bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treating hepatitis C in the prison population is cost-saving
Authors: Tan Jennifer A. , Joseph Tom A. , Saab Sammy 
Published: July 2008

Abstract

The prevalence of chronic hepatitis C infection in U.S. prisons is 12% to 31%. Treatment of this substantial portion of the population has been subject to much controversy, both medically and legally. Studies have demonstrated that treatment of chronic hepatitis C with pegylated interferon (PEG IFN) and ribavirin is a cost-effective measure in the general population; however, no study has addressed whether the same is true of the prison population. The aim of this study was to determine the cost-effectiveness of hepatitis C treatment with PEG IFN and ribavirin in the U.S. prison population. Cost-effectiveness was determined via a decision analysis model employing Markov simulation. The cohort of prisoners had a distribution of genotypes and stages of fibrosis in accordance with prior studies evaluating inmate populations. The probability of transitioning from one health state to another, reinfection rates, in-prison and out-of-prison mortality rates, sustained viral response rates, costs, and quality of life weights were also obtained from the literature. Sensitivity analysis was performed. In a strategy without a pretreatment liver biopsy, treatment was cost-effective for all ages and genotypes. This model was robust to rates of disease progression, mortality rates, reinfection rates, sustained viral response rates, and costs. In a strategy employing a pretreatment liver biopsy, treatment was also cost-saving for prisoners of all ages and genotypes with portal fibrosis, bridging fibrosis, or compensated cirrhosis. Treatment was not cost-effective in patients between the ages of 40 and 49 with no fibrosis and genotype 1.

Conclusion:

Treatment of chronic hepatitis C with PEG IFN and ribavirin in U.S. prisons results in both improved quality of life and savings in cost for almost all segments of the inmate population. If the decision to treat hepatitis C is based on pharmaco-economic measures, this significant proportion of infected individuals should not be denied access to therapy. (Hepatology 2008.)
A study of the energy balance and melt regime on Juncal Norte Glacier, semi‐arid Andes of central Chile, using melt models of different complexity
Authors: Pellicciotti Francesca , Helbing Jakob , Rivera Andrés , Favier Vincent , Corripio Javier , Araos José , Sicart Jean‐Emmanuel , Carenzo Marco 
Published: July 2008

AbstractWe use meteorological data from two automatic weather stations (AWS) on Juncal Norte Glacier, central Chile, to investigate the glacier–climate interaction and to test ablation models of different complexity. The semi‐arid Central Andes are characterized by dry summers, with precipitation close to zero, low relative humidity and intense solar radiation. We show that katabatic forcing is dominant both on the glacier tongue and in the fore field, and that low humidity and absence of clouds cause strong radiative cooling of the glacier surface. Surface albedo is basically constant for snow and ice, because of the scarcity of solid precipitation. The energy balance of the glacier is simulated for a 2‐month period in austral summer using two models of different complexity, which differ in the inclusion of the heat conduction flux into the snowpack and in the parameterization of the incoming longwave radiation. Net shortwave radiation is the dominant component of the energy balance. The sensible heat flux is always positive, while both the net longwave radiation and latent heat flux are negative. Neglecting the subsurface heat flux and corresponding variations in surface temperature leads to an overestimation of ablation of 2% over a total of 3695 mm water equivalent (w.e.) at the end of the season. Correct modelling of incoming longwave radiation is crucial, and we suggest that parameterizations based on vapour pressure and air temperature should be used rather than on computed cloud amount. We also used an enhanced temperature‐index model incorporating the shortwave radiation flux, which has two empirical parameters. We apply it both with values of parameters obtained for Alpine glaciers and recalibrated on Juncal Norte. The model recalibrated against the correct energy balance simulations performs very well. The model parameters respond to the meteorological conditions typical of this climatic setting. Copyright © 2008 John Wiley & Sons, Ltd.
Molecular evidence for a clonal relationship between multiple lesions in patients with unknown primary adenocarcinoma
Authors: Speel Ernst‐Jan M. , van de Wouw Agnes J. , Claessen Sandra M.H. , Haesevoets Annick , Hopman Anton H.N. , van der Wurff Anneke A.M. , Osieka Rainhardt , Buettner Reinhard , Hillen Harry F.P. , Ramaekers Frans C.S. 
Published: July 2008

AbstractUnknown primary adenocarcinoma (UPA) comprises a group of heterogeneous cancers of great clinical and biological interest. UPA presents as metastatic disease without a detectable primary site after medical workup. Here we investigated whether or not a clonal relationship exists between multiple tumors within individual UPA patients. A molecular resemblance would argue for an early clonal outgrowth of tumor cells from the primary lesion, a mutual feature observed within this group of neoplasms. In 14 patients with UPA multiple tumors, obtained at autopsy, were analyzed by molecular allelotyping and immunohistochemistry. In addition, tumors of 4 patients could be analyzed by comparative genomic hybridization (CGH). Similar genetic and phenotypic profiles were used as indicator for a clonal relationship, whereas different profiles implicate independent tumors. The molecular data indicated that the multiple lesions in the 14 UPA patients, including the primary tumors, are clonally related. In agreement with the theory of tumor progression, some metastatic lesions showed additional genetic alterations besides the characteristics that were shared with the primary tumor. Furthermore, 8 UPA patients had tumors with a high frequency of allelic loss and/or imbalance (FALI; 43–71%), while 6 patients demonstrated a lower FALI (14–29%), suggesting the occurrence of chromosomal instability in the former group. Our data provide molecular evidence for a clonal relationship between multiple metastases and the primary tumor within individual UPA patients, independent of the anatomical origin of the cancer. This finding is in agreement with the suggestion that tumor progression is rapid in UPA patients, limiting the chance of clonal divergence. The identification of 2 groups of UPAs with either a high or low FALI indicates that chromosomal instability is not the only driving force behind early tumor cell dissemination. Thus, other molecular mechanisms must underlie the common biology of these tumors. © 2008 Wiley‐Liss, Inc.
Genetic alterations of HLA‐class II in ovarian cancer
Authors: Kübler Kirsten , Arndt Peter F. , Wardelmann Eva , Landwehr Christina , Krebs Dieter , Kuhn Walther , van der Ven Katrin 
Published: July 2008

AbstractThe immune system controls tumor formation through identification and elimination of cellular alterations. Consequently, cancer development in immune competent hosts depends on strategies to evade the immune system. Modulation of tumor antigen‐specific immune responses by aberrant expression of HLA‐class I and II molecules is well documented in a variety of carcinomas including ovarian cancer. To date, little data are available about molecular mechanisms responsible for altered HLA‐class II phenotypes in tumors. In our sample of 10 Caucasian patients with ovarian carcinoma, a semiquantitative analysis was performed for HLA‐class II loci DRB1 and DQB1 in malignant and normal ovarian tissue. Gene amplifications were identified in 62.5% of analyzed alleles and deletions in 17.5%, demonstrating that genomic aberrations of 6p21.3 are common and that copy number gain is more frequent than loss. Moreover, amplifications are most pronounced in advanced‐stage tumors. To evaluate genotype‐phenotype relation, immunohistochemical analyses were performed and revealed de novo expression of HLA‐class II in 30% of tumors with an inverse association between antigen level and HLA copy number. It remains to be elucidated whether the profound changes of the latter quantities are the result of the host's immunological self‐defense, indicate the presence of an oncogene located within the MHC‐complex or merely reflect the increasing loss of differentiation of the tumor tissue. © 2008 Wiley‐Liss, Inc.
Systemic IGF‐I administration stimulates the in vivo growth of early, but not advanced, renal cell carcinoma
Authors: Rosendahl Ann H. , Holly Jeff M.P. , Celander Mona , Forsberg Göran 
Published: July 2008

AbstractInsulin‐like growth factor I (IGF‐I) is a potent mitogen and antiapoptotic factor. Although elevated serum IGF‐I levels have been associated with increased cancer risk, it is not yet clear whether IGF‐I sensitivity is sustained throughout tumor progression. To evaluate the biological effects of IGF‐I during renal cell carcinoma (RCC) establishment and progression, we administered recombinant human IGF‐I to severe combined immuno‐deficient mice bearing early or more established Caki‐2 human RCC tumors. IGF‐I significantly enhanced the tumor growth 2.4‐fold when administered early after tumor inoculation. This IGF‐I‐induced growth was accompanied with enhanced tumor cell proliferation, tumor vascularization, as well as increased intratumoral insulin‐like growth factor binding protein 3 (IGFBP‐3) and pSmad2 levels. In contrast, IGF‐I administrated to more established RCC tumors showed no effect on tumor growth, with subsequently much lower Ki‐67, IGFBP‐3 and pSmad2 levels. Taken together, these data suggest that systemic IGF‐I has potent actions during early RCC tumor development with a sustained long‐term effect on proliferation and neovascularization although with progression, later tumors appear to become desensitized to systemic IGF‐I effects. © 2008 Wiley‐Liss, Inc.
Expression and prognostic impact of PRL‐3 in lymph node metastasis of gastric cancer: Its molecular mechanism was investigated using artificial microRNA interference
Authors: Wang Zhao , He Yu‐Long , Cai Shi‐Rong , Zhan Wen‐Hua , Li Zeng‐Rong , Zhu Bao‐He , Chen Chuang‐Qi , Ma Jin‐Ping , Chen Zheng‐Xuan , Li Wen , Zhang Long‐Juan 
Published: July 2008

AbstractHigh PRL‐3 expression had been reported to have close association with lymph node metastasis (LNM) of gastric cancer. However, the prognostic significance of highly expressing PRL‐3 in LNM of human gastric cancer and the role in the metastasis remain unclear. Our study examined PRL‐3 expression both in the LNM (n = 107) and in the primary lesion (n = 137) of gastric cancer, and compared the overall survival rates. RNA interference, induced by recombinant plasmid pcDNA.rPRL3‐miR expressing artificial PRL‐3 miRNA, was employed to knockdown PRL‐3 expression in human SGC7901 gastric cancer cells. Invasion assay and migration assay in vitro were conducted to determine the role of PRL‐3 in the metastasis. The role of PRL‐3 in the proliferation of SGC7901 cells and tumor growth were also determined. We observed that high PRL‐3 expression was more frequently detected in the LNM than in the matched primary lesion (72.9 vs. 47.7%, p < 0.001). Furthermore, the overall survival rate of the patients with high expression of PRL‐3 in the LNM was significantly less than those with moderate/low expression (p = 0.003). Importantly, knockdown of PRL‐3 can significantly reduce both invasion and migration potencies of SGC7901 cells (p < 0.001), and significantly suppressed the proliferation of SGC7901 cells and slowed down the tumor growth (p < 0.001). It was concluded that high expression of PRL‐3 in the LNM had a negative impact on the prognosis of the patients, and plays important roles in LNM of gastric cancer and the tumor growth, which can be a potential therapeutic target and a prognostic factor. © 2008 Wiley‐Liss, Inc.
Cancer risks among relatives of children with Hodgkin and non‐Hodgkin lymphoma
Authors: Pang Dong , Alston Robert D. , Eden Tim O.B. , Birch Jillian M. 
Published: July 2008

AbstractA role for genetic susceptibility in the aetiology of childhood lymphomas was investigated in 454 families of children with histologically confirmed Hodgkin lymphoma (HL) and non‐Hodgkin lymphoma (NHL) from Northwest England. Cancers in parents were obtained from the UK National Health Service Central Register and in other close relatives by interview with the parents. The cancer incidence among relatives was compared with expected incidence based on cancer registry data for England. There were 197 cancers in relatives (SIR 1.0 95% CI 0.8–1.1). In families of children with HL, there was an excess of HL in the first degree relatives (SIR 5.8 95% CI 1.2–16.9). Excesses of HL diagnosed under population median age (SIR 4.1 95% CI 1.1–10.6) were seen among all relatives and relatives of children who were below the median age at diagnosis (SIR 5.5 95% CI 1.1–16.0). In families of children with NHL, there were non‐significant excesses of central nervous system (CNS) tumours in the first degree relatives (SIR 2.9 95% CI 0.8–7.4) and in the second and third degree relatives (SIR 1.5). There were significant excesses of CNS tumours diagnosed under the population median age (SIR 2.8 95% CI 1.1–5.8) in all relatives. Excess CNS tumours were also seen among relatives of children below the median age at diagnosis (SIR 3.2 95% CI 1.1–7.6). In conclusion, genetic susceptibility in some families of children with lymphoma might be operating, but aetiologies in HL and NHL appear to be different. Possible interpretations of our findings, in the context of putative genetic and infectious aetiologies, are discussed. © 2008 Wiley‐Liss, Inc.
Cancer risks in ulcerative colitis patients
Authors: Hemminki Kari , Li Xinjun , Sundquist Jan , Sundquist Kristina 
Published: July 2008

AbstractPatients diagnosed with ulcerative colitis (UC) are known to be at an increased risk of colorectal and liver cancers and leukemia. UC is an autoimmune disease, which may present a wider spectrum of cancers. We wanted to examine the risk of cancer in a large population of UC patients in order to reach high statistical power. A UC research database was constructed by identifying UC patients from the Swedish Hospital Discharge Register and cancer patients from the Cancer Registry. Follow‐up of 27,606 UC patients hospitalized for the first time during the years 1964–2004 identified 2,058 patients with cancer. Standardized incidence ratios were calculated for cancer in UC patients by comparing to subjects without hospitalization for UC. The novel tumor sites in UC patients included small intestinal (carcinoid), pancreatic, breast and prostate cancers, nonthyroid endocrine gland tumors, non‐Hodgkin lymphoma and multiple myeloma. A total of 11 sites showed an increased risk, which remained at 6 sites when tumors diagnosed in the year of UC hospitalization were excluded; even chronic myeloid leukemia was in excess. Cancer risks depended on the age at first hospitalization for UC. The SIRs for colon, rectal, liver and pancreatic cancers declined by age at hospitalization for UC, while for endocrine tumors the older patients were at higher risk. Our large study identified novel subsequent cancers in UC patients. However, some of these, including small intestinal carcinoids, prostate cancers and nonthyroid endocrine tumors, may be in excess because of intensified medical surveillance of the patients. © 2008 Wiley‐Liss, Inc.
Upregulated expression of complement inhibitory proteins on bladder cancer cells and anti‐MUC1 antibody immune selection
Authors: Varela Juan Carlos , Atkinson Carl , Woolson Robert , Keane Thomas E. , Tomlinson Stephen 
Published: July 2008

AbstractMembrane complement inhibitors (CD46, CD55 and CD59) are upregulated in some human cancers indicating that they play a role in immune evasion. We investigated complement inhibitor expression in bladder cancer and examined the hypothesis that selective pressure of an antibody response (anti‐MUC1) results in the upregulated expression of complement inhibitors on tumor cells. Paired samples of tumor and normal tissue from 22 bladder cancer patients were analyzed for expression of MUC1, CD46, CD55 and CD59, and matched serum samples analyzed for anti‐MUC1 IgM and IgG levels. Relationships between anti‐MUC1 antibody levels and complement inhibitor expression were investigated. MUC1 mRNA was upregulated in 86% of tumor samples. CD46 was upregulated in 77%, CD55 in 55% and CD59 in 59% of tumors. Low titer anti‐MUC1 IgM was detected in normal human sera, but was elevated in 41% of the bladder cancer patients. Anti‐MUC1 IgG was virtually absent from normal sera, but present in 32% of the cancer patients. There was a direct relationship between anti‐MUC1 antibody titer and expression level of complement inhibitors. Analysis of the correlation of each antibody with the expression of each complement inhibitor by Spearman's rank test revealed a strong correlation between both anti‐MUC1 IgM and IgG levels and increased expression of CD46 and CD55, and combined anti‐MUC1 IgM/IgG levels correlated with increased expression of all 3 complement inhibitors. In conclusion, the data demonstrate upregulated complement inhibitor expression and the presence of an anti‐MUC1 antibody response in bladder cancer patients and support the hypothesis of antibody‐mediated immune selection. © 2008 Wiley‐Liss, Inc.
The beginning of the end of the lung cancer epidemic in Dutch women?
Authors: Karim‐Kos Henrike E. , Janssen‐Heijnen Maryska L.G. , van Iersel Carola A. , van der Meer Regina M. , de Vries Esther , Coebergh Jan Willem W. 
Published: July 2008

AbstractIn some European countries, female lung cancer mortality and incidence have started to decrease or flatten out, whereas they are still rising in The Netherlands. We present recent mortality and incidence trends of lung cancer and smoking trends in The Netherlands to show the end of the lung cancer epidemic in Dutch women. Lung cancer mortality and incidence rates by gender were analyzed for 4 age groups (20–44, 45–49, 50–54 and 55–59), and smoking prevalence rates were examined for women using joinpoint regression and birth cohort analysis. Data on mortality were collected for the period 1960–2006, incidence for the period 1989–2003 and smoking prevalence for the period 1988–2007. Because of decreasing lung cancer mortality and incidence rates among males and dramatically increasing rates among females, rates of young males were surpassed by those of females after the mid‐1990s. However, although in young women (20–49) mortality increased with 4–5% per year, it flattened out (no significant in‐ or decreases) since 1999. Among older women, mortality rates were still increasing markedly. Mortality rates and smoking prevalence tended to decrease in women born after the 1950s. This is the first report suggesting that the lung cancer epidemic in Dutch women is coming to an end. Although the increase in lung cancer incidence and mortality among Dutch women has been one of the most dramatic in Europe, the recent decrease in young women is expected to be followed by a future leveling off or a slight decrease in overall female lung cancer rates. © 2008 Wiley‐Liss, Inc.
Pathways from infant exposure to marital conflict to parent–toddler role reversal
Authors: Macfie Jenny , Houts Renate M. , Pressel Abigail S. , Cox Martha J. 
Published: July 2008

AbstractWe know that exposure to marital conflict places infants at risk, but we know less about processes. One process may be role reversal, when a distressed parent looks to the child to meet unmet needs for comfort, intimacy, or companionship. A parent in marital conflict may be particularly prone to role reversal, which in turn adversely affects child development. The current study examined pathways from infants' exposure to marital conflict at 12 months to role reversal at 24 months. We sampled low–middle socioeconomic status (SES) families with their first child (N = 128). Independent observers assessed marital conflict (in a problem‐solving task) and role reversal (in a story‐telling task). We found that each parent's conflict behavior predicted the other parent's role reversal. In a direct pathway, mother's conflict behavior towards father led directly to father's role reversal with the child. In an indirect pathway, father's conflict behavior towards mother led to his withdrawal from her, which in turn led to mother's role reversal with the child. Clinical implications are discussed within a developmental psychopathology framework in terms of preventive interventions to offset the deleterious effect of marital conflict and role reversal on child development.
The Chances for Children Teen Parent–Infant Project: Results of a pilot intervention for teen mothers and their infants in inner city high schools
Authors: Mayers Hillary A. , Hager‐Budny Michaela , Buckner Elizabeth B. 
Published: July 2008

AbstractAdolescent motherhood poses serious challenges to mothers, to infants, and ultimately to society, particularly if the teen mother is part of a minority population living in an urban environment. This study examines the effects of a treatment intervention targeting low‐income, high‐risk teen mothers and their infants in the context of public high schools where daycare is available onsite. Our findings confirm the initial hypothesis that mothers who received intervention would improve their interactions with their infants in the areas of responsiveness, affective availability, and directiveness. In addition, infants in the treatment group were found to increase their interest in mother, respond more positively to physical contact, and improve their general emotional tone, which the comparison infants did not. Importantly, these findings remain even within the subset of mothers who scored above the clinical cutoff for depression on the Center for Epidemiological Studies‐Depression Scale (CES‐D; L. Radloff, 1977), confirming that it is possible to improve mother–infant interaction without altering the mother's underlying depression. The implications of these findings are significant both because it is more difficult and requires more time to alter maternal depression than maternal behavior and because maternal depression has been found to have such devastating effects on infants.
Violated wishes about division of childcare labor predict early coparenting process during stressful and nonstressful family evaluations
Authors: Khazan Inna , McHale James P. , Decourcey Wendy 
Published: July 2008

AbstractPrior research has indicated that expectant parents overestimate the extent to which fathers will take part in the “work” of parenting, with mothers often becoming disenchanted when these expectations are violated following the baby's arrival. In this study, we examine the role of violated wishes concerning childcare involvement in accounting for variability in maternal and paternal marital satisfaction, and in early coparenting behavior as assessed during family‐interaction sessions. The results indicate possible negative effects of violated wishes on the enacted family process and confirm previous findings regarding the effects of marital satisfaction. In addition, we uncovered differences in the way that violated maternal wishes are related to coparenting during playful and mildly stressful family interactions.