tbuckley/cabot-search huggingface dataset:
THE PATHOLOGY OF INTESTINAL AMEBIASIS.
Authors: PAUL G. WOOLLEY
Journal: JAMA (1905)

In former papers, one of us (Musgrave) has dealt with the subjects of the cultivation of amebas, and the etiology, diagnosis, prognosis and treatment of intestinal amebiasis. To complete the series, there remained, then, the pathology, complications and sequelæ, and to the pathology of the intestinal amebic disease the following remarks will be limited. It may be well to state at the outset that we can see no valid reason for departing from the nomenclature of Lösch. He described a<i>pathogenic</i>ameba from a diseased intestine and called it<i>Amœba coli</i>. Why this term should be applied to a supposititious non-pathogenic organism is difficult to say. We shall, in referring to the cause of intestinal amebiasis, use the name introduced by Lösch. Among the many articles in the literature of amebiasis, there are but few which are of special value from the pathologic side. Chief among these are those of
P172Monoamine oxidase inhibition corrects endothelial dysfunction in experimental diabetes
Authors: A Sturza, L Noveanu, O Duicu, DM Muntean
Journal: Cardiovascular Research (2014)

Monoamine oxidases (MAOs) are mitochondrial dehydrogenases with two isoforms, A and B, that catalyze the electron transfer from biogenic amines to molecular oxygen, with the constant generation of hydrogen peroxide (H2O2) as by-product. The resent study was aimed to assess whether MAO-derived H2O2 contributes to the aggravation of oxidative stress-related endothelial dysfunction. We hypothesized that MAO inhibition improves endothelial-dependent relaxation in experimental diabetes, a condition widely recognized as being associated with increased oxidative stress as happens in diseased vessels. Methods. Segments from aorta, carotid and femoral arteries with intact and denuded endothelium (using CHAPS solution) were harvested from Zucker obese diabetic rats and streptozotocin-induced diabetic rats and studied in an organ-bath system. The contractile response was assessed using phenylephrine (0,01-1 microM) in the presence vs. absence of a MAO-A inhibitor, clorgyline (10 microM). H2O2 production was measured by a spectrophotometric method (Feric Oxydation Xylenol Orange assay). The effect of hyperglycemia on MAO gene expression was tested by quantitative RT-PCR technique. Results. MAO inhibition reduced the diabetic-induced aortic H2O2 generation by 30% and partially normalized the contractility of diseased vascular segments. Conclusion. MAO inhibition might be useful in restoring endothelial-dependent relaxation in conditions associated with increased vascular oxidative stress and endothelial dysfunction, including diabetes. Further investigations aimed at characterizing the mechanisms underlying MAO-dependent H2O2 formation are warranted.
A randomised double-blind phase II study of lamivudine (LAM) compared to lamivudine plus adefovir dipovoxil (ADV) for treatment naïve patients with chronic hepatitis B (CHB): Week 52 analysis
Authors: J.J.Y. Sung, J.Y. Lai, S. Zeuzem, W.C. Chow, E. Heathcote, R. Perrillo, C. Brosgart, M. Woessner, S.A. Scott, F.M. Campbell
Journal: Journal of Hepatology (2003)
THORACIC PAIN PERSISTING AFTER CORONARY THROMBOSIS
Authors: LOWELL B. ECKERSON
Journal: JAMA (1928)

That attacks of angina pectoris may cease after the occurrence of coronary thrombosis has been pointed out by McKeen 1 and by Wolff and White. 2 This is probably explained by the fact that the branch of the coronary which, by its narrowed condition, was responsible for pain on an increased demand for function of the heart, is obliterated by the thrombosis. After obliteration of the vessel by a thrombosis there is an infarct of that part of the heart muscle which it supplies and, if the patient survives, this is followed by scar tissue replacement. The infarct or the scar is physiologically inactive and increased physiologic demand on the heart does not result in the attacks of angina pectoris to which the patient was previously subject, unless other coronary branches are involved.  On the other hand, we believe that it is not uncommon for patients who have suffered coronary
Psoriasis, psoriatic arthritis and type 2 diabetes mellitus: a systematic review and meta-analysis
Authors: P. Coto-Segura, N. Eiris-Salvado, L. González-Lara, R. Queiro-Silva, P. Martinez-Camblor, C. Maldonado-Seral, B. García-García, L. Palacios-García, S. Gomez-Bernal, J. Santos-Juanes, E. Coto
Journal: British Journal of Dermatology (2013)

Several observational studies have assessed the association between psoriasis, psoriatic arthritis (PsA) and type 2 diabetes mellitus, with inconclusive results. We set out to investigate the association between psoriasis, PsA and type 2 diabetes mellitus. Observational studies assessing the relationship between psoriasis or PsA and type 2 diabetes mellitus up to December 2012 were identified by electronic and hand searches in Medline, Embase, PubMed, the Cochrane Database of Systematic Reviews and Google Scholar. For each study we collected the first author's last name, publication year, country of origin, study design, characteristics of participants (sample size, age and sex), the variables incorporated into the multivariable analyses, and the odds ratios (ORs) of psoriasis associated with diabetes along with the corresponding 95% confidence intervals (CIs). From the data provided in each article, the crude OR was also calculated. Forty-four observational studies (in 37 articles) were identified for the final analysis. The pooled OR from random-effects analysis was determined to be 1·76 (95% CI 1·59-1·96). The highest risk was for patients suffering from PsA (OR 2·18, 95% CI 1·36-3·50). We also observed a dose effect in the risk of suffering from type 2 diabetes mellitus, as patients considered as having severe psoriasis had higher risk (OR 2·10, 95% CI 1·73-2·55) than the pooled OR. We perform meta-regression and sensitivity analyses to explore sources of heterogeneity among the studies and to determine how they would influence the estimates, and found no significant influence in the results of the meta-analyses. The findings support the association between psoriasis, PsA and type 2 diabetes mellitus. Some caution must be taken in the interpretation of these results because there may be heterogeneity between studies.
Prevalence and significance of isotypes of anti-cyclic citrullinated peptide antibodies in juvenile idiopathic arthritis
Authors: R H Syed, B E Gilliam, T L Moore
Journal: Annals of the Rheumatic Diseases (2008)

Several studies have evaluated the potential role for IgG anti-cyclic citrullinated peptide (anti-CCP) antibodies in juvenile idiopathic arthritis (JIA) concerning diagnosis and disease outcome.1–6 Unlike rheumatoid arthritis (RA),7 8 no study in JIA has evaluated the distribution of anti-CCP antibody isotypes and assessed their significance in the disease process.

We assessed anti-CCP antibody isotype distribution in 72 consecutive patients with JIA (59 female and 13 male), including 14 with IgM RF-positive polyarthritis, 24 with IgM rheumatoid factor (RF)-negative polyarthritis, 21 with oligoarthritis, 11 with systemic-onset arthritis, and 2 with psoriatic arthritis. The mean (SD) age was 12.1 (5.8) years and mean disease duration was 4.8 (4.5) years. The levels of anti-CCP antibody isotypes were measured …
Functional Promiscuity of Squirrel Monkey Growth Hormone Receptor Toward both Primate and Nonprimate Growth Hormones
Authors: Soojin Yi, Bryan Bernat, Gábor Pál, Anthony Kossiakoff, Wen-Hsiung Li
Journal: Molecular Biology and Evolution (2002)

Primate growth hormone (GH) has evolved rapidly, having undergone ∼30% amino acid substitutions from the inferred ancestral eutherian sequence. Nevertheless, human growth hormone (hGH) is physiologically effective when administered to nonprimate mammals. In contrast, its functional counterpart, the human growth hormone receptor (hGHR), has evolved species specificity so that it responds only to Old World primate GHs. It has been proposed that this species specificity of the hGHR is largely caused by the Leu → Arg change at position 43 after a prior His → Asp change at position 171 of the GH. Sequence analyses supported this hypothesis and revealed that the transitional phase in the GH:GHR coevolution still persists in New World monkeys. For example, although the GH of the squirrel monkey has the His → Asp substitution at position 171, residue 43 of its GHR is a Leu, the nonprimate residue. If the squirrel monkey truly represents an intermediate stage of GH:GHR coevolution, its GHR should respond to both hGH and nonprimate GH. Also, if the emergence of species specificity was a result of the selection for a more efficient GH:GHR interaction, then changing residue 43 of the squirrel monkey growth hormone receptor (smGHR) to Arg should increase its binding affinity toward higher primate GH. To test these hypotheses, we performed protein-binding assays between the smGHR and both human and rat GHs, using the surface plasmon resonance methodology. Furthermore, the effects of reciprocal mutations at position 43 of human and squirrel monkey GHRs are measured for their binding affinities toward human and squirrel monkey GHs. The results from the binding kinetic assays clearly demonstrate that the smGHR is in the intermediate state of the evolution of species specificity. Interestingly, the altered residue Arg at position 43 of the smGHR does not lead to an increased binding affinity. The implications of these results on the evolution of the GH:GHR interaction and on functional evolution are discussed.
Extrinsic Barium Collection on Barium Enema Examination
Authors: Emil Gutman
Journal: JAMA (1980)

<h3>History</h3> A 53-year-old man was admitted with epigastric pain of five to six days' duration. Normal stools had become tarry. The patient had a history of surgery 11 years ago for perforated peptic ulcer. Barium enema examination revealed findings as on Fig 1 (preevacuation) and Fig 2 (postevacuation). Figure 3 is a preevacuation spot film. <h3>Diagnosis</h3> Tubular communicating duplication of the descending colon. In this case it was not certain whether the positive guaiac test on stool was caused from duodenal ulcer seen on gastrointestinal examination or duplication of the colon. Gastric surgery (vagotomy and pyloroplasty) and excision of the colon duplication were performed, and the patient was later discharged. He has had a number of subsequent admissions for other problems, the last being Dec 8 to 11, 1975, but has had no difficulties related to the colon and no further bleeding. Note the mobility of the duplicated segment (Fig
Screening of Donor Blood for Alanine Aminotransferase
Authors: Harald Fiedler
Journal: JAMA (1985)

<h3>To the Editor.—</h3> Silverstein et al<sup>1</sup>advocate alanine aminotransferase (ALT) screening of donor blood because it will be cost-effective over a wide range of ALT levels. What the authors obviously did not take into consideration is that many chronic carriers of non-A, non-B hepatitis are asymptomatic with occasionally elevated ALT levels. The percentage of donors without transmissible liver disease in any donor population occasionally exhibiting elevated ALT levels is unknown. It therefore remains difficult to decide whether donors with previous ALT levels of 45 IU or higher should be accepted again as blood donors when their ALT levels have become lower than 45 IU, although transitory periods with normal ALT levels are typical for mild chronic non-A, non-B hepatitis, or whether such donors should be rejected once and for all. The latter course carries the risk of decimating the noninfectious part of the donor population as time goes on.
Preconditioning human ventricular cardiomyocytes with brief periods of simulated ischaemia
Authors: J. S Ikonomidis, L. C Tumiati, R. D Weisel, D. A G Mickle, R.-K. Li
Journal: Cardiovascular Research (1994)

Objective: The aim was to test for "ischaemic" preconditioning in monolayer cultures of quiescent human ventricular cardiomyocytes. Methods: Stabilised cardiomyocytes (n = 8 plates per group) were preconditioned with varying periods of simulated ischaemia and reperfusion, followed in all groups by 90 min of sustained "ischaemia" with or without 30 min of reperfusion. Cellular injury was assessed by trypan blue exclusion and survival was assessed by culturing the cells for 24 h postintervention. In addition, separate groups of cell plates (n = 8 per group) which had first been preconditioned with 20 min ischaemia and 20 min reperfusion were exposed to either 30, 60, or 90 min sustained ischaemia or 90 min sustained ischaemia with 30 min reperfusion. The supernatants and/or cell homogenates were analysed for hydrogen ion, lactate, lactate dehydrogenase (LDH), and adenine nucleotides and degradation products. Results: Preconditioning (PC) decreased trypan blue uptake following subsequent sustained ischaemia, with the 20 min ischaemia/20 min reperfusion (20/20) regimen having the most profound effect [control ischaemia: 37.0(SEM 2.1); 10/10: 23.9(1.5); 20/20: 15.4(1.4); 30/30: 25.8(2.1) percent blue stained cells, p < 0.05 by ANOVA/Duncan]. The 20/20 preconditioning regimen resulted in less hydrogen ion [control: 2.1(0.4); PC: 1.4(0.1) mmol·g−1 protein, p <0.05] and less LDH release [control: 20.7(3.1); PC: 11.9(4.2) units·g−1 protein, p < 0.05]. At 90 min of sustained ischaemia, the control group had produced significantly greater lactate [intracellular: control 1.55(0.62); PC 0.54(0.23) mol·g−1 DNA, p < 0.05; extracellular: control 0.47(0.09); PC 0.33(0.07) mol·g−1 DNA, p < 0.05]. There were no differences in ATP depletion in the two groups. Conclusions: Ischaemic preconditioning can be induced in human cardiomyocytes independent of other cell types. The effect can be established in human cell cultures. Cardiovascular Research 1994;28:1285-1291
124 HEPATITIS DELTA INFECTION IN HUMANIZED UPA/SCID-MICE LEADS TO PRONOUNCED INDUCTION OF HUMAN-SPECIFIC INNATE IMMUNE RESPONSES AND CYTOKINE EXPRESSION IN COMPARISON TO HBV MONO-INFECTION
Authors: K. Giersch, M. Lütgehetmann, T. Volz, L. Allweiss, J.-L. Braunschmidt, A.W. Lohse, J. Petersen, M. Dandri
Journal: Journal of Hepatology (2013)
A Longitudinal Analysis of Electronic Cigarette Use and Smoking Cessation
Authors: Rachel A. Grana, Lucy Popova, Pamela M. Ling
Journal: JAMA Internal Medicine (2014)

Although electronic cigarettes (e-cigarettes) are aggressively promoted as smoking cessation aids,1 studies of their effectiveness for cessation have been unconvincing.2, 3 One randomized trial comparing e-cigarettes with and without nicotine, and nicotine patch found no differences in 6-month quit rates.2 Population-based, longitudinal studies have also not shown associations between e-cigarette use and quitting.4, 5 A longitudinal, international study found that, although 85% of smokers who used e-cigarettes reported using them to quit, e-cigarette users did not quit more frequently than non-users (p=.516).4 Among US quitline callers, e-cigarette users were less likely to have quit at 7 months than non-users.5

We employed a longitudinal analysis of a national sample of current US smokers to determine whether e-cigarette use predicted successful quitting, or reduced cigarette consumption.
Randomized Trial of High Loading Dose of Clopidogrel for Reduction of Periprocedural Myocardial Infarction in Patients Undergoing Coronary Intervention
Authors: Giuseppe Patti, Giuseppe Colonna, Vincenzo Pasceri, Leonardo Lassandro Pepe, Antonio Montinaro, Germano Di Sciascio
Journal: Circulation (2005)

Aggressive platelet inhibition is crucial to reduce myocardial injury and early cardiac events after coronary intervention. Although observational data have suggested that pretreatment with a high loading dose of clopidogrel may be more effective than a conventional dose, this hypothesis has never been tested in a randomized trial.A total of 255 patients scheduled to undergo percutaneous coronary intervention were randomized to a 600-mg (n=126) or 300-mg (n=129) loading regimen of clopidogrel given 4 to 8 hours before the procedure. Creatine kinase MB, troponin I, and myoglobin levels were measured at baseline and at 8 and 24 hours after intervention. The primary end point was the 30-day occurrence of death, myocardial infarction (MI), or target vessel revascularization. The primary end point occurred in 4% of patients in the high loading dose versus 12% of those in the conventional loading dose group (P=0.041) and was due entirely to periprocedural MI. Peak values of all markers were significantly lower in patients treated with the 600-mg regimen (P< or =0.038). Safety end points were similar in the 2 arms. At multivariable analysis, the high loading regimen was associated with a 50% risk reduction of MI (OR 0.48, 95% CI 0.15 to 0.97, P=0.044). An incremental benefit was observed in patients randomized to the 600-mg dose who were receiving statins, with an 80% risk reduction.Pretreatment with a 600-mg loading dose of clopidogrel 4 to 8 hours before the procedure is safe and, as compared with the conventional 300-mg dose, significantly reduced periprocedural MI in patients undergoing percutaneous coronary intervention. These results may influence practice patterns with regard to antiplatelet therapy before percutaneous revascularization.
Subdural haemorrhages in infants
Authors: B. Lloyd
Journal: BMJ (1998)

Papers p 1558 

In this issue Jayawant et al report the results of a study of the incidence, causes, and outcome of subdural haemorrhages in infancy in a defined geographical area in England and Wales from 1993 to 1995 (p 1558).1 This subject is important because, as this study confirms, most subdural haemorrhages are due to abuse. The subdural haemorrhage is just one element of the brain injury in infants who have suffered non-accidental head injury (caused either by shaking alone or by shaking and impact).2

Ascertainment seems to have been thorough and the results are likely to be generalisable to the rest of the United Kingdom. The results suggest that a large district general hospital can expect, on average, to see an infant with a subdural haemorrhage every year. Most of these infants needed intensive care and, as in other studies, the outcome was poor. 3 4 Assuming that the results are generalisable, …
Autoreactive CD4+ LKM-specific and anticlonotypic T-cell responses in LKM-1 antibody-positive autoimmune hepatitis
Authors: H F Lohr, J F Schlaak, A W Lohse, W O Bocher, M Arenz, G Gerken, K M Buschenfelde
Journal: Hepatology (1996)

Peripheral blood mononuclear cells (PBMC) of patients with autoimmune hepatitis (AIH) and controls were studied for their proliferative response to six overlapping synthetic peptides covering the 33–amino acid immunodominant region of cytochrome P450IID6, the main target antigen of LKM–1 antibody–positive type II AIH. PBMC from 8 of 8 type II AIH patients (100%), 6 of 12 LKM–1 antibody–negative type I AIH patients (50%), but only 4 of 31 patients with chronic hepatitis C (12.9%) reacted with a 23–amino acid LKM peptide and mainly with a shorter 18–amino acid LKM peptide. Follow–up showed that LKM–specific T–cell responses decreased after immunosuppression had started. Fine specificity, HLA restriction, and cytokine release of LKM–specific T cells were analyzed with 16 CD4+ peptide–specific T–cell lines and 21 CD4+ T–cell clones isolated and expanded from blood and liver tissue of six AIH patients. Activated LKM–specific T cells released interferon gamma (IFN–γ) but no or little interleukin–4. In three AIH patients, PBMC showed specific recognition of autologous LKM–specific T cells, suggesting the presence of a regulatory T–cell network. These T cells also showed the CD4+ phenotype and secreted large amounts of IFN–γ. Furthermore, it was assessed that the regulatory T–cell response is clonotypic. To conclude, we describe a major T–cell epitope in AIH that was recognized by Th1 helper cells isolated from blood and liver tissue. This autoreactive T–cell response correlated widely with disease activity and LKM–1 antibody status and seemed to be regulated by anticlonotypic T cells.
K:CI cotransport in red cells of transgenic mice expressing high levels of human hemoglobin S
Authors: José R. Romero, Mary E. Fabry, Sandra M. Suzuka, Frank Costantini, Ronald L. Nagel, Mitzy Canessa
Journal: American Journal of Hematology (1997)

K:CI cotransport is involved in generating dense red blood cells (RBCs) in homozygotes for HbS (SS). We report on the properties of this transport system in RBCs from control and transgenic mice expressing high levels of human αH and βS chains. Unlike human SS RBCs, mouse RBCs incubated in isotonic media exhibited a CI−-dependent K+ efflux and therefore have a different set-point for activation. This basal efflux was slightly stimulated by cell swelling to values five times smaller than that in human SS cells; In addition, the delay time for activation was shorter in transgenic than in control mice, but fourtold longer than that of human SS cells. These properties cast doubt on the physiological impact of the mouse K:CI cotransporter on RBC volume regulation in the mouse and suggest that there are intrinsic differences between the human K:CI cotransporter and the putative transporter in mice. Am. J. Hematol. 55:112-114, 1997. © 1997 Wiley-Liss, Inc.
Dr. Taylor's Dressing After Hare-Lip Operation.
Authors: C. B. Stockwell.
Journal: JAMA (1907)

Port Huron, Mich., Dec. 22, 1906. <h3>To the Editor:</h3> —Under tie above heading Dr. Alfred S. Taylor of New York City calls attention<sup>1</sup>to the use of strips of adhesive plaster crossed at a point above the nose, first used by him at the Vanderbilt clinic in 1901. He makes the statement: "So far as I know, it was an original idea." Dr. William H. DeCamp of Grand Rapids, Mich., was the originator, I think, of this idea, and described the method in a paper read before the Michigan State Medical Society in 1886.<sup>2</sup> I saw the method used two years later in one of the London, England, hospitals by one who had heard of Dr. DeCamp's method. Dr. Taylor, nevertheless, should have the gratitude of the medical profession for again bringing this method to its attention, and especially for illustrating it, which is the most efficient way
Advances in targeted therapies: TNFalpha blockade in clinical practice
Authors: F C BREEDVELD, J R KALDEN, J S SMOLEN
Journal: Annals of the Rheumatic Diseases (1999)

constitute summaries of presentations at the first International Symposium on "Advances in Targeted Therapies-TNF Blockade in Clinical Practice", which was held in March 1999.As such they represent the state of the art on the biology, mechanisms of action and pathophysiology of TNF as well as the current knowledge on means and consequences of blocking this important cytokine.We are grateful to Drs CroVord, Feldmann, Klareskog, Lipsky, Maini, Moreland and Weinblatt, the members of the Advisory Board of the Symposium, for their invaluable help towards the success of the conference, the first of a series of similar events planned for the future.We particularly wish to thank all speakers for their excellent presentations, most of which are summarised here in writing, and all participants who have actively contributed to the discussions.Finally, we also wish to thank the sponsors* of this university driven event who have provided unrestricted educational grants that enabled us to invite the leading scientists in the field.Moreover, for the first time a rheumatological audience (and the readers of this supplement) have been able to obtain back to back information on the eYcacy and safety of TNF blocking agents from representatives of the major companies involved with open discussion of issues arising regarding each agent when looked at individually and compared with others.It is also thankfully acknowledged that representatives of both the FDA and EMEA actively participated in this symposium.