tbuckley/cabot-search huggingface dataset:
Requests for Euthanasia/Physician-Assisted Suicide on the Basis of Mental Suffering
Authors: Reginald Deschepper, Wim Distelmans, Johan Bilsen
Journal: JAMA Psychiatry (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Psychiatry HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Psychiatry journal
P146 Cognitive loss in stable non-hypoxaemic patients with moderate chronic obstructive pulmonary disease (COPD)
Authors: J. W. Dodd, M. Van Den Broek, D. Shrikrishna, N. S. Hopkinson, P. W. Jones
Journal: Thorax (2010)

<h3>Background</h3> Cognitive impairment has been demonstrated in up to 77% of patients with COPD and hypoxaemia,1 however it is unclear if this impairment is due to cognitive loss or was present before disease onset. In addition the evidence for impairment is less clear in patients with mild disease without hypoxaemia. <h3>Methods</h3> Detailed neuropsychological testing of 44 non-exacerbating, non-hypoxaemic patients with COPD. Other physiological, and health status data were collected. Standardised neuropsychological scores were generated from age, gender and education related normative population samples. Cognition is considered moderately or severely impaired if a standardised score lie ≥1 or 2 standard deviations (SD) respectively from the normative population mean. The use of population normal range is valid given that the group have a normal estimated Full Scale IQ. Estimates of an individuals predicted cognitive performance in attention and processing speed are derived from their adult reading ability, which is stable over time and largely resistant to cognitive decline. Individuals performing below their predicted performance are judged to have suffered cognitive loss. This methodology has advantages over control group comparisons since the individual acts their own control allowing for calculations of what is ‘normal’ for that individual. <h3>Results</h3> 44 patients, 52% Females, Mean Age 68±8 years, FEV<sub>1pp</sub> 49±20%, PaO<sub>2</sub> 10±2 kPa, Pack Years. smoking 57 (41–69), 6MWD 387m (359–458), BMI 26 (23–29), SGRQ 52±19, Hospital Anxiety and Depression Scale 12 (6–19), Fatigue (FACIT-F) 18 (9–25), Estimated Full Scale IQ 96. In terms of cognitive loss, 25% had significant loss in processing speed and 30% in working memory. The proportion of patients whose cognitive scores were 1 and 2 SD9s below predicted are tabulated. <h3>Conclusion</h3> Up to one third of stable non-hypoxaemic patients with COPD demonstrate significant cognitive loss. A significant proportion have severe impairment of memory and executive function. The cause and implications of this cognitive loss should be the focus of future research.
1005-82 Myocardial and Coronary Vascular Protection After Coronary Occlusion and Reperfusion by Selective Sinoatrial Node Inhibition
Authors: Roger Williams, Wilmer W. Nichols, Liying Chen, Michael S. Stalvey, Linda V. Thompson, Tiffany D. Boyd, Jawahar L. Mehta, Carl J. Pepine
Journal: Journal of the American College of Cardiology (1995)
Phase II Study of Afatinib, an Irreversible ErbB Family Blocker, in EGFR FISH-Positive Non–Small-Cell Lung Cancer
Authors: Federico Cappuzzo, Giovanna Finocchiaro, Francesco Grossi, Paolo Bidoli, Adolfo Favaretto, Antonio Marchetti, Maria Luisa Valente, Agnieszka Cseh, Laura Clementi, Dan Massey, Armando Santoro
Journal: Journal of Thoracic Oncology (2014)
Paramethasone in the Treatment of Systemic Lupus Erythematosus
Authors: Edmund L. Dubois
Journal: JAMA (1963)

A new synthetic corticosteroid was found to be effective without causing sodium retention, even when given to patients with advanced renal disease and hypertension. A dose of 2 mg was equal in potency to 5 mg of prednisone and 4 mg of methylprednisolone. Fifty patients were given paramethasone orally as a single daily dose, usually immediately before breakfast. Forty-five or 90% were able to control their illness by this method. The effect of steroids on the renal lesion was analyzed and, except for benefit in acute toxic lupus nephropathy, the results were disappointing. Long-term antimalarial therapy frequently produced mottled bluish-black hyperpigmentation on the shins which may be confused with ecchymoses associated with steroid therapy. One patient developed muscle weakness due to vacuolar degeneration which clinically resembled steroid-induced myopathy.
Abdomino&amp;ndash;Perineal Repair of Recurrent and Complex Bladder Neck&amp;ndash;Prostatic Urethra Contractures
Authors: Ch. Theodorou, Ch. Katsifotis, P. Stournaras, G. Moutzouris, A. Katsoulis, D. Floratos
Journal: European Urology (2000)
Induction of Adrenal Suppression by Megestrol Acetate in Patients with AIDS
Authors: M C Leinung, R Liporace, C H Miller
Journal: Annals of Internal Medicine (1995)

Objective: To investigate the development of secondary adrenal suppression in a patient with the acquired immunodeficiency syndrome (AIDS) who was receiving megestrol acetate. Design and Patients: Case report of one patient abruptly withdrawn from long-term therapy with megestrol acetate; prospective study of four patients with AIDS who were starting therapy with megestrol acetate for cachexia. Setting: Outpatient clinic of a university hospital. Interventions: Study patients received megestrol acetate, 80 mg three times daily. Measurements: Study patients had cosyntropin-stimulation testing and oral glucose tolerance testing before and after starting therapy with megestrol acetate. Results: The patient described in the case report developed symptoms of adrenal insufficiency after withdrawal of megestrol acetate after 4 years of treatment. His basal cortisol and adrenocorticotropic hormone (ACTH) levels were low. He showed an abnormally diminished response to a short cosyntropin-stimulation test but did respond to a 3-day cosyntropin-stimulation test. The morning cortisol levels of the study patients decreased significantly (from 11.0 ±1.8 µg/dL to 1.5 ±0.9 µg/dL; P < 0.01), and the ACTH levels of these patients decreased to below normal (from 16.6 ±5.5 pg/mL to 6.3 ±3.3 pg/mL; P = 0.02) during treatment with megestrol acetate. Cortisol levels after administration of cosyntropin decreased significantly (from 27.3 ±3.3 pg/mL to 9.3 ±6.3 pg/mL; P = 0.01) during treatment with megestrol acetate. The results of oral glucose tolerance testing in two patients were consistent with the development of insulin resistance, and daily insulin requirements increased 10-fold in a patient who had preexisting diabetes. Conclusions: Prolonged administration of megestrol acetate can induce clinically significant secondary adrenal suppression, and abrupt withdrawal of megestrol acetate after prolonged administration can cause adrenal insufficiency.
SIXTH NATIONAL CONGRESS OF THE JAPAN MEDICAL ASSOCIATION
Authors: Henry Edmund Meleney
Journal: JAMA (1922)

<h3>To the Editor:</h3> —A program consisting of more than 1,600 papers from an attendance of 3,000 delegates is the remarkable record of the Sixth National Congress of the Japan Medical Association, which was held at Kyoto, April 1 to 5, 1922. This record, which, allowing for the presentation of more than one paper by some delegates, represents the participation of nearly 50 per cent. of the delegates of the congress in its proceedings, illustrates the tremendous activity of the Japanese in the medical sciences. Furthermore, the total number of papers presented is not swelled by the usual number which at most medical congresses are "read by title," for practically every one of the sixteen hundred papers at this congress was given its place on the program, and was delivered within its allotted time of ten minutes by its author. The first and fifth days of the congress were occupied with
Role for α3 integrin in EMT and pulmonary fibrosis
Authors: Zea Borok
Journal: Journal of Clinical Investigation (2008)

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive (myo)fibroblast accumulation and collagen deposition. One possible source of (myo)fibroblasts is epithelial cells that undergo epithelial-mesenchymal transition (EMT), a process frequently mediated by TGF-beta. In this issue of the JCI, Kim et al. report that epithelial cell-specific deletion of alpha3 integrin prevents EMT in mice, thereby protecting against bleomycin-induced fibrosis (see the related article beginning on page 213). The authors propose a novel mechanism linking TGF-beta and beta-catenin signaling in EMT through integrin-dependent association of tyrosine-phosphorylated beta-catenin and pSmad2 and suggest targeted disruption of this interaction as a potential therapeutic approach.
Abstract 5156: Obstructive Sleep Apnea, Obesity, and Coronary Artery Calcification in Middle-Aged Men
Authors: Seong Hwan Kim, Goo-Yeong Cho, Koung-Mi Rhee, Seung Yong Shin, Young Hyun Kim, Hong Euy Lim, Sang Yup Lim, Jeong Cheon Ahn, Woo Hyuk Song, Chol Shin
Journal: Circulation (2008)

Obesity is associated with coronary artery calcification (CAC), and obstructive sleep apnea (OSA) is highly prevalent in obese subjects. Although OSA is known to be an independent risk factor for t...
THROMBOSIS OF RENAL ARTERY SIMULATING CORONARY THROMBOSIS
Authors: Joseph B. Wolffe
Journal: JAMA (1942)

We wish to report this case for the following reasons: The patient presented a diagnostic problem on admission. Few cases of thrombosis of the renal artery have been reported in the literature. The clinical manifestations of renal artery thrombosis are as yet not well recognized and therefore not thought of. Early recognition of the syndrome and proper therapy may prevent extensive renal pathologic changes. While many cases of renal infarction due to emboli<sup>1</sup>and thrombosis of the small branches of the renal artery secondary to nephritis,<sup>2</sup>trauma<sup>3</sup>and periarteritis<sup>4</sup>have been reported, we found in the literature only an incomplete description of the syndrome, reported by one of us,<sup>5</sup>and<sup>3</sup>cases of fatal thrombosis of the renal artery<sup>6</sup>associated with general vascular disease. There is no complete description, as far as we can find, in any textbook or periodical of the clinical manifestations
Pregnancy Advisory Services
Authors: B. Brumby
Journal: BMJ (1971)

in sarcoidosis and the normal levels.A fur- *ther study of this interesting condition is called for especially in view of the evidence (reviewed by Drs.Willoughby and Mitchell) that Crohn's disease and ulcerative colitis may sometimes share so many features that the distinction between them has become blurred.-Weare, etc.,
Clinical Associations of 11-Hydroxycorticosteroid Suppression and Non-suppression in Severe Depressive Illnesses
Authors: B. J. Carroll, B. Davies
Journal: BMJ (1970)

Fifty patients with severe depression were separated into two groups by the responses of their plasma 11-hydroxycorticosteriod levels to a midnight dose of 2 mg. of dexamethasone. Clinical and questionary comparisons were made between the two groups of patients, who were similar as regards age, sex, and length of symptoms before admission to hospital. No differences were found between the groups of severely ill patients as regards the severity of their depression and anxiety assessed by questionary. Nevertheless, agitation was significantly greater in the patients whose corticosteroid levels were not suppressed by dexamethasone and adverse childhood experiences in those whose levels were suppressed.
Conservative Management of the Zollinger-Ellison Syndrome
Authors: Thomas T. Long
Journal: JAMA (1980)

Techniques for evaluating ectopic gastrin production associated with the Zollinger-Ellison syndrome are described. The site of gastrin production in this example was a mucinous cystadenoma of the ovary confirmed by immunoperoxidase localization of gastrin within the ovarian tumor cells and by radioimmunoassay of the tumor's gastrin content. These methods, localizing the source of ectopic gastrin, permitted conservative management of the ulcer diathesis with surgical resection of the mucinous cystadenoma. After oophorectomy the patient's serum gastrin level returned to normal, and the ulcer diathesis ceased.
Hypoxia inhibits gene expression of voltage-gated K+ channel alpha subunits in pulmonary artery smooth muscle cells.
Authors: J Wang, M Juhaszova, L J Rubin, X J Yuan
Journal: Journal of Clinical Investigation (1997)

Activity of voltage-gated K+ channels (KV) in pulmonary arterial smooth muscle cells (PASMC) is pivotal in controlling membrane potential, cytoplasmic free Ca2+ concentration ([Ca2+]cyt, and pulmonary vasomotor tone. Acute hypoxia selectively inhibits KV channels, depolarizes PASMC, raises [Ca2+]cyt, and causes pulmonary vasoconstriction and vascular remodeling. Prolonged hypoxia (24-60 h) decreased significantly the mRNA levels of KV channel alpha subunits, KV1.2 and KV1.5. Consistently, the protein levels of KV1.2 and KV1.5 were also decreased significantly by hypoxia (48-72 h). Nevertheless, hypoxia affected negligibly the mRNA levels of KV channel beta subunits (KVbeta1, KVbeta2, and KVbeta3). The native K+ channels are composed of pore-forming alpha and auxiliary beta subunits. Assembly of KV beta subunits with alpha subunits confers rapid inactivation on the slowly or non-inactivating delayed rectifier KV channels. KV beta subunits also function as an open-channel blocker of KV channels. Thus, the diminished transcription and expression of KV alpha subunits may reduce the number of KV channels and decrease KC currents. Unchanged transcription of KV beta subunits may increase the fraction of the KV channel alpha subunits that are associated with beta subunits and further reduce the total KV currents. These data demonstrate a novel mechanism by which chronic hypoxia may cause pulmonary vasoconstriction and hypertension.
Steroid Inhibition of Cytokine-Mediated Vasodilation After Warm Heart Surgery
Authors: Kevin H.T. Teoh, Christine A. Bradley, Jack Gauldie, Heather Burrows
Journal: Circulation (1995)

Background Peripheral vasodilation, a potentially adverse effect of warm heart surgery, may be mediated by the perioperative release of cytokines. Corticosteroids may abolish cytokine production and vasodilation. We investigated cytokine production and its inhibition by steroids in patients undergoing elective coronary bypass surgery. Methods and Results Twenty-five patients undergoing coronary bypass surgery with normothermic cardiopulmonary bypass received either preoperative steroid (Solumedrol 250 mg IV, n=16) or no steroid (n=9, control group). Blood samples were obtained serially for 24 hours and assayed for interleukin-6 (IL-6), tumor necrosis factor (TNF), and interleukin-8 (IL-8). In the control patients, the IL-6, TNF, and IL-8 levels were elevated postoperatively and peaked between 3 and 6 hours after surgery (IL-6, 1330±295 [mean±SEM] pg/mL; TNF, 18.4±9.8 pg/mL; and IL-8, 150±51 pg/mL). Cytokine release was abolished in patients receiving preoperative corticosteroid (IL-6, 75±38 pg/mL; TNF, 2.6±0.5 pg/mL; and IL-8, 33±6.7 pg/mL; P &lt;.05). Patients receiving steroid premedication had higher arterial pressure, lower cardiac index, and higher systemic vascular resistance, indicating less vasodilation. Conclusions Our findings demonstrate that cytokine production occurs after normothermic cardiopulmonary bypass. Preoperative administration of steroids abolishes cytokine release and vasodilation.
Quantitative assessment of nanoparticle surface hydrophobicity and its influence on pulmonary biocompatibility
Authors: Marie-Christine Jones, Stuart A. Jones, Yanira Riffo-Vasquez, Domenico Spina, Ewelina Hoffman, Anna Morgan, Aateka Patel, Clive Page, Ben Forbes, Lea Ann Dailey
Journal: Journal of Controlled Release (2014)
Treatment of Men with Paraphilia
Authors: John M.W. Bradford
Journal: New England Journal of Medicine (1998)

People convicted of sexually abusing children are usually incarcerated, a strategy that has not been successful but for which the costs have been staggering ($2,055,528,000 in the United States in 19901). In this issue of the Journal, Rösler and Witztum describe the results of a study of the treatment of men with pedophilia and other paraphilias with triptorelin, an agonist analogue of gonadotropin-releasing hormone.2 They found that the drug reduced abnormal sexual thoughts and behaviors substantially, presumably as a result of its ability to reduce the secretion of gonadotropin and, therefore, of testosterone. Unfortunately, this was not a randomized, . . .
Basal and glucose- and arginine-stimulated serum concentrations of insulin, C-peptide, and glucagon in hyperthyroid patients
Authors: Elio Roti, Lewis E. Braverman, Giuseppe Robuschi, Mario Salvi, Eliana Gardini, Lorenzo d'Amato, Dante Maestri, Mara Montermini, Elisabetta Borciani, Antonio Pezzarossa, Paolo Chiodera, Attilio Manfredi, Ronald A. Arky, Angelo Gnudi
Journal: Metabolism (1986)
[730] PROSPECTIVE COMPARISON BETWEEN TRANSIENT ELASTOGRAPHY (FIBROSCAN), APRI AND FORNS TEST FOR ASSESSING LIVER FIBROSIS IN PATIENTS WITH HISTOLOGICAL FEATURES OF NAFLD
Authors: J.C. Marin, J. De La Cruz, I. Fernandez, A.M. Martin, R. Munoz, F. Colina, J.A. Soils
Journal: Journal of Hepatology (2007)
ADAMTS13 gene deletion aggravates ischemic brain damage: a possible neuroprotective role of ADAMTS13 by ameliorating postischemic hypoperfusion
Authors: Masayuki Fujioka, Kazuhide Hayakawa, Kenichi Mishima, Ai Kunizawa, Keiichi Irie, Sei Higuchi, Takafumi Nakano, Carl Muroi, Hidetada Fukushima, Mitsuhiko Sugimoto, Fumiaki Banno, Koichi Kokame, Toshiyuki Miyata, Michihiro Fujiwara, Kazuo Okuchi, Kenji Nishio
Journal: Blood (2009)
Localization and cellular source of the extracellular matrix protein tenascin in normal and fibrotic rat liver
Authors: Peter van Eyken, Albert Geerts, Pieter de Bleser, Jean-Marc Lazou, Raf Vrijsen, Raf Sciot, Eddie Wisse, Valeer J. Desmet
Journal: Hepatology (1992)

The distribution and the cellular source of the novel extracellular matrix glycoprotein tenascin were studied in normal and fibrotic rat liver. Cryostat sections of normal rat livers, livers of rats treated with intraperitoneal injections of CCl4 and 4-day-old and 8-day-old primary fat-storing cell cultures were stained for tenascin and desmin using an immunoperoxidase procedure or a double-label immunofluorescence technique. Fat-storing cell cultures were metabolically labeled with H-proline. Radiolabeled proteins were immunoprecipitated from the supernatant with antitenascin antiserum and subjected to polyacrylamide gel electrophoresis. In normal rat livers, tenascin was detected discontinuously along the sinusoids, whereas portal tracts were devoid of staining. In fibrotic rat livers, tenascin was preferentially expressed in areas of cell damage, in slender septa or at connective tissue–parenchymal interfaces. The middle region of broad septa was negative. Desmin-positive fat-storing cells accumulated in areas strongly immunoreactive for tenascin, and double-label immunofluorescence showed cells positive for both tenascin and desmin. In fat-storing cell cultures, both intracellular positivity for tenascin and staining of extracellular fibers were seen. Gel electrophoresis of immunoprecipitated proteins revealed two major and three minor bands with molecular weights consistent with tenascin. We conclude that tenascin is a component of the extracellular matrix of both normal and fibrotic rat livers. The strong expression of tenascin in areas of cell damage, in “early” septa or at septal-parenchymal interfaces, in contrast to its absence from the middle region of mature septa, suggests a role in early matrix organization. Fat-storing cells synthesize and secrete tenascin. (HEPATOLOGY 1992;15:909–916).
EVI1 induces myelodysplastic syndrome in mice
Authors: Silvia Buonamici, Donglan Li, Yiqing Chi, Rui Zhao, Xuerong Wang, Larry Brace, Hongyu Ni, Yogen Saunthararajah, Giuseppina Nucifora
Journal: Journal of Clinical Investigation (2004)

Myelodysplasia is a hematological disease in which genomic abnormalities accumulate in a hematopoietic stem cell leading to severe pancytopenia, multilineage differentiation impairment, and bone marrow (BM) apoptosis. Mortality in the disease results from pancytopenia or transformation to acute myeloid leukemia. There are frequent cytogenetic abnormalities, including deletions of chromosomes 5, 7, or both. Recurring chromosomal translocations in myelodysplasia are rare, but the most frequent are the t(3;3)(q21;q26) and the inv(3)(q21q26), which lead to the inappropriate activation of the EVI1 gene located at 3q26. To better understand the role of EVI1 in this disease, we have generated a murine model of EVI1-positive myelodysplasia by BM infection and transplantation. We find that EVI1 induces a fatal disease of several stages that is characterized by severe pancytopenia. The disease does not progress to acute myeloid leukemia. Comparison of in vitro and in vivo results suggests that EVI1 acts at two levels. The immediate effects of EVI1 are hyperproliferation of BM cells and downregulation of EpoR and c-Mpl, which are important for terminal erythroid differentiation and platelet formation. These defects are not fatal, and the mice survive for about 10 months with compensated hematopoiesis. Over this time, compensation fails, and the mice succumb to fatal peripheral cytopenia.
Poliomyelitis Due to West Nile Virus
Authors: Jonathan D. Glass, Owen Samuels, Mark M. Rich
Journal: New England Journal of Medicine (2002)

To the Editor: Muscle weakness is a common finding and an important predictor of death in patients with West Nile virus encephalitis. 1,2 Yet this important sign does not have a defined pathological basis.In monkeys, horses, and birds, West Nile virus causes poliomyelitis. [3]4][5] Our clinical and electrodiagnostic findings in three consecutive patients withThe New England Journal of Medicine Downloaded from nejm.org