rat small intestine were prepared. Lipid‐extracted porcine aortic valves, or cells cultured from those same valves, were placed in intestinal pouches, sealed, fixed with GA, and grafted in rat subcutis. Cells in the pouches calcified in 3 weeks whereas the valvular matrix did not calcify for 9 weeks. Cellular calcification spread to the wall of the intestinal pouches and grew heavier after 9 weeks. Similarly, smooth muscle cells calcified exclusively in GA‐treated rat aorta grafted in rat subcutis for 3 weeks. Calcification of extracellular matrix was seen after 9 weeks. Cells initiate calcification and extracellular matrix serves as a substrate for the subsequent growth of apatite in GA‐treated vascular tissue. © 2001 Wiley Periodicals, Inc., J Biomed Mater Res 59: 639–645, 2002
Anticoagulant activity of sulfonated polyrotaxanes as blood‐compatible materials
Authors: Park Hyung Dal , Lee Won Kyu , Ooya Tooru , Park Ki Dong , Kim Young Ha , Yui Nobuhiko 
Published: August 2002

AbstractPolyrotaxanes, in which α‐cyclodextrins (α‐CDs) are threaded onto poly(ethylene glycol)‐b‐poly(propylene glycol)‐b‐poly(ethylene glycol) triblock copolymers (Pluronic) capped with benzyloxycarbonyl(Z)‐L‐phenylalanine (Z‐L‐Phe), were prepared, and sulfopropyl groups were introduced to hydroxyl groups of α‐CDs in the polyrotaxanes. The supramolecular structure and the chemical composition of the polyrotaxanes after the sulfonation were confirmed by 1H‐NMR, 13C‐NMR, and elemental analysis. Anticoagulant activity of the polyrotaxanes and sulfonated polyrotaxanes was measured by activated partial thromboplastin time (APTT). It was found that the polyrotaxanes and the sulfonated polyrotaxanes showed greater anticoagulant activity than Pluronic itself, suggesting that both the supramolecular structure of the polyrotaxanes and the sulfonated groups contribute to the inhibition of intrinsic coagulation factors. Finally, our designed polyrotaxanes are suggested to be a promising candidate when fabricating blood‐compatible medical devices by blending with or coating on clinically used polymers. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 60: 186–190, 2002
Regulation of the GST mu‐1 isoenzyme in Y1 cells by adrenocorticotropic hormone is primarily transcriptional
Authors: Stark Tuula , Mankowitz Louise , DePierre Joseph W. 
Published: August 2002

AbstractIn earlier experiments, adrenocorticotropic hormone (ACTH) was shown to decrease the level of glutathione transferase M1 (murine glutathione transferase mu‐1) (mGSTM1), as well as of the corresponding mRNA, in a murine adrenocortical cell line. In the present study, the effect of ACTH on mGSTM1 gene transcription was examined using two techniques. First, a cDNA that coded for the mGSTM1 subunit but lacked the corresponding promoter sequences was transfected into the adrenocortical cell line, and the effect of ACTH on the level of the corresponding transcript was compared to that of endogenous mGSTM1 mRNA. The other technique used was nuclear run‐on transcription, where the rate of transcription of endogenous mGSTM1 mRNA in ACTH‐treated cells was compared to that in untreated control cells. These experimental approaches indicated that the rate of transcription of the mGSTM1 gene is regulated by ACTH in adrenocortical cells. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:128–132, 2001
Altering interface detector positioning in combination with prestorage filtration to achieve a better quality of single donor platelet concentrates using the CS 3000 plus blood separator
Authors: Lydaki E. , Nikoloudi E. , Bolonaki E. , Mavroudis D. , Kandidaki E. 
Published: August 2002

AbstractThe interface detector (ID) is an optical density sensor that affects the quality of single donor platelet collection using the CS 3000 Plus blood separator. The purpose of this study was to evaluate the effect of altering ID position on platelet yields and the contamination of leukocytes (WBC) in platelet concentrates (PCs). Dual‐needle apheresis procedures (n = 93) were performed using an A35 collection chamber. Plateletpheresis products were separated according to interface detector offset (IDO) positioning into four groups: A: IDO = 6 (n = 33), B: IDO = 10 (n = 28), C: IDO = 12 (n = 18), D: IDO = 18 (n = 14). For 32% of the collections, the closed system apheresis kit with integral Sepacell filter (Baxter) was used and 33% of them were leukodepleted using the LRP‐6 (PALL) filter. Our results showed that: (1) Although the mean blood volume and the time of apheresis were significantly higher, the mean platelet (PLT) yields were significantly lower in PCs of group A as compared to all other groups (P < 0.0001). (2) The mean WBC content was significantly higher in PCs of group D as compared to all other groups (P < 0.0001). (3) With the LRP‐6 filter, a significantly higher WBC reduction as well as PLT loss in PCs was observed as compared to Sepacell leukapheresis filter. A higher PLT loss was observed with both filters when leukoreduction was performed within the first 6 hours as compared to 24 hours after the procedure. Conclusively, an IDO setting of 10 or 12 results in better platelet yields in PCs without increasing the WBC contamination. An IDO positioning of 18 or higher must be avoided or should be always combined with PCs leukodepletion. Finally, the best timing for leukoreduction is 24 hours after the plateletpheresis. J. Clin. Apheresis, 17:21–26, 2002. © 2002 Wiley‐Liss, Inc.
Apheresis treatment of recurrent focal segmental glomerulosclerosis after kidney transplantation: Re‐analysis of published case‐reports and case‐series
Authors: Davenport Robertson D. 
Published: August 2002

AbstractA systematic re‐analysis of published cases was performed to better define the role of plasmapheresis in the treatment recurrent focal segmental glomerulosclerosis after renal transplantation. Forty‐four cases were identified, of which 32 responded to apheresis. The median number of treatments to response was 9. There was no difference between responders and nonresponders in the total number of treatments performed. The presence of sclerosis on biopsy predicted treatment failure. Relapse after first successful treatment was reported in 10 cases. The median number of treatments received was less and the time from diagnosis to first treatment was greater for patients who relapsed than for patients in whom relapse was not reported, but the differences were not statistically significant. On the basis of this analysis, we recommend early treatment after diagnosis with a regimen of three daily plasmapheresis treatments followed by 6 treatments on an every other day basis. J. Clin. Apheresis 16:175–178, 2001. © 2001 Wiley‐Liss, Inc.
Ex vivo expansion of apheresis‐derived peripheral blood hematopoietic progenitors
Authors: Estrov Zeev , Huh Yang O. , Ginsberg Cheryl F. , Harris David , Van Quin , Mirza Nadeem Q. , Talpaz Moshe , Korbling Martin 
Published: August 2002

AbstractBecause the administration of hematopoietic growth factors and the use of stem cell support often fails to alleviate the neutropenic phase induced by cytotoxic drugs, several investigators have attempted to expand ex vivo hematopoietic progenitors for clinical use. These attempts have clearly shown that the cultured cells are functional and can be safely administered to patients, but that the in vivo performance is disappointing and the concept as a whole is not yet clinically useful. The major reasons for these unsuccessful attempts are thought to be cumbersome cell fractionation techniques, contamination, prolonged incubation, and the use of less than ideal cytokine combinations. In response, we have developed a simple procedure for ex vivo expansion of myeloid progenitor cells. In this assay, unfractionated mononuclear cells from apheresis donors are incubated in nonpyrogenic plastic bags for 7 days in the presence of culture medium either containing fetal calf serum or human plasma, granulocyte colony‐stimulating factor, and stem cell factor. We have demonstrated that under these conditions the number of colony‐forming units (CFU) granulocyte‐macrophage (CFU‐GM) and of CFU‐granulocyte‐macrophage‐erythroid‐megakaryocyte (CFU‐GEMM) increased 7‐ and 9‐fold, respectively, by day 7 and the number of burst‐forming units‐erythroid (BFU‐E) increased 2.7‐fold by day 5 of culture. Significant increases in the numbers of cells expressing CD34+, CD34+/CD38+, CD34+/CD33+, CD34+/CD15+, and CD34+/CD90+ and significant declines in the numbers of cells expressing CD34+/CD38‐ and CD19 surface antigens were also observed. The relative numbers of cells expressing T‐cell markers and CD56 surface antigen did not change. By using different concentrations of various hematopoietic growth factor combinations, we can increase the number of mature and immature cells of different hematopoietic lineages. J. Clin. Apheresis 17:7–16, 2002. © 2002 Wiley‐Liss, Inc.
Donor lymphocyte apheresis for adoptive immunotherapy compared with blood stem cell apheresis
Authors: Körbling M. , Giralt S. , Khouri I. , Mirza N. , Donato M. , Anderlini P. , Fischer H. , Andreeff M. , McMannis J. , Champlin R. 
Published: August 2002

AbstractDonor lymphocyte transfusion has gained considerable interest as adoptive cellular immunotherapy for prevention or treatment of relapse after allogeneic stem cell transplantation. This study was designed to compare the yield of CD3+, CD3+4+, CD3+8+, CD19+, CD3−56+16+, and CD34+ cells contained in apheresis products from 61 consecutive non‐cytokine treated, human leukocyte antigen (HLA)‐matched donors for lymphocyte collection with the corresponding apheresis‐derived cell yield from 112 consecutive, HLA‐matched donors for blood stem cell collection who received recombinant human granulocyte colony stimulating factor (rhG‐CSF, filgrastim) 6 μg/kg every 12 hours until cell collection was completed. Apheresis was started on day 4 or 5 of rhG‐CSF treatment. The yield of lymphoid subsets was significantly different in the two sample groups, rhG‐CSF treated product yields exceeding untreated product yields by a median of 2.1‐fold (range: 1.3–2.6). However, the CD34+ cell yield in rhG‐CSF‐treated apheresis products exceeded untreated products by 26‐fold. A single untreated apheresis procedure was usually sufficient to collect a target dose of 1 × 108/kg CD3+ cells. Untreated apheresis products contained a median of 0.2 × 106/kg CD34+ cells. A potential engraftment dose of ≥0.5 × 106 CD34+ cells per kg of recipient body weight was contained in 16% of 57 untreated apheresis products. One single apheresis performed in a normal, untreated donor provides a sufficient amount of CD3+ cells for adoptive immunotherapy. Compared with that of an rhG‐CSF stimulated apheresis product, the CD34+ cell count is usually, but not always, below the engraftment dose range. RhG‐CSF treatment has little effect on the yield of lymphoid subsets collected by apheresis but is highly selective of the release of CD34+ cells. This report provides baseline data for studies that will show whether other cytokines such as granulocyte macrophage colony stimulating factor (GM‐CSF) and/or Flt‐3 Ligand can immunomodulate allotransfusates in vivo to improve the graft‐vs.‐leukemia (GVL) effect after allogeneic stem cell transplantation, while lowering the incidence and severity of graft‐vs.‐host disease (GVHD). J. Clin. Apheresis. 16:82–87, 2001. © 2001 Wiley‐Liss, Inc.
Parathyroid hormone (hPTH 1–38) stimulates the expression of UBP41, an ubiquitin‐specific protease, in bone
Authors: Miles R.R. , Sluka J.P. , Halladay D.L. , Santerre R.F. , Hale L.V. , Bloem L. , Patanjali S.R. , Galvin R.J.S. , Ma L. , Hock J.M. , Onyia J.E. 
Published: August 2002

AbstractParathyroid hormone (PTH) stimulates bone formation in both animals and humans, and the expression of a number of genes has been implicated in the mediation of this effect. To discover new bone factors that initiate and support this phenomenon, we used differential display reverse transcription polymerase chain reaction (DDRT‐PCR) and screened for genes, which are differentially expressed in osteoblast‐enriched femoral metaphyseal primary spongiosa of young male rats after a single subcutaneous (s.c.) injection of hPTH (1–38) (8 μg/100 g). We found and cloned one full‐length cDNA, which encodes a putative 348 amino acid protein. Sequence analysis of this protein demonstrates a 98, 93.7, and 82.5% identity with mouse, human, and chicken ubiquitin‐specific protease UBP41, respectively. Northern blot analysis confirmed that a 3.8–4 kb UBP41 mRNA transcript was rapidly increased 1 h after acute hPTH (1–38) exposure in both metaphyseal (6‐ to 8‐fold) and diaphyseal (3‐fold) bone, but returned to control levels by 24 h after exposure. In contrast, continuous exposure to hPTH (1–38), resulted in a rapid and sustained elevation of UBP41 mRNA. PTH (1–31), which stimulates intracellular cAMP, and PTHrP (1–34) both induced UBP41 mRNA expression; whereas PTH analogs (3–34) and (7–34), that do not stimulate cAMP, had no effect on UBP41 expression. UBP41 mRNA expression was also rapidly induced 1 h after injection of PGE2, but returned to the control level by 6 to 24 h. In vitro, UBP41 mRNA is expressed in primary osteoblasts (metaphyseal and diaphyseal derived) and in the osteoblast‐like cell lines UMR106, ROS17/2.8, and BALC. PTH (1–38) treatment induced UPB41 expression (3.6‐ to 13‐fold) in both primary cultures of osteoblasts and in UMR106 cells. Further analysis in UMR 106 cells demonstrated that PGE2, forskolin and dibutyryl cAMP increased UBP41 mRNA expression 4‐, 4.5‐, and 2.4‐fold, respectively. Tissue distribution analysis of UBP41 mRNA detected transcripts in brain, heart, skeletal muscle, kidney, liver, and testis. Together, these results demonstrate that UBP41, an ubiquitin‐specific protease, is selectively upregulated in bone by the osteotropic agents PTH, PTHrP, and PGE2, possibly via the PKA/cAMP pathway. We speculate that the rapid induction of UBP41 in response to these physiological regulators contributes to the mechanism by which either the structure, activity, half‐life or localization of essential proteins are modified to maintain bone homeostasis. J. Cell. Biochem. 85: 229–242, 2002. © 2002 Wiley‐Liss, Inc.
Augmented synthesis and differential localization of heparan sulfate proteoglycans in Duchenne muscular dystrophy
Authors: Alvarez Karin , Fadic Ricardo , Brandan Enrique 
Published: August 2002

AbstractMuscular dystrophies are characterized by continuous cycles of degeneration and regeneration that result in extensive fibrosis and a progressive diminution of muscle mass. Cell surface heparan sulfate proteoglycans are found almost ubiquitously on the surface and in the extracellular matrix (ECM) of mammalian cells. These macromolecules interact with a great variety of ligands, including ECM constituents, adhesion molecules, and growth factors. In this study, we evaluated the expression and localization of three heparan sulfate proteoglycans in the biopsies of Duchenne muscular dystrophy (DMD) patients. Through SDS–PAGE analyses followed by specific identification of heparitinase‐digested proteins with an anti‐Δ‐heparan sulfate specific monoclonal antibodies, we observed an increase of three forms of heparan sulfate proteoglycans, corresponding to perlecan, syndecan‐3, and glypican‐1. Immunohistochemistry analyses indicated a differential localization for these proteoglycans: glypican‐1 and perlecan were found mainly associated to ECM structures, while syndecan‐3 was associated to muscle fibers. These results suggest that the amount of specific heparan sulfate proteoglycans is augmented in skeletal muscle in DMD patients presenting a differential localization. J. Cell. Biochem. 85: 703–713, 2002. © 2002 Wiley‐Liss, Inc.
Serum suppresses myeloid progenitor apoptosis by regulating iron homeostasis
Authors: Maclean Kirsteen , Yang Hui , Cleveland John L. 
Published: August 2002

AbstractThe growth and survival of committed hematopoietic progenitors is dependent upon cytokine signaling. However, serum is also required for optimal growth of these progenitors in culture ex vivo. Here we report that serum withdrawal leads to myeloid progenitor cell apoptosis. Although serum deprivation‐induced cell death has many hallmarks typical of apoptosis, these cell deaths were not inhibited by hemopoietins, survival factors such as IGF‐I, or treatment with a broad‐spectrum caspase inhibitor. Rather, apoptosis due to serum withdrawal was associated with damage to mitochondria. Surprisingly the serum factor required for myeloid cell survival was identified as iron, and loss of iron led to marked reductions in ATP production. Furthermore, supplementing serum‐deprived myeloid cells with bound or free iron promoted cell survival and prevented mitochondrial damage. Therefore, serum suppresses hematopoietic cell apoptosis by providing an obligate source of iron and iron homeostasis is critical for proper myeloid cell metabolism and survival. J. Cell. Biochem. 82: 171–186, 2001. © 2001 Wiley‐Liss, Inc.
Butyrate stimulates ApoA‐IV‐containing lipoprotein secretion in differentiated Caco‐2 cells: Role in cholesterol efflux
Authors: Nazih Hassan , Nazih‐Sanderson Françoise , Krempf Michel , Michel Huvelin Jean , Mercier Sabine , Marie Bard Jean 
Published: August 2002

AbstractThe aim of this study was to determine: (1) whether the Short Chain Fatty Acids (SCFA) Acetate, Propionate, and Butyrate enhance the synthesis and secretion of intestinal apolipoprotein A‐IV‐containing lipoproteins and (2) if so, whether these particles are able to promote cholesterol efflux in vitro. For this purpose Caco‐2 cells were used for their functional properties of differentiated enterocytes. They were incubated with the three SCFA (2, 4, and 8 mM) for 48 h. Only butyrate stimulated apoA‐IV gene expression and this was associated with an increase in apoA‐IV secretion. A nondenaturing 2D‐PAGE (agarose gel was followed by PAGE) was used to identify apoA‐IV‐containing lipoproteins in various media, and showed that butyrate stimulated the secretion of two small HDL sized particles. The influence of these secreted particles on cholesterol efflux was investigated using incubation of media with 3H‐cholesterol‐labeled Fu5AH cells. The data indicate that conditioned media from Caco‐2 cells treated with butyrate resulted in an increase of 20–30% in cholesterol efflux. We conclude that butyrate may regulate apoA‐IV secretion and, therefore, modulate reverse cholesterol transport. J. Cell. Biochem. 83: 230–238, 2001. © 2001 Wiley‐Liss, Inc.
Ovarian carcinoma cells synthesize both chondroitin sulfate and heparan sulfate cell surface proteoglycans that mediate cell adhesion to interstitial matrix
Authors: Kokenyesi Robert 
Published: August 2002

AbstractMetastatic ovarian carcinoma metastasizes by intra‐peritoneal, non‐hematogenous dissemination. The adhesion of the ovarian carcinoma cells to extracellular matrix components, such as types I and III collagen and cellular fibronectin, is essential for intra‐peritoneal dissemination. The purpose of this study was to determine whether cell surface proteoglycans (a class of matrix receptors) are produced by ovarian carcinoma cells, and whether these proteoglycans have a role in the adhesion of ovarian carcinoma cells to types I and III collagen and fibronectin. Proteoglycans were metabolically labeled for biochemical studies. Both phosphatidylinositol‐anchored and integral membrane‐type cell surface proteoglycans were found to be present on the SK‐OV‐3 and NIH:OVCAR‐3 cell lines. Three proteoglycan populations of differing hydrodynamic size were detected in both SK‐OV‐3 and NIH:OVCAR‐3 cells. Digestions with heparitinase and chondroitinase ABC showed that cell surface proteoglycans of SK‐OV‐3 cells had higher proportion of chondroitin sulfate proteoglycans (75:25 of chondroitin sulfate:heparan sulfate ratio), while NIH:OVCAR‐3 cells had higher proportion of heparan sulfate proteoglycans (10:90 of chondroitin sulfate:heparan sulfate ratio). RT‐PCR indicated the synthesis of a unique assortment of syndecans, glypicans, and CD44 by the two cell lines. In adhesion assays performed on matrix‐coated titer plates both cell lines adhered to types I and III collagen and cellular fibronectin, and cell adhesion was inhibited by preincubation of the matrix with heparin, heparan sulfate, chondroitin sulfate, dermatan sulfate, or chondroitin glycosaminoglycans. Treatment of the cells with heparitinase, chondroitinase ABC, or methylumbelliferyl xyloside also interfered with adhesion confirming the role of both heparan sulfate and chondroitin sulfate cell surface proteoglycans as matrix receptors on ovarian carcinoma cells. J. Cell. Biochem. 83: 259–270, 2001. © 2001 Wiley‐Liss, Inc.