bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glycolysis and glucose transporter 1 as markers of response to hormonal therapy in breast cancer
Authors: Rivenzon‐Segal Dalia , Boldin‐Adamsky Swetlana , Seger Dalia , Seger Rony , Degani Hadassa 
Published: August 2003

AbstractEstrogen plays a key role in the development and progression of breast cancer; hence, antiestrogens, such as tamoxifen, have a marked impact on the treatment and outcome of breast cancer patients. Estrogen‐induced growth requires continuous replenishment of energy, predominantly generated by glycolysis. Previous work from this laboratory demonstrated estrogen induction and tamoxifen inhibition of glycolysis in MCF7 human breast cancer cells in vitro (Furman et al., J Steroid Biochem Mol Biol 1992;43:189–95). We present here studies of estrogen vs. tamoxifen regulation of glycolysis in orthotopic MCF7 human breast cancer xenografts in vivo. In addition we investigated mediation of this metabolic regulation through glucose transporter 1, in the same cells, in vitro, as well as in 2 other hormone‐responsive human breast cancer cells. Tumor response and glycolysis were monitored noninvasively by means of magnetic resonance imaging and 13C spectroscopy, respectively. During estrogen‐stimulated tumor growth (from ≈0.5 to ≈1.3 cm3 in 10 days), the rate of glucose metabolism through glycolysis in vivo was high at 40 ± 4 μmole/g/min. However, treatment for 10 days with tamoxifen induced growth arrest and a concomitant decrease of 2‐fold in the rate of glycolysis. In congruence, glucose transporter 1 expression was stimulated by estrogen, reaching after 72 hr a 2‐ to 3‐fold higher level of expression relative to that in tamoxifen‐treated cells. Thus, estrogen‐induced changes in glycolysis appeared to be mediated via its regulation of glucose transporter 1 expression. The in vivo monitoring of glycolysis may serve as a tool to expose hormonal regulation of glucose transporter 1 expression in breast cancer tumors, as well as to assess response to hormonal therapy. © 2003 Wiley‐Liss, Inc.
Physical activity and breast cancer risk among female physical education and language teachers: A 34‐year follow‐up
Authors: Rintala Pirjo , Pukkala Eero , Läärä Esa , Vihko Veikko 
Published: August 2003

AbstractThe cohort consisted of 1,489 Finnish female physical education and 8,560 language teachers born after 1920 and alive in 1967. The 2 study populations were similar in social class and way of living and clearly discordant in physical activity both during their university studies and later in life. The incidence of breast cancer among these teachers up to the year 2000 was assessed through a record linkage with the Finnish Cancer Registry. The number of breast cancer cases among physical education teachers was 61 in 32,862 person‐years and among language teachers was 404 in 177,188 person‐years. In Poisson‐regression analysis, the incidence rate ratio—adjusted for age, calendar time, number of children and age at first birth—for physical education vs. language teachers was overall 0.83 (95% confidence interval 0.63–1.09). This relative rate was 0.79 (0.46–1.36) in ages <50 years and 0.86 (0.62–1.18) in ages ≥50 years. Our study is concordant with the hypothesis that life‐long physical activity may reduce the risk of breast cancer. © 2003 Wiley‐Liss, Inc.
Identification of TDE2 gene and its expression in non‐small cell lung cancer
Authors: Player Audrey , Gillespie John , Fujii Takeshi , Fukuoka Junya , Dracheva Tatiana , Meerzaman Dauod , Hong Kyeong Man , Curran John , Attoh Goziam , Travis William , Jen Jin 
Published: August 2003

AbstractTDE2, a gene with sequence similarity to the mouse testicular tumor‐differentially‐expressed (Tde1/MUSTETU) gene, was identified by serial analysis of gene expression (SAGE) in nonsmall cell lung cancers (NSCLC). Here we characterized the TDE2 gene and determined its transcript levels in a panel of lung tumors, adjacent nonmalignant lung tissues and a variety of normal human tissues. In addition, we show that TDE2 is a potential transmembrane protein with 11 putative transmembrane helices. Using real‐time quantitative PCR, we showed that TDE2 transcript levels were higher in NSCLC compared to nonmalignant samples. In nonpulmonary normal tissues, the level of TDE2 was the highest in bladder, kidney and muscle; moderate to low in stomach, liver, skin, placenta and ovary tissues; and undetectable in brain, spleen and heart. By in situ hybridization, we showed that 10 of 18 lung tumors and only 1 of 14 adjacent nonmalignant regions had high levels of TDE2 transcripts. Alternatively, only 2 of 18 tumors and 8 of 14 adjacent nonmalignant bronchiole epithelium regions demonstrated negative to low levels of TDE2 signals. © 2003 Wiley‐Liss, Inc.
Overexpression of BAD preferentially augments anoikis
Authors: Idogawa Masashi , Adachi Masaaki , Minami Takae , Yasui Hiroshi , Imai Kohzoh 
Published: August 2003

AbstractBAD is a BH3‐only protein, and its proapoptotic activity is negatively regulated by serine phosphorylation. Here, we show that overexpression of BAD preferentially augments anchorage loss–induced apoptosis (anoikis). Gene transfer–mediated BAD overexpression alone did not induce apoptosis in attached MDCK cells but strongly augmented apoptosis when cells were cultured in suspension. In contrast, overexpression of another BH3‐only protein, BID, displayed much lower augmentation of anoikis, suggesting a preferential contribution of BAD to anoikis. During suspension culture, unphosphorylated BAD was gradually increased and targeted to the mitochondria. Cotransfection of BAD with constitutively active Akt cDNA strongly inhibited this change. In contrast, the increase of unphosphorylated BAD was not significantly inhibited by several phosphatase inhibitors or cotransfection with a dominant negative calcineurin cDNA, implying that the increase may be mainly due to a decrease of serine kinase activity, such as that of Akt. Similar results were observed in COS‐7 cells, suggesting that BAD overexpression can increase sensitivity of anchorage‐dependent cancer cells to anoikis. Thus, we propose that BAD can serve as a valuable gene therapeutic molecule to inhibit carcinoma progression. © 2003 Wiley‐Liss, Inc.
Radiation‐related mortality among offspring of atomic bomb survivors: A half‐century of follow‐up
Authors: Izumi Shizue , Suyama Akihiko , Koyama Kojiro 
Published: August 2003

AbstractOur objective was to examine whether parental exposure to atomic bomb radiation has led to increased cancer and/or noncancer mortality rates among the offspring. We studied 41,010 subjects born from May 1946 through December 1984 (i.e., conceived between 1 month and 38 years after the bombings) and surviving for at least 1 year. One or both parents were in Hiroshima or Nagasaki at the time of the bombings and childbirth. We analyzed mortality data from 1946 to 1999 using the Japanese family registry system by Cox regression model and examined the effects of paternal and maternal irradiation with adjustment for city, sex, year of birth and parental age at childbirth. During follow‐up, 314 cancer deaths and 1,125 noncancer disease deaths occurred. The mean age of living subjects was 45.7 years. Median doses were 143 mSv for 12,722 exposed fathers and 132 mSv for 7,726 exposed mothers. Cancer and noncancer mortality rates were no higher for subjects with exposed parents (5+ mSv or unknown dose) than for reference subjects (0–4 mSv), and mortality did not increase with increasing dose. For subjects with both parents exposed, the adjusted hazard ratios were 1.16 [95% confidence interval (CI) 0.92‐1.46] for noncancer and 0.96 (95% CI 0.59–1.55) for cancer. This was true of deaths occurring both before and after 20 years of age. However, because of uncertainty due to the small number of deaths and relatively young ages of subjects, we cannot rule out an increase in disease mortality at this time. © 2003 Wiley‐Liss, Inc.
Expression of prostate specific membrane antigen and three alternatively spliced variants of PSMA in prostate cancer patients
Authors: Schmittgen Thomas D. , Teske Sabine , Vessella Robert L. , True Lawrence D. , Zakrajsek Brian A. 
Published: August 2003

AbstractProstate specific membrane antigen (PSMA) is a folate γ glutamyl carboxypeptidase that is oriented on the plasma membrane of normal and prostate cancer cells. A cytosolic version of PSMA, PSM′, results from alternative splicing of the PSMA gene. Two additional alternatively spliced variants of PSMA, PSM‐C and PSM‐D, have been described recently. The ratio of PSMA to PSM′ mRNA was higher in a small number of prostate cancer specimens compared to normal prostate cancer and benign prostatic hypertrophy (Su et al. Cancer Res 1995;55:1441). The intent of our study was to measure the gene expression of PSMA and the 3 PSMA splice variants in a large number of patient's tissues. A real‐time, quantitative PCR assay was developed to quantify PSMA, PSM′, PSM‐C and PSM‐D. Discrimination among the variants was achieved by designing unique primers and TaqMan probes for each gene. Amplification and detection was specific for the desired splice variant and was sensitive to one gene copy per reaction. The assay was used to quantify the gene expression in specimens of normal, benign, primary and metastatic prostate cancer from 72 patients. The mean PSMA expression (relative to 18S rRNA) was 2‐ to 3‐fold lower in normal prostate (n = 4) compared to primary (n = 55, p = 0.31) and metastatic (n = 20, p = 0.33) prostate cancer. There was no difference in the PSMA expression between benign and cancerous prostate tissue from the same patients (n = 35). The ratio of PSMA to PSM′ was lowest in the normal prostate and increased with increasing Gleason score (p < 0.001). The increased ratio in these tissues was a reflection of both increasing PSMA levels and decreasing PSM′ mRNA. The expression of PSM‐C did not differ in any of the tissue categories studied. The expression of PSM‐D was similar in normal and primary prostate cancer but was 2‐fold higher in lymph node (p < 0.005) and bone metastases (p < 0.05) compared to the primary tumors. Our results of the first detailed quantitative analysis of PSMA mRNA expression in patient's tissues demonstrate that PSMA and the 3 PSMA splice variants are expressed in normal, benign, cancerous and metastatic prostate cancer. We note increased PSMA expression in some malignant tissues, however, these increases are modest in magnitude. We also report that the expression of a novel splice variant, PSM‐D, is elevated in prostate cancer metastases. © 2003 Wiley‐Liss, Inc.
Dimensional versus categorical classification of prototypic and nonprototypic cases of personality disorder
Authors: Sprock June 
Published: August 2003

AbstractThis study examined interrater reliability and ratings of confidence and clinical utility (professional communication, case conceptualization, treatment planning) of categorical and dimensional approaches to diagnosing prototypic and nonprototypic personality disorder cases. Two national samples of psychologists (n= 93,n= 92) participated. Interrater reliability was higher for prototypic cases than nonprototypic cases for the categorical system, but similar for prototypic and nonprototypic cases using dimensional ratings. Across cases, interrater reliability and confidence were highest for the categorical model, hybrid models, and the five‐factor model. However, ratings of clinical utility were highest for the categorical and the hybrid models, even when interrater reliability was inadequate, suggesting clinician preference for a classification based on the existing categories. Mean ratings for the prototypic cases supported the theorized relationships between the dimensional models and the personality disorders. Reasons for these findings and implications for moving towards a dimensional model of personality disorder are discussed. © 2003 Wiley Periodicals, Inc. J Clin Psychol.
The Schizophrenia Proneness (SzP) scale: An MMPI‐2 measure of schizophrenia liability
Authors: Bolinskey P. Kevin , Gottesman Irving I. , Nichols David S. 
Published: August 2003

AbstractWe examined the psychometric properties and construct validity for a Minnesota Multiphasic Personality Inventory–2 Schizophrenia Proneness (SzP) scale (Bolinskey et al., 2001) and provided normative statistics. Premorbid participants were offspring of parents with schizophrenia‐related illness (SRI), with comparison groups of offspring of parents with major affective disorders and offspring of normals. Postmorbid participants were twins affected with SRI; their unaffected relatives served as a comparison group. Results suggest that an SzP T score of 65 or above is an effective indicator of personality processes associated with increased liability to developing SRI. © 2003 Wiley Periodicals, Inc. J Clin Psychol
Personality traits predicting long‐term adjustment after surgery for ulcerative colitis
Authors: Weinryb Robert M. , Gustavsson J. Petter , Barber Jacques P. 
Published: August 2003

AbstractVery few studies have examined the relationship between personality traits and long‐term postoperative psychosocial adjustment. In a sample of 46 patients, we examined the relation between personality traits before pelvic pouch surgery for ulcerative colitis and psychosocial adjustment seven years postoperatively, controlling for the effects of surgical functional outcome. The Karolinska Psychodynamic Profile (KAPP) was used for personality assessment. Surgical functional outcome scales and the Psychosocial Adjustment to Illness Scale were also used. As assessed by the KAPP, poor frustration tolerance, long‐standing preoperative problems in sexual functioning, perfectionistic body ideals, and lack of alexithymia predicted poorer postoperative long‐term psychosocial adjustment in the areas of health concerns, sexuality, family relations, and psychological distress. Surgical functional outcome itself was a poor predictor of long‐term adjustment. The results indicate that it may be beneficial to take personality factors into account in preoperative assessment. © 2003 Wiley Periodicals, Inc. J Clin Psychol.
MMPI‐2 based classification of forensic psychiatric outpatients: An exploratory cluster analytic study
Authors: Nieberding Ron J. , Gacono Carl B. , Pirie Mark , Bannatyne Lynne A. , Viglione Donald J. , Cooper Bruce , Bodholdt Robert H. , Frackowiak Marita 
Published: August 2003

AbstractThe Minnesota Multiphasic Personality Inventory (MMPI), and now the MMPI‐2, are the most widely researched personality assessment tools in correctional and related forensic settings (MMPI; Hathaway & McKinley, 1940; MMPI‐2; Butcher, Dahlstrom, Graham, Tellegen, & Kaemmer, 1989). Using the original MMPI, Megargee (1977a) and colleagues (Megargee & Bohn, 1977; Megargee & Dorhout, 1977) developed an extensive and meaningful classification system for correctional inmates. However, few studies, with the exception of Toch and Adams (1994) cluster analytic study of emotionally disturbed violent offenders, have explored possibilities of a statistically derived categorical classification paradigm within the growing population of forensic psychiatric patients awaiting discharge into the community (Bannatyne, 1996). The present exploratory study investigates the utility of a commonly employed and replicable cluster analytic method in establishing an MMPI‐2‐based categorical classification system within a substantial forensic psychiatric outpatient sample (N = 300). Here, we present results of a seven‐cluster solution, augmented by contemporaneous Rorschach inkblot data utilizing Exner's Comprehensive System (Exner, 1991; Exner et al., 1995). Descriptive cluster characteristics are provided along with potential clinical correlates in an attempt to move closer to the goal of pairing informed assessment with effective treatment in this growing, but unique, population. © 2003 Wiley Periodicals, Inc. J Clin Psychol.
Adaptation to the sky: Defining the feather with integument fossils from mesozoic China and experimental evidence from molecular laboratories
Authors: Chuong Cheng‐Ming , Wu Ping , Zhang Fu‐Cheng , Xu Xing , Yu Minke , Widelitz Randall B. , Jiang Ting‐Xin , Hou Lianhai 
Published: August 2003

AbstractIn this special issue on the Evo‐Devo of amniote integuments, Alibardi has discussed the adaptation of the integument to the land. Here we will discuss the adaptation to the sky. We first review a series of fossil discoveries representing intermediate forms of feathers or feather‐like appendages from dinosaurs and Mesozoic birds from the Jehol Biota of China. We then discuss the molecular and developmental biological experiments using chicken integuments as the model. Feather forms can be modulated using retrovirus mediated gene mis‐expression that mimics those found in nature today and in the evolutionary past. The molecular conversions among different types of integument appendages (feather, scale, tooth) are discussed. From this evidence, we recognize that not all organisms with feathers are birds, and that not all skin appendages with hierarchical branches are feathers. We develop a set of criteria for true avian feathers: 1) possessing actively proliferating cells in the proximal follicle for proximo‐distal growth mode; 2) forming hierarchical branches of rachis, barbs, and barbules, with barbs formed by differential cell death and bilaterally or radially symmetric; 3) having a follicle structure, with mesenchyme core during development; 4) when mature, consisting of epithelia without mesenchyme core and with two sides of the vane facing the previous basal and supra‐basal layers, respectively; and 5) having stem cells and dermal papilla in the follicle and hence the ability to molt and regenerate. A model of feather evolution from feather bud → barbs → barbules → rachis is presented, which is opposite to the old view of scale plate → rachis → barbs → barbules (Regal, '75; Q Rev Biol 50:35). J. Exp. Zool. (Mol. Dev. Evol.) 298B:42–56, 2003. © 2003 Wiley‐Liss, Inc.
A hierarchical model of plumage: Morphology, development, and evolution
Authors: Prum Richard O. , Dyck Jan 
Published: August 2003

AbstractPlumage is a complex component of the avian phenotype. The plumage of an individual is composed of numerous hierarchically arranged developmental and morphological modules. We present a hierarchical model of plumage that provides an intellectual framework for understanding the development and evolution of feathers. Independence, covariation, and interaction among plumage modules create numerous opportunities for developmental and evolutionary diversification of feather complexity and function. The hierarchical relationships among plumage modules are characterized by both top‐down and bottom‐up effects in which properties of modules at one level of the hierarchy determine or influence the properties of modules at lower or higher levels of the hierarchy. Plumage metamodules are created by covariation or interaction among modules at different levels of the hierarchy. J. Exp. Zool. (Mol. Dev. Evol.) 298B: 73–90, 2003. © 2003 Wiley‐Liss, Inc.
Variations in the morphology, distribution, and arrangement of feathers in domesticated birds
Authors: Bartels Thomas 
Published: August 2003

AbstractDomesticated birds exhibit a greater diversity in the morphology of their integument and its appendages than their wild ancestors. Many of these variations affect the appearance of a bird significantly and have been bred selectively by poultry and pigeon fanciers and aviculturists for the sake of visual appeal. Variations in feather distribution (e.g., feathering of legs and feet, featherless areas in normally feather‐bearing skin) are widespread in chickens and pigeons. Variations in the number of feathers (e.g., increased number of tail feathers, lack of tail feathers) occur in certain pigeon and poultry breeds. Variations in feather length can affect certain body regions or the entire plumage. Variations in feather structure (e.g., silkiness, frilled feathering) can be found in exhibition poultry as well as in pet birds. Variations in feather arrangement (e.g., feather crests and vortices) occur in many domesticated bird species as a results of mutation and intense selective breeding. The causes of variations in the structure, distribution, length and arrangement of feathers is often unknown and opens a wide field for scientific research under various points of view (e.g., morphogenesis, pathogenesis, ethology, etc.). To that extent, variations in the morphology, distribution and arrangement of feathers in domesticated birds require also a concern for animal welfare because certain alleles responsible for integumentary variations in domesticated birds have pleiotropic effects, which often affect normal behaviour and viability. J. Exp. Zool. (Mol. Dev. Evol.) 298B:91–108, 2003. © 2003 Wiley‐Liss, Inc.
Evolution and development of mammalian limb integumentary structures
Authors: Hamrick Mark W. 
Published: August 2003

AbstractThe adaptive radiation of mammalian clades has involved marked changes in limb morphology that have affected not only the skeleton but also the integumentary structures. For example, didelphid marsupials show distinct differences in nail and claw morphology that are functionally related to the evolution of arboreal, terrestrial, and aquatic foraging behaviors. Vespertilionoid bats have evolved different volar pad structures such as adhesive discs, scales, and skin folds, whereas didelphid marsupials have apical pads covered either with scales, ridges, or small cones. Comparative analysis of pad and claw development reveals subtle differences in mesenchymal and ectodermal patterning underlying interspecific variation in morphology. Analysis of gene expression during pad and claw development reveals that signaling molecules such as Msx1 and Hoxc13 play important roles in the morphogenesis of these integumentary structures. These findings suggest that evolutionary change in the expression of these molecules, and in the response of mesenchymal and ectodermal cells to these signaling factors, may underlie interspecific differences in nail, claw, and volar pad morphology. Evidence from comparative morphology, development, and functional genomics therefore sheds new light on both the patterns and mechanisms of evolutionary change in mammalian limb integumentary structures. J. Exp. Zool. (Mol. Dev. Evol.) 298B:152–163, 2003. © 2003 Wiley‐Liss, Inc.
Molecular biology of hair morphogenesis: Development and cycling
Authors: Botchkarev Vladimir A. , Paus Ralf 
Published: August 2003

AbstractIn mammals, hair follicles produce hairs that fulfill a number of functions including thermoregulation, collecting sensory information, protection against environmental trauma, social communication, and mimicry. Hair follicles develop as a result of epithelial‐mesenchymal interactions between epidermal keratinocytes committed to hair‐specific differentiation and cluster of dermal fibroblasts that form follicular papilla. During postnatal life, hair follicles show patterns of cyclic activity with periods of active growth and hair production (anagen), apoptosis‐driven involution (catagen), and relative resting (telogen). During last decade, substantial progress has been achieved in delineating molecular mechanisms that control hair follicle development and cyclic activity. In this review, we summarize the data demonstrating that regulation of hair follicle development in the embryo and control of hair follicle growth during postnatal life are highly conserved and both require involvement of similar molecular mechanisms. Since many of the molecules that control hair follicle development and cycling are also involved in regulating morphogenesis and postnatal biology of other ectodermal derivatives, such as teeth, feathers, and mammary glands, basic principles and molecular mechanisms that govern hair follicle development and growth may also be applicable for other developmental systems. J. Exp. Zool. (Mol. Dev. Evol.) 298B: 164–180, 2003. © 2003 Wiley‐Liss, Inc.