tbuckley/cabot-search huggingface dataset:
Manometric evaluation of rectal prolapse and faecal incontinence.
Authors: D M Matheson, M R Keighley
Journal: Gut (1981)

Sixty-three patients with complete rectal prolapse and/or faecal incontinence have undergone anal manometry and the results have been compared with an equal number of age- and sex-matched controls. Maximal basal pressure (MBP) and maximum squeeze pressure (MSP) were measured before and at four months and a year after treatment. The anal pressures of normal subjects are presented. Patients with rectal prolapse alone had normal anal pressures, whereas patients with incontinence with or without prolapse had significantly lower basal and squeeze pressures than controls. Successful surgical treatment of prolapse or incontinence did not produce significant change in anal canal pressures, whereas the combination of pelvic floor exercises and a continence aid was associated with a significant rise in MSP.
Infusion of suicide-gene-engineered donor lymphocytes after family haploidentical haemopoietic stem-cell transplantation for leukaemia (the TK007 trial): a non-randomised phase I–II study
Authors: Fabio Ciceri, Chiara Bonini, Maria Teresa Lupo Stanghellini, Attilio Bondanza, Catia Traversari, Monica Salomoni, Lucia Turchetto, Scialini Colombi, Massimo Bernardi, Jacopo Peccatori, Alessandra Pescarollo, Paolo Servida, Zulma Magnani, Serena K Perna, Veronica Valtolina, Fulvio Crippa, Luciano Callegaro, Elena Spoldi, Roberto Crocchiolo, Katharina Fleischhauer, Maurilio Ponzoni, Luca Vago, Silvano Rossini, Armando Santoro, Elisabetta Todisco, Jane Apperley, Eduardo Olavarria, Shimon Slavin, Eva M Weissinger, Arnold Ganser, Michael Stadler, Evangelia Yannaki, Athanasios Fassas, Achilles Anagnostopoulos, Marco Bregni, Corrado Gallo Stampino, Paolo Bruzzi, Claudio Bordignon
Journal: The Lancet Oncology (2009)
Steroid sulphatase activity in the skin biopsies of various types of ichthyosis
Authors: A. RUOKONEN, A. OIKARINEN
Journal: British Journal of Dermatology (1981)

A simple method was developed for the determination of steroid sulphatase activity in a skin biopsy for routine use. In this method, 6 mg of minced tissue is incubated in 1 ml of Krebs-Ringer bicarbonate buffer with radioactive dehydroepiandrosterone sulphate (20,000 c.p.m., S.A. 1.1 Ci/mmol) for 4 h. After the incubation the liberated unconjugated dehydroepiandrosterone and its possible metabolites are separated from the conjugated compound by extraction with ethyl acetate-ethyl ether 10:90 (v/v). The organic phase is counted in a scintillation counter. The results are expressed as c.p.m. values per 6 mg tissue wet weight. Steroid sulphatase activity was measured in skin biopsies from nine control subjects and from thirteen patients with various types of ichthyosis. In the different groups studied, the ranges of the c.p.m. values were as follows: controls (n = 9) 377-1802; X-linked ichthyosis (n = 5) 140-214; ichthyosis vulgaris (n = 5) 607-1320; ichthyosiform erythroderma (n = 2) 2146-2214; lamellar ichthyosis (n = 1) 2185. The reagent blank varied from 180 to 259 c.p.m. In X-linked ichthyosis the c.p.m. values were always less than in the corresponding reagent blank, indicating that no enzyme activity was present in the tissue. In other types of ichthyosis, steroid sulphatase activity was normal. The method described is easy to accomplish in any clinical laboratory where scintillation counting is possible.
Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP
Authors: Marisa R. Bonsignore, G. Parati, G. Insalaco, P. Castiglioni, O. Marrone, S. Romano, A. Salvaggio, G. Mancia, G. Bonsignore, M. Di Rienzo
Journal: European Respiratory Journal (2005)

Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.
THE REQUIREMENT FOR HYDROCORTISONE IN ANTIBODY-FORMING TISSUE CULTIVATED IN SERUM-FREE MEDIUM
Authors: Charles T. Ambrose
Journal: The Journal of Experimental Medicine (1964)

It was previously reported from this laboratory that the secondary antibody response can regularly be elicited in vitro from fragments of rabbit lymph node node cultured in Eagle's medium supplemented with normal rabbit serum. Evidence is now presented that physiological levels of hydrocortisone (0.01 to 1.0 microM) can substitute for serum in the culture medium. However, with the omission of serum, serine (0.1 mM) must be included among Eagle's "essential" amino acids for consistent optimal antibody production. In some experiments the addition of insulin (0.5 unit/ml) and vitamin B(12) (0.5 microg/ml) has further enhanced the secondary response in this serum-free medium.
How does interferon inhibit HCV cell entry?
Authors: M. Jones, J. S. Owen
Journal: Gut (2008)

Hepatitis C virus (HCV), the sole member of the Hepacivirus genus of the Flaviviridae family, is an enveloped virus with a positive-sense single-stranded RNA genome of 9600 nucleotides. HCV virions mainly infect hepatocytes, entering via specific receptors and clathrin-mediated endocytosis to release their genome from acidified endosomes.1 Over 170 million people worldwide are infected with HCV, and 80–85% of these develop chronic hepatitis C, which in a sizeable portion (up to 20%) leads to cirrhosis, hepatic failure or hepatocellular carcinoma. Current HCV treatment is based on the antiviral action of interferon α (IFNα) in combination with ribavirin, although this clears the virus in only 40–55% of patients.

IFNα plays a central role in the innate immune system by inducing an antiviral state in target cells,2 most notably for HCV by inhibiting viral replication.3 However, it is less clear whether IFNα initiates specific actions to limit HCV infections, such as restricting virion attachment and/or entry into hepatocytes. In this edition of Gut ( see page 10.1136/gut.2006.111443 ), Murao et al 4 demonstrate in vitro that IFNα decreases cell surface expression of scavenger receptor class B type I (SR-BI), a pivotal molecule in early stages of the HCV life cycle. Before discussing their findings, however, we first describe the molecular ensemble of host cellular factors which orchestrate HCV entry.

Until the last decade, HCV research was hampered by lack of infectious clones and an inability to propagate the virus in cultured liver cells. Introduction of the HCV replicon system (a self-replicating subgenomic construct)5 allowed studies of viral replication, …
Characterization of 148 Ovarian Cancer tumografts (Avatars) using BROCA-HR deep sequencing
Authors: K. Lodhia, M. Becker, X. Hou, K. Kalli, M. Harrell, K. Wilcoxen, E. Swisher, S. Weroha, P. Halsuka
Journal: Annals of Oncology (2015)
Prognostic classification of pediatric medulloblastoma based on chromosome 17p loss, expression of MYCC and MYCN, and Wnt pathway activation
Authors: A. K. Park, S.-J. Lee, J. H. Phi, K.-C. Wang, D. G. Kim, B.-K. Cho, C. Haberler, S. Fattet, C. Dufour, S. Puget, C. Sainte-Rose, F. Bourdeaut, J. Grill, O. Delattre, S.-K. Kim, W.-Y. Park
Journal: Neuro-Oncology (2011)

Pediatric medulloblastoma is considered a highly heterogeneous disease and a new strategy of risk stratification to optimize therapeutic outcomes is required. We aimed to investigate a new risk-stratification approach based on expression profiles of medulloblastoma cohorts. We analyzed gene expression profiles of 30 primary medulloblastomas and detected strong evidence that poor survival outcome was significantly associated with mRNA expression profiles of 17p loss. However, it was not supported in independent cohorts from previously published data (n = 100). We speculated that this discrepancy might come from complex conditions of two important prognostic determinants: loss of tumor suppressors (chromosome 17p) and high expression of oncogenes c-myc (MYCC) or N-myc (MYCN). When patients were stratified into 5 or 7 subgroups based on simultaneous consideration of these 2 factors while defining the Wnt group as independent, obviously different survival expectancies were detected between the subgroups. For instance, predicted 5-year survival probabilities ranged from 19% to 81% in the 5 subgroups. We also found that age became a significant prognostic marker after adjusting for 17p, MYCC, and MYCN status. Diminished survival in age <3 years was more substantial in subgroups with high expression of MYCC, MYCN, or 17p loss but not in other subgroups, indicating that poor survival outcome might be synergistically affected by these 3 factors. Here we suggest a more tailored subgrouping system based on expression profiles of chromosome 17p, MYCC, and MYCN, which could provide the basis for a novel risk-stratification strategy in pediatric medulloblastoma.
Antiretroviral Drug Resistance Testing in Adult HIV-1 Infection
Authors: Martin S. Hirsch, Françoise Brun-Vézinet, Richard T. D'Aquila, Scott M. Hammer, Victoria A. Johnson, Daniel R. Kuritzkes, Clive Loveday, John W. Mellors, Bonaventura Clotet, Brian Conway, Lisa M. Demeter, Stefano Vella, Donna M. Jacobsen, Douglas D. Richman
Journal: JAMA (2000)

Assays for drug resistance testing in human immunodeficiency virus type 1 (HIV-1) infection are now available and clinical studies suggest that viral drug resistance is correlated with poor virologic response to new therapy. The International AIDS Society-USA sought to update prior recommendations to provide guidance for clinicians regarding indications for HIV-1 resistance testing.An International AIDS Society-USA 13-member physician panel with expertise in basic science, clinical research, and patient care involving HIV resistance to antiretroviral drugs was reconvened to provide recommendations for the clinical use of drug resistance testing.The full panel met regularly between January and October 1999. Resistance and resistance testing data appearing in the last decade through April 2000 and presentations at national and international research conferences were reviewed. Recommendations and considerations were developed by 100% group consensus, acknowledging that definitive data to support final recommendations are not yet available.Emerging data indicate that despite limitations, resistance testing should be incorporated into patient management in some settings. Resistance testing is recommended to help guide the choice of new regimens after treatment failure and for guiding therapy for pregnant women. It should be considered in treatment-naive patients with established infection, but cannot be firmly recommended in this setting. Testing also should be considered prior to initiating therapy in patients with acute HIV infection, although therapy should not be delayed pending the results. Expert interpretation is recommended given the complexity of results and assay limitations.
Primary Smallpox Vaccination Temporally Associated with New Onset Urticaria-Angioedema (UrtAng) Evolving to Chronic Disease
Authors: R.J.M. Engler, A. Marini, J. Green, M. Klote, L. Collins, P.V. Belandres, S.T. Chang, J.F. Williams, M.R. Nelson
Journal: Journal of Allergy and Clinical Immunology (2007)
Impact of Reporting Delay and Reporting Error on Cancer Incidence Rates and Trends
Authors: L. X. Clegg
Journal: JNCI Journal of the National Cancer Institute (2002)

Background: Cancer incidence rates and trends are a measure of the cancer burden in the general population. We studied the impact of reporting delay and reporting error on incidence rates and trends for cancers of the female breast, colorectal, lung/bronchus, prostate, and melanoma. Methods: Based on statistical models, we obtained reporting-adjusted (i.e., adjusted for both reporting delay and reporting error) case counts for each diagnosis year beginning in 1981 using reporting information for patients diagnosed with cancer in 1981–1998 from nine cancer registries that participate in the Surveillance, Epidemiology, and End Results (SEER) program. Joinpoint linear regression was used for trend analysis. All statistical tests are two-sided. Results: Initial incidence case counts (i.e., after the standard 2-year delay) accounted for only 88%–97% of the estimated final counts; it would take 4–17 years for 99% or more of the cancer cases to be reported. The percent change between reporting-adjusted and unadjusted cancer incidence rates for the 1998 diagnosis year ranged from 3% for colorectal cancers to 14% for melanoma in whites and for prostate cancer in black males. Reporting-adjusted current incidence trends for breast cancer and lung/bronchus cancer in white females showed statistically significant increases (estimated annual percent change [EAPC] = 0.6%, 95% confidence interval [CI] = 0.1% to 1.2%) and 1.2%, 95% CI = 0.7% to 1.6%, respectively), whereas trends for these cancers using unadjusted incidence rates were not statistically significantly different from zero (EAPC = 0.4%, 95% CI = –0.1% to 0.9% and 0.5%, 95% CI = –0.1% to 1.1%, respectively). Reporting-adjusted melanoma incidence rates for white males showed a statistically significant increase since 1981 (EAPC = 4.1%, 95% CI = 3.8% to 4.4%) in contrast to the unadjusted incidence rate, which was most consistent with a flat or downward trend (EAPC = –4.2%, 95% CI = –11.1% to 3.3%) after 1996. Conclusions: Reporting-adjusted cancer incidence rates are valuable in precisely determining current cancer incidence rates and trends and in monitoring the timeliness of data collection. Ignoring reporting delay and reporting error may produce downwardly biased cancer incidence trends, particularly in the most recent diagnosis years.
CO<sub>2</sub> laser debridement of sulphur mustard (bis-2-chloroethyl sulphide) induced cutaneous lesions accelerates production of a normal epidermis with elimination of cytological atypia
Authors: K.J. SMITH, H.G. SKELTON, J.L. MARTIN, C.G. HURST, B.E. HACKLEY
Journal: British Journal of Dermatology (1997)

Sulphur mustard (bis-2-chloroethyl sulphide; HD) exposure acutely produces lesions that vary from mild erythema, to blister formation, to necrosis. When blisters occur, with or without necrosis, healing of the lesions is delayed. Weanling pigs exposed to a mild erythema-producing dose of HD and to a moderate erythema-producing dose that consistently gave microblister formation were treated with CO2 laser (Tru-Pulse) debridement at 6, 24 or 48 h after exposure. The histopathological features observed at 14 days after exposure in control skin and skin exposed to both HD doses were compared with the features observed in CO2 laser-debrided skin in non-exposed and HD-exposed skin sites. The overlying epidermis in the non-laser treated lesions was thin, with cytological atypia and squamoid changes within the basal cell layer, as well as scattered apoptotic/necrotic keratinocytes. An increased inflammatory infiltrate and necrobiotic changes in the dermis were seen at the higher HD dose. All laser-treated lesions appeared identical, with a thick, differentiated epidermis and a well-formed basal cell layer. There was minimal inflammatory infiltrate. In the papillary dermis there were increased stromal cells. Laser debridement of mild clinical lesions induced by HD produced a more functional epidermis by 14 days as well as clearing the epidermis of damaged keratinocytes.
Symptoms and Cancer Outcome in Adjuvant Endocrine Therapy for Breast Cancer: Why Are They Associated?
Authors: Kathleen I. Pritchard
Journal: Journal of Clinical Oncology (2013)

may predict or be associated with breast cancer outcome. It is tempting to speculate that patients who report more adverse effects are somehow getting higher levels or more effects from the endocrine drugsinvolved,bothontheirgeneralbodysystems(vasomotorsymptoms, musculoskeletal symptoms, vulvovaginal symptoms) and on any remaining breast cancer cells. However, something about these analyses does not quite fit with that conclusion. In both a previous paper by Cuzick et al in Lancet Oncology 3 and the current paper, 1 patients seem to have fewer recurrences if they have musculoskeletal symptoms in both the tamoxifen and the aromatase inhibitor arms, even though musculoskeletal symptoms are not a reported adverse effect of tamoxifen. Similar results are seen in an International Breast Cancer Study GroupB1to98report. 4 Why should this be true? These data suggest, as I postulated in my editorial 5 in relation to Cuzick’s article, that there may be something similar about patients who both report more adverse effects and have fewer recurrences. In Cuzick’s paper, counterintuitively, more adverse effects were associated with better compliance with endocrine therapy. In the current TamoxifenExemestaneAdjuvantMultinational(TEAM)trialpaper, 1 whiletheauthorsdonotreportcomplianceinthesamewayasCuzick did, they suggest that the adverse effect association with better outcomes persists despite treatment discontinuation. It may be that women who note and report their adverse effects in a more detailed wayareperhapsinturnalsomorelikelytopursueotherhealthyhabits
Moderate Increase of Secondary Hematologic Malignancies After Myeloablative Radiochemotherapy and Autologous Stem-Cell Transplantation in Patients With Indolent Lymphoma: Results of a Prospective Randomized Trial of the German Low Grade Lymphoma Study Group
Authors: Georg Lenz, Martin Dreyling, Eva Schiegnitz, Torsten Haferlach, Joerg Hasford, Michael Unterhalt, Wolfgang Hiddemann
Journal: Journal of Clinical Oncology (2004)

Purpose An increased risk of therapy-related myelodysplastic syndrome (t-MDS) and acute myeloid leukemia (t-AML) after high-dose therapy and autologous stem-cell transplantation (ASCT) for malignant lymphoma has been described by several studies, reporting a highly variable incidence ranging from 1% to 12%. To assess this risk more precisely, the German Low Grade Lymphoma Study Group investigated the incidence of t-MDS/t-AML after ASCT on the basis of a randomized comparison of ASCT versus interferon alfa (IFN-α) maintenance in indolent lymphoma. Patients and Methods Between 1996 and 2002, 440 patients with indolent lymphoma were randomly assigned after a cyclophosphamide, doxorubicin, vincristine, and prednisone–like induction therapy regimen to myeloablative radiochemotherapy followed by ASCT or IFN-α. The incidence of secondary hematologic malignancies was determined by standardized follow-up of all study patients. Bone marrow samples from patients with proven or suspected t-MDS/t-AML were centrally reviewed. Results After a median follow-up of 44 months, 431 patients were assessable. Five of 195 patients developed a secondary hematologic malignancy after ASCT. Two of these patients developed a secondary AML. Accordingly, the estimated 5-year risk for secondary hematologic neoplasias after ASCT was 3.8%. In contrast, in the IFN-α arm, the 5-year risk of hematologic neoplasias was 0.0% (P = .0248). Conclusion The data of this randomized trial demonstrate an increased risk of secondary hematologic malignancies after myeloablative radiochemotherapy and ASCT compared with conventional chemotherapy. However, as ASCT significantly improves progression-free survival, it is currently not evident to what extent the higher rate of t-MDS/t-AML will diminish the benefit of ASCT in indolent lymphoma.
Fertility regulator seeks views on donation compensation
Authors: A. O'Dowd
Journal: BMJ (2010)

People who donate eggs or sperm for other people to be able to conceive could receive higher financial compensation after a review by the UK’s fertility regulator.

The Human Fertilisation and Embryology Authority (HFEA) has launched a review to seek opinions on whether the money paid to egg and sperm donors should be increased to deal with current shortages.

The review will also look at the number of families that donors can donate to; donation between family members; the conditions that donors can place on the use of their gametes or embryos; and the upper age limit for sperm donation.

In the UK, egg and …
Circulatory Consequences of Changes in Cardiac Rhythm Produced in Patients by Transthoracic Direct-Current Shock*
Authors: John S. Graettinger, Richard A. Carleton, Joseph J. Muenster
Journal: Journal of Clinical Investigation (1964)

NSR mos 1 9a.A.L. 46 F RHD-MSt 1 AF 2 mos 58.0 NSR AF days 1 b.A.L.
The interaction of Herpes Simplex Virus with murine lymphocytes. I. Mitogenic properties of herpes simplex virus.
Authors: D Mochizuki, S Hedrick, J Watson, D T Kingsbury
Journal: The Journal of Experimental Medicine (1977)

Herpes simplex virus (HSV) stimulates DNA synthesis in mouse spleen cultures prepared from normal, macrophage-depleted, and T-cell-depleted spleen cells, but not from thymocytes. In addition, a polyclonal antibody response is observed in HSV-infected spleen cultures. These findings indicate that the cells stimulated to undergo DNA synthesis after HSV infection appear to be the bone marrow-derived lymphocytes. The newly synthesized DNA is host cell and not of viral origin. Heat treatment and ultraviolet irradiation of HSV before addition to spleen cultures prevents the induction of DNA synthesis. We consider the use of this system as assay for the study of cell transformation by HSV and also for the study of host cell control of the expression of the viral genome.
Carcinogenicity of Tumor Cell Populations: Origin of a Putative H-2 Isoantigenic Loss Variant Tumor&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: R S Kerbel, M Florian, M S Man, J Dennis, I F McKenzie
Journal: JNCI Journal of the National Cancer Institute (1980)

Journal Article Carcinogenicity of Tumor Cell Populations: Origin of a Putative H-2 Isoantigenic Loss Variant Tumor Get access R. S. Kerbel, R. S. Kerbel Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Florian, M. Florian Search for other works by this author on: Oxford Academic PubMed Google Scholar M. S. Man, M. S. Man Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Dennis, J. Dennis Search for other works by this author on: Oxford Academic PubMed Google Scholar I. F. C. McKenzie I. F. C. McKenzie Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 64, Issue 5, May 1980, Pages 1221–1230, https://doi.org/10.1093/jnci/64.5.1221 Published: 01 May 1980 Article history Received: 18 July 1979 Accepted: 16 October 1979 Published: 01 May 1980