bluuebunny/crossref_metadata_2025_split huggingface dataset:
Screening for breast cancer in pre‐menopausal women. Who should decide?
Authors: Berrino Franco , Bouchardy Christine , Sasco Annie J. 
Published: September 2008

AbstractThe recent UICC meeting on breast cancer screening in pre‐menopausal women showed that experts disagree: some would recommend that screening begin at age 40, others would postpone it until after age 50 (Eckhardt et al., 1994). There is full consensus that screening at ages 40 to 49 may detect a substantial fraction of breast‐cancer cases before their clinical manifestation, but the trials carried out have not indicated a significant reduction in subsequent mortality. As stated in the report of the UICC meeting, “this issue is too large for it to remain only the concern of experts.” In our opinion, women should be provided with full information to enable them to decide themselves what is better for them. This means that the available scientific evidence both on benefits and on risks should be made quantitatively explicit. As recently reviewed by Hurley and Kaldor (1992), potential benefits include saved lives, increased use of conservative therapies, and reassurance of women without pre‐clinical cancer; risks include radiationinduced breast cancer, unnecessary investigations for false positives, useless early diagnosis and treatment, diagnosis and treatment of lesions not requiring treatment (over‐diagnosis), false reassurance, and psychological and social morbidity such as anxiety and the stigmatization of women with positive diagnosis. © 1995 Wiley‐Liss, Inc.
Cancer risk following primary hemochromatosis: A population‐based cohort study in Denmark
Authors: Hsing Ann W. , McLaughlin Joseph K. , Olsen Jorgcn H. , Mellemkjar Lenc , Wacholder Sholom , Fraumeni Joseph F. 
Published: September 2008

AbstractA population‐based cohort of 120 Danish men, discharged with a hospital diagnosis of primary hemochromatosis from 1977 to 1989, was followed up to 1989 for subsequent cancer risk. Nineteen subjects (including 6 with primary liver cancers) were excluded from the analysis, either because they died within the same month of hemochromatosis diagnosis or because they had cancer prior to diagnosis of hemochromatosis. Among the 101 remaining subjects, 4 primary liver cancers occurred one year or more after the diagnosis of hemochromatosis, far surpassing the expected number based on incidence rates from the Danish population (standardized incidence ratio 92.9, 95% confidence interval 25.0 to 237.9). The excess of liver cancer was associated with cirrhosis and included cholangiocarcinoma as well as hepatocellular carcinoma. Significantly elevated risks were also observed for non‐hepatic cancers (13 cases; SIR 3.5, 95% CI 1.9 to 6.0), notably esophageal cancer (2 cases; SIR 42.9, 95% CI 4.8 to 154.9) and skin melanoma (2 cases; SIR 27.8, 95% CI 3.1 to 100.3). The results of this population‐based study are in accordance with the hypothesis that patients with primary hemochromatosis have a substantial risk of primary liver cancer. Further studies of hemochromatosis may be useful in clarifying the relation of non‐hepatic malignancies to body iron stores in the general population. © 1995 Wiley‐Liss, Inc.
Expression of PDGF and PDGF receptors in human astrocytoma operation specimens supports the existence of an autocrine loop
Authors: Guha Abhijit , Dashner Kathleen , Mc Black Peter L. , Wagner John A. , Stiles Charles D. 
Published: September 2008

AbstractEstablished cell lines derived from human malignant astrocytomas typically express a combination of platelet‐derived growth factor (PDGF) and PDGF receptor which could form an autocrine loop. In this study, we screened for the essential components of a PDGF autocrine loop in fresh surgical isolates of human astrocytomas, using in situ hybridization and immunohis‐tochemical techniques. Eight malignant astrocytomas (6 glioblastomas and 2 anaplastic astrocytomas), 5 low‐grade astrocytomas and 4 non‐neoplastic glial specimens (mesial temporal sclerosis) were evaluated. Malignant astrocytomas, and to a lesser extent low‐grade astrocytomas, expressed more PDGF‐A and PDGF‐B than non‐neoplastic glia. PDGF‐α‐receptor expression was elevated both in malignant and in iow‐grade astrocytomas. These data support the argument that PDGF autocrine loops contribute to the unregulated growth of human astrocytomas. Expression of PDGF and PDGF receptor in low‐grade astrocytomas suggests that activation of PDGF autocrine loops may be an early event in the pathogenesis of malignant astrocytomas. © 1995 Wiley‐Liss, Inc.
International renal‐cell cancer study. I. Tobacco use
Authors: McLaughlin Joseph K. , Lindblad Per , Mellemgaard Anders , McCredie Margaret , Mandel Jack S. , Schlehofer Brigitte , Pommer Wolfgang , Adami Hans‐Olov 
Published: September 2008

AbstractThe relationship between renal‐cell cancer (RCC) and tobacco use was investigated in an international, multicenter, population‐based case‐control stud/. Coordinated studies were conducted in Australia, Denmark, Germany, Sweden and the United States using a shared protocol and questionnaire. A total of 1,732 cases (1,050 men, 682 women) and 2,309 controls (1,429 men, 880 women) were interviewed for the study. No association was observed between risk and use of cigars, pipes or smokeless tobacco. A statistically significant association was observed for cigarette smoking, with current smokers having a 40% increase in risk [relative risk (RR) = 1.4, 95% confidence interval (CI) 1.2–1.7]. Risk increased with intensity (number of cigarettes) and duration (years smoked). Among current smokers the RR for pack‐years rose from I.I (95% CI 0.8–1.5) for <15.9 pack years to 2.0 (95% CI 1.6–2.7) for >42 pack years (p for trend < 0.001). Long‐term quitters (> 15 years) experienced a reduction in risk of about 15–25% relative to current smokers. Those who started smoking late (>24 years of age) had about two‐thirds the risk of those who started young (< 12 years of age). Overall, the findings of this pooled analysis confirm that cigarette smoking is a causal factor in the etiology of RCC. © 1995 Wiley‐Liss, Inc.
IFN‐α1 gene transfection completely abolishes the tumorigenicity of murine B16 melanoma cells in allogeneic DBA/2 mice and decreases their tumorigenicity in syngeneic C57BL/6 mice
Authors: Kaido Thomas , Bandu Marie‐Thérèse , Maury Chantal , Ferrantini Maria , Belardelli Filippo , Gresser Ion 
Published: September 2008

AbstractThe murine B16 melanoma (H‐2b) was transfected with a retroviral vector containing the mouse IFN‐α1 gene. IFN‐α1‐transfected cells produced IFN‐α in vitro and exhibited an altered phenotype characterized by a decreased rate of multiplication, enhanced expression of H‐2 antigens, an antiviral state to VSV, and decreased pigmentation. Control and IFN‐α1‐transfected cells were tested for their ability to grow in syngeneic (H‐2b) CS7B1/6 and allogeneic (H‐2d) DBA/2 mice. IFN‐α1producing B16 clones were less tumorigenic after s.c, i.p., and i.v. routes of injection than IFN‐non‐producer BI6 clones in syngeneic CS7B1/6 mice. IFN‐α1‐producing B16 cells were, however, totally rejected by allogeneic DBA/2 mice regardless of the routes and inocula tested, while control B16 cells grew in and killed DBA/2 mice. The total rejection of IFN‐α1‐transfected B16 cells in allogeneic mice appeared to be dependent on T cells as these cells grew in DBA/2 nude mice. Incubation of IFN‐α‐producing clones with anti‐mouse IFN‐α/β prior to injection into C57BI/6 mice did not enhance their tumorigenicity. Likewise, injection of C57BI/6 and DBA/2 mice with antibody to IFN‐α/β did not enhance the tumorigenicity of IFN‐α1‐transfected cells. C57B1/6 mice immunized with irradiated IFN‐α1 cells were only slightly protected against a subsequent challenge with parental B16 cells. In contrast, DBA/2 mice immunized with irradiated IFN‐α1 cells exhibited tumor‐specific, long‐lasting immunity to subsequent challenge with parental B16 cells. © 1995 Wiley‐Liss, Inc.
Loss of chromosome 3p arm differentiating tumorigenic from non‐tumorigenic cells derived from the same SV40‐transformed human mammary epithelial cells
Authors: Lebeau Jérocme , Gerbault‐Seureau Michèle , Lemieux Nicole , Apiou Francloise , Calvo Fabien , Berthon Philippe , Goubin Gerard , Dutrillaux Bernard 
Published: September 2008

AbstractAfter immortalization of human normal mammary epithelial cells by replication‐defective SV40 genome integration, 2 cultures were developed independently. Both had the same integration site, in band 9q21, but rapidly diverged karyotypically. After a few passages, one, designated SC2T2, exhibited near‐diploid (a) and the other, designated SL2T2, near‐tetraploid (b) karyotypes. The simplest formulas were 44, X, ‐X, der(3;22) (q10;q10), der(4)t(4;9)(q34;q12), +8, +9, add(13)(pl), der(19) t(8; 19)(q21;p 13.3), add(22)(p 1) for karyotype (a) and 93, XXXX, add(1)(q12), add(11)(q13), +20 for karyotype (b). A number of alterations were further acquired with passages. Both cell cultures were tumorigenic, but their efficiency of grafting in nude mice largely differed: it was low for SL2T2 and high for SC2T2 cultures. All cultures of the xenografted tumors, obtained from either SL2T2 or SC2T2, exhibited the same clonal anomalies as those characterizing karyotype (a). It was concluded that only cells with karyotype (a) were tumorigenic, and that the difference in the tumorigenic potential of cultures SC2T2 and SL2T2 was related to their richness in cells with this karyotype. The comparison of the various karyotypes, together with data obtained in other cell types transformed by SV40, suggests that the acquisition of tumorigenicity in S2T2 mammary epithelial cells may be related to the loss of chromosome 3p arm. © 1995 Wiley‐Liss, Inc.
Effects of granulocyte‐monocyte colony‐stimulating factor (GM‐CSF) on expression of adhesion molecules and production of cytokines in blood monocytes and ovarian cancer‐associated macrophages
Authors: Bernasconi Sergio , Matteucci Christian , Sironi Marina , Conni Mario , Colotta Francesco , Mosca Monica , Colombo Nicoletta , Bonazzi Cristina , Landoni Fabio , Corbetta Giuseppe , Mantovani Alberto , Allavena Paola 
Published: September 2008

AbstractThe present study was aimed at characterizing the effects of in vitro exposure to GM‐CSF on blood monocytes and tumor‐associated macrophages (TAM) in human ovarian cancer. Purified populations of TAM from ovarian cancer patients were studied in terms of expression of surface molecules, cytokine production and tumor cytotoxicity after overnight incubation with GM‐CSF or IFNγ and LPS, used as reference activators. GM‐CSF augmented the surface expression of ICAM‐I and CD 18 in TAM and in blood monocytes. Stimulation was more prominent in monocytes than in TAM, which showed higher baseline expression of this adhesion molecule. ICAM‐3 was not influenced by GM‐CSF or by IFNγ/LPS. GM‐CSF‐augmented ICAM‐I expression was associated with higher levels of mRNA transcripts. The protein synthesis inhibitor cycloheximide superinduced basal and GM‐CSF‐induced ICAM‐I transcripts, thus excluding a role for secondary polypeptide mediators. In the absence of stimuli, TAM produced higher levels, compared to monocytes, of IL‐6 and IL‐8 but not of IL‐1 and TNF. GM‐CSF augmented the production of IL‐6 and IL‐8 (but not that of IL‐1 and TNF) in TAM, whereas it had little effect on blood monocyte. Tumoricidal activity was tested against two ovarian tumor cell lines (OVCAR3 and SW626). GM‐CSF more prominently augmented monocyte cytotoxicity, while only 2 of 6 TAM preparations were stimulated by GM‐CSF. These results suggest that GM‐CSF selectively regulates the function of blood monocytes and TAM, the effect of this cytokine varying with the parameter and cell population examined. These data provide a rational and biological endpoint for further studies with GM‐CSF as an activator of mononuclear phagocyte function in ovarian cancer. © 1995 Wiley‐Liss, Inc.
International renal‐cell cancer study. II. Analgesics
Authors: McCredie Margaret , Pommer Wolfgang , McLaughlin Joseph K. , Stewart John H. , Lindblad Per , Mandel Jack S. , Mellemgaard Anders , Schlehofer Brigitte , Niwa Shelley 
Published: September 2008

AbstractThere has been concern about the role of analgesics in the development of renal‐cell cancer, although a few studies have reported moderately elevated risks with regular or long‐term use. In a large international case‐control study of renal‐cell cancer we examined, among other hypotheses, the effect of phenacetin‐containing and of other types of analgesics: paracetamol (acetaminophen), salicylates (mainly aspirin) and pyrazolones (e.g., antipyrine or phenazone). Relative risks, adjusted for the effects of age, sex, body‐mass index, tobacco smoking and study centre, were not significantly increased with intake of phenacetin, either when lifetime consumption was categorized at the level of >0.1 kg or when subjects were subdivided further by amount. Nor were paracetamol, salicylates or pyrazolones linked with renal‐cell cancer. No consistently increasing risks with consumption level was found. The lack of association was not altered by restricting analgesic use to that which occurred 5 or 10 years before the defined “cut‐off” date or when analysis was restricted to exclusive users of a particular type of analgesic. Neither was the risk influenced by the rate of consumption or whether the consumption had occurred at a young age. Our study provides clear evidence that aspirin is unrelated to renal‐cell cancer risk, and our findings do not support the hypothesis that analgesics containing phenacetin or paracetamol increase the risk, although the number of “regular” users and the amount of these types of analgesic consumed were too small to confidently rule out a minor carcinogenic effect of phenacetin and paracetamol. © 1995 Wiley‐Liss, Inc.
Treatment of postpartum depression in mothers: Secondary benefits to the infants
Authors: Goodman Sherryl H. , Broth Michelle R. , Hall Christine M. , Stowe Zachary N. 
Published: September 2008

AbstractThis study examined the quality of mother–infant interaction and levels of perceived stress and parenting efficacy in association with mothers' levels of depression among mothers with significant depressive symptoms during the postpartum period, who were followed prospectively during treatment, and their infants less than 6 months old. Mothers with postpartum depression (n = 19) were treated with medication, and the mothers were observed with their infants prior to treatment and 3 and 6 months later. A comparison group of nondepressed mothers (n = 25) was included to control for the normal developmental changes associated with the postpartum period. The depressed women experienced a significant reduction in depressive symptoms and did not differ significantly from well mothers 6 months after beginning treatment. Despite initial levels of parenting quality and depression, mothers' reduced levels of depression, after 12 weeks of treatment, were associated with improvements in the quality of their interactions with their infants and with improvements in their infants' quality of play. For both perceived stress and parenting efficacy beliefs, both depressed and well mothers showed a significant improvement from the initial to the 12‐week visit, and there were no significant differences between depressed and well mothers' perceived stress or efficacy beliefs at the 12‐week visit. Depression at the 12‐week visit did not predict perceived stress or efficacy beliefs beyond the variance accounted for by initial levels of those variables and depression. The impact of reducing levels of maternal depression symptoms supports theoretical models of the role of parenting in the association between maternal depression and child functioning. Further, these findings support the benefits to infants of reducing depression in mothers.
Dyadic intervention during pregnancy? Treating pregnant women and possibly reaching the future baby
Authors: Bergner Sharone , Monk Catherine , Werner Elizabeth A. 
Published: September 2008

AbstractIt is well established that postnatally, maternal psychopathology greatly increases a child's risk for emotional disorders. This article addresses the formative phase that precedes the mother–infant mutually regulating dyad. Biopsychological data presented here suggest that women's affective states during pregnancy—specifically depression, anxiety, and elevated life‐stress—are associated with subtle alterations in the neurobiological substrate of the fetus' emerging affect regulation system. The article moves to a general discussion of the emotional experience of pregnancy, and to the use of psychodynamic psychotherapy when problematic aspects of women's representational world lead to negative or dysregulated affect. Two case vignettes are presented: one described in brief and the other in greater detail. This kind of therapeutic intervention aims to achieve mood improvement, address women's emerging relationship with her baby, and potentially, influence the course of fetal development. Winnicott (1960) said there is no such thing as a baby alone; all the more so during pregnancy.
Maternal depression and anxiety effects on the human fetus: Preliminary findings and clinical implications
Authors: Dieter John N.I. , Emory Eugene K. , Johnson Katrina C. , Raynor B. Denise 
Published: September 2008

AbstractNewborns of depressed and anxious mothers show biobehavioral abnormalities suggesting that maternal psychological distress has negative effects on the fetus. Two studies examined the fetuses of depressed and nondepressed mothers: (a) a cross‐sectional investigation of fetal activity during the second and third trimesters and (b) an examination of behavioral and heart rate response to vibratory stimulation in late‐gestation fetuses. Fetuses of depressed mothers were more active during the fifth, sixth, and seventh gestational months. Assessment of late‐term fetuses consisted of a baseline, trials of vibratory stimulation directed towards measuring habituation, and a poststimulation period. During baseline, the fetuses of depressed mothers exhibited a lower heart rate. During stimulation trials, they showed less total movement and appeared to habituate more often. Approximately 35% of the variance in fetal behavior was accounted for by the mothers' depression and anxiety symptoms. Maternal depression may be linked to greater fetal activity during the second and third trimesters and decreased behavioral responsivity during late gestation. The response of late‐term fetuses of depressed mothers to vibratory stimulation may reflect “receptor adaptation/effector fatigue” and not true habitation. Future studies should examine the value of clinical interventions provided to the pregnant mother.
Chromosome instability and tumor lethality suppression in carcinogenesis
Authors: Shen Changxian , Zhou Yonggang , Zhan Jun , Reske Sven N. , Buck Andreas K. 
Published: September 2008

AbstractThe maintenance and survival of each organism depends on its genome integrity. Alterations of essential genes, or aberrant chromosome number and structure lead to cell death. Paradoxically, cancer cells, especially in solid tumors, contain somatic gene mutations and are chromosome instability (CIN), suggesting a mechanism that cancer cells have acquired to suppress the lethal mutations and/or CIN. Herein we will discuss a tumor lethality suppression concept based on the studies of yeast genetic interactions and transgenic mice. During the early stages of the multistep process of tumorigenesis, incipient cancer cells probably have adopted genetic and epigenetic alterations to tolerate the lethal mutations of other genes that ensue, and to a larger extent CIN. In turn, CIN mediated massive gain and loss of genes provides a wider buffer for further genetic reshuffling, resulting in cancer cell heterogeneity, drug resistance and evasion of oncogene addiction, thus CIN may be both the effector and inducer of tumorigenesis. Accordingly, interfering with tumor lethality suppression could lead to cancer cell death or growth defects. Further validation of the tumor lethality suppression concept would help to elucidate the role of CIN in tumorigenesis, the relationship between CIN and somatic gene mutations, and would impact the design of anticancer drug development. J. Cell. Biochem. 105: 1327–1341, 2008. © 2008 Wiley‐Liss, Inc.
Truncation of small matrix elements based on the Euclidean norm for blocked data structures
Authors: Rubensson Emanuel H. , Rudberg Elias , Sałek Paweł 
Published: September 2008

AbstractMethods for the removal of small symmetric matrix elements based on the Euclidean norm of the error matrix are presented in this article. In large scale Hartree–Fock and Kohn–Sham calculations it is important to be able to enforce matrix sparsity while keeping errors under control. Truncation based on some unitary‐invariant norm allows for control of errors in the occupied subspace as described in (Rubensson et al. J Math Phys 49, 032103). The Euclidean norm is unitary‐invariant and does not grow intrinsically with system size and is thus suitable for error control in large scale calculations. The presented truncation schemes repetitively use the Lanczos method to compute the Euclidean norms of the error matrix candidates. Ritz value convergence patterns are utilized to reduce the total number of Lanczos iterations. © 2008 Wiley Periodicals, Inc. J Comput Chem, 2009
Epidermal glands in the abdomen of a basal ant Dinoponera lucida (Formicidae: Ponerinae)
Authors: Serrão José Eduardo , Castro Rafael Cunha A. , Zanuncio José Cola , Mariano Cléa Santos Ferreira , Delabie Jacques Hubert Charles 
Published: September 2008

AbstractThe basal ant Dinoponera (Hymenoptera: Ponerinae) has lost the morphologic queen caste so that all females may be potential reproductive individuals, and the nestmate recognition results from cuticular hydrocarbons cues. However, data about the origin of that substance in Ponerinae ants are scarce. This study reports the occurrence of epidermal glands in the abdomen of the ant Dinoponera lucida. In this ant, the epidermis of the abdominal sternites has tall cells with well‐developed nucleus contrasting with flattened and collapsed epidermis in the tergites, suggesting a glandular function in the epidermis of the sternites. The possible role of the glandular epidermis in the synthesis of cuticular hydrocarbons for the nestmate recognition is discussed. Microsc. Res. Tech., 2009. © 2008 Wiley‐Liss, Inc.