tbuckley/cabot-search huggingface dataset:
Prevalence of War-Related Sexual Violence and Other Human Rights Abuses Among Internally Displaced Persons in Sierra Leone
Authors: Lynn L. Amowitz
Journal: JAMA (2002)

ContextSierra Leone's decade-long conflict has cost tens of thousands of lives and all parties to the conflict have committed abuses.ObjectiveTo assess the prevalence and impact of war-related sexual violence and other human rights abuses among internally displaced persons (IDPs) in Sierra Leone.Design and SettingA cross-sectional, randomized survey, using structured interviews and questionnaires, of internally displaced Sierra Leone women who were living in 3 IDP camps and 1 town, which were conducted over a 4-week period in 2001.ParticipantsA total of 991 women provided information on 9166 household members. The mean (SE) age of the respondents was 34 (0.48) years (range, 14-80 years). The majority of the women sampled were poorly educated (mean [SE], 1.9 [0.11] years of formal education); 814 were Muslim (82%), and 622 were married (63%).Main Outcome MeasuresAccounts of war-related sexual assault and other human rights abuses.ResultsOverall, 13% (1157) of household members reported incidents of war-related human rights abuses in the last 10 years, including abductions, beatings, killings, sexual assaults and other abuses. Ninety-four (9%) of 991 respondents and 396 (8%) of 5001 female household members reported war-related sexual assaults. The lifetime prevalence of non–war-related sexual assault committed by family members, friends, or civilians among these respondents was also 9%, which increased to 17% with the addition of war-related sexual assaults (excluding 1% of participants who reported both war-related and non–war-related sexual assault). Eighty-seven percent of women believed that there should be legal protection for women's human rights. More than 60% of respondents believed a man has a right to beat his wife if she disobeys, and that it is a wife's duty/obligation to have sex with her husband even if she does not want to.ConclusionsSexual violence committed by combatants in Sierra Leone was widespread and was perpetrated in the context of a high level of human rights abuses against the civilian population.
Fluid dynamics of coronary artery stenosis.
Authors: R E Mates, R L Gupta, A C Bell, F J Klocke
Journal: Circulation Research (1978)

A large-scale model of the coronary circulation, instrumented to permit detailed pressure and velocity measurements, has been used to study flow through isolated stenotic elements in large coronary arteries. Pulsatile aortic and instantaneous peripheral resistance were stimulated with servovalves. A variety of axisymmetric and asymmetric stenoses were studied and flow separation was found to occur for all but very mild stenoses. Pressure recovery downstream of the stenosis throat was limited and, in some cases, no recovery was observed. Pressure drop was primarily dependent upon the minimum area of the stenosis and relatively independent of stenosis geometry. Flow was quasi-steady at normal heart rates, and simple steady flow theory proved adequate to describe the pressure drop through the stenosis. The theory yielded results that agreed well with published data for dogs and appears promising for predicting effects of hemodynamic variables on a given stenotic lesion. Thus, principal findings of the study are that a relatively severe stenosis behaves essentially like an orifice and that a simple quasi-steady theory appears adequate to predict effects of a stenosis on coronary flow.
Identification of the Bile Canalicular Cell Surface Molecule Gp110 As the Ectopeptidase Dipeptidyl Peptidase Iv: An Analysis by Tissue Distribution, Purification And N –Terminal Amino Acid Sequence
Authors: Geoffrey W. McCaughan, Julie E. Wickson, Paul F. Creswick, Mark D. Gorrell
Journal: Hepatology (1990)

This paper describes the tissue distribution, purification and N–terminal amino acid sequence of the bile canalicular cell surface molecule dipeptidyl peptidase IV. Immunoperoxidase staining of cryostat sections of rat liver with a monoclonal antibody, Medical Research Council OX–61, indicated specific binding to hepatocyte bile canalicular domains and brush borders of bile ducts. Additional staining was seen in other epithelial brush borders (small intestine, kidney, colon, pancreatic duct); acinar structures in salivary glands; endothelial structures and T cell areas in thymus, spleen and lymph node. The tissue distribution suggested that monoclonal antibody OX–61 binds to the ectoenzyme dipeptidyl peptidase IV. This was confirmed by depletion of dipeptidyl peptidase IV activity from tissue homogenates by monoclonal antibody OX–61 coupled to Sepharose. The molecule recognized by OX–61 was then purified from liver and kidney by monoclonal antibody affinity chromatography. The molecule had a molecular weight of 110 kD under reducing conditions. The purified molecule was subsequently analyzed for amino acid composition and N–terminal amino acid sequence. Thirty–one N–terminal amino acids were sequenced and indicated identity with part of the predicted N–terminus of the previously cloned bile canalicular molecule GP110. On review, other similarities between dipeptidyl peptidase IV and GP110 were detected: molecular weight, deglycosylated from and metabolic half–life. Finally, the recent cloning of dipeptidyl peptidase IV permitted a comparison between the molecule recognized by monoclonal antibody OX–61, GP110 and dipeptidyl peptidase IV. It is concluded that these three molecules are almost certainly identical.(HEPATOLOGY 1990; 11:534:544.)
Chromosome Instability as an Indicator of Malignant Progression in Laryngeal Mucosa
Authors: Joris A. Veltman, Fredrik J. Bot, Ference C. Huynen, Frans C. S. Ramaekers, Johannes J. Manni, Anton H. N. Hopman
Journal: Journal of Clinical Oncology (2000)

Routine histologic examination cannot predict whether premalignant laryngeal lesions will progress toward invasive growth. The acquisition of changes in chromosome constitution has been suggested to be essential for driving tumor progression by enhancing mutagenic mechanisms. The aim of the present study was to determine whether chromosomal changes occur in the subsequent stages of early laryngeal carcinogenesis and, if so, whether these changes can be of prognostic value.Numerical aberrations for chromosomes 1 and 7 were detected in tissue sections from archival material using an improved in situ hybridization protocol. In total, eight benign laryngeal lesions, 37 premalignant laryngeal lesions, and 16 specimens containing histologically normal epithelia adjacent to laryngeal squamous cell carcinomas were studied. Both the histologic and the cytogenetic classifications were correlated with progression to laryngeal cancer.No evidence for chromosome alterations was obtained in the control group, nor in histologically normal epithelia adjacent to laryngeal squamous cell carcinomas, nor in all but one hyperplastic lesion (n = 11). In contrast, 14 of 15 dysplastic lesions and nine of 11 carcinomas-in-situ contained numerical chromosomal aberrations. Tetrasomy was present in the majority of the dysplastic lesions. An unstable chromosome content (indicated by the presence of chromosome imbalances and/or polyploidization) in the premalignant lesion strongly predicted its malignant progression.Our results show that laryngeal tumor development involves chromosome tetraploidization. The further change from a stable to an unstable chromosome constitution is of importance for malignant progression.
Inhibition by secretin of the gastric acid responses to meals and to pentagastrin in duodenal ulcer patients
Authors: S. J. Konturek, J. Biernat, T. Grzelec
Journal: Gut (1973)

The inhibitory effects of intravenous secretion on the gastric acid responses to a meal and to pentagastrin were studied in seven duodenal ulcer patients. A test meal of 10% peptone adjusted to pH 5·0 was introduced into the stomach and the Fordtran and Walsh method was used to measure the gastric acid output by monitoring the rate at which a solution of 0·3 M sodium bicarbonate had to be added to keep the pH of the gastric content constant at the value of 5·0. A constant dose of secretin (1 U/kg-hr) significantly depressed the serum gastrin response to a meal and produced an inhibition of acid secretion by about 70% of the control level. Secretin inhibited the acid response induced by pentagastrin by about 60% and simultaneously provoked a pancreatic bicarbonate output sufficient to neutralize about 60% of the gastric acid output to pentagastrin. We conclude that secretin is a strong inhibitor of gastric secretion in duodenal ulcer patients induced by a meal and by pentagastrin.
Association of Reference Payment for Colonoscopy With Consumer Choices, Insurer Spending, and Procedural Complications
Authors: James C. Robinson, Timothy T. Brown, Christopher Whaley, Emily Finlayson
Journal: JAMA Internal Medicine (2015)

Regulatory limits on consumer cost sharing permit wide variation in the prices charged for screening and diagnostic tests such as colonoscopy. Employers are experimenting with reference payment initiatives that offer full insurance coverage at low-priced facilities but require substantial cost sharing if patients select high-priced alternatives.
Research authors' reply to Campillo-Soto and Freedhoff
Authors: P. Lagiou, S. Sandin, M. Lof, D. Trichopoulos, H.-O. Adami, E. Weiderpass
Journal: BMJ (2012)

Campillo-Soto repeatedly mentions “biases” but uses this epidemiological term loosely and unconventionally.1 2 Selection bias is not really a concern in a cohort study and neither is measurement bias—assessment of exposures cannot be differentially affected by the outcome if it is not known when the exposure is reported. In his …
Mortality Among Men Using Homeless Shelters in Toronto, Ontario
Authors: Stephen W. Hwang
Journal: JAMA (2000)

ContextHomeless persons in US cities have high mortality rates. However, few comparison data exist for death rates among homeless persons in other developed countries.ObjectivesTo compare mortality rates among men using homeless shelters and the general population in Toronto, Ontario, and to determine whether mortality rates differ significantly among men using homeless shelters in Canadian and US cities.DesignCohort study conducted from 1995 through 1997, with a mean follow-up of 2.6 years.ParticipantsMen aged 18 years or older who used homeless shelters in Toronto in 1995 (n=8933).Main Outcome MeasureMortality rate ratios comparing age-specific mortality rates among men using homeless shelters in Toronto with those of men in the general population of Toronto and of men using homeless shelters in New York, NY; Boston, Mass; and Philadelphia, Pa.ResultsMen using homeless shelters in Toronto were more likely to die than men in the city's general population. Mortality rate ratios were 8.3 (95% confidence interval [CI], 4.4-15.6) for men aged 18 to 24 years, 3.7 (95% CI, 3.0-4.6) for men aged 25 to 44 years, and 2.3 (95% CI, 1.8-3.0) for men aged 45 to 64 years. In most cases, however, the risk of death was significantly lower for men using homeless shelters in Toronto than for those in US cities. For men aged 25 to 44 years using homeless shelters, mortality rate ratios were 0.52 (95% CI, 0.41-0.65) for Toronto compared with Boston and 0.61 (95% CI, 0.44-0.85) for Toronto compared with New York City. For men aged 35 to 54 years using homeless shelters, the mortality rate ratio was 0.42 (95% CI, 0.27-0.66) for Toronto compared with Philadelphia.ConclusionsMortality rates among men who use homeless shelters in Toronto, while higher than in the general population of Toronto, are much lower than mortality rates observed among men using homeless shelters in 3 major US cities. Further study is needed to identify the reasons for this disparity.
Noninvasive Measurement of Shortening in the Fiber and Cross-Fiber Directions in the Normal Human Left Ventricle and in Idiopathic Dilated Cardiomyopathy
Authors: Guy A. MacGowan, Edward P. Shapiro, Haim Azhari, Cynthia O. Siu, Paul S. Hees, Grover M. Hutchins, James L. Weiss, Frank E. Rademakers
Journal: Circulation (1997)

Background Studies in anesthetized dogs have shown that myocardial fibers shorten ≈8%. However, in the endocardium, shortening occurs to a much greater extent at 90° to the fiber orientation (“cross-fiber shortening”) than it does along the fiber direction. The purpose of this study was to estimate the extent of fiber and cross-fiber shortening in the normal human left ventricle and in patients with idiopathic dilated cardiomyopathy (IDC). Methods and Results Ten normal subjects and nine patients with IDC were imaged with magnetic resonance tissue tagging. Finite strain analysis was used to calculate endocardial and epicardial shortening in the fiber and cross-fiber directions using anatomic fiber angles from representative autopsy specimens as references. Anatomic fiber angles were not different between normal subjects and IDC patients. Epicardial fiber strain was −0.14±0.01 in normal subjects and −0.08±0.01 in IDC patients ( P &lt;.0001 versus normal subjects). Epicardial cross-fiber strain was −0.08±0.01 in normal subjects and −0.06±0.01 in IDC patients ( P =NS). Endocardial fiber strain was −0.16±0.01 in normal subjects and −0.09±0.01 in IDC patients ( P &lt;.0001), and endocardial cross-fiber strain was −0.26±0.01 in normal subjects and −0.15±0.01 in IDC patients ( P &lt;.0001). Cross-fiber shortening was greater than fiber shortening at the endocardium in both normal subjects ( P &lt;.0001) and IDC patients ( P &lt;.05). Conclusions In normal humans, the direction of maximal deformation aligns with the fiber direction in the epicardium but is perpendicular to the fiber direction in the endocardium. When strain in a coordinate system aligned to the fibers is estimated, cross-fiber shortening is found to be the dominant shortening strain at the endocardium. Normal fiber shortening is ≈15%, and this is markedly reduced in IDC. The normal transition in fiber orientation through the wall is not altered in IDC, and cross-fiber shortening is still the dominant strain at the endocardium, suggesting that interactions between myocardial layers persist in these patients.
Malignant Germ Cell Tumors Display Common MicroRNA Profiles Resulting in Global Changes in Expression of Messenger RNA Targets
Authors: Roger D. Palmer, Matthew J. Murray, Harpreet K. Saini, Stijn van Dongen, Cei Abreu-Goodger, Balaji Muralidhar, Mark R. Pett, Claire M. Thornton, James C. Nicholson, Anton J. Enright, Nicholas Coleman
Journal: Cancer Research (2010)

Despite their extensive clinical and pathologic heterogeneity, all malignant germ cell tumors (GCT) are thought to originate from primordial germ cells. However, no common biological abnormalities have been identified to date. We profiled 615 microRNAs (miRNA) in pediatric malignant GCTs, controls, and GCT cell lines (48 samples in total) and re-analyzed available miRNA expression data in adult gonadal malignant GCTs. We applied the bioinformatic algorithm Sylamer to identify miRNAs that are of biological importance by inducing global shifts in mRNA levels. The most significant differentially expressed miRNAs in malignant GCTs were all from the miR-371-373 and miR-302 clusters (adjusted P < 0.00005), which were overexpressed regardless of histologic subtype [yolk sac tumor (YST)/seminoma/embryonal carcinoma (EC)], site (gonadal/extragonadal), or patient age (pediatric/adult). Sylamer revealed that the hexamer GCACTT, complementary to the 2- to 7-nucleotide miRNA seed AAGUGC shared by six members of the miR-371-373 and miR-302 clusters, was the only sequence significantly enriched in the 3'-untranslated region of mRNAs downregulated in pediatric malignant GCTs (as a group), YSTs and ECs, and in adult YSTs (all versus nonmalignant tissue controls; P < 0.05). For the pediatric samples, downregulated genes containing the 3'-untranslated region GCACTT showed significant overrepresentation of Gene Ontology terms related to cancer-associated processes, whereas for downregulated genes lacking GCACTT, Gene Ontology terms generally represented metabolic processes only, with few genes per term (adjusted P < 0.05). We conclude that the miR-371-373 and miR-302 clusters are universally overexpressed in malignant GCTs and coordinately downregulate mRNAs involved in biologically significant pathways.
Vascular endothelial growth factor and receptor interaction is a prerequisite for murine hepatic fibrogenesis
Authors: H Yoshiji
Journal: Gut (2003)

<b>Background:</b> It has been shown that expression of the potent angiogenic factor, vascular endothelial growth factor (VEGF), and its receptors, flt-1 (VEGFR-1) and KDR/Flk-1 (VEGFR-2), increased during the development of liver fibrosis. <b>Aims:</b> To elucidate the in vivo role of interaction between VEGF and its receptors in liver fibrogenesis. <b>Methods:</b> A model of CCl<sub>4</sub> induced hepatic fibrosis was used to assess the role of VEGFR-1 and VEGFR-2 by means of specific neutralising monoclonal antibodies (R-1mAb and R-2mAb, respectively). R-1mAb and R-2mAb were administered after two weeks of treatment with CCl<sub>4</sub>, and indices of fibrosis were assessed at eight weeks. <b>Results:</b> Hepatic VEGF mRNA expression significantly increased during the development of liver fibrosis. Both R-1mAb and R-2mAb treatments significantly attenuated the development of fibrosis associated with suppression of neovascularisation in the liver. Hepatic hydroxyproline and serum fibrosis markers were also suppressed. Furthermore, the number of α-smooth muscle actin positive cells and α1(I)-procollagen mRNA expression were significantly suppressed by R-1mAb and R-2mAb treatment. The inhibitory effect of R-2mAb was more potent than that of R-1mAb, and combination treatment with both mAbs almost completely attenuated fibrosis development. Our in vitro study showed that VEGF treatment significantly stimulated proliferation of both activated hepatic stellate cells (HSC) and sinusoidal endothelial cells (SEC). VEGF also significantly increased α1(I)-procollagen mRNA expression in activated HSC. <b>Conclusions:</b> These results suggest that the interaction of VEGF and its receptor, which reflected the combined effects of both on HSC and SEC, was a prerequisite for liver fibrosis development.
Trans Fatty Acids and Cardiovascular Disease
Authors: Dariush Mozaffarian, Martijn B. Katan, Alberto Ascherio, Meir J. Stampfer, Walter C. Willett
Journal: New England Journal of Medicine (2006)

The intake of trans fat has been associated with coronary heart disease, sudden death from cardiac causes, and diabetes. This article reviews the evidence for physiological and cellular effects of trans fatty acids, unsaturated fatty acids with at least one double bond in the trans configuration. The authors consider the feasibility and potential implications of reducing or eliminating the consumption of trans fatty acids from partially hydrogenated vegetable oils in the United States.
Mutant p53 Induces the GEF-H1 Oncogene, a Guanine Nucleotide Exchange Factor-H1 for RhoA, Resulting in Accelerated Cell Proliferation in Tumor Cells
Authors: Shinji Mizuarai, Kazunori Yamanaka, Hidehito Kotani
Journal: Cancer Research (2006)

The tumor suppressor gene p53 is known to induce G1-S and G2-M cell cycle arrest and apoptosis by transactivating various wild-type (WT) p53 regulatory genes. Mutational inactivation of p53 is detected in more than half of human cancers, depriving the p53 protein of its tumor-suppressive functions. Recent studies have shown that mutant p53 provides tumor cells with gain-of-function properties, such as accelerated cell proliferation, increased metastasis, and apoptosis resistance. However, the mechanism underlying the elevated tumorigenicity by p53 mutation remains to be elucidated. In the present study, we showed that GEF-H1, a guanine exchange factor-H1 for RhoA, is transcriptionally activated by the induction of mutant p53 proteins, thereby accelerating tumor cell proliferation. Osteosarcoma U2OS cell lines, which express inducible p53 mutants (V157F, R175H, and R248Q), were established, and the expression profiles of each cell line were then analyzed to detect genes specifically induced by mutant p53. We identified GEF-H1 as one of the consensus genes whose expression was significantly induced by the three mutants. The GEF-H1 expression level strongly correlated with p53 status in a panel of 32 cancer cell lines, and GEF-H1 induction caused activation of RhoA. Furthermore, growth of mutant p53 cells was dependent on GEF-H1 expression, whereas that of WT p53 cells was not. These results suggest that increased GEF-H1 expression contributes to the tumor progression phenotype associated with the p53 mutation.
Which patients are likely to die in an accident and emergency department?
Authors: M J Shalley, A B Cross
Journal: BMJ (1984)

Four hundred and eighty-eight deaths occurring in an accident and emergency department over five years were analysed. Their causes were categorised as medical, surgical, or traumatic. Medical causes accounted for 87% of the deaths, of which 60% were from cardiac conditions. Blood loss was an important factor in over half the deaths from surgical and traumatic causes. Lives might have been saved by considering infectious disease in patients with medical conditions and by undertaking more rapid blood transfusion, earlier chest drainage, and lateral cervical spine x rays in appropriate surgical or traumatic cases. The admission to casualty departments of people with terminal neoplasms should be discouraged. The management of medical emergencies should be emphasised when training accident and emergency department staff.
Comparative study of the effects of different glucocorticosteroids on eosinophil survival primed by cultured epithelial cell supernatants obtained from nasal mucosa and nasal polyps.
Authors: J Mullol, A Xaubet, E Lopez, J Roca-Ferrer, C Picado
Journal: Thorax (1995)

Supernatants from epithelial cell cultures enhance eosinophil survival in vitro, this effect being abrogated by previous incubation of eosinophils with glucocorticosteroids. This property has resulted in the development of an in vitro test to compare the potency of these drugs. A comparative study was performed with dexamethasone, methylprednisolone, deflazacort, and budesonide.Human epithelial cell conditioned media (HECM) was generated from cultured epithelial cells obtained from healthy nasal mucosa and polyps. Eosinophils isolated from the peripheral blood were incubated with different corticosteroids for one hour before the addition of HECM. The inhibitory potency of the four steroids on the eosinophil survival index was compared using the concentration of steroid causing 50% inhibition (IC50).Eosinophil survival was increased by HECM from both healthy nasal mucosa and polyps. All four steroids blocked HECM-induced eosinophil survival in a dose-dependent manner. On healthy nasal mucosa methylprednisolone was the least potent (IC50 = 536 nM), deflazacort (IC50 = 264 nM) was twice as potent as methylprednisolone, while budesonide and dexamethasone were approximately nine times as potent (both IC50 = 58 nM). When potency was evaluated on the promoting effects of the HECM obtained from nasal polyps, the inhibitory potencies were lower and consequently the IC50 values were higher when compared with HECM generated from healthy nasal mucosa: methylprednisolone (IC50 = 546 nM), deflazacort (IC50 = 390 nM), dexamethasone (IC50 = 76 nM), and budesonide (IC50 = 78 nM).The potencies of glucocorticosteroids can be compared by evaluating their effects on the survival of eosinophils previously primed by supernatants obtained from epithelial cell culture. The different effects of steroids on eosinophils primed by HECM obtained from healthy nasal mucosa compared with HECM obtained from nasal polyps suggest that polyps might represent more active tissue which is relatively resistant to treatment with corticosteroids.