tbuckley/cabot-search huggingface dataset:
Social and Racial Differences in Selection of Breast Cancer Adjuvant Chemotherapy Regimens
Authors: Jennifer J. Griggs, Eva Culakova, Melony E.S. Sorbero, Marek S. Poniewierski, Debra A. Wolff, Jeffrey Crawford, David C. Dale, Gary H. Lyman
Journal: Journal of Clinical Oncology (2007)

Purpose Breast cancer outcomes are worse among black women and women of lower socioeconomic status. The purpose of this study was to investigate racial and social differences in selection of breast cancer adjuvant chemotherapy regimens. Methods Detailed information on patient, disease, and treatment factors was collected prospectively on 957 patients who were receiving breast cancer adjuvant chemotherapy in 101 oncology practices throughout the United States. Adjuvant chemotherapy regimens included in any of several published guidelines were considered standard. Receipt of nonstandard regimens was examined according to clinical and nonclinical factors. Differences between groups were assessed using χ 2 tests. Multivariate logistic regression was used to identify factors associated with use of nonstandard regimens. Results Black race (P = .008), lower educational attainment (P = .003), age ≥ 70 years (P = .001), higher stage (P &lt; .0001), insurance type (P = .048), employment status (P = .045), employment type (P = .025), and geographic location (P = .021) were associated with the use of nonstandard regimens in univariate analyses. In multivariate analysis, black race (P = .020), lower educational attainment (P = .024), age ≥ 70 years (P = .032), and higher stage (P &lt; .0001) were associated with receipt of nonstandard regimens. Conclusion The more frequent use of non–guideline-concordant adjuvant chemotherapy regimens in black women and women with lower educational attainment may contribute to less favorable outcomes in these populations. Addressing such differences in care may improve cancer outcomes in vulnerable populations.
Randomized Phase II Trial Comparing Bevacizumab Plus Carboplatin and Paclitaxel With Carboplatin and Paclitaxel Alone in Previously Untreated Locally Advanced or Metastatic Non-Small-Cell Lung Cancer
Authors: David H. Johnson, Louis Fehrenbacher, William F. Novotny, Roy S. Herbst, John J. Nemunaitis, David M. Jablons, Corey J. Langer, Russell F. DeVore, Jacques Gaudreault, Lisa A. Damico, Eric Holmgren, Fairooz Kabbinavar
Journal: Journal of Clinical Oncology (2004)

To investigate the efficacy and safety of bevacizumab plus carboplatin and paclitaxel in patients with advanced or recurrent non-small-cell lung cancer.
CDX-2 should be included in the work-up of patients with lung metastases from unknown primary
Authors: N. Fazio, T. De Pas, F. de Braud, L. Spaggiari, G. Mazzarol, R. Biffi, B. Andreoni, M. Zampino, G. Curigliano, K. Lorizzo, G. Di Meglio, A. Goldhirsch
Journal: Annals of Oncology (2004)
Prevention of Preterm Delivery
Authors: Hyagriv N. Simhan, Steve N. Caritis
Journal: New England Journal of Medicine (2007)

Although preterm birth (at <37 weeks' gestation) is sometimes indicated for the health of the mother or her fetus, spontaneous preterm births occur as a consequence of spontaneous preterm labor or preterm rupture of fetal membranes before the onset of labor. This review focuses on therapeutic strategies for the prevention and treatment of spontaneous preterm labor and delivery.
Heart Failure and Lung Disease
Authors: HANS H. HECHT
Journal: Circulation (1956)

The confusing and complex interplay of factors leading to "cor pulmonale" may be somewhat clarified if the effects of excessive pulmonary hypertension causing right heart overloading ("pulmonary hypertensive heart disease") are separated from the ventilatory defects that result in arterial desaturation, erythrocytosis, and moderate pulmonary hypertension ("emphysema heart"). In the former group, heart failure dominates the clinical picture; in the latter, it is assumed that heart failure occurs on the basis of a "myocardial factor"—presumably arteriosclerotic heart disease—whose manifestations are colored and modified by the coexisting and contributing respiratory dysfunction. Overlapping of these two distinct forms occurs frequently, and pulmonary hypertension may be severe enough to be the chief precipitating cause of failure in emphysema, particularly in young subjects and in patients with kyphoscoliosis. Respiratory disturbances, fibrosis, and loss of pulmonary elasticity may accompany heart failure secondary to right ventricular overloading which may ultimately lead to significant arterial desaturation at rest and the development of polycythemia, even in this group. It is typical, however, that the disturbances leading to cor pulmonale rarely, if ever, involve the actual pulmonary function of alveolar-capillary gas exchange; they are confined to the abnormalities of the precapillary pulmonary vasculature and to the mechanical apparatus of the chest cage and of the pulmonary parenchyma concerned with breathing mechanisms. Pulmonary hypertensive heart disease, whatever its cause, has a monotonous symptomatology that is dominated by the signs of heart failure. In cor pulmonale due to emphysema and its allied types, the clinical picture is varied, and oxygen deficiency with arterial desaturation is of central significance. It raises pulmonary artery pressure by a mechanism not fully understood, and it stimulates erythropoiesis. When erythrocytosis has occurred, heart failure from cor pulmonale will soon make its appearance. Unless the arterial oxygen content falls sharply on exercise, resting oxygen saturation values in excess of 80 per cent do not cause this type of polycythemia; nor does polycythemia as such, as in erythremia ("vera"), result in significant arterial desaturation, pulmonary hypertension, or heart failure. However, little is known concerning the hemodynamic load imposed by an increase in blood viscosity. The management of cor pulmonale must recognize the multiplicity of factors that are concerned and should weigh their relative significance in any given subject. The kaleidoscopic appearance of cor pulmonale requires flexibility of therapy based on a grasp of the individual pathophysiologic interrelations, which may differ from patient to patient.
Risk Assessment, Genetic Counseling, and Genetic Testing for BRCA-Related Cancer in Women: U.S. Preventive Services Task Force Recommendation Statement
Authors: Virginia A. Moyer
Journal: Annals of Internal Medicine (2013)

Description: Update of the 2005 U.S. Preventive Services Task Force (USPSTF) recommendation on genetic risk assessment and BRCA mutation testing for breast and ovarian cancer susceptibility. Methods: The USPSTF reviewed the evidence on risk assessment, genetic counseling, and genetic testing for potentially harmful BRCA mutations in asymptomatic women with a family history of breast or ovarian cancer but no personal history of cancer or known potentially harmful BRCA mutations in the family. The USPSTF also reviewed interventions aimed at reducing the risk for BRCA-related cancer in women with potentially harmful BRCA mutations, including intensive cancer screening, medications, and risk-reducing surgery. Population: This recommendation applies to asymptomatic women who have not been diagnosed with BRCA-related cancer. Recommendation: The USPSTF recommends that primary care providers screen women who have family members with breast, ovarian, tubal, or peritoneal cancer with 1 of several screening tools designed to identify a family history that may be associated with an increased risk for potentially harmful mutations in breast cancer susceptibility genes (BRCA1 or BRCA2). Women with positive screening results should receive genetic counseling and, if indicated after counseling, BRCA testing. (B recommendation) The USPSTF recommends against routine genetic counseling or BRCA testing for women whose family history is not associated with an increased risk for potentially harmful mutations in the BRCA1 or BRCA2 genes. (D recommendation)
Expression of Membrane Type 1 Matrix Metalloproteinase Is Associated with Cervical Carcinoma Progression and Invasion
Authors: Yali Zhai, Kevin B. Hotary, Bin Nan, F. Xavier Bosch, Nubia Muñoz, Stephen J. Weiss, Kathleen R. Cho
Journal: Cancer Research (2005)

Abstract Membrane type 1 matrix metalloproteinase (MT1-MMP) is frequently expressed by cancer cells and is believed to play an important role in cancer cell invasion and metastasis. However, little is known about the role of MT1-MMP in mediating invasiveness of cervical cancer cells. In this study, we examined MT1-MMP expression in 58 primary human cervical tissue specimens, including normal cervix, low-grade squamous intraepithelial lesions (LSIL), high-grade SILs (HSIL), and invasive carcinomas. We also evaluated MT1-MMP, MMP-2, and tissue inhibitor of metalloproteinase-2 expression in several cervical cancer–derived cell lines, human papillomavirus (HPV)–immortalized keratinocytes, and keratinocytes derived from a LSIL. Using in situ hybridization techniques to study the cervical tissue specimens, we found that MT1-MMP expression increases with cervical tumor progression (Spearman correlation coefficient = 0.66; P &amp;lt; 0.0001, exact test). Specifically, MT1-MMP expression is very low or absent in normal cervix and LSILs, is readily detectable in HSILs, and is very strongly expressed in nearly all invasive carcinomas. Most but not all cervical cancer–derived cell lines also expressed significant levels of MT1-MMP and MMP-2. Constitutive expression of exogenous MT1-MMP in cervical carcinoma–derived cells and HPV-immortalized keratinocytes with low endogenous levels of MT1-MMP induced invasiveness in collagen I, but this effect was not observed in LSIL-derived keratinocytes. Our results show that MT1-MMP is a key enzyme mediating cervical cancer progression. However, MT1-MMP alone is not always sufficient for inducing keratinocyte invasiveness at least in the collagen I invasion assay used in this study. Further studies of gene expression in preinvasive and invasive cervical cancers should assist with identification of additional critical factors mediating cervical cancer progression.
Diuretics, potassium, and ventricular arrhythmias
Authors: A. M. Clarfield
Journal: JAMA (1992)

To the Editor.  —It is now abundantly clear that hypertension is a problem for both young and old. In fact, one can argue that it is an even more serious condition for the elderly, given that the sequelae of hypertension are found mostly in those over the age of 65. 1  JAMA , as well as other medical journals, has recognized the importance of hypertension in the elderly and published numerous articles on this subject over the past few years. The Systolic Hypertension in the Elderly Program study 2 is only one recent example.  Thus, it is with surprise and some consternation that we examined the recent article by Siegel et al 3 on diuretics, serum and intracellular electrolyte levels, and ventricular arrhythmias in hypertensive men. This was a first-class piece of research. For some reason, however, the sample population was restricted to patients under the age of 70.  The exclusion
Compliance in clinical trials.
Authors: T Pullar, S Kumar, M Feely
Journal: Annals of the Rheumatic Diseases (1989)

Compliance with treatment can be an important determinant of the outcome of clinical trials. To date there is no completely satisfactory method of measuring compliance and some of the most widely used methods are inadequate. The various methods of measuring compliance and how they have been applied to clinical trials are described, and improvements in the standard of the measurement and reporting of compliance in clinical trials are suggested.
The profile of cardiac patients with renal artery stenosis
Authors: Christopher E Buller, Jorge G Nogareda, Krishnan Ramanathan, Donald R Ricci, Ognjenka Djurdjev, Kathryn J Tinckam, Ian M Penn, Rebecca S Fox, Lesley A Stevens, John A Duncan, Adeera Levin
Journal: Journal of the American College of Cardiology (2004)
Telomerase Activity and Survival of Patients With Node-Positive Breast Cancer
Authors: G. M. Clark, C. K. Osborne, D. Levitt, F. Wu, N. W. Kim
Journal: JNCI Journal of the National Cancer Institute (1997)

Background: Shortening of telomeres (specialized structures at the ends of chromosomes) beyond a certain length may signal a cell to stop dividing and to enter senescence. A ribonucleoprotein enzyme, telomerase, is a key component in maintaining telomere length. Because the majority of cancers express telomerase but most normal somatic tissues do not, we measured the level of telomerase expression in primary breast cancer specimens for correlation with traditional prognostic indicators and disease outcome. Methods: Telomerase activity was measured in frozen human breast cancer specimens by use of the Telomerec Repeat Amplification Protocol (TRAP) assay. The level of telomerase activity was expressed as total product generated (TPG) and was corrected for specimen cellularity by expressing it as a ratio of TPG to the sample's 28S ribosomal RNA content. Results: A preliminary study of 150 breast cancer specimens demonstrated that telomerase activity correlated with the fraction of cells in S phase of the cell cycle (rsp = .23). In a larger prognostic study of 398 tumors from patients with lymph node-positive breast cancer, telomerase expression correlated with S-phase fraction, progesterone receptor level, DNA ploidy, and lymph node status. After correcting for sample cellularity, increasing TPG levels were associated with decreased disease-free survival (P = .041) and overall survival (P = .009) of the patients. The telomerase activity level remained strongly predictive of death (P = .027) and marginally predictive of disease recurrence (P = .08) after adjustment for other prognostic factors. All P values are two-sided. Conclusions: Telomerase activity in human breast cancers is associated with a more agressive tumor phenotype in patients.
Formation of eosinophilic and monocytic intradermal inflammatory sites in the dog by injection of human RANTES but not human monocyte chemoattractant protein 1, human macrophage inflammatory protein 1 alpha, or human interleukin 8.
Authors: R Meurer, G Van Riper, W Feeney, P Cunningham, D Hora, M S Springer, D E MacIntyre, H Rosen
Journal: The Journal of Experimental Medicine (1993)

Equilibrium binding studies on canine mononuclear and granulocytic cells allow the identification of a single high affinity receptor for the human C-C chemokine RANTES (dissociation constant, 14 +/- 8 pM), that, in contrast to the human RANTES receptor, has no affinity for human macrophage inflammatory protein 1 alpha (hMIP-1 alpha). A single intradermal injection of hRANTES in dog resulted in eosinophil- and macrophage-rich inflammatory sites within 4 h. Cell infiltration peaked at 16-24 h after hRANTES injection. There was histological evidence of intravascular activation of eosinophils at 4 h, although eosinophils in the vasculature and interstitium contained apparently intact granules. Monocytes were the predominant cells adherent to venular endothelium at 16-24 h. Human MIP-1 alpha elicited no response in canine dermis, whereas monocyte chemoattractant protein 1 caused mild perivascular cuffing with monocytes. In contrast, human interleukin 8 induced a neutrophilic dermal infiltrate that was maximal by 4 h after challenge. This provides the first direct evidence in vivo that RANTES has significant proinflammatory activity and, in addition, could be a mediator in atopic pathologies characterized by eosinophilic and monocytic inflammatory responses.
Impact of Cardiac Contractility Modulation on Left Ventricular Global and Regional Function and Remodeling
Authors: Cheuk-Man Yu, Joseph Yat-Sun Chan, Qing Zhang, Gabriel W.K. Yip, Yat-Yin Lam, Anna Chan, Daniel Burkhoff, Pui-Wai Lee, Jeffrey Wing-Hong Fung
Journal: JACC. Cardiovascular imaging (2009)
INTESTINAL PUTREFACTION AND THE PULSE IN RHEUMATOID ARTHRITIS
Authors: F. Hernaman-Johnson
Journal: BMJ (1909)

Microdeletion of a region in chromosome 16p11.2 increases susceptibility to autism. Although this region contains exons of 29 genes, disrupting only a small segment of the region, which spans 5 genes, is sufficient to cause autistic traits. One candidate gene in this critical segment is <i>MVP</i>, which encodes for the major vault protein (MVP) that has been implicated in regulation of cellular transport mechanisms. MVP expression levels in <i>MVP</i><sup>+/-</sup> mice closely phenocopy those of 16p11.2 mutant mice, suggesting that <i>MVP</i><sup>+/-</sup> mice may serve as a model of MVP function in 16p11.2 microdeletion. Here we show that MVP regulates the homeostatic component of ocular dominance (OD) plasticity in primary visual cortex (V1). <i>MVP</i><sup>+/-</sup> mice of both sexes show impairment in strengthening of open-eye responses after several days of monocular deprivation (MD) while closed-eye responses are weakened as normal, resulting in reduced overall OD plasticity. The frequency of mEPSCs in pyramidal neurons is decreased in <i>MVP</i><sup>+/-</sup> mice after extended MD, suggesting a reduction of functional synapses. Correspondingly, upregulation of surface GluA1 AMPA receptors is reduced in <i>MVP</i><sup>+/-</sup> mice after extended MD, and is accompanied by altered expression of STAT1 and phosphorylated ERK, which have been previously implicated in OD plasticity. Normalization of STAT1 levels by introducing STAT1 shRNA rescues surface GluA1 and open-eye responses, implicating STAT1 as a downstream effector of MVP. These findings demonstrate a specific role for MVP as a key molecule influencing the homeostatic component of activity-dependent synaptic plasticity, and potentially the corresponding phenotypes of 16p11.2 microdeletion syndrome. <b>Significance Statement</b> Major vault protein (MVP), a candidate gene in 16p11.2 microdeletion syndrome, has been implicated in the regulation of several cellular processes including transport mechanisms and scaffold signaling. However, its role in brain function and plasticity remains unknown. In this study, we identified MVP as an important regulator of the homeostatic component of experience-dependent plasticity, via regulation of STAT1 and ERK signaling. This study helps reveal a new mechanism for an autism-related gene in brain function, and suggests a broader role for neuro-immune interactions in circuit level plasticity. Importantly, our findings might explain specific components of the pathophysiology of 16p11.2 microdeletion syndrome.
Association between body mass index and the colorectal cancer risk in Japan: pooled analysis of population-based cohort studies in Japan
Authors: K. Matsuo, T. Mizoue, K. Tanaka, I. Tsuji, Y. Sugawara, S. Sasazuki, C. Nagata, A. Tamakoshi, K. Wakai, M. Inoue, S. Tsugane
Journal: Annals of Oncology (2011)
Use of mini-mental state examination by GPs to diagnose dementia may be unnecessary
Authors: H. van Hout, M. Vernooij-Dassen, W. Hoefnagels, R. Grol
Journal: BMJ (1999)

EDITOR—We have a critical comment on the North of England dementia guideline's emphasis on the use of cognitive screening tests such as the mini-mental state examination by general practitioners.1 We do not oppose the use of screening tests but emphasise that in a primary care setting general practitioners have different and equally effective means of diagnosing dementia. To illustrate this we report on an evaluation study …
Adenovirus-Mediated <i>Calponin h1</i> Gene Therapy Directed against Peritoneal Dissemination of Ovarian Cancer: Bifunctional Therapeutic Effects on Peritoneal Cell Layer and Cancer Cells
Authors: Tomonori Ogura, Hiroaki Kobayashi, Yousuke Ueoka, Kaoru Okugawa, Kiyoko Kato, Toshio Hirakawa, Shigenari Hashimoto, Shun'ichiro Taniguchi, Norio Wake, Hitoo Nakano
Journal: Clinical Cancer Research (2006)

Abstract Purpose: Calponin h1 (CNh1), one of the family of actin-binding proteins, stabilizes the filaments of actin and modulates various cellular biological phenotypes. Recent studies revealed the close correlation between the invasive tumor spread and the reduced expression of CNh1 and α-smooth muscle actin in the surrounding stromal cells. The purpose of this study is to evaluate the efficacy of i.p. CNh1 gene therapy against peritoneal dissemination of ovarian cancer. Experimental Design: We used an adenoviral vector to induce the CNh1 gene into peritoneal cells and ovarian cancer cells as a means of enhancing or inducing the expression of α-smooth muscle actin as well as CNh1. The efficacy of gene transfer was examined by in vitro cell culture and in vivo animal experiments. Results: The formation of longer and thicker actin fibers was observed in each transfected cell line, and the localization of these fibers coincided with that of externally transducted CNh1. With respect to changes in cell behavior, the CNh1-transfected peritoneal cells acquired an ability to resist ovarian cancer-induced shrinkage in cell shape; thus, cancer cell invasion through the monolayer of peritoneal cells was inhibited. In addition, CNh1-transfected ovarian cancer cells showed suppressed anchorage-independent growth and invasiveness, the latter of which accompanied impaired cell motility. The concomitant CNh1 transfection into both peritoneal cells and ovarian cancer cells produced an additive inhibitory effect with respect to cancer cell invasion through the peritoneal cell monolayer. By in vivo experiments designed to treat nude mice that had been i.p. inoculated with ovarian cancer cells, we found that the i.p. injected CNh1 adenovirus successfully blocked cancer-induced morphologic changes in peritoneal cell surface and significantly prolonged the survival time of tumor-bearing mice. Moreover, CNh1 adenovirus could successfully enhance the therapeutic effect of an anticancer drug without increase in side effects. Conclusions: Thus, CNh1 gene therapy against peritoneal dissemination of ovarian cancer is bifunctionally effective (i.e., through inhibitory effects on the infected peritoneal cell layers that suppress cancer invasion and through direct antitumor effects against invasion and growth properties of cancer cells).
Papillary cystic neoplasm of the pancreas: presentation and natural history in two cases.
Authors: A N Kingsnorth, S W Galloway, H Lewis-Jones, J R Nash, P A Smith
Journal: Gut (1992)

Two young women, one white and one Chinese, with the rare but increasingly recognised papillary and cystic neoplasm of the pancreas are reported. The initial symptom in both was non-specific abdominal pain which, after investigation, was found to be caused by a pancreatic tumour. One patient did not come to surgery until five years after the initial diagnosis when she developed jaundice. In the five year interval between diagnosis and the development of jaundice computed tomography showed no change in the size (20 cm) of the pancreatic mass. Histology after resection, however, showed signs of lymphatic invasion. Cystic neoplasm of the pancreas can thus be regarded as an indolent, very slow growing tumour with potential for local invasion and hence metastatic spread.