tbuckley/cabot-search huggingface dataset:
Screening for Ovarian Cancer: U.S. Preventive Services Task Force Reaffirmation Recommendation Statement
Authors: Virginia A. Moyer
Journal: Annals of Internal Medicine (2012)

Chinese translation Description: Reaffirmation of the 2004 U.S. Preventive Services Task Force (USPSTF) recommendation statement on screening for ovarian cancer. Methods: A 2008 review of the literature commissioned by the USPSTF revealed no new evidence about the benefits of screening for ovarian cancer but provided some new data about observed harms of screening. A bridge search to 2011 focused on evidence from randomized, controlled trials. Population: This recommendation applies to asymptomatic women. It does not apply to women with known genetic mutations that increase their risk for ovarian cancer (for example, BRCA mutations). Recommendation: The USPSTF recommends against screening for ovarian cancer in women (D recommendation).
MILITARY ORTHOPAEDIC HOSPITALS
Authors: W. C. Mackenzie
Journal: BMJ (1917)

THE contributions made to surgical science by Great lBritain in the last hundred or hundred and twenty years have placed the world for ever under a debt to the savants of this country.The discovery, about the year 1799, by Sir IHumphry Davy that anaesthesia could be induced by yapour inhalation and the suggestion that nitrous oxide might be used with advantage during surgical operations;l the introduction of the antiseptic system by Lister, and the publication of the Origin of Species by Darwin which ;irmly establishled the principles of the law -of evolution- these all effected a complete revolution on medical thought both as regards its theory and its practice.To show how great the revolution was a reference may be made to Lister's papers and more especially to the year 1873.2At ,that time a Scottish medical student was receiving his training in surgical wards from which hospital gangrene, blood poisoning and erysipelas had been banished, and lhe 4was witnessing operations under chloroform anaesthesia, the mortality from which in Syme's first series of 5,000 cases was nil.In anatomy not only could he, like Hunter, study man in relation to the animal world, but, thanks to the genius of Darwin, could study each animal in its sequence to some other.Tlle law and order of function and structure took the place of chaos.It is interesting to note that about that time a com- mission was sent to Edinburgh from Germany under Lind- painter.The wards of the hospitals of that country were foul with sepsis, and the magnificent hospital in Muinich was about to be destroyed owing to the prevalence of blood poisoning, 80 per cent. of all wounds being affected by hospital gangrene.From this country, after a year spent in acquiring principles and methods, the German Com- mission took away a sound knowledge of the antiseptic system, anaesthesia, and of comparative biology-the three factors to which modern surgery owes its existence.After Lindpainter's return from Edinburgh not a single pase of hospital gangrene occurred in the Munich Krankenhaus, and pyaemia and erysipelas were banished.The effects on surgery of the introduction of the anti- septic-or, as called later, the aseptic-system were im- mediate.Its greatness was recognized throughout the *..orld, and everywhere surgical wards and operating theatres were modelleq on the British principle.The cranium, thorax, and abdomen could now be explored, Wnd cases always regarded formerly as hopeless were rendered curable.
Prevalence of Cerebral Amyloid Pathology in Persons Without Dementia
Authors: Willemijn J. Jansen, Rik Ossenkoppele, Dirk L. Knol, Betty M. Tijms, Philip Scheltens, Frans R. J. Verhey, Pieter Jelle Visser, Pauline Aalten, Dag Aarsland, Daniel Alcolea, Myriam Alexander, Ina S. Almdahl, Steven E. Arnold, Inês Baldeiras, Henryk Barthel, Bart N. M. van Berckel, Kristen Bibeau, Kaj Blennow, David J. Brooks, Mark A. van Buchem, Vincent Camus, Enrica Cavedo, Kewei Chen, Gael Chetelat, Ann D. Cohen, Alexander Drzezga, Sebastiaan Engelborghs, Anne M. Fagan, Tormod Fladby, Adam S. Fleisher, Wiesje M. van der Flier, Lisa Ford, Stefan Förster, Juan Fortea, Nadia Foskett, Kristian S. Frederiksen, Yvonne Freund-Levi, Giovanni B. Frisoni, Lutz Froelich, Tomasz Gabryelewicz, Kiran Dip Gill, Olymbia Gkatzima, Estrella Gómez-Tortosa, Mark Forrest Gordon, Timo Grimmer, Harald Hampel, Lucrezia Hausner, Sabine Hellwig, Sanna-Kaisa Herukka, Helmut Hildebrandt, Lianna Ishihara, Adrian Ivanoiu, William J. Jagust, Peter Johannsen, Ramesh Kandimalla, Elisabeth Kapaki, Aleksandra Klimkowicz-Mrowiec, William E. Klunk, Sebastian Köhler, Norman Koglin, Johannes Kornhuber, Milica G. Kramberger, Koen Van Laere, Susan M. Landau, Dong Young Lee, Mony de Leon, Viviana Lisetti, Alberto Lleó, Karine Madsen, Wolfgang Maier, Jan Marcusson, Niklas Mattsson, Alexandre de Mendonça, Olga Meulenbroek, Philipp T. Meyer, Mark A. Mintun, Vincent Mok, José Luis Molinuevo, Hanne M. Møllergård, John C. Morris, Barbara Mroczko, Stefan Van der Mussele, Duk L. Na, Andrew Newberg, Agneta Nordberg, Arto Nordlund, Gerald P. Novak, George P. Paraskevas, Lucilla Parnetti, Gayan Perera, Oliver Peters, Julius Popp, Sudesh Prabhakar, Gil D. Rabinovici, Inez H. G. B. Ramakers, Lorena Rami, Catarina Resende de Oliveira, Juha O. Rinne, Karen M. Rodrigue, Eloy Rodríguez-Rodríguez, Catherine M. Roe, Uros Rot, Christopher C. Rowe, Eckart Rüther, Osama Sabri, Páscual Sanchez-Juan, Isabel Santana, Marie Sarazin, Johannes Schröder, Christin Schütte, Sang W. Seo, Femke Soetewey, Hilkka Soininen, Luiza Spiru, Hanne Struyfs, Charlotte E. Teunissen, Magda Tsolaki, Rik Vandenberghe, Marcel M. Verbeek, Victor L. Villemagne, Stephanie J. B. Vos, Linda J. C. van Waalwijk van Doorn, Gunhild Waldemar, Anders Wallin, Åsa K. Wallin, Jens Wiltfang, David A. Wolk, Marzena Zboch, Henrik Zetterberg
Journal: JAMA (2015)

Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies.
Whole-genome sequencing to delineate Mycobacterium tuberculosis outbreaks: a retrospective observational study
Authors: Timothy M Walker, Camilla LC Ip, Ruth H Harrell, Jason T Evans, Georgia Kapatai, Martin J Dedicoat, David W Eyre, Daniel J Wilson, Peter M Hawkey, Derrick W Crook, Julian Parkhill, David Harris, A Sarah Walker, Rory Bowden, Philip Monk, E Grace Smith, Tim EA Peto
Journal: The Lancet Infectious Diseases (2012)

BackgroundTuberculosis incidence in the UK has risen in the past decade. Disease control depends on epidemiological data, which can be difficult to obtain. Whole-genome sequencing can detect microevolution within Mycobacterium tuberculosis strains. We aimed to estimate the genetic diversity of related M tuberculosis strains in the UK Midlands and to investigate how this measurement might be used to investigate community outbreaks.MethodsIn a retrospective observational study, we used Illumina technology to sequence M tuberculosis genomes from an archive of frozen cultures. We characterised isolates into four groups: cross-sectional, longitudinal, household, and community. We measured pairwise nucleotide differences within hosts and between hosts in household outbreaks and estimated the rate of change in DNA sequences. We used the findings to interpret network diagrams constructed from 11 community clusters derived from mycobacterial interspersed repetitive-unit–variable-number tandem-repeat data.FindingsWe sequenced 390 separate isolates from 254 patients, including representatives from all five major lineages of M tuberculosis. The estimated rate of change in DNA sequences was 0·5 single nucleotide polymorphisms (SNPs) per genome per year (95% CI 0·3–0·7) in longitudinal isolates from 30 individuals and 25 families. Divergence is rarely higher than five SNPs in 3 years. 109 (96%) of 114 paired isolates from individuals and households differed by five or fewer SNPs. More than five SNPs separated isolates from none of 69 epidemiologically linked patients, two (15%) of 13 possibly linked patients, and 13 (17%) of 75 epidemiologically unlinked patients (three-way comparison exact p<0·0001). Genetic trees and clinical and epidemiological data suggest that super-spreaders were present in two community clusters.InterpretationWhole-genome sequencing can delineate outbreaks of tuberculosis and allows inference about direction of transmission between cases. The technique could identify super-spreaders and predict the existence of undiagnosed cases, potentially leading to early treatment of infectious patients and their contacts.FundingMedical Research Council, Wellcome Trust, National Institute for Health Research, and the Health Protection Agency.
Hereditary Angioneurotic Edema
Authors: JOHN J. DENNEHY
Journal: Annals of Internal Medicine (1970)

Of 39 individuals in a family with hereditary angioneurotic edema, 11 are clinically affected in 4 generations, with 2 deaths from laryngeal edema; those still living have abnormally low levels of C′1 esterase inhibitor. Five children have the biochemical defect but as yet no symptoms. Four members of the family have symptoms suggestive of the disease but have normal sera; they may have other illnesses. Two patients have shown marked improvement with testosterone treatment. The known biologic reactions involved are discussed, the recent literature is reviewed, and a previously unnoticed historical reference is added.
Detection of carriers of classic hemophilia using an immunologic assay for antihemophilic factor (factor VIII)
Authors: Theodore S. Zimmerman, Oscar D. Ratnoff, Arthur S. Littell
Journal: Journal of Clinical Investigation (1971)

The relation between functional antihemophilic factor (AHF) activity and AHF-like antigen was studied in the plasma of 25 known carriers of hemophilia. In 23 cases, this relationship was significantly different from that in normal women, at the 99% limit of confidence. In contrast, among families in which only one case of hemophilia had occurred, only five of nine mothers could be identified as carriers. This observation suggests that in some instances the hemophilia arose from a newly mutant gene. The data are consistent with the hypothesis that the proportion of antigen to AHF activity in carriers is determined by random activation or inactivation of the X chromosome.
Oesophageal changes in systemic sclerosis.
Authors: M Atkinson, M D Summerling
Journal: Gut (1966)

EDITORIAL COMMENT These studies provide evidence for the primary lesion in the oesophagus in cases of systemic sclerosis being in the smooth muscle fibres rather than in the neural plexus.The loss of oesophageal peristalsis could often be demonstrated by cine-radiography and manometry before symptoms appeared.By the same techniques it was shown that as the disease progresses the oesophageal wave becomes incoordinated and finally disappears and muscle is atrophied early.on July 8,
Tuberculosis diagnosed during pregnancy: a prospective study from London
Authors: M. Llewelyn
Journal: Thorax (2000)

A study was undertaken to characterise the presentation of tuberculosis in pregnancy and the difficulties in diagnosis in an area of the UK with a high incidence of tuberculosis.A prospective case series was investigated at Northwick Park Hospital, a university affiliated district general hospital in Brent and Harrow health authority in north-west London which incorporates a regional infectious diseases unit. Patients diagnosed with tuberculosis over the study period were included if the onset of symptoms occurred during pregnancy.Thirteen patients were diagnosed during a 30 month period from December 1995 to May 1998 during which 9069 mothers were delivered, a prevalence of 143.3/100 000 deliveries. Symptoms began at a median of 22 weeks gestation (range 9-40 weeks). All patients were recent immigrants of Indian subcontinent or Somali origin and their median duration of residence in the UK was 31 months (range 1-72). Prevalence broken down for racial origin of mothers was 466.3/100 000 for mothers of black African origin and 239.1/100 000 for mothers of Indian origin. Nine of the 13 patients had extrapulmonary tuberculosis. Four patients with widely disseminated disease had a negative Mantoux response and five with localised disease had a strongly positive Mantoux response. HIV co-infection was absent. The median delay between the onset of symptoms and diagnosis was seven weeks (range 2-30). The response to standard treatment was excellent and all patients were cured.Tuberculosis occurring in pregnancy is common in recent immigrants. Diagnosis during pregnancy is delayed because the disease is frequently extrapulmonary with few symptoms.
Nature of socioeconomic inequalities in neonatal mortality: population based study
Authors: L. K. Smith, B. N. Manktelow, E. S. Draper, A. Springett, D. J. Field
Journal: BMJ (2010)

<b>Objective</b> To investigate time trends in socioeconomic inequalities in cause specific neonatal mortality in order to assess changing patterns in mortality due to different causes, particularly prematurity, and identify key areas of focus for future intervention strategies. <b>Design</b> Retrospective cohort study. <b>Setting</b> England. <b>Participants</b> All neonatal deaths in singleton infants born between 1 January 1997 and 31 December 2007. <b>Main outcome measure</b> Cause specific neonatal mortality per 10 000 births by deprivation tenth (deprivation measured with UK index of multiple deprivation 2004 at super output area level). <b>Results</b> 18 524 neonatal deaths occurred in singleton infants born in the 11 year study period. Neonatal mortality fell between 1997-9 and 2006-7 (from 31.4 to 25.1 per 10 000 live births). The relative deprivation gap (ratio of mortality in the most deprived tenth compared with the least deprived tenth) increased from 2.08 in 1997-9 to 2.68 in 2003-5, before a fall to 2.35 in 2006-7. The most common causes of death were immaturity and congenital anomalies. Mortality due to immaturity before 24 weeks’ gestation did not decrease over time and showed the widest relative deprivation gap (2.98 in 1997-9; 4.14 in 2003-5; 3.16 in 2006-7). Mortality rates for all other causes fell over time. For congenital anomalies, immaturity, and accidents and other specific causes, the relative deprivation gap widened between 1997-9 and 2003-5, before a slight fall in 2006-7. For intrapartum events and sudden infant deaths (only 13.5% of deaths) the relative deprivation gap narrowed slightly. <b>Conclusions</b> Almost 80% of the relative deprivation gap in all cause mortality was explained by premature birth and congenital anomalies. To reduce socioeconomic inequalities in mortality, a change in focus is needed to concentrate on these two influential causes of death. Understanding the link between deprivation and preterm birth should be a major research priority to identify interventions to reduce preterm birth.
Non-traumatic paraplegia in northern Tanzania
Authors: J George
Journal: BMJ (1981)

hypertensive drugs and claim that "no data exist showing that these drugs might interfere with the synthesis or metabolism of PGI2...." This is not true.A significant increase in plasma levels of 6-keto-PGF,cx has been demonstrated in hypertensive patients receiv- ing bendrofluazide.1This would tend to bias the Finnish data towards higher levels of immunoreactive 6-keto-PGF, a in their diabetic group.The effects of other antihypertensive drugs on PGI metabolism are unknown but also represent a potentially important group difference.The claim that plasma levels of 6-keto-PGF,co are higher in patients with angiopathy than without is in conflict with previously reported data.'However, in the Finnish study the patients without angiopathy were also older.It has been reported that plasma levels of 6-keto-PGF,x decline with age3 and the failure to match patients for age may explain at least part of the difference reported by Dr Ylikorkala and others.The validity of measurement of 6-keto- PGF,o in plasma as an index of PGI2 bio- synthesis is at present in dispute and undue weight should not be placed on absolute values.Group differences may yet be of considerable importance; but it is essential that such comparisons be made only between groups which are scrupulously matched for age and concurrent drug therapy, among other things.
Cellular Senescence Impairs Circadian Expression of Clock Genes In Vitro and In Vivo
Authors: Takeshige Kunieda, Tohru Minamino, Taro Katsuno, Kaoru Tateno, Jun-ichiro Nishi, Hideyuki Miyauchi, Masayuki Orimo, Sho Okada, Issei Komuro
Journal: Circulation Research (2006)

Circadian rhythms are regulated by a set of clock genes that form transcriptional feedback loops and generate circadian oscillation with a 24-hour cycle. Aging alters a broad spectrum of physiological, endocrine, and behavioral rhythms. Although recent evidence suggests that cellular aging contributes to various age-associated diseases, its effects on the circadian rhythms have not been examined. We report here that cellular senescence impairs circadian rhythmicity both in vitro and in vivo. Circadian expression of clock genes in serum-stimulated senescent cells was significantly weaker compared with that in young cells. Introduction of telomerase completely prevented this reduction of clock gene expression associated with senescence. Stimulation by serum activated the cAMP response element-binding protein, but the activation of this signaling pathway was significantly weaker in senescent cells. Treatment with activators of this pathway effectively restored the impaired clock gene expression of senescent cells. When young cells were implanted into young mice or old mice, the implanted cells were effectively entrained by the circadian rhythm of the recipients. In contrast, the entrainment of implanted senescent cells was markedly impaired. These results suggest that senescence decreases the ability of cells to transmit circadian signals to their clocks and that regulation of clock gene expression may be a novel strategy for the treatment of age-associated impairment of circadian rhythmicity.
Structural Evaluation of the Prefrontal Cortex in Schizophrenia
Authors: R W Buchanan, K Vladar, P E Barta, G D Pearlson
Journal: American Journal of Psychiatry (1998)

OBJECTIVE: Altered prefrontal cortical function has been repeatedly implicated in the pathophysiology of schizophrenia. Attempts to determine whether this altered function is associated with structural changes in the prefrontal cortex have been hampered by the failure to examine more anatomically and functionally homogeneous regions. The authors have developed a reliable set of anatomical landmarks for subdividing the prefrontal cortex into superior, middle, inferior, and orbital regions, in order to determine whether patients with schizophrenia exhibit selective morphological abnormalities of the prefrontal cortex. METHOD: Magnetic resonance imaging (MRI) studies were obtained in 24 normal control subjects (14 men and 10 women) and 18 patients with schizophrenia (12 men and six women) by using a high-resolution thin spoiled-gradient recall acquisition in the steady-state protocol. The MRI images were used to determine prefrontal gray matter volumes for the four prefrontal regions and prefrontal total gray and white volumes. RESULTS: Patients with schizophrenia exhibited selective gray matter volume reductions in the right and left inferior prefrontal cortex. There were no significant group differences in the other prefrontal regions. Patients with schizophrenia also exhibited decreased prefrontal total white matter and total volumes; there was no significant difference in prefrontal total gray matter volume. CONCLUSIONS: Patients with schizophrenia are characterized by relatively selective reductions in inferior prefrontal cortex gray matter volumes. (Am J Psychiatry 1998; 155:1049–1055)
The development of the intrahepatic bile ducts in man: A keratin-immunohistochemical study
Authors: Peter Van Eyken, Raf Sciot, Francesco Callea, Kris Van Der Steen, Philip Moerman, Valeer J. Desmet
Journal: Hepatology (1988)

The development of the intrahepatic bile ducts in man was studied using an immunohistochemical technique on 56 liver specimens ranging in age from 6 weeks of gestation to 8 months after birth. On paraffin sections, two monoclonal anticytokeratin antibodies (CAM 5.2 and KL-1) that normally stain both hepatocytes and bile duct cells and two polyclonal anticytokeratin antisera that in normal adult liver stain bile ducts only were applied. For immunohistochemical staining of cryostat sections (only available from 14 weeks of gestation on), four monoclonal antibodies specifically directed against individual cytokeratin polypeptides 7,8, 18 and 19 were used. Adult human hepatocytes contain cytokeratin 8 and 18 whereas bile duct cells also express cytokeratin 7 and 19 in addition to cytokeratin 8 and 18. On paraffin sections, primitive hepatocytes were stained with monoclonal antibodies CAM 5.2 and KL-1 from 6 weeks of gestation on. On cryostat sections, they were positive with monoclonal antibodies anticytokeratin 8 and 18 from the earliest time point examined (14 weeks). From 9 weeks of gestation on, portal vein branches were surrounded by a layer of cells showing a stronger positive reaction with monoclonal antibodies CAM 5.2 and KL-1 on paraffin sections and with monoclonal antibodies anti-cytokeratin 8 and 18 on cryostat sections (only available from 14 weeks on). This layer, referred to as the ductal plate, first appeared around large portal vein branches close to the hilum and subsequently around more peripheral branches. The duct plates became duplicated over variably long segments of their perimeter, lumina appeared and tubular structures were formed. The latter gradually became incorporated in the connective tissue surrounding the portal vein, resulting in the appearance of individualized bile ducts. Ductal plate cells were stained by both polyclonal anticytokeratin antisera on paraffin sections. On cryostat sections (available from 14 weeks of gestation on), they were immunoreactive for cytokeratin 19 but negative with the monoclonal antibody directed against cytokeratin 7 until 20 weeks of gestation. From then on, weakly positive staining for cytokeratin 7 was detected, but staining intensity subsequently increased and reached the level observed in adult liver at 1 month after birth. At birth, the smallest branches of the portal vein were still surrounded by a discontinuous ductal plate. We conclude that intrahepatic bile duct cells develop from hepatocytes around branches of the portal vein.(ABSTRACT TRUNCATED AT 400 WORDS)
Ly49A Transgenic Mice Provide Evidence for a Major Histocompatibility Complex–dependent Education Process in Natural Killer Cell Development
Authors: Werner Held, David H. Raulet
Journal: The Journal of Experimental Medicine (1997)

The Ly49 natural killer (NK) cell receptors are class I MHC–specific inhibitory receptors that are distributed to overlapping NK cell subsets. The formation of the Ly49 receptor repertoire was examined with transgenic mice that express Ly49A in all NK cells. In MHC class I–deficient mice, the Ly49A transgene did not prevent expression of endogenous Ly49 genes. However, in H-2d mice that express a Ly49A ligand, the transgene caused clear alterations in the endogenous Ly49 repertoire. The frequency of NK cells expressing another H-2d–specific receptor, Ly49G2+, was substantially reduced. Reduced numbers of cells expressing endogenous Ly49A was suggested by reduced endogenous Ly49A mRNA levels. These results support the existence of an MHC-dependent education process that limits the number of NK cells that coexpress multiple self-specific Ly49 receptors. Ligand-dependent downregulation of Ly49 cell surface levels was also examined. Cell-surface downregulation occurred even when the transgene was expressed at low levels. The results demonstrate that downregulation of Ly49A cell surface levels is a posttranscriptional event, and argue against a model in which Ly49 receptors are calibrated to specific cell surface levels depending on the available class I ligands.