tbuckley/cabot-search huggingface dataset:
Comparative Effectiveness of Robotic Versus Laparoscopic Hysterectomy for Endometrial Cancer
Authors: Jason D. Wright, William M. Burke, Elizabeth T. Wilde, Sharyn N. Lewin, Abigail S. Charles, Jin Hee Kim, Noah Goldman, Alfred I. Neugut, Thomas J. Herzog, Dawn L. Hershman
Journal: Journal of Clinical Oncology (2012)

Purpose Use of robotics in oncologic surgery is increasing; however, reports of safety and efficacy are from highly experienced surgeons and centers. We performed a population-based analysis to compare laparoscopic hysterectomy and robotic hysterectomy for endometrial cancer. Patients and Methods The Perspective database was used to identify women who underwent a minimally invasive hysterectomy for endometrial cancer from 2008 to 2010. Morbidity, mortality, and cost were evaluated using multivariable logistic and linear regression models. Results We identified 2,464 women, including 1,027 (41.7%) who underwent laparoscopic hysterectomy and 1,437 (58.3%) who underwent robotic hysterectomy. Women treated at larger hospitals, nonteaching hospitals, and centers outside of the northeast were more likely to undergo a robotic hysterectomy procedure, whereas black women, those without insurance, and women in rural areas were less likely to undergo a robotic hysterectomy procedure (P &lt; .05 for all). The overall complication rate was 9.8% for laparoscopic hysterectomy versus 8.1% for robotic hysterectomy (P = .13). The adjusted odds ratio (OR) for any morbidity for robotic hysterectomy was 0.76 (95% CI, 0.56 to 1.03). After adjusting for patient, surgeon, and hospital characteristics, there were no significant differences in the rates of intraoperative complications (OR, 0.68; 95% CI, 0.42 to 1.08), surgical site complications (OR, 1.49; 95% CI, 0.81 to 2.73), medical complications (OR, 0.64; 95% CI, 0.40 to 1.01), or prolonged hospitalization (OR, 0.85; 95% CI, 0.64 to 1.14) between the procedures. The mean cost for robotic hysterectomy was $10,618 versus $8,996 for laparoscopic hysterectomy (P &lt; .001). In a multivariable model, robotic hysterectomy was significantly more costly ($1,291; 95% CI, $985 to $1,597). Conclusion Despite claims of decreased complications with robotic hysterectomy, we found similar morbidity but increased cost compared with laparoscopic hysterectomy. Comparative long-term efficacy data are needed to justify its widespread use.
Trevo versus Merci retrievers for thrombectomy revascularisation of large vessel occlusions in acute ischaemic stroke (TREVO 2): a randomised trial
Authors: Raul G Nogueira, Helmi L Lutsep, Rishi Gupta, Tudor G Jovin, Gregory W Albers, Gary A Walker, David S Liebeskind, Wade S Smith
Journal: The Lancet (2012)
Occupational asthma due to sodium iso-nonanoyl oxybenzene sulphonate, a newly developed detergent ingredient.
Authors: D J Hendrick, M J Connolly, S C Stenton, A G Bird, I S Winterton, E H Walters
Journal: Thorax (1988)

Research with sodium iso-nonanoyl oxybenzene sulphonate (SINOS) for use in a detergent product was complicated by the development of asthma in an atopic 38 year old laboratory technician. Inhalation challenge tests with nebulised SINOS solutions over a dose range of 0.01-32 micrograms gave reproducible late asthmatic reactions after the higher doses and an increase in bronchial responsiveness to methacholine. The magnitude of the late reaction was related to the challenge dose.
Protection by verapamil of mitochondrial glutathione equilibrium and phospholipid changes during reperfusion of ischemic canine myocardium.
Authors: K Kajiyama, D F Pauly, H Hughes, S B Yoon, M L Entman, J B McMillin-Wood
Journal: Circulation Research (1987)

Pretreatment of the ischemic myocardium with verapamil protects against mitochondrial respiratory depression observed during ischemic arrest as well as during reperfusion. Since ischemic mitochondrial function appears not to be altered further by reperfusion, the purpose of this study is to identify a biochemical event affecting mitochondria that is specifically associated with reperfusion injury. It has been proposed that increased cellular Ca2+ influx and oxygen toxicity may result from reintroduction of coronary flow. Increased cytosolic Ca2+ is transmitted to the mitochondria with subsequent activation of Ca2+-dependent events, including phospholipase A2. Net production of lysophospholipids (and loss of total diacylphospholipids from the mitochondria) will proceed when reacylation mechanisms are inhibited. Since acyl-CoA:lysophospholipid acyltransferase is a sulfhydryl-sensitive enzyme and since increased activity of glutathione peroxidase shifts the levels of the mitochondrial sulfhydryl buffer, glutathione, towards oxidation, levels of glutathione and its oxidation state were measured during reperfusion in the absence or presence of verapamil pretreatment. Ischemia lowers total glutathione and reduces the redox ratio (reduced glutathione: oxidized glutathione) by 85%. Reperfusion partially returns the redox ratio to control by causing oxidized glutathione to disappear from the matrix. Verapamil maintains both the concentration and the redox potential of glutathione at control levels. Concomitant with alterations in reduced glutathione:oxidized glutathione is a decrease in ischemic mitochondrial phospholipid content. During reperfusion, phosphatidylethanolamine and its major constituent fatty acids (C 18:0 and C 20:4) are specifically lost from the mitochondrial membrane. Accompanying the significant loss of arachidonic acid during reperfusion is the decreased content of 11-OH, 12-OH, and 15-OH arachidonate. These lipid peroxidation products are not increased in ischemia. It is proposed that oxidation of matrix glutathione to glutathione disulfide during ischemia results in formation of glutathione-protein mixed disulfides and inhibition of sulfhydryl-sensitive proteins, including acyl-CoA lysophosphatide acyltransferase. Thus, metabolic events occurring within the ischemic period set the stage for prolonged dysfunction during reperfusion.
Transcriptional Profiles of CD133+ and CD133− Glioblastoma-Derived Cancer Stem Cell Lines Suggest Different Cells of Origin
Authors: Claudio Lottaz, Dagmar Beier, Katharina Meyer, Praveen Kumar, Andreas Hermann, Johannes Schwarz, Markus Junker, Peter J. Oefner, Ulrich Bogdahn, Jörg Wischhusen, Rainer Spang, Alexander Storch, Christoph P. Beier
Journal: Cancer Research (2010)

Glioblastoma multiforme (GBM) is paradigmatic for the investigation of cancer stem cells (CSC) in solid tumors. Growing evidence suggests that different types of CSC lead to the formation of GBM. This has prompted the present comparison of gene expression profiles between 17 GBM CSC lines and their different putative founder cells. Using a newly derived 24-gene signature, we can now distinguish two subgroups of GBM: Type I CSC lines display "proneural" signature genes and resemble fetal neural stem cell (fNSC) lines, whereas type II CSC lines show "mesenchymal" transcriptional profiles similar to adult NSC (aNSC) lines. Phenotypically, type I CSC lines are CD133 positive and grow as neurospheres. Type II CSC lines, in contrast, display (semi-)adherent growth and lack CD133 expression. Molecular differences between type I and type II CSC lines include the expression of extracellular matrix molecules and the transcriptional activity of the WNT and the transforming growth factor-beta/bone morphogenetic protein signaling pathways. Importantly, these characteristics were not affected by induced adherence on laminin. Comparing CSC lines with their putative cells of origin, we observed greatly increased proliferation and impaired differentiation capacity in both types of CSC lines but no cancer-associated activation of otherwise silent signaling pathways. Thus, our data suggest that the heterogeneous tumor entity GBM may derive from cells that have preserved or acquired properties of either fNSC or aNSC but lost the corresponding differentiation potential. Moreover, we propose a gene signature that enables the subclassification of GBM according to their putative cells of origin.
Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats
Authors: Timothy J. Aitman, Anne M. Glazier, Caroline A. Wallace, Lisa D. Cooper, Penny J. Norsworthy, Faisal N. Wahid, Khulood M. Al-Majali, Paul M. Trembling, Christopher J. Mann, Carol C. Shoulders, Daniel Graf, Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Michal Pravenec, Azeddine Ibrahimi, Nada A. Abumrad, Lawrence W. Stanton, James Scott
Journal: Nature Genetics (1999)
Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice
Authors: J-K Kim
Journal: Gut (2004)

<b>Background:</b> Id2, an inhibitor of basic helix-loop-helix transcription factors, regulates cell differentiation. Id2<sup>−/−</sup> mice exhibit a variety of phenotypes in the immune system. <b>Aims:</b> In this study we investigated whether Id2 plays a role in intestinal intraepithelial lymphocytes (IELs), which constitute the main defence against pathogens in the intestinal tract. <b>Methods:</b> Flow cytometry and bone marrow transplantation were used to analyse and characterise subsets of IELs of Id2<sup>−/−</sup> mice. Gene expression was analysed by real-time polymerase chain reaction. Intestinal barrier function was evaluated by treating mice with 5-fluorouracil (5-FU). <b>Results:</b> Among the four members of the Id gene family, Id2 was selectively expressed in all T cell subsets in the small intestinal IELs. Id2<sup>−/−</sup> mice showed alteration in the proportions of T cell subsets and a substantial reduction in the number of IELs, especially those of the CD4<sup>+</sup> and CD8αβ<sup>+</sup> T cell subsets, indicating a more pronounced effect on thymus derived IELs. Expression of α<sub>E</sub> integrin was reduced in CD4<sup>+</sup> and CD8αβ<sup>+</sup> T cell subsets in IELs of Id2<sup>−/−</sup> mice. IELs isolated from C57BL/6 mice reconstituted with Id2<sup>−/−</sup> bone marrow cells showed a similar phenotype to that of Id2<sup>−/−</sup> mice, indicating that the defects are intrinsic to bone marrow derived cells. Expression of genes encoding intestinal epithelial cell derived cytokines was reduced in Id2<sup>−/−</sup> mice. The 5-FU treatment revealed impaired intestinal barrier function of Id2<sup>−/−</sup> mice. <b>Conclusions:</b> The Id2 gene is essential for constituting the intestinal mucosal barrier, particularly with respect to IELs. Id2 null mutant mice may provide a good experimental model for studying the ontogeny of IELs and intestinal inflammation and infection.
Chronic disease management for tobacco dependence
Authors: Harshani M Chandrasekera
Journal: Thorax (2012)

This randomised control trial compared the efficacy of utilising chronic disease management principles for tobacco dependence using a tailored intervention with standard care. As tobacco dependence is a chronic relapsing condition, the tailored intervention was chosen to account for possible interim setbacks.

Four hundred and forty-three eligible participants received five telephone-counselling calls and 4 weeks of nicotine …
Evaluating Vitamin D Status in Ill Patients
Authors: Fabiana V. Raimundo, Gustavo A.M. Faulhaber, Tania W. Furlanetto
Journal: Journal of Clinical Oncology (2011)

We appreciate the commentary from Pinsky, 1 one of the lead authors from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.We agree with his point about the importance of including estimates of uncertainty for calculations such as number needed to screen and number needed to treat (NNT).Using a bootstrap approach to provide a measure of uncertainty (ie, CIs) with respect to the number needed to treat/screen would be fully justified if in fact the values shown in Table 1 of our article were likelihood-based estimates that were derived from the actual European Randomized Study of Screening for Prostate Cancer (ERSPC) data set. 2 However, estimates of uncertainty were not included in our analysis precisely because we did not have access to the actual data.Rather, we created a model that was based on visual estimates from the figure in the original ERSPC publication.Thus, the goal of our study was not to conduct an in-depth analysis of NNT, but instead to illustrate the point that estimates of NNT change over time when determined on the basis of a survival-type analysis.It is noteworthy that even the original publications of the ERSPC and Go ¨teborg trials, 2,3 which contained raw data, did not include an estimate of uncertainty for NNT.Moreover, despite the inherent limitations that are associated with our statistical model being based on extrapolated data, it is encouraging that our results were highly consistent with the actual ERSPC data.Indeed, our point estimate for NNT of 18 at 12 years was well corroborated by the subsequent report of NNT of 12 to prevent one prostate cancer death at 14 years in the Go ¨teborg screening trial. 3Furthermore, a recent update from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial reported an NNT of 5 (without an estimate of uncertainty) to prevent one prostate cancer death with screening at 10 years for men with no or minimal comorbidity; this also illustrated the sensitivity of NNT to comorbidity status at baseline. 4 Therefore, despite Pinsky's concerns over our admittedly limited exercise, we believe that we have effectively achieved our stated goal, which was to demonstrate that an estimate of number needed to screen or NNT at a single point in time can be misleading, regardless of whether that estimate includes a measure of uncertainty.Overall, updated follow-up data from the overall ERSPC are forthcoming and will help to shed additional light on this important issue.
Alterations in thyroid hormone economy in patients with hydatidiform mole
Authors: Valerie Anne Galton, Sidney H. Ingbar, Jesus Jimenez-Fonseca, Jerome M. Hershman
Journal: Journal of Clinical Investigation (1971)

Studies of several aspects of thyroid hormone economy have been conducted in 11 patients before and after removal of a molar pregnancy. Before evacuation of the mole, all patients demonstrated moderately to greatly elevated values for thyroidal (131)I uptake, absolute iodine uptake, and serum protein-bound-(131)I. Values for serum PBI and serum thyroxine (T(4)) concentration were consistently and often greatly increased, averaging more than twice those found in normal pregnancy and three times those in normal controls. On the other hand, the maximum binding capacity of the T(4)-binding globulin (TBG) was variably affected, and ranged between the values found in normal controls and those found in normal pregnancy. Values for the absolute concentration of free T(4) in serum were, on the average, only moderately elevated, since the proportion of free T(4) was moderately low, although not as low as in normal pregnancy. Sera of patients with molar pregnancy contained high levels of thyroid stimulating activity, as assessed in the McKenzie mouse bioassay system. The stimulator displayed a more prolonged duration of action than that of TSH and did not reveal a major immunological cross-reactivity with either human or bovine TSH, differing in the latter respect from the chorionic thyrotropin of normal human placenta. Abnormalities in iodine metabolism were rapidly ameliorated after removal of the molar pregnancy, and this was associated with the disappearance from serum of the thyroid stimulator. Despite the foregoing evidence of thyroid hyperfunction and hypersecretion of T(4), patients with molar pregnancy were neither goitrous nor overtly thyrotoxic. They did display, however, high values of the urinary pigment/creatinine ratio, a possible indication of the presence of a hypermetabolic state. It is concluded that in patients with molar pregnancy, thyroid function and T(4) secretion are stimulated, often greatly so, by an unusual thyroid stimulator which is demonstrable in the blood and which is probably of molar origin. The nature of the stimulator, as well as the reasons for both the variability of the increase in TBG which occurs in molar pregnancy and the lack of frank thyrotoxicosis, remain to be clarified.
Gene expression analysis in pregnant women and their infants identifies unique fetal biomarkers that circulate in maternal blood
Authors: Jill L. Maron, Kirby L. Johnson, Donna Slonim, Chao-Qiang Lai, Marco Ramoni, Gil Alterovitz, Zina Jarrah, Zinger Yang, Diana W. Bianchi
Journal: Journal of Clinical Investigation (2007)

The discovery of fetal mRNA transcripts in the maternal circulation holds great promise for noninvasive prenatal diagnosis. To identify potential fetal biomarkers, we studied whole blood and plasma gene transcripts that were common to 9 term pregnant women and their newborns but absent or reduced in the mothers postpartum. RNA was isolated from peripheral or umbilical blood and hybridized to gene expression arrays. Gene expression, paired Student's t test, and pathway analyses were performed. In whole blood, 157 gene transcripts met statistical significance. These fetal biomarkers included 27 developmental genes, 5 sensory perception genes, and 22 genes involved in neonatal physiology. Transcripts were predominantly expressed or restricted to the fetus, the embryo, or the neonate. Real-time RT-PCR amplification confirmed the presence of specific gene transcripts; SNP analysis demonstrated the presence of 3 fetal transcripts in maternal antepartum blood. Comparison of whole blood and plasma samples from the same pregnant woman suggested that placental genes are more easily detected in plasma. We conclude that fetal and placental mRNA circulates in the blood of pregnant women. Transcriptional analysis of maternal whole blood identifies a unique set of biologically diverse fetal genes and has a multitude of clinical applications.
Fate of surrogate light chains in B lineage cells.
Authors: K Lassoued, H Illges, K Benlagha, M D Cooper
Journal: The Journal of Experimental Medicine (1996)

Biosynthesis of the immunoglobulin (Ig) receptor components and their assembly were examined in cell lines representative of early stages in human B lineage development. In pro-B cells, the nascent surrogate light chain proteins form a complex that transiently associates in the endoplasmic reticulum with a spectrum of unidentified proteins (40, 60, and 98 kD) and Bip, a heat shock protein family member. Lacking companion heavy chains, the surrogate light chains in pro-B cells do not associate with either the Ig(alpha) or Ig(beta) signal transduction units, undergo rapid degradation, and fail to reach the pro-B cell surface. In pre-B cells, by contrast, a significant portion of the surrogate light chain proteins associate with mu heavy chains, Ig(alpha), and Ig(beta) to form a stable receptor complex with a relatively long half-life. Early in this assembly process, Bip/GRP78, calnexin, GRP94, and a protein of approximately 17 kD differentially bind to the nascent mu heavy chains. The 17-kD intermediate is gradually replaced by the surrogate light chain protein complex, and the Ig(alpha) and Ig(beta) chains bind progressively to the mu heavy chains during the complex and relatively inefficient process of pre-B receptor assembly. The results suggest that, in humans, heavy chain association is essential for surrogate light chain survival and transport to the cell surface as an integral receptor component.
Gastric MALT Lymphoma Treated With Primary Radiotherapy in the Setting of Autoimmune Disease
Authors: Chelsea C. Pinnix, Valerie Reed, Bouthaina Dabaja
Journal: Journal of the National Comprehensive Cancer Network (2012)

Autoimmune and microbial-induced immune reactions are associated with lymphomagenesis, particularly of extranodal marginal zone B-cell lymphomas. This report presents a case of Helicobacter pylori–negative gastric extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) in the setting of Sjögren syndrome and Hashimoto thyroiditis treated with primary involved-field radiotherapy. This report describes etiologic data, diagnostic and treatment considerations, and sophisticated radiation therapy techniques aimed at reducing long-term toxicity in this indolent disease.
Mimicking Pregnancy To Reduce Breast Cancer Risk
Authors: R. Tuma
Journal: JNCI Journal of the National Cancer Institute (2010)

Women who have a full-term pregnancy before their mid-20s substantially reduce their lifetime risk of breast cancer, compared with women who either have children later in life or do not have children, according to many epidemiological studies. Women who breastfeed their babies further reduce that risk. Now breast cancer researchers are asking whether those observations can be transformed into a feasible breast cancer prevention strategy. Some investigators contend that the goal should be at the forefront of breast cancer research, whereas others express concern that pregnancy is too complex to mimic. Despite the challenges, several research groups are trying to tackle the question, and a few are even starting to test their hypotheses in women at high risk for breast cancer. Scientists once believed that a woman’s age at her fi rst full-term pregnancy is the most important factor, in terms of pregnancy’s role in breast cancer risk. But recent studies have shown that it plays less of a role than the number of births and duration of breast-feeding, said Valeria Beral, M.D., director of the cancer epidemiology unit at the University of Oxford, during her presentation at the San Antonio Breast Cancer Symposium in December. The role of multiple pregnancies became clear in 2002 when the Collaborative Group on Hormonal Factors in Breast Cancer, an international research group based at the University of Oxford, published a pooled analysis of 47 studies that included approximately 50,000 breast cancer patients and 96,000 healthy women. The team, of which Beral is a member, reported that when they held the age at fi rst birth constant, each birth was associated with a 7% lower relative risk of breast cancer and each 12 months of breastfeeding was associated with a 4.3% lower risk. One can see the association of lower risk and early, multiple pregnancies by comparing the rate of breast cancer in developed and developing countries. The incidence of breast cancer in the United States and Europe is 6.3% among women up to age 70 years. By contrast, the rate is 1.2% in rural Africa and Asia. Although diet and environment may account for some of that difference, the Collaborative Group estimates that the incidence in developed countries could theoretically drop to 2.7% if women adopted the same reproductive patterns as women in developing countries have. Beral is careful to emphasize that no one is