bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pancreatic Pseudocysts Transpapillaryand Transmural Drainage
Authors: Libera E. Della , Siqueira E. S. , Morais M. , Rohr M. R. S. , Brant C. Q. , Ardengh J. C. , Ferrari A. P. 
Published: September 2007

Background: Pancreatic pseudocyst endoscopic drainage
has been described as a good treatment option,
with morbidity and mortality rates that are lower
than surgery. The aim of our study is to describe the
efficacy of different forms of endoscopic drainage
and estimate pseudocyst recurrence rate after short
follow up period.Patients and Methods: We studied 30 patients with
pancreatic pseudocyst that presented some indication
for treatment: persistent abdominal pain, infection
or cholestasis. Clinical evaluation was performed
with a pain scale, 0 meaning absence of pain
and 4 meaning continuous pain. Pseudocysts were
first evaluated by abdominal CT scan, and after
endoscopic retrograde pancreatography the patients
were treated by transpapillary or transmural (cystduodenostomy
or cystgastrostomy) drainage. Pseudocyst
resolution was documented by serial CT
scans.Results: 25/30 patients could be treated. Drainage
was successful in 21 (70% in an ‘intention to treat’
basis). After a mean follow‐up of 42±35.82 weeks,
there was only 1 (4.2%) recurrence. A total of 6 complications
occurred in 37 procedures (16.2%), and all
but 2 were managed clinically and/or endoscopically:
there was no mortality related to the procedure.
Patients submitted to combined drainage
needed more procedures than the other groups.
There was no difference in the efficacy when we
compared the three different drainage methods.Conclusions: We concluded that pancreatic pseudocyst
endoscopic drainage is possible in most
patients, with high success rate and low morbidity.
Cholecystectomy, Conversion and Complications
Authors: Thompson M. H. , Benger J. R. 
Published: September 2007

Background Faced with a difficult laparoscopic
cholecystectomy the surgeon may feel that conversion
to open operation would risk greater complications
because of the laparotomy. Information on the
effect of conversion is lacking. The purpose of this
study is to measure the complications of laparoscopic
cholecystectomy and observe the effect of the
conversion rate.Methods A total of 957 patients were studied.
There were three consecutive series of patients; the
first undergoing open cholecystectomy (384 patients),
the second laparoscopic cholecystectomy with a 5.8%
conversion rate (412 patients) and the third laparoscopic
cholecystectomy with a 1.3% conversion rate
(161 patients). Data was collected prospectively using
a continuous audit, and the complication rate
compared on an intention to treat basis. In addition a
panel of experienced surgeons was asked to score the
complications depending on their severity and a
composite complication score calculated. Comparison
between the 3 groups was then undertaken.
Results Open cholecystectomy produced a postoperative
complication rate of 6%. Initially this
appeared to fall to 3.1% with the introduction of
laparoscopic cholecystectomy, but when the complications
occurring in the converted patients were
included (i.e., on an intention to treat basis) the rate
increased to 5.6% in the first group of laparoscopically‐
treated patients and 3.1% in the second. These
differences were not statistically significant. A similar
pattern emerged when scoring the severity of the
complications as judged by the expert panel. The
inclusion of intra‐operative complications appears
to remove any small advantage for laparoscopic
cholecystectomy. The reduction in the conversion
rate between the two laparoscopic groups from 5.8%
to 1.2% was statistically significant.Conclusion When considered on an intention to
treat basis laparoscopic cholecystectomy offers no
advantage over open operation in terms of the frequency
or severity of complications. Reducing the
frequency of conversion from a laparoscopic to an
open procedure also has no significant effect on the
complications encountered. We conclude, therefore,
that the complication rate is independent of the conversion
rate and that the surgeon, when faced with
difficulty at laparoscopic cholecystectomy, should
not be deterred from converting to open operation
for fear of the post‐operative consequences.
Adenoma of the Papillae of Vater.Report of Eleven Cases
Authors: Kiviniemi Heikki , Mäkelä Jyrki , Palm Jukka , Saarela Arto 
Published: September 2007

Eleven patients with a preoperative diagnosis of
adenoma of the papillae of Vater were followed up
during the fifteen‐year period from 1984 till 1998 in
the Oulu University Hospital. Seven patients were
treated primarily by transduodenal excision without
any recurrences so far. One of these seven patients
was found to have adenocarcinoma in a histological
examination.Active surgery for adenoma of the papillae of
Vater is recommended because of the precancerous
nature of the lesion, and because malignancy cannot
always be detected by endoscopic biopsies. Transduodenal
excision could be recommend for patients
at high operative risk, especially in cases with small
adenomas and low‐grade dysplasia, where histologically
free resection margins can be achieved, but
pancreaticoduodenectomy should still be performed
on patients at low operative risk.
Standardization of Steroid Hormone Assays: Why, How, and When?
Authors: Stanczyk Frank Z. , Lee Jennifer S. , Santen Richard J. 
Published: September 2007

Abstract
Lack of standardization of high-quality steroid hormone assays is a major deficiency in epidemiologic studies. In postmenopausal women, reported levels of serum 17β-estradiol (E2) are highly variable and median normal values differ by approximately a 6-fold factor. A particular problem is the use of E2 assays for prediction of breast cancer risk and osteoporotic fractures, where assay sensitivity may be the most important factor. Identification of women in the lowest categories of E2 levels will likely provide prognostic information that would not be available in a large group of women in whom E2 levels are undetectable by less sensitive assays. Detailed and costly methods involving extraction and chromatography in conjunction with RIA provide generally acceptable E2 results in postmenopausal serum, whereas less tedious, direct immunoassays suffer from inadequate specificity and sensitivity. Studies comparing the two types of methods generally report higher E2 values with the direct methods as a result of cross-reactivity with other steroids and reduced correlation with biological variables such as body mass index. Similar problems exist with measurements of E2 and estrone in men, and estrone and testosterone in women. Interest in mass spectrometry–based assays is increasing as potential gold standard methods with enhanced sensitivity and specificity; however, these assays require costly instrumentation and highly trained personnel. Taking all of these issues into consideration, we propose establishment of standard pools of premenopausal, postmenopausal, and male serum, and utilization of these for cross-comparison of various methods on an international basis. An oversight group could then establish standards based on these comparisons and set agreed upon confidence limits of various hormones in the pools. These criteria would allow validation of sensitivity, specificity, precision, and accuracy of current steroid hormone assay methodology and provide surrogates until a true gold standard can be developed. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1713–9)
Weight Gain Prior to Diagnosis and Survival from Breast Cancer
Authors: Cleveland Rebecca J. , Eng Sybil M. , Abrahamson Page E. , Britton Julie A. , Teitelbaum Susan L. , Neugut Alfred I. , Gammon Marilie D. 
Published: September 2007

Abstract
Background: To examine the effects of prediagnostic obesity and weight gain throughout the life course on survival after a breast cancer diagnosis, we conducted a follow-up study among a population-based sample of women diagnosed with first, primary invasive, and in situ breast cancer between 1996 and 1997 (n = 1,508).
Methods: In-person interviews were conducted shortly after diagnosis to obtain information on height and weight at each decade of life from age 20 years until 1 year before diagnosis. Patients were followed to determine all-cause (n = 196) and breast cancer–specific (n = 127) mortality through December 31, 2002.
Results: In multivariate Cox proportional hazards models, obese women had increased mortality due to breast cancer compared with ideal weight women among those who were premenopausal at diagnosis [hazard ratio (HR), 2.85; 95% confidence interval (95% CI), 1.30-6.23] and postmenopausal at diagnosis (HR, 1.91; 95% CI, 1.06-3.46). Among women diagnosed with premenopausal breast cancer, those who gained &gt;16 kg between age 20 years and 1 year before diagnosis, compared with those whose weight remained stable (±3 kg), had more than a 2-fold elevation in all-cause (HR, 2.45; 95% CI, 0.96-6.27) and breast cancer–specific mortality (HR, 2.09; 95% CI, 0.80-5.48). Women diagnosed with postmenopausal breast cancer who gained more than 12.7 kg after age of 50 years up to the year before diagnosis had a 2- to 3-fold increased risk of death due to all-causes (HR, 2.69; 95% CI, 1.63-4.43) and breast cancer (HR, 2.95; 95% CI, 1.36-6.43).
Conclusions: These results indicate that high levels of prediagnostic weight and substantial weight gain throughout life can decrease survival in premenopausal and postmenopausal breast cancer patients. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1803–11)
Excess Body Weight and Colorectal Cancer Risk in Canada: Associations in Subgroups of Clinically Defined Familial Risk of Cancer
Authors: Campbell Peter T. , Cotterchio Michelle , Dicks Elizabeth , Parfrey Patrick , Gallinger Steven , McLaughlin John R. 
Published: September 2007

Abstract
Overweight and obesity are linked with several chronic diseases, including colorectal cancer, among men, but results among women are equivocal. Previous evidence suggests that menopausal status, postmenopausal hormone use, and family history of cancer may modify the link between adiposity and colorectal cancer. In data from two population-based case-control studies (cases: 1,292 males and 1,404 females; controls: 1,465 males and 1,203 females) in Ontario and Newfoundland, Canada, we examined the link between colorectal cancer and body mass index (BMI) at two reference periods (BMI 2 years prior and BMI at age 20 years), weight gain since age 20 years, and height. Based on recent BMI indices among men, obesity (BMI ≥30 kg/m2) was associated with an 80% [95% confidence interval (95% CI), 1.43-2.27] increased risk of colorectal cancer relative to a normal BMI (18.5-24.9 kg/m2). The same comparison for BMI at age 20 years suggested a 94% increased risk of colorectal cancer (95% CI, 1.19-3.16). Odds ratios were similar among subgroups of men with and without a clinically defined familial risk of cancer (according to the Amsterdam or revised Bethesda criteria for Lynch syndrome). Associations were moderately stronger for cancer of the colon than cancer of the rectum. Among women, BMI and weight gain were not linked with colorectal cancer; the null associations were persistent in subgroups of familial risk of cancer, menopausal status, estrogenic status, and subsite. Tall height (&gt;1.75 m), however, was linked with increased risk of colorectal cancer among women (odds ratio, 2.27; 95% CI, 1.46-3.59) but not among men. This study suggests that obesity is associated with increased risk of sporadic and Lynch syndrome–related colon and rectal cancers among men but not among women, whereas height is directly linked with all such cancers among women but not among men. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1735–44)
Associations between Androgen and Vitamin D Receptor Microsatellites and Postmenopausal Breast Cancer
Authors: Wedrén Sara , Magnusson Cecilia , Humphreys Keith , Melhus Håkan , Kindmark Andreas , Stiger Fredrik , Branting Maria , Persson Ingemar , Baron John , Weiderpass Elisabete 
Published: September 2007

AbstractWe investigated the association between polymorphism in the androgen receptor (AR) and vitamin D receptor (VDR) genes and breast cancer risk in a large population-based case-control study of genetically homogenous Swedish women. We successfully determined both AR CAGn and VDR An genotype in 1,502 women with invasive breast cancer and in 1,510 control women. We did not find any associations between AR or VDR microsatellite lengths and breast cancer when we used a priori determined cutoffs (≤21 or ≥22 repeats for AR and ≤18 or ≥19 for VDR) to define long and short alleles. There was statistically significant interaction between VDR genotype and parity, such that women with two short alleles had a halved risk for breast cancer, irrespective of parity, compared with nulliparous women with two long alleles. Homozygosity for the long VDR allele was associated with a more advanced clinical stage at diagnosis. In exploratory analyses, we determined cutoffs based on visual inspection of distributions of allele lengths among cases and controls and found that women carrying two alleles with &lt;20 AR CAGn repeats had an increased risk for breast cancer, odds ratio of 1.67 (95% confidence interval, 1.17-2.38), compared with those with two alleles with ≥20 repeats. Women carrying two VDR alleles with &lt;21 An were also at an increased risk, odds ratio of 1.26 (95% confidence interval, 1.04-1.51). Our data do not support major roles for AR or VDR polymorphism as breast cancer risk factors. However, we did find an interaction between VDR genotype and parity that remains to be corroborated. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1775–83)
Dose-Response Modeling of Occupational Exposure to Polycyclic Aromatic Hydrocarbons with Biomarkers of Exposure and Effect
Authors: Pesch Beate , Kappler Martin , Straif Kurt , Marczynski Boleslaw , Preuss Ralf , Roβbach Bernd , Rihs Hans-Peter , Weiss Tobias , Rabstein Sylvia , Pierl Christiane , Scherenberg Michael , Adams Ansgar , Käfferlein Heiko Udo , Angerer Jürgen , Wilhelm Michael , Seidel Albrecht , Brüning Thomas 
Published: September 2007

AbstractIn regulatory toxicology, the dose-response relationship between occupational exposure and biomarkers is of importance in setting threshold values. We analyzed the relationships between occupational exposure to polycyclic aromatic hydrocarbons (PAH) and various biomarkers of internal exposure and DNA damage with data from 284 highly exposed male workers. Personal exposure to phenanthrene and other PAHs was measured during shift and correlated with the sum of 1−, 2+9−, 3−, and 4-hydroxyphenanthrenes in post-shift urine. PAHs and hydroxyphenanthrenes were associated with DNA damage assessed in WBC as 8-oxo-7,8-dihydro-2′-deoxyguanosine/106 dGuo and strand breaks by Comet assay as Olive tail moment. Hydroxyphenanthrenes correlated with phenanthrene (Spearman rs = 0.70; P &lt; 0.0001). No correlations could be found between strand breaks and exposure (rs = 0.01, P &lt; 0.0001 for PAHs; rs = −0.03, P = 0.68 for hydroxyphenanthrenes). Correlations with 8-oxo-7,8-dihydro-2′-deoxyguanosine/106 dGuo were weakly negative (rs = −0.22, P = 0.004 for PAHs) or flat (rs = −0.08, P = 0.31 for hydroxyphenanthrenes). Linear splines were applied to assess the relationships between the log-transformed variables. All regression models were adjusted for smoking and type of industry. For hydroxyphenanthrenes, 51.7% of the variance could be explained by phenanthrene and other predictors. Up to 0.77 μg/m3 phenanthrene, no association could be found with hydroxyphenanthrenes. Above that point, hydroxyphenanthrenes increased by a factor of 1.47 under a doubling of phenanthrene exposure (slope, 0.56; 95% confidence interval, 0.47-0.64). Hydroxyphenanthrenes may be recommended as biomarker of occupational PAH exposure, whereas biomarkers of DNA damage in blood did not show a dose-response relation to PAH exposure. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1863–73)
Exploring the Underlying Hormonal Mechanisms of Prenatal Risk Factors for Breast Cancer: A Review and Commentary
Authors: Troisi Rebecca , Potischman Nancy , Hoover Robert N. 
Published: September 2007

AbstractPrenatal factors have been hypothesized to influence subsequent breast cancer development. Directly evaluating the associations of in utero exposures with risk, however, presents several methodologic and theoretical challenges, including the long induction period between exposure and disease and the lack of certainty regarding the critical timing of exposure. Indirect evaluation of these associations has been achieved by use of proxies such as gestational and neonatal characteristics. Evidence suggests that preeclampsia is associated with a reduced breast cancer risk, whereas high birth weight and dizygotic twinning seem associated with an increased risk. Asians born in Asia have substantially lower breast cancer risks than women born in the West. Although data thus far are few, what exists is not consistent with a unifying hypothesis for a particular biological exposure (such as estrogens or androgens) during pregnancy as mediating the observed associations between pregnancy factors and breast cancer risk. This suggests that additional studies of prenatal factors should seek to broaden the range of hormones, growth, and other endocrine factors that are evaluated in utero. Once candidate biomarkers are identified, assessing them with respect to breast cancer and with intermediate end points in carcinogenesis should be a priority. In addition, investigations should explore the possibility that in utero exposures may not act directly on the breast, but may alter other physiologic pathways such as hormone metabolism that have their effect on risk later in life. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1700–12)
GLIOGENE—an International Consortium to Understand Familial Glioma
Authors: Malmer Beatrice , Adatto Phyllis , Armstrong Georgina , Barnholtz-Sloan Jill , Bernstein Jonine L. , Claus Elizabeth , Davis Faith , Houlston Richard , Il'yasova Dora , Jenkins Robert , Johansen Christoffer , Lai Rose , Lau Ching , McCarthy Bridget , Nielsen Hanne , Olson Sara H. , Sadetzki Siegal , Shete Sanjay , Wiklund Fredrik , Wrensch Margaret , Yang Ping , Bondy Melissa 
Published: September 2007

AbstractEvidence for familial aggregation of glioma has been documented in both case-control and cohort studies and occurs apart from the well-described rare inherited genetic syndromes involving glioma: neurofibromatosis type 1 and 2, tuberous sclerosis, Turcot's syndrome, and Li-Fraumeni syndrome. Nonsyndromic glioma families have been studied but no genes have been identified in the two published linkage studies of familial glioma probably due to the small number of families. Because glioma is a rare but devastating cancer, and a family history of glioma has been observed in ∼5% of the cases, we initiated an international consortium to identify glioma families not affected by syndromes to better understand the inherited factors related to this disease. The international consortium GLIOGENE is an acronym for “glioma gene” and includes 15 research groups in North America, Europe, and Israel to study familial glioma. The overarching goal is to characterize genes in glioma families using a genome-wide single-nucleotide polymorphism approach and conducting linkage analysis to identify new genomic regions or loci that could harbor genes important for gliomagenesis. Here, we review the rationale for studying familial glioma and our proposed strategy for the GLIOGENE study. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1730–4)
Validation of Self-Reported Smoking Status Using Saliva Cotinine: A Rapid Semiquantitative Dipstick Method
Authors: Montalto Norman J. , Wells Wayne O. 
Published: September 2007

Abstract
Purpose: This study evaluated the performance characteristics of a novel rapid method for verifying smoking status in individuals by measurement of cotinine, the primary metabolite of nicotine, in saliva samples using an immunochromatographic strip in a “dipstick” format compared with liquid chromatography/mass spectrometry (LC/MS).
Materials and Methods: A prospective comparison was made of smoking status as determined by measurement of cotinine in urine by LC/MS (the gold standard) and in saliva using a semiquantitative dipstick assay that uses cotinine-specific monoclonal antibodies attached to gold particles and a series of avidity traps to measure cotinine levels (saliva NicAlert®). One hundred seventy-two individuals from a family practice/general medical setting agreed to participate after informed consent and institutional review board approval. Saliva NicAlert® tests were done by untrained operators who followed written directions.
Results: Comparison of smoking status as determined by urine cotinine measurement by LC/MS (50 ng/mL cutoff) with the saliva strip test results, averaged over the two operators, indicated that the saliva test strip results had a sensitivity of 99% and a specificity of 96%. Saliva NicAlert® also identified four smokers who reported being nonsmokers but were confirmed to be smokers by LC/MS.
Conclusions: The saliva NicAlert® assay seems to be a valid, highly sensitive, and specific method for validating self-reported smoking status and may have clinical applications in selected medical settings. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1858–62)
Detection of Cotinine in Newborn Dried Blood Spots
Authors: Spector Logan G. , Hecht Stephen S. , Ognjanovic Simona , Carmella Steven G. , Ross Julie A. 
Published: September 2007

AbstractMaternal smoking while pregnant is a plausible risk factor for childhood cancers because many seem to initiate in utero and tobacco-specific carcinogens cross the placenta. Social desirability bias may affect maternal report of smoking in case-control studies and could explain inconsistently observed associations with offspring cancer. Detection of tobacco smoke biomarkers in dried blood spots (DBS), which are increasingly stored by newborn screening programs, may improve retrospective assessment of fetal tobacco exposure. As proof-of-principle, we examined cotinine in DBS of 20 infants enrolled in a pilot study of pregnancy among low-income women. We recruited 107 pregnant women (&lt;30 weeks of gestation) from six Women, Infants, and Children clinics in Minneapolis and St. Paul in 1999. Blood samples obtained at enrollment were tested for total cotinine using gas chromatography/mass spectrometry. Women were then interviewed at 7 months of gestation to determine current smoking habits. DBS were obtained from the Minnesota Department of Health. We tested DBS from 10 infants whose mothers had detectable serum cotinine at baseline and 10 control infants whose mothers had none. One quarter of each DBS was assayed for cotinine using gas chromatography/mass spectrometry; levels were estimated assuming 50 μL blood per sample. Mean cotinine was 29 ng/mL (SD, 7.5), 45 ng/mL (SD, 9.7), and 9 ng/mL (SD, 7.4), respectively, among infants of all smokers, infants of four women who acknowledged smoking at 7 months of gestation, and infants of nonsmokers. These results suggest that DBS analysis may identify infants of women who smoke throughout pregnancy. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1902–5)