tbuckley/cabot-search huggingface dataset:
Restraint and seclusion: a review of the literature
Authors: W A Fisher
Journal: American Journal of Psychiatry (1994)

The author reviewed the literature published since 1972 concerning restraint and seclusion.The review began with a computerized literature search. Further sources were located through citations from articles identified in the original search.The author synthesized the contents of the articles reviewed using the categories of indications and contraindications; rates of seclusion and restraint as well as demographic, clinical, and environmental factors that affect these rates; effects on patients and staff; implementation; and training.The literature on restraint and seclusion supports the following. 1) Seclusion and restraint are basically efficacious in preventing injury and reducing agitation. 2) It is nearly impossible to operate a program for severely symptomatic individuals without some form of seclusion or physical or mechanical restraint. 3) Restraint and seclusion have deleterious physical and psychological effects on patients and staff, and the psychiatric consumer/survivor movement has emphasized these effects. 4) Demographic and clinical factors have limited influence on rates of restraint and seclusion. 5) Local nonclinical factors, such as cultural biases, staff role perceptions, and the attitude of the hospital administration, have a greater influence on rates of restraint and seclusion. 6) Training in prediction and prevention of violence, in self-defense, and in implementation of restraint and/or seclusion is valuable in reducing rates and untoward effects. 7) Studies comparing well-defined training programs have potential usefulness.
Acute Illnesses Associated With Pesticide Exposure at Schools
Authors: Walter A. Alarcon, Geoffrey M. Calvert, Jerome M. Blondell, Louise N. Mehler, Jennifer Sievert, Maria Propeck, Dorothy S. Tibbetts, Alan Becker, Michelle Lackovic, Shannon B. Soileau, Rupali Das, John Beckman, Dorilee P. Male, Catherine L. Thomsen, Martha Stanbury
Journal: JAMA (2005)

Pesticides continue to be used on school property, and some schools are at risk of pesticide drift exposure from neighboring farms, which leads to pesticide exposure among students and school employees. However, information on the magnitude of illnesses and risk factors associated with these pesticide exposures is not available.To estimate the magnitude of and associated risk factors for pesticide-related illnesses at schools.Analysis of surveillance data from 1998 to 2002 of 2593 persons with acute pesticide-related illnesses associated with exposure at schools. Nationwide information on pesticide-related illnesses is routinely collected by 3 national pesticide surveillance systems: the National Institute for Occupational Safety and Health's Sentinel Event Notification System for Occupational Risks pesticides program, the California Department of Pesticide Regulation, and the Toxic Exposure Surveillance System.Incidence rates and severity of acute pesticide-related illnesses.Incidence rates for 1998-2002 were 7.4 cases per million children and 27.3 cases per million school employee full-time equivalents. The incidence rates among children increased significantly from 1998 to 2002. Illness of high severity was found in 3 cases (0.1%), moderate severity in 275 cases (11%), and low severity in 2315 cases (89%). Most illnesses were associated with insecticides (n = 895, 35%), disinfectants (n = 830, 32%), repellents (n = 335, 13%), or herbicides (n = 279, 11%). Among 406 cases with detailed information on the source of pesticide exposure, 281 (69%) were associated with pesticides used at schools and 125 (31%) were associated with pesticide drift exposure from farmland.Pesticide exposure at schools produces acute illnesses among school employees and students. To prevent pesticide-related illnesses at schools, implementation of integrated pest management programs in schools, practices to reduce pesticide drift, and adoption of pesticide spray buffer zones around schools are recommended.
Ischaemic strictures of the small intestine in Nigeria.
Authors: S G Subbuswamy, F I Iweze
Journal: Gut (1977)

Eleven specimens of small intestinal strictures were seen at the Pathology Department of the University of Benin Teaching Hospital, Benin City, Nigeria, during a period of two and a half years. Eight of them were ischaemic in origin and the clinical and pathological features of these eight cases are described. In five of the cases, the ischaemia could be related to inguinal hernia, with herniorrhaphy a few weeks before surgery for stricture in four cases. The most important factor in making a clinical or pathological diagnosis of ischaemic stricture of the small intestine appears to be awareness of the condition. The importance is emphasised of studying the mesentery, with particular attention to lymph nodes and blood vessels, before making a final diagnosis on intestinal lesions.
Adenine Arabinoside Monophosphate (Vidarabine Phosphate) in Combination with Human Leukocyte Interferon in the Treatment of Chronic Hepatitis B
Authors: G Garcia, C I Smith, J I Weissberg, M Eisenberg, J Bissett, P V Nair, B Mastre, S Rosno, D Roskamp, K Waterman
Journal: Annals of Internal Medicine (1987)

Study Objective: To determine the efficacy of adenine arabinoside monophosphate (Ara-AMP; vidarabine phosphate) with or without human leukocyte interferon in chronic hepatitis B. Study Design: Randomized, double-blinded, placebo-controlled trial with 6-month treatment and an 18-month follow-up. Setting: Referral-based liver-disease clinics at three university medical centers. Patients: Twenty-five patients with chronic active hepatitis or cirrhosis and 39 with chronic persistent hepatitis. Interventions: Thirteen patients received intramuscular Ara-AMP, 2.5 mg/kg body weight, twice daily, alternated monthly for 6 months with subcutaneous human leukocyte interferon, 5 million units, twice daily. Painful paresthesia of the legs necessitated dosage reduction and early discontinuation of enrollment. Twenty-four patients received intramuscular Ara-AMP, 2.5 mg/kg, twice daily, alternated monthly for 6 months with a matching placebo given subcutaneously twice daily. Twenty-seven patients received placebo by intramuscular and subcutaneous injections twice daily for 6 months. Measurements and Main Results: Of the 64 patients, 95% had symptomatic and virologic data available and 64% had biopsies at 12 months; at 24 months, 77% had data available and 56% had repeat biopsies. The highest dropout rate was seen in the group receiving Ara-AMP. The group receiving the placebo was less symptomatic (Karnofsky score of 96% compared with 91% in the group receiving Ara-AMP/ placebo and 92% in the group receiving Ara-AMP/human leukocyte interferon, p = 0.02) at 12 but not at 24 months. Loss of DNA polymerase, the hepatitis B e antigen, and the serum hepatitis B virus DNA was similar in all three groups. Histologically, erosion of the limiting plate and lobular activity favored Ara-AMP at 12 but not at 24 months and these differences did not result in differences in the histologic diagnosis. Conclusion: These results do not support the use of Ara-AMP and human leukocyte interferon in chronic persistent or chronic active hepatitis B.
Primary cutaneous B-cell lymphoma associated with actinic prurigo
Authors: C.M. Perrett, C.A. Harwood, M. Khorshid, R. Cerio, J.M. McGregor
Journal: British Journal of Dermatology (2005)

We describe two patients with a diagnosis of actinic prurigo who subsequently developed cutaneous B-cell lymphoma. This is the first report, to our knowledge, of this association. We propose that chronic antigenic stimulation by ultraviolet radiation, in the context of actinic prurigo, may have been causal in the development of these unusual lymphomas.
Somatic<i>HIF2A</i>Gain-of-Function Mutations in Paraganglioma with Polycythemia
Authors: Zhengping Zhuang, Chunzhang Yang, Felipe Lorenzo, Maria Merino, Tito Fojo, Electron Kebebew, Vera Popovic, Constantine A. Stratakis, Josef T. Prchal, Karel Pacak
Journal: New England Journal of Medicine (2012)

Hypoxia-inducible factors are transcription factors controlling energy, iron metabolism, erythropoiesis, and development. When these proteins are dysregulated, they contribute to tumorigenesis and cancer progression. However, mutations in genes encoding α subunits of hypoxia-inducible factors (HIF-α) have not previously been identified in any cancer. Here we report two novel somatic gain-of-function mutations in the gene encoding hypoxia-inducible factor 2α (HIF2A) in two patients, one presenting with paraganglioma and the other with paraganglioma and somatostatinoma, both of whom had polycythemia. The two mutations were associated with increased HIF-2α activity and increased protein half-life.
Prevalence and Predictors of Concomitant Carotid and Coronary Artery Atherosclerotic Disease
Authors: Arie Steinvil, Ben Sadeh, Yaron Arbel, Dan Justo, Anca Belei, Natan Borenstein, Shmuel Banai, Amir Halkin
Journal: Journal of the American College of Cardiology (2011)
Authors’ response: impaired duodenal mucosal integrity and low-grade inflammation in functional dyspepsia
Authors: Hanne Vanheel, Tim Vanuytsel, Ricard Farré, Jan Tack
Journal: Gut (2014)

We thank Prof Rodrigo and colleagues for their comments1 on our recent paper on increased permeability and low-grade inflammation in functional dyspepsia (FD).2 

However, we disagree that our study is underpowered, which was confirmed by highly significant differences between the groups. As indicated in the manuscript, we calculated the minimum sample size and even included more subjects than statistically required. We also want to point out that our n-values are in the upper range for a study that combines functional and structural measurements of epithelial integrity.

Questions were raised about the absence of Helicobacter pylori (HP) in our participants. Ten years ago, the prevalence of HP in the FD patient population of Belgium was low (17%), and has decreased even further since then.3 All patients were found to be negative for HP using immunohistochemical staining of gastric biopsies and had never received eradication therapy. HP status was not evaluated in the control group, but none of them had gastrointestinal complaints.

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Decreased Contractile and Metabolic Reserve in Peroxisome Proliferator–Activated Receptor-α–Null Hearts Can Be Rescued by Increasing Glucose Transport and Utilization
Authors: Ivan Luptak, James A. Balschi, Yanqiu Xing, Teresa C. Leone, Daniel P. Kelly, Rong Tian
Journal: Circulation (2005)

Downregulation of peroxisome proliferator-activated receptor-alpha (PPARalpha) in hypertrophied and failing hearts leads to the reappearance of the fetal metabolic pattern, ie, decreased fatty acid oxidation and increased reliance on carbohydrates. Here, we sought to elucidate the functional significance of this shift in substrate preference.We assessed contractile function and substrate utilization using 13C nuclear magnetic resonance spectroscopy and high-energy phosphate metabolism using 31P nuclear magnetic resonance spectroscopy in perfused hearts isolated from genetically modified mice (PPARalpha(-/-)) that mimic the metabolic profile in myocardial hypertrophy. We found that the substrate switch from fatty acid to glucose (3-fold down) and lactate (3-fold up) in PPARalpha(-/-) hearts was sufficient for sustaining normal energy metabolism and contractile function at baseline but depleted the metabolic reserve for supporting high workload. Decreased ATP synthesis (measured by 31P magnetization transfer) during high workload challenge resulted in progressive depletion of high-energy phosphate content and failure to sustain high contractile performance. Interestingly, the metabolic and functional defects in PPARalpha(-/-) hearts could be corrected by overexpressing the insulin-independent glucose transporter GLUT1, which increased the capacity for glucose utilization beyond the intrinsic response to PPARalpha deficiency.These findings demonstrate that metabolic remodeling in hearts deficient in PPARalpha increases the susceptibility to functional deterioration during hemodynamic overload. Moreover, our results suggest that normalization of myocardial energetics by further enhancing myocardial glucose utilization is an effective strategy for preventing the progression of cardiac dysfunction in hearts with impaired PPARalpha activity such as hearts with pathological hypertrophy.
Childhood Schizophrenia and 47, XXY Klinefelter's Syndrome
Authors: MICHAEL A. SPERBER, LUCY SALOMON, MARY H. COLLINS, MORRIS STAMBLER
Journal: American Journal of Psychiatry (1972)

Klinefelter's syndrome is a genetically transmitted endocrinological disorder characterized by a complement of 44 autosomes with an XXY sex-chromosome complex; it is frequently accompanied by neuropsychiatric disorders, although childhood schizophrenia has not been previously reported. Noting a statistically significant increase in the incidence of Klinefelter's syndrome in a schizophrenic population, the authors advance several verifiable hypotheses: adult Klinefelter schizophrenics may have psychotic processes of early origin, a high percentage of children currently diagnosed as psychotic may have Klinefelter's syndrome, and those with Klinefelter's syndrome may have increased susceptibility to develop schizophrenia.
Increased DNA fragmentation and ultrastructural changes in fibromyalgic muscle fibres
Authors: H Sprott
Journal: Annals of the Rheumatic Diseases (2004)

<b>Objective:</b> To determine whether there is evidence of increased DNA fragmentation and ultrastructural changes in muscle tissue of patients with fibromyalgia (FM) compared with healthy controls. <b>Methods:</b> Muscle tissues from 10 community residents with FM and 10 age and sex matched healthy controls were examined "blindly" for the presence of DNA fragmentation by two different methods: terminal deoxynucleotidyl transferase (TdT) staining (TUNEL) and the FragEL-Klenow DNA fragmentation detection kit. Ultrastructural analysis of tissue was performed by electron microscopy. <b>Results:</b> DNA fragmentation was detected by both methods in 55.4 (SEM 2.5)% of the nuclei in muscle tissue of patients with FM compared with 16.1 (4.1)% (p&lt;0.001) of the nuclei in healthy controls. Contrary to expectation, no typical features of apoptosis could be detected by electron microscopy. The myofibres and actin filaments were disorganised and lipofuscin bodies were seen; glycogen and lipid accumulation were also found. The number of mitochondria was significantly lower in patients with FM than in controls and seemed to be morphologically altered. <b>Conclusion:</b> The ultrastructural changes described suggest that patients with FM are characterised by abnormalities in muscle tissue that include increased DNA fragmentation and changes in the number and size of mitochondria. These cellular changes are not signs of apoptosis. Persistent focal contractions in muscle may contribute to ultrastructural tissue abnormalities as well as to the induction and/or chronicity of nociceptive transmission from muscle to the central nervous system.
Structural aspects of cross‐reactivity and its relation to antibody affinity
Authors: Rob C. Aalberse, Ilona Kleine Budde, Steven O. Stapel, Ronald Van Ree
Journal: Allergy (2001)

In the context of IgE/allergen interactions, affinity is largely determined by the stability of the allergen‐IgE complex: a low affinity is usually equated with a rapid dissociation of the complex. Regular solid‐phase assays are not well suited for affinity estimates because of multivalency effects, “unstirred layer” effects and “invisible” antibodies. Elution of IgE bound to solid‐phase coupled allergen might be a good measure of intrinsic affinity, provided that reassociation of antibodies is prevented by a high concentration of soluble allergen. Allergen‐mediated IgE‐dependent triggering of a mast cell is presumably a two‐step process. During the first step, the allergen is bound to a cell‐bound IgE antibody and dragged over the cell surface. The second step is the interaction between this cell‐bound allergen and another IgE antibody. The hypothesis is that the affinity requirements for the first step are higher than for the second. The implication is that a mast cell can be triggered by a single high‐affinity antibody in combination with one or more low‐affinity antibodies.
A novel mechanism of retrovirus inactivation in human serum mediated by anti-alpha-galactosyl natural antibody.
Authors: R P Rother, W L Fodor, J P Springhorn, C W Birks, E Setter, M S Sandrin, S P Squinto, S A Rollins
Journal: The Journal of Experimental Medicine (1995)

Type C retroviruses endogenous to various nonprimate species can infect human cells in vitro, yet the transmission of these viruses to humans is restricted. This has been attributed to direct binding of the complement component C1q to the viral envelope protein p15E, which leads to classical pathway-mediated virolysis in human serum. Here we report a novel mechanism of complement-mediated type C retrovirus inactivation that is initiated by the binding of "natural antibody" [Ab] (anti-alpha-galactosyl Ab) to the carbohydrate epitope Gal alpha 1-3Gal beta 1-4GlcNAc-R expressed on the retroviral envelope. Complement-mediated inactivation of amphotropic retroviral particles was found to be restricted to human and other Old World primate sera, which parallels the presence of anti-alpha-galactosyl natural Ab. Blockade or depletion of anti-alpha-galactosyl Ab in human serum prevented inactivation of both amphotropic and ecotropic murine retroviruses. Similarly, retrovirus was not killed by New World primate serum except in the presence of exogenous anti-alpha-galactosyl Ab. Enzyme-linked immunosorbent assays revealed that the alpha-galactosyl epitope was expressed on the surface of amphotropic and ecotropic retroviruses, and Western blot analysis further localized this epitope to the retroviral envelope glycoprotein gp70. Finally, down-regulation of this epitope on the surface of murine retroviral particle producer cells rendered them, as well as the particles liberated from these cells, resistant to inactivation by human serum complement. Our data suggest that anti-alpha-galactosyl Ab may provide a barrier for the horizontal transmission of retrovirus from species that express the alpha-galactosyl epitope to humans and to other Old World primates. Further, these data provide a mechanism for the generation of complement-resistant retroviral vectors for in vivo gene therapy applications where exposure to human complement is unavoidable.
Use of glycosylated recombinant human G-CSF (lenograstim) during and/or after induction chemotherapy in patients 61 years of age and older with acute myeloid leukemia: final results of AML-13, a randomized phase-3 study
Authors: Sergio Amadori, Stefan Suciu, Ulrich Jehn, Roberto Stasi, Xavier Thomas, Jean-Pierre Marie, Petra Muus, François Lefrère, Zwi Berneman, Georges Fillet, Claudio Denzlinger, Roel Willemze, Pietro Leoni, Giuseppe Leone, Marco Casini, Francesco Ricciuti, Marco Vignetti, Filip Beeldens, Franco Mandelli, Theo de Witte
Journal: Blood (2005)
Ulipristal acetate versus levonorgestrel for emergency contraception: a randomised non-inferiority trial and meta-analysis
Authors: Anna F Glasier, Sharon T Cameron, Paul M Fine, Susan JS Logan, William Casale, Jennifer Van Horn, Laszlo Sogor, Diana L Blithe, Bruno Scherrer, Henri Mathe, Amelie Jaspart, Andre Ulmann, Erin Gainer
Journal: The Lancet (2010)
Association between Obstructive Sleep Apnea and Cancer Incidence in a Large Multicenter Spanish Cohort
Authors: Francisco Campos-Rodriguez, Miguel A. Martinez-Garcia, Montserrat Martinez, Joaquin Duran-Cantolla, Monica de la Peña, María J. Masdeu, Monica Gonzalez, Felix del Campo, Inmaculada Gallego, Jose M. Marin, Ferran Barbe, Jose M. Montserrat, Ramon Farre
Journal: American Journal of Respiratory and Critical Care Medicine (2012)

Obstructive sleep apnea (OSA) has been associated with increased cancer mortality, but whether it is also associated with cancer incidence is unknown.To investigate whether OSA is associated with increased cancer incidence in a large clinical cohort.A multicenter, clinical cohort study including consecutive patients investigated for suspected OSA between 2003 and 2007 in seven Spanish teaching hospitals. Apnea-hypopnea index (AHI) and percent nighttime with oxygen saturation less than 90% (TSat(90)) were used as surrogates of OSA severity, both as continuous variables and categorized by tertiles. Cox proportional hazards regression analyses were used to calculate hazard ratio (HR) and 95% confidence interval (CI) for cancer incidence after adjusting for confounding variables.A total of 4,910 patients were analyzed (median follow-up, 4.5 yr; interquartile range, 3.4-5.2). Compared with the lower TSat(90) category (<1.2%), the adjusted hazards (95% CI) of cancer incidence for increasing categories were 1.58 (1.07-2.34) for TSat(90) 1.2-12% and 2.33 (1.57-3.46) for TSat(90) greater than 12%. Continuous TSat(90) was also associated with cancer incidence (adjusted HR, 1.07 [1.02-1.13] per 10-unit increase in TSat(90)). In stratified analyses, TSat(90) was associated with cancer incidence in patients younger than 65 years (adjusted HR, 1.13 [95% CI, 1.06-1.21] per 10-unit increase in TSat(90)) and males (adjusted HR, 1.11 [95% CI, 1.04-1.17] per 10-unit increase in TSat(90)). AHI was not associated with cancer incidence in the adjusted analyses, except for patients younger than 65 years (adjusted HR for AHI >43 vs. <18.7, 1.66; 95% CI, 1.04-2.64).Increased overnight hypoxia as a surrogate of OSA severity was associated with increased cancer incidence. This association seems to be limited to men and patients younger than 65 years of age.
Role of CXCR2/CXCR2 ligands in vascular remodeling during bronchiolitis obliterans syndrome
Authors: John A. Belperio, Michael P. Keane, Marie D. Burdick, Brigitte Gomperts, Ying Ying Xue, Kurt Hong, Javier Mestas, Abbas Ardehali, Borna Mehrad, Rajan Saggar, Joseph P. Lynch, David J. Ross, Robert M. Strieter
Journal: Journal of Clinical Investigation (2005)

Angiogenesis and vascular remodeling support fibroproliferative processes; however, no study has addressed the importance of angiogenesis during fibro-obliteration of the allograft airway during bronchiolitis obliterans syndrome (BOS) that occurs after lung transplantation. The ELR(+) CXC chemokines both mediate neutrophil recruitment and promote angiogenesis. Their shared endothelial cell receptor is the G-coupled protein receptor CXC chemokine receptor 2 (CXCR2). We found that elevated levels of multiple ELR(+) CXC chemokines correlated with the presence of BOS. Proof-of-concept studies using a murine model of BOS not only demonstrated an early neutrophil infiltration but also marked vascular remodeling in the tracheal allografts. In addition, tracheal allograft ELR(+) CXC chemokines were persistently expressed even in the absence of significant neutrophil infiltration and were temporally associated with vascular remodeling during fibro-obliteration of the tracheal allograft. Furthermore, in neutralizing studies, treatment with anti-CXCR2 Abs inhibited early neutrophil infiltration and later vascular remodeling, which resulted in the attenuation of murine BOS. A more profound attenuation of fibro-obliteration was seen when CXCR2(-/-) mice received cyclosporin A. This supports the notion that the CXCR2/CXCR2 ligand biological axis has a bimodal function during the course of BOS: early, it is important for neutrophil recruitment and later, during fibro-obliteration, it is important for vascular remodeling independent of neutrophil recruitment.