tbuckley/cabot-search huggingface dataset:
Clozapine-Associated Reduction in Arrest Rates of Psychotic Patients With Criminal Histories
Authors: W Frankle, D Shera, H Berger-Hershkowitz, A Eden Evins, C Connolly, D Goff, D Henderson
Journal: American Journal of Psychiatry (2001)

OBJECTIVE: The authors examined the relationship between treatment with clozapine and rates of arrest of psychotic outpatients with criminal histories. METHOD: Patients who had been given a DSM-IV psychotic diagnosis were selected from an urban outpatient clinic database. Background checks performed on 360 patients identified 165 (45.8%) with positive criminal histories in Massachusetts. The authors reviewed the charts of these patients to determine several variables, including whether and when they had received clozapine. A Poisson regression model was used to regress arrest rates against the variables of age, sex, onset of illness, birth cohort, and clozapine treatment. Risk ratios (i.e., percent change in arrest rates) were then calculated by computing the exponential of the Poisson regression coefficients. RESULTS: The 165 patients included in the analysis had a total of 1,126 arrests. The mean number of arrests was 6.8. Differences were found between the 65 patients who received clozapine and the 100 patients who did not in number of arrests, sex, and onset of illness. The regression revealed significantly higher arrest rate estimates associated with more recent birth cohort (4.8%) and with onset of illness (64.6%) and lower arrest rate estimates associated with higher levels of education (11.6%), receiving clozapine (32.6%), and receiving clozapine during specific periods of time (68.9%). CONCLUSIONS: Clozapine's effect on arrest rates in this group of patients is large enough to warrant further investigation. The data indicate that clozapine may reduce recidivism in subjects with criminal histories who are in need of antipsychotic medication.
Mitochondrial glutathione content determines the rate of liver regeneration after partial hepatectomy in eu- and hypothyroid rats
Authors: Ignazio Grattagliano, Bernhard H Lauterburg, Piero Portincasa, Maria Lucia Caruso, Gianluigi Vendemiale, Anna Maria Valentini, Vincenzo O Palmieri, Giuseppe Palasciano
Journal: Journal of Hepatology (2003)
Inactivating mutations in MFSD2A, required for omega-3 fatty acid transport in brain, cause a lethal microcephaly syndrome
Authors: Alicia Guemez-Gamboa, Long N Nguyen, Hongbo Yang, Maha S Zaki, Majdi Kara, Tawfeg Ben-Omran, Naiara Akizu, Rasim Ozgur Rosti, Basak Rosti, Eric Scott, Jana Schroth, Brett Copeland, Keith K Vaux, Amaury Cazenave-Gassiot, Debra Q Y Quek, Bernice H Wong, Bryan C Tan, Markus R Wenk, Murat Gunel, Stacey Gabriel, Neil C Chi, David L Silver, Joseph G Gleeson
Journal: Nature Genetics (2015)
Panhematin provides a therapeutic benefit in experimental pancreatitis
Authors: A. Habtezion, R. Kwan, E. Akhtar, S. P. Wanaski, S. D. Collins, R. J. Wong, D. K. Stevenson, E. C. Butcher, M. B. Omary
Journal: Gut (2010)

<h3>Background and aim</h3> Acute pancreatitis (AP) can result in pancreatic necrosis and inflammation, with subsequent multi-organ failure. AP is associated with increased neutrophil recruitment and a rise in pro-inflammatory cytokines such as TNFα. Pretreatment with haemin, results in recruitment of haem-oxygenase-1 (HO-1)<sup>+</sup> macrophages and protects against experimental pancreatitis. It is not clear whether modulation of HO-1 after onset of disease has a protective role. In this study, we tested the utility of Panhematin, a water-soluble haemin formulation, in activating and inducing pancreatic HO-1, and as a therapeutic agent in treating mouse acute pancreatitis. <h3>Methods</h3> We defined the distribution of radiolabelled haemin, then used in vivo HO-1–luciferase bioluminescence imaging and the CO-release assay to test Panhematin-induced upregulation of HO-1 transcription and activity, respectively. Using two well-defined AP murine models, we tested the therapeutic benefit of Panhematin, and quantified cytokine release using a luminex assay. <h3>Results</h3> Intravenously administered Panhematin induces rapid recruitment of HO-1<sup>+</sup> cells to the pancreas within 2 h and de novo splenic HO-1 transcription by 12 h. Despite high baseline spleen HO-1 activity, the pancreas is particularly responsive to Panhematin-mediated HO-1 induction. Panhematin-treated mice, at various time points after AP induction had significant reduction in mortality, pancreatic injury, together with upregulation of HO-1 and downregulation of pro-inflammatory cytokines and CXCL1, a potent neutrophil chemoattractant. <h3>Conclusions</h3> Despite AP-associated mortality and morbidity, no effective treatment other than supportive care exists. We demonstrate that Panhematin leads to: (i) rapid induction and activation of pancreatic HO-1 with recruitment of HO-1<sup>+</sup> cells to the pancreas, (ii) amelioration of AP even when given late during the course of disease, and (iii) a decrease in leucocyte infiltration and pro-inflammatory cytokines including CXCL1. The utility of Panhematin at modest doses as a therapeutic in experimental pancreatitis, coupled with its current use and safety in humans, raises the potential of its applicability to human pancreatitis.
Cell and Molecular Biology of Simian Virus 40: Implications for Human Infections and Disease
Authors: J. S. Butel, J. A. Lednicky
Journal: JNCI Journal of the National Cancer Institute (1999)

Simian virus 40 (SV40), a polyomavirus of rhesus macaque origin, was discovered in 1960 as a contaminant of polio vaccines that were distributed to millions of people from 1955 through early 1963. SV40 is a potent DNA tumor virus that induces tumors in rodents and transforms many types of cells in culture, including those of human origin. This virus has been a favored laboratory model for mechanistic studies of molecular processes in eukaryotic cells and of cellular transformation. The viral replication protein, named large T antigen (T-ag), is also the viral oncoprotein. There is a single serotype of SV40, but multiple strains of virus exist that are distinguishable by nucleotide differences in the regulatory region of the viral genome and in the part of the T-ag gene that encodes the protein's carboxyl terminus. Natural infections in monkeys by SV40 are usually benign but may become pathogenic in immunocompromised animals, and multiple tissues can be infected. SV40 can replicate in certain types of simian and human cells. SV40-neutralizing antibodies have been detected in individuals not exposed to contaminated polio vaccines. SV40 DNA has been identified in some normal human tissues, and there are accumulating reports of detection of SV40 DNA and/or T-ag in a variety of human tumors. This review presents aspects of replication and cell transformation by SV40 and considers their implications for human infections and disease pathogenesis by the virus. Critical assessment of virologic and epidemiologic data suggests a probable causative role for SV40 in certain human cancers, but additional studies are necessary to prove etiology.
Insulin-like growth factor receptor 1 (IGF1R) expression and survival in surgically resected non-small-cell lung cancer (NSCLC) patients
Authors: F. Cappuzzo, G. Tallini, G. Finocchiaro, R.S. Wilson, C. Ligorio, L. Giordano, L. Toschi, M. Incarbone, R. Cavina, L. Terracciano, M. Roncalli, M. Alloisio, M. Varella-Garcia, W.A. Franklin, A. Santoro
Journal: Annals of Oncology (2009)
Thymocytes may persist and differentiate without any input from bone marrow progenitors
Authors: Laetitia Peaudecerf, Sara Lemos, Alessia Galgano, Gerald Krenn, Florence Vasseur, James P. Di Santo, Sophie Ezine, Benedita Rocha
Journal: The Journal of Experimental Medicine (2012)

Thymus transplants can correct deficiencies of the thymus epithelium caused by the complete DiGeorge syndrome or FOXN1 mutations. However, thymus transplants were never used to correct T cell–intrinsic deficiencies because it is generally believed that thymocytes have short intrinsic lifespans. This notion is based on thymus transplantation experiments where it was shown that thymus-resident cells were rapidly replaced by progenitors originating in the bone marrow. In contrast, here we show that neonatal thymi transplanted into interleukin 7 receptor–deficient hosts harbor populations with extensive capacity to self-renew, and maintain continuous thymocyte generation and export. These thymus transplants reconstitute the full diversity of peripheral T cell repertoires one month after surgery, which is the earliest time point studied. Moreover, transplantation experiments performed across major histocompatibility barriers show that allogeneic transplanted thymi are not rejected, and allogeneic cells do not induce graft-versus-host disease; transplants induced partial or total protection to infection. These results challenge the current dogma that thymocytes cannot self-renew, and indicate a potential use of neonatal thymus transplants to correct T cell–intrinsic deficiencies. Finally, as found with mature T cells, they show that thymocyte survival is determined by the competition between incoming progenitors and resident cells.
Reflex regulation of sympathetic activity in the spontaneously hypertensive rat.
Authors: J H Coote, Y Sato
Journal: Circulation Research (1977)

The influence that the pressure-sensitive receptors in the cardiovascular system have on renal nerve activity and on heart rate was compared in normotensive rats (NTR) and spontaneously hypertensive rats (SHR). The cardiovascular receptors were stimulated by raising the blood pressure (BP) with intravenous phenylephrine. The duration of silence in the record of renal sympathetic nerve activity produced by a number of different rises in BP was measured. We found that the pressure that was just able to produce a silence in the nerve activity (threshold pressure) was higher in the SHR (170 mm Hg) than in the NTR (130 mm Hg). Also, comparable rises in BP above the threshold pressure in the SHR and NTR were less effective in the SHR in producing a complete inhibition of sympathetic nerve activity as judged by the short duration of inhibition. In contrast, we found that the changes in heart rate produced by rises in BP above threshold pressure were similar in NTR and SHR although the threshold pressure was somewhat higher in the latter. It was, therefore, concluded that the cardiovascular pressure receptors, apart from being reset to operate at a higher pressure level in the SHR, are less able to inhibit ongoing sympathetic activity than in the NTR. It is suggested that this is most likely due to a high sympathetic activity in the SHR.
THE STABILITY OF VARIOLA VIRUS PROPAGATED IN EMBRYONATED EGGS
Authors: John B. Nelson
Journal: The Journal of Experimental Medicine (1943)

After 24 transfers in embryonated eggs a strain of variola virus (Chinese) was established in the testis of the rabbit and maintained for 11 passages at intervals of 7 days. Residence in the rabbit testis was not accompanied by any significant alteration in the species identity of the virus. A second strain of variola virus (Minnesota) was transferred 180 times in embryonated eggs with no apparent change in its behavior. Subsequent attempts, however, to maintain this strain in the rabbit by serial testicular passage were unsuccessful. These observations are discussed in relation to the so called transformation of variola to vaccinia virus by animal passage.
De-novo mutations of the sodium channel gene SCN1A in alleged vaccine encephalopathy: a retrospective study
Authors: Samuel F Berkovic, Louise Harkin, Jacinta M McMahon, James T Pelekanos, Sameer M Zuberi, Elaine C Wirrell, Deepak S Gill, Xenia Iona, John C Mulley, Ingrid E Scheffer
Journal: The Lancet Neurology (2006)
Patients' characteristics associated with unsuccessful sputum induction in asthma
Authors: Hirofumi Matsuoka, Akio Niimi, Hisako Matsumoto, Tetsuya Ueda, Masaya Takemura, Masafumi Yamaguchi, Makiko Jinnai, Liang Chang, Kojiro Otsuka, Tsuyoshi Oguma, Tomoshi Takeda, Kazuo Chin, Michiaki Mishima
Journal: Journal of Allergy and Clinical Immunology (2008)
Naproxen With Cyclobenzaprine, Oxycodone/Acetaminophen, or Placebo for Treating Acute Low Back Pain
Authors: Benjamin W. Friedman, Andrew A. Dym, Michelle Davitt, Lynne Holden, Clemencia Solorzano, David Esses, Polly E. Bijur, E. John Gallagher
Journal: JAMA (2015)

Low back pain (LBP) is responsible for more than 2.5 million visits to US emergency departments (EDs) annually. These patients are usually treated with nonsteroidal anti-inflammatory drugs, acetaminophen, opioids, or skeletal muscle relaxants, often in combination.To compare functional outcomes and pain at 1 week and 3 months after an ED visit for acute LBP among patients randomized to a 10-day course of (1) naproxen + placebo; (2) naproxen + cyclobenzaprine; or (3) naproxen + oxycodone/acetaminophen.This randomized, double-blind, 3-group study was conducted at one urban ED in the Bronx, New York City. Patients who presented with nontraumatic, nonradicular LBP of 2 weeks' duration or less were eligible for enrollment upon ED discharge if they had a score greater than 5 on the Roland-Morris Disability Questionnaire (RMDQ). The RMDQ is a 24-item questionnaire commonly used to measure LBP and related functional impairment on which 0 indicates no functional impairment and 24 indicates maximum impairment. Beginning in April 2012, a total of 2588 patients were approached for enrollment. Of the 323 deemed eligible for participation, 107 were randomized to receive placebo and 108 each to cyclobenzaprine and to oxycodone/acetaminophen. Follow-up was completed in December 2014.All participants were given 20 tablets of naproxen, 500 mg, to be taken twice a day. They were randomized to receive either 60 tablets of placebo; cyclobenzaprine, 5 mg; or oxycodone, 5 mg/acetaminophen, 325 mg. Participants were instructed to take 1 or 2 of these tablets every 8 hours, as needed for LBP. They also received a standardized 10-minute LBP educational session prior to discharge.The primary outcome was improvement in RMDQ between ED discharge and 1 week later.Demographic characteristics were comparable among the 3 groups. At baseline, median RMDQ score in the placebo group was 20 (interquartile range [IQR],17-21), in the cyclobenzaprine group 19 (IQR,17-21), and in the oxycodone/acetaminophen group 20 (IQR,17-22). At 1-week follow-up, the mean RMDQ improvement was 9.8 in the placebo group, 10.1 in the cyclobenzaprine group, and 11.1 in the oxycodone/acetaminophen group. Between-group difference in mean RMDQ improvement for cyclobenzaprine vs placebo was 0.3 (98.3% CI, -2.6 to 3.2; P = .77), for oxycodone/acetaminophen vs placebo, 1.3 (98.3% CI, -1.5 to 4.1; P = .28), and for oxycodone/acetaminophen vs cyclobenzaprine, 0.9 (98.3% CI, -2.1 to 3.9; P = .45).Among patients with acute, nontraumatic, nonradicular LBP presenting to the ED, adding cyclobenzaprine or oxycodone/acetaminophen to naproxen alone did not improve functional outcomes or pain at 1-week follow-up. These findings do not support use of these additional medications in this setting.clinicaltrials.gov Identifier: NCT01587274.
Effects of 24 hours of aspirin, Bufferin, paracetamol and placebo on normal human gastroduodenal mucosa.
Authors: J W Hoftiezer, J C O'Laughlin, K J Ivey
Journal: Gut (1982)

Aspirin causes gastroduodenal erosions and/or ulcers in man when taken for prolonged periods. The effects of shorter periods of aspirin, Bufferin, or paracetamol (acetaminophen) intake as used for self-medication are unknown. In a four way, crossover, blinded endoscopic study, we compared the effects of aspirin, Bufferin, paracetamol, and placebo, two tablets four times a day for 24 hours, on the gastroduodenal mucosa of 10 normal volunteers. Both regular aspirin and bufferin produced multiple gastric (p less than 0.005) and duodenal erosions (p less than 0.05, compared with baseline and placebo studies). Paracetamol did not cause significant gastric or duodenal mucosal damage. Two subjects developed duodenal ulcer-like lesions in the course of the study. We conclude that the use of unbuffered aspirin and Bufferin, but not paracetamol, in recommended doses for one day causes significant gastroduodenal mucosal damage.
Anticoagulation Therapy for Stroke Prevention in Atrial Fibrillation
Authors: Alan S. Go, Elaine M. Hylek, Yuchiao Chang, Kathleen A. Phillips, Lori E. Henault, Angela M. Capra, Nancy G. Jensvold, Joe V. Selby, Daniel E. Singer
Journal: JAMA (2003)

Warfarin has been shown to be highly efficacious for preventing thromboembolism in atrial fibrillation in randomized trials, but its effectiveness and safety in clinical practice is less clear.To evaluate the effect of warfarin on risk of thromboembolism, hemorrhage, and death in atrial fibrillation within a usual care setting.Cohort study assembled between July 1, 1996, and December 31, 1997, and followed up through August 31, 1999.Large integrated health care system in Northern California.Of 13,559 adults with nonvalvular atrial fibrillation, 11,526 were studied, 43% of whom were women, mean age 71 years, with no known contraindications to anticoagulation at baseline.Ischemic stroke, peripheral embolism, hemorrhage, and death according to warfarin use and comorbidity status, as determined by automated databases, review of medical records, and state mortality files.Among 11,526 patients, 397 incident thromboembolic events (372 ischemic strokes, 25 peripheral embolism) occurred during 25,341 person-years of follow-up, and warfarin therapy was associated with a 51% (95% confidence interval [CI], 39%-60%) lower risk of thromboembolism compared with no warfarin therapy (either no antithrombotic therapy or aspirin) after adjusting for potential confounders and likelihood of receiving warfarin. Warfarin was effective in reducing thromboembolic risk in the presence or absence of risk factors for stroke. A nested case-control analysis estimated a 64% reduction in odds of thromboembolism with warfarin compared with no antithrombotic therapy. Warfarin was also associated with a reduced risk of all-cause mortality (adjusted hazard ratio, 0.69; 95% CI, 0.61-0.77). Intracranial hemorrhage was uncommon, but the rate was moderately higher among those taking vs those not taking warfarin (0.46 vs 0.23 per 100 person-years, respectively; P =.003, adjusted hazard ratio, 1.97; 95% CI, 1.24-3.13). However, warfarin therapy was not associated with an increased adjusted risk of nonintracranial major hemorrhage. The effects of warfarin were similar when patients with contraindications at baseline were analyzed separately or combined with those without contraindications (total cohort of 13,559).Warfarin is very effective for preventing ischemic stroke in patients with atrial fibrillation in clinical practice while the absolute increase in the risk of intracranial hemorrhage is small. Results of randomized trials of anticoagulation translate well into clinical care for patients with atrial fibrillation.
1143-136 Prosthetic valve endocarditis: Report of 214 cases from the intracardiac echocardiography prospective cohort study
Authors: Christopher H Cabell, G.Ralph Corey, Bruno Hoen, Jose M Miro, Diana Iarussi, Christine Selton-Suty, Andrew Wang, Eugene Athan, Sandra Braun, Philip Jones, Stamatios Lerakis, Shabaz Hasan, Miguel Oyonarte, Vance G Fowler
Journal: Journal of the American College of Cardiology (2004)
Negative antineutrophil cytoplasmic antibodies in Behcet's disease.
Authors: M Hamza, O Meyer
Journal: Annals of the Rheumatic Diseases (1990)

Negative antineutrophil cytoplasmic antibodies in Behqet's disease Sir: Antineutrophil cytoplasmic antibodies have been detected in patients with idiopathic necrotising and crescentic glomerulonephritis, active Wegener's granulomatosis, and micro- scopic polyarteritis nodosa.'Behcet's disease, an inflammatory disorder of unknown cause, is characterised by oral and genital ulcerations associated with systemic manifestations due to large and small vessel vasculitis.Ocular, cutaneous, and central nervous system involvement are often the translation of small vessel vasculitis.2Crescen- tic glomerulonephritis has also been reported.3
Prognostic Significance of p16 Protein Levels in Oropharyngeal Squamous Cell Cancer
Authors: Paul M. Weinberger, Z. Yu, B.G. Haffty, D. Kowalski, M. Harigopal, C. Sasaki, D. L. Rimm, A. Psyrri
Journal: Clinical Cancer Research (2004)

Functional inactivation of p16 is an early and frequent event in head and neck squamous cell cancers. In this study, we sought to determine whether p16 expression is of prognostic importance in oropharyngeal squamous cell carcinoma.p16 protein expression was evaluated by immunohistochemistry in a tissue microarray composed of 123 oropharyngeal squamous cell cancers with a mean patient follow-up time of 33 months.p16 overexpression was associated with more advanced Tumor-Node-Metastasis stage and higher histologic grade. Despite this association with unfavorable features, p16 overexpression was associated with decreased 5-year local recurrence rates (11 versus 53%) and increased 5-year disease-free survival (62 versus 19%) and overall survival (60 versus 21%). In multivariate analysis, p16 expression status remained an independent prognostic factor for local recurrence, disease-free survival, and overall survival.In patients with oropharyngeal squamous cell carcinoma, overexpression of p16 as determined by immunohistochemistry is associated with significantly improved prognosis and lower local recurrence rates.
Signal transduction by Fc gamma RIII (CD16) is mediated through the gamma chain.
Authors: U Wirthmueller, T Kurosaki, M S Murakami, J V Ravetch
Journal: The Journal of Experimental Medicine (1992)

To determine the functional role of the two isoforms of Fc gamma RIII (CD16) (IIIA, IIIB), the signal transduction capabilities of wild-type and mutant forms of these receptors were analyzed in transfected lymphoid, myeloid, and fibroblastic cell lines. Functional reconstitution of receptor signalling was observed in hematopoietic T and mast cells, and was absent in nonhematopoietic (CHO) cells. Fc gamma RIIIA, a hetero-oligomeric receptor composed of a ligand-binding subunit alpha and dimeric gamma chains, generated both proximal and distal responses in Jurkat and P815 cells, typical of what is seen in natural killer cells and macrophages upon receptor activation. In contrast, Fc gamma RIIIB, which is normally attached to the cell surface via a glycosyl-phosphatidylinositol anchor, was incapable of transducing signals. After crosslinking, Fc gamma RIIIA signalling was dependent only upon the gamma chain. Fc gamma RIIIA chimeras in which the alpha subunit transmembrane and cytoplasmic domains were substituted with the corresponding gamma chain sequences functioned as well as wild-type hetero-oligomeric receptors. These data indicate that the ability of the Fc gamma RIIIA complex to activate the appropriate pathways for cell activation is cell-type restricted and independent of the transmembrane and cytoplasmic domains of the alpha subunit. The presence of the gamma chain is responsible for the assembly of, as well as the signal transduction by, the functional cell surface complex.