tbuckley/cabot-search huggingface dataset:
Chronic Inhalation of Nitric Oxide Inhibits Neointimal Formation After Balloon-Induced Arterial Injury
Authors: Joon S. Lee, Christophe Adrie, Howard J. Jacob, Jesse D. Roberts, Warren M. Zapol, Kenneth D. Bloch
Journal: Circulation Research (1996)

Abstract Systemic and local intravascular NO administration inhibits neointimal formation after vascular injury in animal models. NO appears to attenuate smooth muscle proliferation both directly and indirectly by preventing the release of growth factors. Inhalation of low concentrations of NO dilates pulmonary vascular smooth muscle but does not cause systemic vasodilatation. Recently, NO inhalation was found to inhibit platelet function in vivo. We studied the effects of NO inhalation on neointimal formation after balloon-induced injury of the adult rat carotid artery. Beginning 60 minutes before carotid injury, rats breathed either air with 0 or 80 ppm NO for 14 days. Rats were killed, carotid arteries were fixed and paraffin-embedded, and neointimal formation was measured by analyzing the ratio of intimal to medial areas (I/M ratio) in carotid artery cross sections. Intimal hyperplasia was evident in both groups of animals, but I/M ratios were 43% less in animals breathing 80 ppm NO for 2 weeks than in animals breathing air alone (0.78±0.12 and 1.37±0.11 [mean±SE], respectively; P &lt;.02). Similarly, 1 week after carotid injury, neointimal formation was less in rats breathing 80 ppm NO than in rats breathing air alone (I/M ratio, 0.39±0.11 versus 0.76±0.06; P &lt;.02). Breathing 20 ppm NO for 2 weeks or 80 ppm NO for 1 week followed by air alone for 1 week did not attenuate neointimal formation measured at 14 days. In anesthetized rats breathing 80 ppm NO or air alone for 1 hour, neither systemic blood pressure nor bleeding time differed. These observations demonstrate that inhaling 80 ppm NO inhibits neointimal formation after balloon-induced carotid artery injury in rats. NO inhalation may represent a safe and novel method of preventing restenosis after percutaneous angioplasty.
Qualitative interview study of communication between parents and children about maternal breast cancer
Authors: J. Barnes
Journal: BMJ (2000)

<h3>Abstract</h3> <b>Objective:</b> To examine parents9 communication with their children about the diagnosis and initial treatment of breast cancer in the mother. <b>Design:</b> Qualitative interview study within cross sectional cohort. <b>Setting:</b> Two breast cancer treatment centres. <b>Participants:</b> 32 women with stage I or stage II breast cancer with a total of 56 school aged children. <b>Main outcome measures:</b> Semistructured interview regarding timing and extent of communication with children about the diagnosis and initial treatment of the mother9s illness, reasons for talking to children or withholding information, and help available and requested from health professionals. <b>Results:</b> Women were most likely to begin talking to their children after their diagnosis had been confirmed by biopsy, but a minority waited until after surgery or said nothing at all. Family discussion did not necessarily include mention of cancer. There was considerable consistency in the reasons given for either discussing or not discussing the diagnosis. The most common reason for not communicating was avoidance of children9s questions and particularly those about death. While most mothers experienced helpful discussion with a doctor concerning their illness, few were offered help with talking to children; many would have liked help, particularly the opportunity for both parents to talk to a health professional with experience in understanding and talking to children. <b>Conclusions:</b> Parents diagnosed with cancer or other serious illnesses should be offered help to think about whether, what, and how to tell their children and about what children can understand, especially as they may well be struggling themselves to come to terms with their illness.
Who Should Be Sent for Genetic Testing in Hereditary Colorectal Cancer Syndromes?
Authors: Henry T. Lynch, C. Richard Boland, Miguel A. Rodriguez-Bigas, Christopher Amos, Jane F. Lynch, Patrick M. Lynch
Journal: Journal of Clinical Oncology (2007)

Genetic testing is being adopted increasingly to identify individuals with germline mutations that predispose to hereditary colorectal cancer syndromes. Deciding who to test and for which syndrome is of concern to members of the GI oncology community, molecular geneticists, and genetic counselors. The purpose of this review is to help provide guidelines for testing, given that the results influence syndrome diagnosis and clinical management. Although family history may determine whether testing is appropriate and may direct testing to the most informative family member, evolving clinicopathologic features can identify individual patients who warrant testing. Thus, although the usual absence of clinical premonitory signs in hereditary nonpolyposis colorectal cancer (or Lynch syndrome) adds difficulty to its diagnosis, use of the Amsterdam Criteria and Bethesda Guidelines can prove helpful. In contrast, premonitory stigmata such as pigmentations in Peutz-Jeghers syndrome and the phenotypic features of familial adenomatous polyposis aid significantly in syndrome diagnosis. We conclude that the physician's role in advising DNA testing is no small matter, given that a hereditary cancer syndrome's sequelae may be far reaching. Genetic counselors may be extremely helpful to the practicing gastroenterologist, oncologist, or surgeon; when more specialized knowledge is called for, referral can be made to a medical geneticist and/or a medical genetics clinic.
Nonclassical behavior of the thymus leukemia antigen: peptide transporter-independent expression of a nonclassical class I molecule.
Authors: H R Holcombe, A R Castaño, H Cheroutre, M Teitell, J K Maher, P A Peterson, M Kronenberg
Journal: The Journal of Experimental Medicine (1995)

The thymus leukemia (TL) antigen is a major histocompatibility complex-encoded nonclassical class I molecule. Here we present data demonstrating that expression of the TL antigen, unlike other class I molecules, is completely independent of the function of the transporter associated with antigen processing (TAP). The TL antigen is expressed by transfected TAP-2-deficient RMA-S cells when these cells are grown at 37 degrees C. In transfected RMA cells, the kinetics of arrival of TL antigen on the cell surface are similar to those of a classical class I molecule. The kinetics are not altered in TAP-deficient RMA-S cells, demonstrating that surface TL expression in TAP-deficient cells is not due to the stable expression of a few molecules that leak out by a TAP-independent pathway. Soluble TL molecules produced by Drosophila melanogaster cells are highly resistant to thermal denaturation, unlike peptide-free classical class I molecules synthesized by these insect cells. In addition, these soluble TL molecules are devoid of detectable bound peptides. The results demonstrate that the TL antigen is capable of reaching the surface without bound peptide, although acquisition of peptide or some other ligand through a TAP-independent pathway cannot be formally excluded. We speculate that the ability of the TL antigen to reach the cell surface, under conditions in which other class I molecules do not, may be related to a specialized function of the TL molecule in the mucosal immune system, and possibly in the stimulation of intestinal gamma delta T cells.
Unrecognized Pattern of von Willebrand Factor Abnormalities in Hemolytic Uremic Syndrome and Thrombotic Thrombocytopenic Purpura
Authors: MIRIAM GALBUSERA, ARIELA BENIGNI, SIMONA PARIS, PIERO RUGGENENTI, CARLA ZOJA, CHIARA ROSSI, GIUSEPPE REMUZZI
Journal: Journal of the American Society of Nephrology (1999)

Heterogeneous abnormalities in multimeric structure and fragmentation of endothelial-derived von Willebrand factor (vWF) have been reported in hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). This study was conducted to establish whether different patterns of vWF abnormalities were associated with different clinical syndromes. Plasmatic levels of vWF antigen (vWF:Ag), vWF release from endothelial cells (EC) exposed to patient sera, and vWF multimeric pattern were studied during episodes and again in remission in three groups of patients with severe forms of HUS and TTP paradigmatic of the most common clinical patterns of disease presentation: (1) plasma-responsive; (2) plasma-resistant; and (3) frequently relapsing. Plasma vWF:Ag and serum-induced vWF release from EC were increased in the acute phase of either plasma-responsive and plasma-resistant HUS and TTP, but normalized at remission only in plasma-responsive cases. Both indices were persistently normal in the relapsing forms. Enhanced vWF fragmentation as defined by disappearance of high molecular weight and increase in low molecular weight forms was a consistent finding of the acute phases, and always normalized in remission in all three groups. Unusually large vWF multimers were found exclusively in plasma of relapsing forms of HUS and TTP both during and between relapses. Enhanced levels of vWF:Ag and serum capability to induce vWF release in vitro are markers of disease activity and may reflect systemic endothelial injury and consequent activation. Their presence discriminates acute single-episode cases from relapsing forms and, when failing to normalize with plasma therapy, predicts plasma resistance. Enhanced low molecular weight multimers that closely paralleled disease activity suggest a permissive role of fragmented vWF in the formation of microvascular thrombi. Finally, finding of unusually large multimers exclusively in relapsing forms of HUS and TTP even between relapses, when no other clinical signs of disease activity could be detected, suggests that they cannot be the only factor in microvascular thrombosis.
Do emergency tests help in the management of acute medical admissions?
Authors: R T. Jones
Journal: BMJ (1984)

dstress Metabolic ackiosis Hyperpyrexia Hyperglycoeamia R if nmpicin Bright red skin pigmentation Red discoloumtion d plasma and urine Liver damage Ethambutol Nausea Abdominal pain Fever Mental confusion Visual hallucinations Optic neuropathyCompound cough mixtures and cold remedies may contain a variety of opioids, antihistamines, and sympathomimetic and mucolytic agents.The management of opioid and antihistamine overdose is covered elsewhere.The various sympathomimetic agents cause acute behavioural disturbances including visual and auditory hallucinations as well as features of cc and i overactivity.These may require specific treatment in the form of sedation or sympathomimetic blocking agents, or both.Chronic use of these drugs may cause behavioural disorders and hallucinations which remit on withdrawal of the drug.Anticholinergic drugs-Agents such as ipratropium bromide are being used increasingly in the treatment of asthma.When administered by inhalation these have a wide safety margin, but accidental or deliberate self-poisoning with nebuliser fluid may cause pronounced anticholinergic poisoning.There have been a few reports of paradoxical bronchoconstriction after both aerosol or high dose nebulised anticholinergic compounds.The reaction to the aerosol is thought to be an allergic response, but the reaction to the nebulised solution may be due to inhalation of a non-isotonic solution.Corticosteroids are occasionally taken in acute overdose but toxic effects are unlikely.Sodium cromoglycate is of low toxicity and overdose needs no specific
A solution to the tag-assignment problem for neural networks
Authors: Gary W. Strong, Bruce A. Whitehead
Journal: Behavioral and Brain Sciences (1989)

Abstract Purely parallel neural networks can model object recognition in brief displays – the same conditions under which illusory conjunctions (the incorrect combination of features into perceived objects in a stimulus array) have been demonstrated empirically (Treisman 1986; Treisman &amp; Gelade 1980). Correcting errors of illusory conjunction is the “tag-assignment” problem for a purely parallel processor: the problem of assigning a spatial tag to nonspatial features, feature combinations, and objects. This problem must be solved to model human object recognition over a longer time scale. Our model simulates both the parallel processes that may underlie illusory conjunctions and the serial processes that may solve the tag-assignment problem in normal perception. One component of the model extracts pooled features and another provides attentional tags that correct illusory conjunctions. Our approach addresses two questions: (i) How can objects be identified from simultaneously attended features in a parallel, distributed representation? (ii) How can the spatial selectional requirements of such an attentional process be met by a separation of pathways for spatial and nonspatial processing? Our analysis of these questions yields a neurally plausible simulation of tag assignment based on synchronizing feature processing activity in a spatial focus of attention.
Cheap Labor from Poor Nations
Authors: E. FULLER TORREY, ROBERT L. TAYLOR
Journal: American Journal of Psychiatry (1973)

In the authors' opinion, one of the most serious problems facing American psychiatry is the importation of large numbers of foreign medical graduates to staff the country's mental hospitals. This paper reviews the magnitude of the problem, the utilization of these doctors as cheap labor, the quality of care provided, and the effects of the brain drain on the countries of origin. It discusses possible roots of the problem and suggests some solutions.
Neurogenic pruritus: a case of pruritus induced by transverse myelitis
Authors: L.D. Bond, G.C. Keough
Journal: British Journal of Dermatology (2003)

Sir, Pruritus without a primary skin eruption generally indicates an underlying medical disorder.1 Pruritus is a well‐known complaint in some medical illnesses such as cholestasis, uraemia, diabetes mellitus, malignancy, lymphoma, polycythaemia vera and other myeloproliferative disorders. Neurogenic pruritus is rare. We report the first case of pruritus induced by transverse myelitis, an uncommon neurological condition which initially presents with bilateral lower extremity weakness, sensory loss with a distinct dermatomal distribution, and urinary retention.2 A 43‐year‐old black woman initially presented with pain and paraesthesiae in her legs. Three weeks after initial presentation, she complained of terrible pruritus and hyperaesthesia of a well‐demarcated area of her proximal upper extremities, associated with difficulty in urinating. The pruritus and allodynia were so severe that they prevented her from falling asleep at night. Intravenous and oral medications, including steroids, hydroxyzine, doxepin and moisturizers, did not alleviate the symptoms. Oxycodone, however, was an effective analgesic for her pain and pruritus. Our patient's past medical history was unremarkable. She reported no history of any other medical problems including multiple sclerosis or nerve tumours, recent upper respiratory tract infection or recent vaccinations.
Pneumoperitoneum After Hysterectomy
Authors: Lyman B. Spaulding
Journal: JAMA (1979)

PNEUMOPERITONEUM usually presents as a surgical emergency owing to perforation of a hollow viscus. Closure of the perforation in the stomach, duodenum, or colon must be accomplished immediately to halt peritoneal contamination. Often celiotomy fails to disclose a perforation site. In these cases, the origin of air has been ascribed to a small perforated duodenal ulcer, a minute leak from a colon diverticulum, a rupture of an emphysematous bleb, or an insufflation of air via the female genital tract in association with postpartum exercises, douching, and even pelvic examination.<sup>1</sup>Oral-genital sex, normal daily exercises, salpingitis, and prolapsed fallopian tube have also been reported in conjunction with pneumoperitoneum.<sup>2</sup>The following case is unusual, as the pneumoperitoneum occurred one year after hysterectomy. <h3>Report of a Case</h3> A 34-year-old woman, gravida 3, para 3, came to the emergency room complaining of severe abdominal pain that radiated to her left shoulder when
Depression and Glycemic Control in Elderly Ethnically Diverse Patients With Diabetes
Authors: Paula M. Trief, Philip C. Morin, Roberto Izquierdo, Jeanne A. Teresi, Joseph P. Eimicke, Robin Goland, Justin Starren, Steven Shea, Ruth S. Weinstock
Journal: Diabetes Care (2006)

OBJECTIVE—The purpose of the study was to investigate the effect of comorbid depression on glycemic control and on response to a telemedicine case management intervention for elderly, ethnically diverse diabetic patients. RESEARCH DESIGN AND METHODS—Medicare beneficiaries in underserved areas were participants (n = 1,665) in the Informatics for Diabetes Education and Telemedicine (IDEATel) project and randomized to a telemedicine case management intervention or usual care. The data analyzed include baseline demographics (age, sex, race/ethnicity, marital status, insulin use, years of education, years of diabetes, and pack-years smoked) and measures of glycemic control (HbA1c [A1C]), comorbidity, diabetes symptom severity, functional disability and depression, and 1-year (n = 1,578) A1C. The association between depression and glycemic control was analyzed cross-sectionally and prospectively. RESULTS—At baseline, there was a significant correlation between depression and A1C and a trend for depression to predict A1C when other factors were controlled. However, in prospective analyses, depression did not predict change in A1C, either in the control or intervention group. CONCLUSIONS—In this large sample of elderly diabetic patients, a weak relationship between depression and A1C was found, but depression did not prospectively predict change in glycemic control. Thus, there is no evidence that depression should be used to exclude patients from interventions. Also, we should evaluate the impact of depression on outcomes other than glycemic control.
Treatment of young children with localized medulloblastoma by chemotherapy alone: Results of the prospective, multicenter trial HIT 2000 confirming the prognostic impact of histology
Authors: A. O. von Bueren, K. von Hoff, T. Pietsch, N. U. Gerber, M. Warmuth-Metz, F. Deinlein, I. Zwiener, A. Faldum, G. Fleischhack, M. Benesch, J. Krauss, J. Kuehl, R. D. Kortmann, S. Rutkowski
Journal: Neuro-Oncology (2011)

This study was designed to confirm the previously observed favorable survival rates and prognostic factors in young children with nonmetastatic medulloblastoma (MB) treated with postoperative chemotherapy alone. Patients who received a diagnosis during the period January 2001 through December 2005 and who were aged <4 years received 3 cycles of postoperative systemic multiagent chemotherapy and intraventricular methotrexate. In cases of complete remission, treatment was terminated after 2 additional cycles of chemotherapy. Otherwise, secondary surgery, radiotherapy, and consolidation chemotherapy were recommended. At a median follow-up of 4.5 years, the 5-year event-free survival (EFS) and overall survival (OS) rates (± standard error) for 45 patients (median age, 2.5 years) were 57% ± 8% and 80% ± 6%, respectively. Nineteen patients with desmoplastic/nodular MB variants had better 5-year EFS and OS rates (90% ± 7% and 100% ± 0%, respectively) than did 23 patients with classic MB (30% ± 11% and 68% ± 10%, respectively; P < .001 for EFS; P = .008 for OS). Five-year EFS and OS rates for 3 children with anaplastic MB were 33% ± 27%. Desmoplastic/nodular histology was an independent prognostic factor for EFS. Twenty-nine of 30 patients without postoperative residual tumor remained in continuous complete remission. Our results confirm that histology of MB variants is a strong prognostic factor in this age group. Sustained tumor control can be achieved by this chemotherapy regimen in young children with desmoplastic/nodular MB variants. For children with non-desmoplastic/nonnodular MB variants, for which predominantly local relapses lead to less favorable survival rates, local radiotherapy has been introduced after chemotherapy since 2006.
Homocysteine lowering by B vitamins and the secondary prevention of deep vein thrombosis and pulmonary embolism: a randomized, placebo-controlled, double-blind trial
Authors: Martin den Heijer, Huub P. J. Willems, Henk J. Blom, Wim B. J. Gerrits, Marco Cattaneo, Sabine Eichinger, Frits R. Rosendaal, Gerard M. J. Bos
Journal: Blood (2006)
Premature Atherosclerosis Associated With Monogenic Insulin Resistance
Authors: Robert A. Hegele
Journal: Circulation (2001)

Background —The common insulin resistance syndrome, with obesity, dyslipidemia, hyperglycemia, and hypertension, is associated with increased risk of atherosclerosis. Early atherosclerosis in rare monogenic forms of insulin resistance, however, has not been extensively documented. Cardiovascular end points were thus evaluated in subjects with Dunnigan-type familial partial lipodystrophy (FPLD) due to mutations at LMNA codon 482. Methods and Results —FPLD subjects ≥35 years old were stratified by genotype for either the LMNA R482Q or R482W mutation. Twenty-three subjects were heterozygous mutation carriers, and 17 were R482/R482 homozygous family control subjects. All LMNA mutation carriers had FPLD with insulin resistance. In addition, LMNA mutation carriers had significantly more type 2 diabetes, hypertension, and dyslipidemia than normal family control subjects. Eight LMNA mutation carriers had coronary heart disease (CHD), compared with 1 normal control subject (OR 5.9, 95% CI 1.2 to 30.2). Six LMNA mutation carriers had CHD end points before age 55 years, and 4 of these, all women, had been hospitalized for CABG surgery between the ages of 35 and 54 years. Conclusions —Rare LMNA mutations that underlie FPLD with insulin resistance and hyperinsulinemia are also associated with early CHD, notably in women. This suggests that abnormalities of the nuclear envelope can result in a phenotype that recapitulates most of the important attributes of the common insulin resistance syndrome, including accelerated cardiovascular disease. FPLD thus appears to be an appropriate human monogenic model for the common insulin resistance syndrome.
Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression
Authors: Antonio F. Santidrian, Akemi Matsuno-Yagi, Melissa Ritland, Byoung B. Seo, Sarah E. LeBoeuf, Laurie J. Gay, Takao Yagi, Brunhilde Felding-Habermann
Journal: Journal of Clinical Investigation (2013)

Despite advances in clinical therapy, metastasis remains the leading cause of death in breast cancer patients. Mutations in mitochondrial DNA, including those affecting complex I and oxidative phosphorylation, are found in breast tumors and could facilitate metastasis. This study identifies mitochondrial complex I as critical for defining an aggressive phenotype in breast cancer cells. Specific enhancement of mitochondrial complex I activity inhibited tumor growth and metastasis through regulation of the tumor cell NAD+/NADH redox balance, mTORC1 activity, and autophagy. Conversely, nonlethal reduction of NAD+ levels by interfering with nicotinamide phosphoribosyltransferase expression rendered tumor cells more aggressive and increased metastasis. The results translate into a new therapeutic strategy: enhancement of the NAD+/NADH balance through treatment with NAD+ precursors inhibited metastasis in xenograft models, increased animal survival, and strongly interfered with oncogene-driven breast cancer progression in the MMTV-PyMT mouse model. Thus, aberration in mitochondrial complex I NADH dehydrogenase activity can profoundly enhance the aggressiveness of human breast cancer cells, while therapeutic normalization of the NAD+/NADH balance can inhibit metastasis and prevent disease progression.