bluuebunny/crossref_metadata_2025_split huggingface dataset:
Oral cancer in southern India: The influence of smoking, drinking, paan‐chewing and oral hygiene
Authors: Balaram Prabha , Sridhar Hema , Rajkumar Thangarajan , Vaccarella Salvatore , Herrero Rolando , Nandakumar Ambakumar , Ravichandran Kandaswamy , Ramdas Kunnambath , Sankaranarayanan Rengaswamy , Gajalakshmi Vendhan , Muñoz Nubia , Franceschi Silvia 
Published: August 2002

AbstractBetween 1996 and 1999 we carried out a case‐control study in 3 areas in Southern India (Bangalore, Madras and Trivandrum) including 591 incident cases of cancer of the oral cavity (282 women) and 582 hospital controls (290 women), frequency‐matched with cases by age and gender. Odds ratios (ORs) and 95% confidence intervals (CIs) were obtained from unconditional multiple logistic regressions and adjusted for age, gender, center, education, chewing habit and (men only) smoking and drinking habits. Low educational attainment, occupation as a farmer or manual worker and various indicators of poor oral hygiene were associated with significantly increased risk. An OR of 2.5 (95% CI 1.4–4.4) was found in men for smoking ≥ 20 bidi or equivalents versus 0/day. The OR for alcohol drinking was 2.2 (95% CI 1.4–3.3). The OR for paan chewing was more elevated among women (OR 42; 95% CI 24–76) than among men (OR 5.1; 95% CI 3.4–7.8). A similar OR was found among chewers of paan with (OR 6.1 in men and 46 in women) and without tobacco (OR 4.2 in men and 16.4 in women). Among men, 35% of oral cancer is attributable to the combination of smoking and alcohol drinking and 49% to pan‐tobacco chewing. Among women, chewing and poor oral hygiene explained 95% of oral cancer. © 2002 Wiley‐Liss, Inc.
ZD1839 (IRESSA), an EGFR‐selective tyrosine kinase inhibitor, enhances taxane activity in bcl‐2 overexpressing, multidrug‐resistant MCF‐7 ADR human breast cancer cells
Authors: Ciardiello Fortunato , Caputo Rosa , Borriello Gaetano , Del Bufalo Donatella , Biroccio Annamaria , Zupi Gabriella , Bianco A. Raffaele , Tortora Giampaolo 
Published: August 2002

AbstractConstitutive bcl‐2 overexpression increases the tumorigenic and metastatic potential of doxorubicin‐resistant, estrogen‐independent, MCF‐7 ADR human breast cancer cells. We evaluated the sensitivity to taxanes (paclitaxel, docetaxel and IDN 5109) of 2 bcl‐2‐overexpressing MCF‐7 ADR clones and control neomycin‐transfected MCF‐7 ADR neo cells. The 2 bcl‐2‐overexpressing MCF‐7 ADR clones were relatively resistant to all 3 taxanes, whereas the MCF‐7 ADR neo cells were relatively resistant to paclitaxel and docetaxel, but sensitive to IDN 5109. We found that both MCF‐7 ADR neo and bcl‐2‐overexpressing MCF‐7 ADR clones express high levels of the epidermal growth factor receptor (EGFR) and its ligand, transforming growth factor‐α (TGF‐α). Therefore, we tested the growth inhibitory effect of ZD1839 (Iressa™, AstraZeneca, Macclesfield, UK), an orally active, selective EGFR tyrosine kinase inhibitor (EGFR‐TKI) that is in clinical development. ZD1839 inhibited the growth in soft agar of all 3 clones in a dose‐dependent manner (IC50 of approximately 0.1 μM). This effect was accompanied by a dose‐dependent inhibition of EGFR tyrosine autophosphorylation and of the production of TGF‐α, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF). To determine whether the blockade of EGFR signaling might affect the sensitivity of bcl‐2‐overexpressing MCF‐7 ADR cells to taxanes, cells were treated with ZD1839 in combination with paclitaxel, docetaxel or IDN 5109, and dose‐dependent cooperative growth inhibition as well as apoptosis potentiation were observed. Combined treatment with IDN 5109 and ZD1839 also resulted in a significant inhibition of bcl‐2 expression in bcl‐2‐overexpressing MCF‐7 ADR cells. These results demonstrate the ability of ZD1839 to overcome taxane resistance in a model of hormone‐independent, multidrug‐resistant, human breast cancer. © 2002 Wiley‐Liss, Inc.
αv‐Integrin antagonist EMD 121974 induces apoptosis in brain tumor cells growing on vitronectin and tenascin
Authors: Taga Takashi , Suzuki Atsushi , Gonzalez‐Gomez Ignacio , Gilles Floyd H. , Stins Monique , Shimada Hiroyuki , Barsky Lora , Weinberg Kenneth I. , Laug Walter E. 
Published: August 2002

AbstractOrthotopic brain tumor growth is inhibited in athymic mice by the daily systemic administration of the αv‐integrin antagonist EMD 121974. This compound, a cyclic RGD‐penta‐peptide, is a potent inhibitor of angiogenesis, which induces apoptosis of growing endothelial cells through inhibition of their αv‐integrin interaction with the matrix proteins vitronectin and tenascin. Here we show that EMD 121974 also induces apoptosis in the αv‐integrin‐expressing tumor cell lines U87 MG and DAOY by detaching them from vitronectin and tenascin, matrix proteins known to be essential for brain tumor growth and invasion. These matrix proteins are shown to be produced by the brain tumor cells in vitro and in vivo. Furthermore, only tumor cells expressing αv‐integrins responded to the treatment with EMD 121974, after xenotransplantation into the forebrain of nude mice, supporting the importance of tumor cell‐matrix interactions in tumor cell survival in the brain. Thus, the αv‐antagonist EMD 121974 suppresses brain tumor growth through induction of apoptosis in both brain capillary and brain tumor cells by preventing their interaction with the matrix proteins vitronectin and tenascin. The dual action of this peptide explains its potent growth suppression of orthotopically transplanted brain tumors. © 2002 Wiley‐Liss, Inc.
UV‐B‐type mutations and chromosomal imbalances indicate common pathways for the development of Merkel and skin squamous cell carcinomas
Authors: Popp Susanne , Waltering Stefan , Herbst Christel , Moll Ingrid , Boukamp Petra 
Published: August 2002

AbstractTwo developmentally highly divergent nonmelanoma skin cancers, the epidermal squamous cell carcinomas (SCC) and the neuroendocrine Merkel cell carcinomas (MCC), occur late in life at sun‐exposed body sites. To determine whether these similarities may indicate common genetic alterations, we studied the genetic profile of 10 MCCs and analyzed 6 derived cell lines and 5 skin SCC lines by comparative genomic hybridization (CGH) and molecular genetic analyses. Although the MCCs were highly divergent—only 3 of the 10 tumors exhibited common gains and losses—they shared gain of 8q21‐q22 and loss of 4p15‐pter with the genetically much more homogeneous SCC lines. In addition, 2 of 5 SCC and 2 of 6 MCC lines exhibited UV‐B‐type‐specific mutations in the p53 tumor‐suppressor gene and a high frequency (9/11) of CC→TT double base changes in codon 27 of the Harvey (Ha)‐ras gene. Since 45% of the tumor lines were homozygous for this nucleotide substitution compared to 14% of the controls and in 1 MCC patient the wild‐type allele was lost in the tumor, this novel polymorphism may contribute to tumor development. On the other hand, loss of 3p, characteristic for SCCs, was rare in MCCs. Although in 2 of 3 SCC lines 3p loss was correlated with reduced expression of the FHIT (fragile histidine triad) gene, the potential tumor suppressor mapped to 3p14.2 and 2 MCC lines with normal 3p showed aberrant or no FHIT transcripts. Taken together, in addition to the common UV‐B‐specific mutations in the p53 and Ha‐ras gene, MCCs and SCCs also share chromosomal imbalances that may point to a common environmental‐derived (e.g., UV‐A) oxidative damage. © 2002 Wiley‐Liss, Inc.
Financial development and poverty reduction in developing countries
Authors: Jalilian Hossein , Kirkpatrick Colin 
Published: August 2002

AbstractEmpirical investigation of the link between financial development and economic growth has established that finance exerts a significant and positive influence on growth. This paper extends this line of analysis by examining the contribution that financial development makes to poverty reduction in low‐income countries. The results reported support the contention that financial sector development policy can contribute to achieving the goal of poverty reduction in developing countries. Copyright © 2002 John Wiley & Sons, Ltd.
Space–time evolution of the fertility transition in India, 1961–1991
Authors: Balabdaoui F. , Bocquet‐Appel J.‐P. , Lajaunie C. , Irudaya Rajan S. 
Published: August 2002

AbstractA fertility index has been estimated which takes into account the space–time variations of mortality rates of children and women and the different fertility rates of women across age groups. The basic data are the recorded frequencies at district level for four decennial census dates (1961 to 1991) of children aged 0–4 years and women aged 15–49 years. On that basis, we have 326, 349, 400 and 454 data points on the map for each decennial census, respectively. To construct fertility surfaces on the map, the kriging technique of spatial interpolation was applied. To highlight on these surfaces the areas of regional homogeneity and zones of major change, on a subcontinental scale, a technique of image analysis and the wombling procedure of detection of the zones of abrupt change were used. The fertility maps and the variogram surfaces show that the transition took place by an expansion of heterogeneity starting from the southwestern zones. This expansion reduced the extent of the pre‐transition area of homogeneity in such a way that its original transverse SW–NE direction turned into a longitudinal direction by 1991 and its size became appreciably smaller. In 1961 a long zone of abrupt change detected by wombling was observed crossing the Indian subcontinent transversely. From west to east, it extended longitudinally for a length of nearly 2500 km, including Bangladesh. This zone of abrupt fertility change divided the subcontinent into two regions, one of high fertility in the north and the other of lower fertility in the south. This latter zone is separated partially by State boundaries and geographical landmarks. A procedure of regression trees (classic AID tree) applied to the co‐variables shows that this zone also corresponds to a major regional change in the female literacy rate. From 1961 to 1991, with a general fall in fertility rates all over the country, this zone of abrupt change has progressively disappeared. Copyright © 2001 John Wiley & Sons, Ltd.
Gender preference, contraceptive use and fertility in India: regional and development influences
Authors: Arokiasamy Perianayagam 
Published: August 2002

AbstractThe low status of women and a strong preference for male children are two patriarchal constraints in the northern states of India. This analysis explores the regional influence of culture and that of development factors on gender preference effects towards contraception and fertility. Gender preference effects on contraception are the strongest in the western region, followed by the northern and north central regions, and lowest in the south followed by the eastern region. Gender preference effects on fertility also follow a similar regional pattern. Across the regions of India, there is a close correspondence between the degree of son preference and its effects on contraception and fertility, regardless of the level of fertility. Given that key variables that account for socio‐economic status variations have been held constant in the models, the region‐wise gender preference effects represent the regional influence of culture. However, development factors also have a very substantial counteracting effect on gender preference. There is a reduction in son preference effects on contraception and fertility with increasing levels of women's education and household economic conditions, particularly in the three regions where son preference effects are strongest. Development factors also have a significant independent influence on the use of contraception and recent fertility. However, here also there is a regional pattern relating to this. In summary, women's education and exposure to the mass media are two important developmental indicators that bear a highly significant positive relationship with contraception and a negative relationship with fertility through all regions. However, household economic status as measured by an index of living conditions indicated a strong demand‐driven effect on contraception in the northern and north central regions where women have a lower social position. In contrast, in the southern region where contraception is quickly embraced, facilitated by good access to healthcare, economic conditions barely have any effect at all on the use of contraception or recent fertility. Copyright
© 2002 John Wiley & Sons, Ltd.
Differential effects of dihalogenated and trihalogenated acetates in the liver of B6C3F1 mice
Authors: Kato‐Weinstein J. , Stauber A. J. , Orner G. A. , Thrall B. D. , Bull R. J. 
Published: August 2002

AbstractHaloacetates are produced in the chlorination of drinking water in the range 10–100 μg l−1. As bromide concentrations increase, brominated haloacetates such as bromodichloroacetate (BDCA), bromochloroacetate (BCA) and dibromoacetate (DBA) appear at higher concentrations than the chlorinated haloacetates: dichloroacetate (DCA) or trichloroacetate (TCA). Both DCA and TCA differ in their hepatic effects; TCA produces peroxisome proliferation as measured by increases in cyanide‐insensitive acyl CoA oxidase activity, whereas DCA increases glycogen concentrations. In order to determine whether the brominated haloacetates DBA, BCA and BDCA resemble DCA or TCA more closely, mice were administered DBA, BCA and BDCA in the drinking water at concentrations of 0.2–3 g l−1. Both BCA and DBA caused liver glycogen accumulation to a similar degree as DCA (12 weeks). The accumulation of glycogen occurred in cells scattered throughout the acinus in a pattern very similar to that observed in control mice. In contrast, TCA and low concentrations of BDCA (0.3 g l−1) reduced liver glycogen content, especially in the central lobular region. The high concentration of BDCA (3 g l−1) produced a pattern of glycogen distribution similar to that in DCA‐treated and control mice. This effect with a high concentration of BDCA may be attributable to the metabolism of BDCA to DCA. All dihaloacetates reduced serum insulin levels. Conversely, trihaloacetates had no significant effects on serum insulin levels. Dibromoacetate was the only brominated haloacetate that consistently increased acyl‐CoA oxidase activity and rates of cell replication in the liver. These results further distinguish the effects of the dihaloacetates from those of peroxisome proliferators like TCA. Copyright © 2001 John Wiley & Sons, Ltd.
Lead‐induced cell death in testes of young rats
Authors: Adhikari Neeta , Sinha Neelima , Narayan Ram , Saxena D. K. 
Published: August 2002

AbstractLead is a well‐documented testicular toxicant. The present work was planned to study the occurrence of germ cell death after lead administration. Young growing rats were treated with 5, 10 and 20 mg kg−1 body weight of lead for 2 weeks. Cell death was assessed by employing in situ TUNEL staining, DNA electrophoresis and morphological examination of the tubules. The results showed that Pb induced significant numbers of germ cells to undergo apoptosis in the seminiferous tubules of rats treated with 20 mg kg−1 body weight. However, DNA fragmentation was not detected at any of the doses. The level of lead accumulation in the testis increased in a dose‐dependent manner. Copyright © 2001 John Wiley & Sons, Ltd.
Effect of sodium hypochlorite on dentin bonding with a polyalkenoic acid‐containing adhesive system
Authors: Osorio Raquel , Ceballos Laura , Tay Franklin , Cabrerizo‐Vilchez Miguel A. , Toledano Manuel 
Published: August 2002

AbstractThe purpose of this study was to evaluate the effect of sodium hypochlorite (NaOCl) treatment on dentin bonding by means of contact angle (CA), shear bond strength (SBS), and microleakage (ML) measurements. Ultrastructure and nanoleakage (NL) of the interfaces were examined by transmission electron microscopy (TEM). For CA, SBS, and TEM evaluation, human molars were sectioned to expose dentin surfaces and were either acid‐etched (35% H3PO4) or further treated with 5% NaOCl for 2 min before the application of Single Bond adhesive. CAs were measured using the Axisymmetric Drop Shape Analysis technique. The Watanabe testing assembly was used for SBS evaluation. ML was assessed by a dye penetration method. NL was examined using a silver‐staining technique. The results showed that CA values decreased after acid etching and even more after NaOCl treatment. NaOCl treatment produced lower SBS than acid‐etched dentin. Both ML values and NL manifestations were similar for NaOCl‐treated and acid‐etched dentin. NaOCl did not completely remove the collagen matrix. NL was manifested along the base of hybrid layers and within the polyalkenoic acid copolymer in both groups. Adverse chemical interactions could have occurred between the remnant collagen matrix and/or mineralized dentin after NaOCl treatment. There is no additional advantage in using NaOCl treatment with this adhesive. © 2002 John Wiley & Sons, Inc. J Biomed Mater Res 60: 316–324, 2002; DOI 10.1002/jbm.10074
Preparation of macroporous biodegradable PLGA scaffolds for cell attachment with the use of mixed salts as porogen additives
Authors: Lin Hong‐Ru , Kuo Chun‐Jung , Yang C. Y. , Shaw Shyh‐Yu , Wu Yu‐Jun 
Published: August 2002

AbstractIn the present study, a mixture of ammonium‐bicarbonate (NH4HCO3) and sodium‐chloride (NaCl) particles was used as a porogen additive to fabricate highly macroporous biodegradable poly(lactic‐co‐glycolic acid) (PLGA) scaffolds. A two‐step salt‐leaching process was performed after the sample had become semisolidified. Compared to the standard solvent‐casting/particulate‐leaching (SC/PL) technique, the processing time of this approach was significantly shorter: Instead of several days, only half a day was required. In addition, the polymer/salts/solvent mixture can be easily handled and molded into scaffolds of any specific shape—for example, thin sheet, cylindrical, or bone‐shaped—for special applications in tissue engineering. Our results demonstrate that these scaffolds have a highly interconnected open‐pore structure as well as greater mechanical properties than those made using the standard SC/PL technique. Primary rat osteoblasts seeded into the scaffolds exhibited good seeding efficiency. The method presented here is a promising approach for fabricating scaffolds for tissue engineering applications. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res (Appl Biomater) 62:271–279, 2002
Drug‐releasing scaffolds fabricated from drug‐loaded microspheres
Authors: Nof Moriah , Shea Lonnie D. 
Published: August 2002

AbstractBiodegradable scaffolds serve a central role in many strategies for engineering tissue replacements or in guiding tissue regeneration. Typically, these scaffolds function to create and maintain a space and to provide a support for cell adhesion. However, these scaffolds also can serve as vehicles for the delivery of bioactive factors (e.g., protein or DNA) in order to manipulate cellular processes within the scaffold microenvironment. This study presents a novel approach to fabricate tissue‐engineering scaffolds capable of sustained drug delivery whereby drug‐loaded microspheres are fabricated into structures with controlled porosity. A double‐emulsion process was used to fabricate microspheres with encapsulated DNA that retained its integrity and was released from the microspheres within 24 h. These DNA‐loaded microspheres subsequently were formed into a nonporous disk or an interconnected open‐pore scaffold (>94% porosity) via a gas‐foaming process. The disks and scaffolds exhibited sustained plasmid release for at least 21 days and had minimal burst during the initial phase of release. This approach of assembling drug‐loaded microspheres into porous and nonporous structures may find great utility in the fabrication of synthetic matrices that direct tissue formation. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 349–356, 2002
The effect of particle wear debris on NFκB activation and pro‐inflammatory cytokine release in differentiated THP‐1 cells
Authors: Akisue Toshihiro , Bauer Thomas W. , Farver Carol F. , Mochida Yuichi 
Published: August 2002

AbstractOrthopedic wear debris has been thought to be an important factor associated with osteolysis and loosening of total joint arthroplasties. Previous in vitro studies have reported that particles of wear debris induce the release of pro‐inflammatory cytokines and other inflammatory mediators from macrophages and other cells. Several recent investigations, however, have suggested that the wear particles themselves may not be primarily responsible for the inflammatory cellular responses, but that the observed cytokine release in vitro may be caused by endotoxin adsorbed to commercially available particle preparations. The intracellular pathways involved in macrophage signal transduction also are poorly understood. The purposes of this study are to use isolated orthopedic wear debris particles to evaluate pro‐inflammatory cytokine release and nuclear factor kappa B (NFκB) activation from macrophages. Cells from human monocyte/macrophage cell line (THP‐1) were differentiated and incubated with particles of debris that had been isolated from a failed human total hip arthroplasty. The titanium‐alloy particles did not evoke release of TNF‐α or IL‐1β whereas lipopolysaccharide (LPS) or LPS‐treated debris particles induced both TNF‐α and IL‐1β. LPS‐treated particles, but not particles alone, stimulated NFκB activation. Our results suggest that at the concentrations tested in this study, endotoxin‐free wear debris particles may not themselves initiate inflammatory cellular responses in differentiated THP‐1 cells. It is unclear whether adsorbed endotoxin is clinically associated with osteolysis and/or loosening in total joint arthroplasties, but several factors, including adsorbed endotoxin, need to be investigated to explore the cellular responses responsible for osteolysis and/or loosening. © 2001 Wiley Periodicals, Inc. J Biomed Mater Res 59: 507–515, 2002
Real‐time and quantitative PCR: applications to mechanism‐based toxicology
Authors: Walker Nigel J. 
Published: August 2002

AbstractThere is increasing awareness that quantitative analysis of changes in molecular targets plays a key role in addressing scientific questions in molecular toxicology, molecular epidemiology, and human risk assessment. One of the emerging technologies that is being used to analyze these molecular targets is real‐time and quantitative (RTAQ) polymerase chain reaction (PCR). The aim of this review is to provide the reader with an overview of this technology and to highlight specific applications of this technology to some key areas of molecular toxicology. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:121–127, 2001