tbuckley/cabot-search huggingface dataset:
Change in Systolic Left Ventricular Performance After 3 Years of Antihypertensive Treatment
Authors: Kristian Wachtell, Vittorio Palmieri, Michael H. Olsen, Eva Gerdts, Vasilios Papademetriou, Markku S. Nieminen, Gunnar Smith, Björn Dahlöf, Gerard P. Aurigemma, Richard B. Devereux
Journal: Circulation (2002)

Background — We have shown that hypertensive patients with left ventricular (LV) hypertrophy have decreased LV midwall mechanics, but the effect of antihypertensive therapy remains unclear. Methods and Results — Echocardiograms were recorded at baseline in 679 hypertensive patients and ECG LV hypertrophy and repeated yearly during 3 years of blinded treatment to achieve target blood pressures (BPs) of 140/90 mm Hg. On average, BP was reduced from 174±21 to 147±19 over 95±11 to 82±10 mm Hg and LV mass from 234±56 to 194±50 g. Endocardial fractional shortening (FS) decreased slightly, whereas midwall FS increased from 15.4±2.0% to 16.8±2.1% and stress-corrected midwall FS increased from 97±13 to 105±12% (all P &lt;0.001). Change in midwall FS was related inversely to change in LV mass (LVM), relative wall thickness (RWT), and diastolic BP and directly to change in Doppler stroke volume (SV, all P &lt;0.001). Multivariate analysis showed that change in MWS was independently inversely related to changes in LVM (β=−0.211), RWT (β=−0.334, all P &lt;0.001), and diastolic BP (β=−0.088, P &lt;0.05) and directly related to SV (β=0.192, P &lt;0.001) with control for blinded therapy. Change in stress-corrected midwall shortening was inversely independently associated with changes in LVM (β=−0.153) and RWT (β=−0.562) and directly with changes in SV (β=0.145) and systolic BP (β=0.s221, all P &lt;0.001) with control for blinded therapy. Conclusions — Antihypertensive therapy reduced LVM and increased LV midwall shortening and contractility with a small decrease in LV chamber function and significant increase in SV. Change in systolic LV performance was independently associated inversely with change in LVM, RWT, and BP and directly with change in SV.
Vagotomy for peptic ulceration.
Authors: M Lee
Journal: BMJ (1970)

culation is indicated by our findingsl 2 that in blood obtained from the uterine veins this factor was greater than that in the arterial blood.Plasminogen activator levels were estimated by the euglobulin lysis time (E.L.T.) method.3Evidence supporting our findings is provided by the observations published by bination of phenformin-stanozolol is as Maki et al.4These workers, investigating the fibrinolytic activity in blood from the vasa efferentia of the uterus and comparing it with that in blood from a cubital vein, found that this activity was considerably increased in the blood from the uterus.They suggested that this constituted indirect evidence that the uterus contributed activators to the systemic circulation.Moreover, in a comparative study of blood from a uterine vein and a uterine artery in 14 patients, Cash,5 using the E.L.T. method, found marked increased fibrinolytic activity in the former.-Iam, etc.,
Cerebral Microembolism Is Blocked by Tirofiban, a Selective Nonpeptide Platelet Glycoprotein IIb/IIIa Receptor Antagonist
Authors: Ulrich Junghans, Mario Siebler
Journal: Circulation (2003)

Microembolic signals (MES) as detected by transcranial Doppler ultrasound define an individual stroke risk in patients with carotid artery disease. To study the composition of MES in vivo, we used the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonist tirofiban, a highly selective platelet aggregation inhibitor.Twenty-four patients with recent cerebral or retinal embolism of arterial origin and a MES rate >6 per hour on initial transcranial Doppler ultrasonography recording received the short-acting GPIIb/IIIa antagonist tirofiban. With tirofiban, the MES rate dropped from a median (range) of 38 (9 to 324) to zero in all patients. After cessation of infusion, the inhibitory effect of tirofiban was reversible, with a significant increase of MES (median 13.5; range, 0 to 35; n=16; P=0.001). Six patients received overlapping oral antiplatelet agents and remained MES-negative.Cerebral microembolism of arterial origin has the property of solid emboli, with platelet-fibrinogen units as predominant constituent parts. GPIIb/IIIa antagonists may have the potential to bridge the ischemic risk in patients with unstable carotid disease.
Immunoglobulin A1 Protease, an Exoenzyme of Pathogenic <i>Neisseriae</i>, Is a Potent Inducer of Proinflammatory Cytokines
Authors: Dirk R. Lorenzen, Frank Düx, Uwe Wölk, Anastasios Tsirpouchtsidis, Gaby Haas, Thomas F. Meyer
Journal: The Journal of Experimental Medicine (1999)

A characteristic of human pathogenic Neisseriae is the production and secretion of an immunoglobulin (Ig)A1-specific serine protease (IgA1 protease) that cleaves preferentially human IgA1 and other target proteins. Here we show a novel function for native IgA1 protease, i.e., the induction of proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 from peripheral blood mononuclear cells. The capacity of IgA1 protease to elicit such cytokine responses in monocytes was enhanced in the presence of T lymphocytes. IgA1 protease did not induce the regulatory cytokine IL-10, which was, however, found in response to lipopolysaccharide and phytohemagglutinin. The immunomodulatory effects caused by IgA1 protease require a native form of the enzyme, and denaturation abolished cytokine induction. However, the proteolytic activity is not required for the cytokine induction by IgA1 protease. Our results indicate that IgA1 protease exhibits important immunostimulatory properties and may contribute substantially to the pathogenesis of neisserial infections by inducing large amounts of TNF-α and other proinflammatory cytokines. In particular, IgA1 protease may represent a key virulence determinant of bacterial meningitis.
Effects of dithranol on neutrophil superoxide generation in patients with psoriasis
Authors: G.M. KAVANAGH, J.L. BURTON, V.O. DONNELL
Journal: British Journal of Dermatology (1996)

The effect of dithranol on superoxide generation in vivo has not been studied previously. Neutrophils produce large amounts of superoxide following stimulation by phorbol 12-myristate-13-acetate (PMA). We studied the effect of dithranol on PMA-activated superoxide generation by isolated neutrophils from normal subjects, and measured whole blood luminescence in response to PMA, using samples from 13 psoriatic patients before and during dithranol treatment. Oxidized dithranol had no effect on the PMA-stimulated superoxide generation in neutrophils, but there was a modest dose-related increase in superoxide generation by neutrophils exposed to dithranol before activation. Similar results were found with neutrophils obtained from the 13 psoriasis patients. Three of these patients suffered a dithranol burn and developed a neutrophilia, with a marked increase in stimulated superoxide generating ability. Our findings suggest that dithranol treatment of a psoriasis plaque is associated with a decrease in oxygen radical generating capacity in vivo. However, where inflammation of perilesional and uninvolved skin occurs, neutrophils appear to become semi-activated or primed.
Prevention of Air Embolism During Subclavian Venipuncture
Authors: Ashiq H. Tahir
Journal: JAMA (1973)

To the Editor.—  Air embolism is a serious complication of percutaneous cannulation of the branches of the superior vena cava and has caused numerous deaths. 1-5 Having the patient in Trendelenburg's position, deep expiration at the time of venipuncture, and occluding the needle hub with a finger after disconnecting the syringe while preparing to insert the catheter have been suggested as preventive measures. 2-4 Use of Trendelenburg's position helps filling and distension of the vein, but air embolism can still occur. 4 Even a brief exposure of the catheter hub to the atmosphere may result in a significant aero-embolus. Using Poiseuille's law, Flanagan and co-workers calculated that 100 cc of air per second could easily pass through a 14-gauge needle. 5 Air embolism can also occur when the intravenous tubing is disconnected from the catheter hub during irrigation or flushing of the system or while drawing a blood sample. In
C5a/C5aR pathway is essential for the pathogenesis of murine viral fulminant hepatitis by way of potentiating Fgl2/fibroleukin expression
Authors: Gui-lian Xu, Jian Chen, Fei Yang, Gui-qing Li, Li-xin Zheng, Yu-zhang Wu
Journal: Hepatology (2014)

Viral fulminant hepatitis (FH) remains a serious clinical problem with very high mortality. Lacking understanding of FH pathogenesis has in essence hindered efficient clinical treatment. Inferring from a correlation observed between the genetic differences in the complement component 5 (C5) and the susceptibility of mouse strains to murine hepatitis virus strain-3 (MHV-3) infections, we propose that excessive complement activation plays a critical role in the development of FH. We show that MHV-3 infection causes massive complement activation, along with a rapid increase in serum C5a levels and quick development of FH in susceptible strains. Mice deficient in the C5a receptor (C5aR) or the susceptible strains treated with C5aR antagonists (C5aRa) exhibit significant attenuation of the disease, accompanied by a remarkable reduction of hepatic fibrinogen-like protein 2 (Fgl2), a hallmark protein that causes necrosis of infected livers. In accordance, biopsy of FH patients shows a dramatic increase of Fgl2 expression, which correlates with C5aR up-regulation in the liver. In vitro C5a administration accelerates MHV-3-induced Fgl2 secretion by macrophages. Furthermore, inhibiting ERK1/2 and p38 efficiently blocks C5a-mediated Fgl2 production during viral infections. Conclusion : These data provide evidence that mouse susceptibility to MHV-3-induced FH may rely on C5a/C5aR interactions, for which ERK1/2 and p38 pathways participate in up-regulating Fgl2 expression. Inhibition of C5a/C5aR interactions is expected to be beneficial in the clinical treatment of FH patients. (Hepatology 2014;60:114–124)
Stable Levels of Long-Term Transgene Expression Driven by the Latency-Associated Transcript Promoter in a Herpes Simplex Virus Type 1 Vector
Authors: B.K. Berges, J.H. Wolfe, N.W. Fraser
Journal: Molecular Therapy (2005)

Previous gene transfer studies of the herpes simplex virus type 1 (HSV-1) using the latency-associated transcript (LAT) promoter have reported a decrease in transgene expression in the brain over time, but the extent of this decrease has not been measured and it is unknown if expression eventually stabilizes. We examined LAT promoter-mediated transgene expression in the mouse brain for 1 year following intracranial injection with a HSV-1 vector expressing human β-glucuronidase (GUSB). The vector genome copy number remained stable from 2 to 52 weeks. Quantitative reverse transcriptase PCR detected a peak of LAT intron expression at 2 weeks (corresponding to the end of the acute phase of viral infection), followed by stable expression during latency (13–52 weeks). The number of GUSB-positive cells also had a peak in the acute phase and then was stable during latency (13–52 weeks). GUSB enzymatic activity was maintained at 11% of normal at 6 and 12 months, indicating that the LAT promoter is capable of driving stable transgene expression in the brain.
Acute lipodermatosclerosis is associated with venous insufficiency
Authors: Adam S Greenberg, Anthony Hasan, Berta M Montalvo, Anne Falabella, Vincent Falanga
Journal: Journal of the American Academy of Dermatology (1996)

Background: Acute lipodermatosclerosis is characterized by pain and tenderness in the medial aspect of the leg. It is thought to be the result of venous insufficiency and to be the acute counterpart of chronic lipodermatosclerosis, a hallmark of venous disease. However, there is no direct evidence linking acute lipodermatosclerosis to venous disease. Objective: Our purpose was to determine whether acute lipodermatosclerosis is associated with venous insufficiency. Methods: With air plethysmography, we determined the venous filling index, the ejection fraction, and the residual volume fraction in 15 sequential patients with acute lipodermatosclerosis. Results: Ten of the 15 patients (67%) had at least one abnormal result, eight (53%) had two, and two (13%) had three. In four patients (27%), abnormalities of both reflux and ejection were noted. Duplex venous ultrasonography, in two of the patients with normal results from air plethysmography, showed incompetent perforators at sites of lipodermatosclerosis. Conclusion: Acute lipodermatosclerosis is associated with objective findings of venous insufficiency in a high percentage of patients. It is likely that this condition is the result of venous disease.
AB0741 Multidimensional Health Related Quality of Life Assessment Using PROMIS (Patient Reported Outcome Measurement Information System) Measures in Psoriatic Arthritis Flares: Table 1.
Authors: A.-M. Orbai, S. Bartlett, T. Duncan, E. de Leon, M. Jones, C.O. Bingham
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Psoriatic arthritis (PsA) impacts health and health related quality of life (HRQL). Patients (pts) with PsA have periods of exacerbation or flares, but there is limited characterization from the pt9s perspective. PROMIS is an IRT calibrated item bank covering physical, mental, and social health with population-normalized T scores (Mean 50, SD 10). PROMIS measures provide precise estimates using computer adaptive tests (CAT). PROMIS evaluation in specific diseases is limited and not studied in PsA. <h3>Objectives</h3> To gather preliminary data on HRQL in PsA patient-reported flare using multiple PROMIS measures. <h3>Methods</h3> Participants with PsA completed 10 PROMIS CATs (pain interference, fatigue, physical function, sleep disturbance, sleep related impairment, depression, anxiety, anger, ability to participate social, satisfaction social roles) administered on a tablet. Routine PROs were collected (pt global/pain/fatigue VAS, mHAQ, and flare self-report). <h3>Results</h3> We report on the first 42 pts with PsA: White 90%, Female 63%, Mean (SD) age 49 (11) yrs, PsA duration 14 (9) yrs. In the overall PsA population [mean CDAI 7.6 (9)] PROMIS pain interference, fatigue, function and sleep were worse than population norms. Pts reporting PsA flare (n=15) had worse scores across all PROMIS domains compared to no flare (n=27), with statistically significant differences for most domains tested (see Table). <h3>Conclusions</h3> These preliminary data on PROMIS CAT assessments of physical, mental, and social health in PsA, which provide population normalized estimates, suggest pts with PsA and self-reported flare suffer impairment in health and HRQL areas encompassing pain, fatigue, function, sleep, mood and participation. PROMIS CATs may help differentiate flare vs non flare states in PsA. Our results highlight impact of PsA on HRQL areas not traditionally assessed in clinical care and research. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1131
Gonadotropin-Releasing Hormone: Role of Pulsatile Secretion in the Regulation of Reproduction
Authors: Jeffrey S. Flier, Lisa H. Underhill, John C. Marshall, Robert P. Kelch
Journal: New England Journal of Medicine (1986)

Reproductive function in humans changes markedly during life and is usually divided into four stages. During the initial stage, which begins early in fetal life and ends in infancy, gonadotropins and gonadal steroids are secreted at levels similar to those seen in early and mid-adolescence. In the second stage, which lasts from infancy through the first decade of life, reproductive function first regresses and then becomes quiescent. Puberty, the third stage, is heralded by a nocturnal increase in the secretion of gonadotropins and sex steroids. This nocturnal predominance gradually diminishes and disappears during the fourth stage — adulthood. In men, . . .
Mechanisms of increased acid secretion after eradication of Helicobacter pylori infection
Authors: E M El-Omar
Journal: Gut (2006)

Eradication of Helicobacter pylori infection leads to recovery of gastric acid secretion in some individuals but the mechanism is not fully understood. In the short term, there is an impressive increase in expression of H+/K+-ATPase pumps without an increase in the number of parietal cells. Longer follow up studies are needed to see if the parietal cell mass eventually recovers.
Teaching rheumatology to nurses
Authors: V. Wright, R. Hopkins
Journal: Annals of the Rheumatic Diseases (1978)

Seven different types of lecturing technique were assessed in 14 groups of nurses at 2 hospitals. Two lectures in rheumatology were given to each group and a multiple choice questionnaire answered by the nurses immediately after the lecture and 3 months later. A significant amount of knowledge was imparted by the lecturer. About a third of the knowledge, however, was lost within a minute of the end of the lecture, and a half to two-thirds within 3 months. There was no correlation between scores and the row on which the students sat. There was no significant difference between the scores of overseas students and those of British nurses. At immediate recall the techniques differed little. The techniques which scored best were giving the questionnaire before the lectures, giving handouts and using the blackboard. At delayed recall 100% differences in marks were seen between the worst and best techniques in the second lecture. The same techniques which scored best at immediate recall did so on delayed recall. The lowest score occurred where note taking was forbidden. Some questions scored significantly better with note taking. When note taking was forbidden, it made no difference if the student was an habitual notetaker or not. Nor did it make any difference if she was frustrated by the ban. There was no correlation between entry qualifications and the scores obtained. Nurses at a non-teaching hospital did just as well as those at a teaching hospital. It should be emphasised that teaching endeavours to influence 3 aspects-knowledge, skills and attitudes. This series of experiments largely tests the first, but does suggest that a technique which scores highly on information recall may be less helpful in forming constructive attitudes to the patient.
Carbohydrate Metabolism in Pregnancy
Authors: Sheldon J. Bleicher, John B. O'Sullivan, Norbert Freinkel
Journal: New England Journal of Medicine (1964)

COMPELLING evidence that gestation taxes ma > ternal insulin economy is afforded by the usual clinical course in pregnant subjects with marginal or absent pancreatic reserve. Thus, in prediabetes, pregnancy may unmask chemical diabetes mellitus, and, in patients known to have the disease, pregnancy may increase the maintenance requirements for insulin.1 , 2 Previous work from this laboratory has indicated that augmented catabolism of insulin may contribute, at least in part, to these diabetogenic effects of gestation. It has been shown that all portions of the conceptus contain enzymatic mechanisms for the proteolytic inactivation of insulin,3 , 4 that maternal insulin has free access . . .
DERMATITIS PRODUCED BY COSMETICS (LA GERARDINE)
Authors: LESTER HOLLANDER
Journal: JAMA (1933)

Dermatitis produced by cosmetics through direct contact is becoming a more frequently established and recognized condition, but the specific agent responsible for this eruption has to be ferreted out of an almost endless number of these so-called beautifying preparations. As the eruption may develop either immediately after the use of a new preparation as a result of specific hypersensitivity or of chemical irritation, or only after a long period of use, as a result of sensibilization, created through frequent and constant use, difficulty arises in finding the cause. A subconscious defensive attitude on the part of the patient when the subject of cosmetics is broached adds further hindrance. It may be profitable to mention what arouses one's suspicion of a dermatitis produced by contact with cosmetics: Location of the eruption. Sudden appearance. Intense subjective symptoms (burning and itching). Time element. Type of skin eruption. These points need further elucidation: <h3>1.</h3>
Differential role of ethanol and acetaldehyde in the induction of oxidative stress in HEP G2 cells: Effect on transcription factors AP-1 and NF-κB
Authors: Juan Román, Anna Colell, Carmen Blasco, Joan Caballeria, Albert Parés, Joan Rodés, José C. Fernández-Checa
Journal: Hepatology (1999)

The oxidative metabolism of ethanol by the cytochrome P450 2E1 (CYP2E1) has been recognized to contribute to the ethanol-induced deleterious effects through the induction of oxidative stress. This study compared the effect of ethanol and acetaldehyde in the induction of oxidative stress and activation of transcription factors nuclear factor-κB (NF-κB) and activating protein 1 (AP-1) in HepG2 cells, which do not express CYP2E1, and HepG2 cells transfected with CYP2E1 (E47 cells). Neither ethanol (80 mmol/L) nor acetaldehyde (25-200 μmol/L) caused oxidative stress in HepG2 cells, an effect that was independent of blocking reduced glutathione (GSH) synthesis with buthionine- l -sulfoximine (BSO). However, BSO preincubation caused an overproduction of peroxides and activation of NF-κB and AP-1 in E47 cells even in the absence of ethanol. Furthermore, the incubation of E47 cells with ethanol (80 mmol/L for up to 5 days) depleted cellular GSH stores in both cytosol and mitochondria, reflecting the induction of oxidative stress. Ethanol activated NF-κB and AP-1 in E47 cells, an effect that was prevented by 4-methylpyrazole, potentiated by cyanamide, and attenuated by trolox C. Interestingly, however, despite the inability of acetaldehyde to induce oxidative stress in HepG2, acetaldehyde activated NF-κB and AP-1; in contrast, ethanol failed to activate these transcription factors in HepG2. Thus, our findings indicate that activation of NF-κB and AP-1 by ethanol and acetaldehyde occurs through distinct mechanisms. CYP2E1 is indispensable in the induction of oxidative stress from ethanol, whereas the activation of NF-κB and AP-1 by acetaldehyde is independent of oxidative stress.
Cirrhosis and haemolysis complicating methyldopa treatment.
Authors: S L Myer, A J Knell
Journal: BMJ (1977)

Cirrhosis and haemolysis complicating methyldopa treatmentHaemolysis is a recognised complication of methyldopa treatment.'Chronic hepatitis may also be induced by methyldopa and progress to cirrhosis if the drug is continued.2We describe here a patient who developed severe haemolytic anaemia after two years on methyldopa and was also found to have active cirrhosis. Case reportA 68-year-old English woman had suffered from psoriasis for many years.It was usually mild and had needed intermittent treatment with various topical ointments, including betamethasone.A severe exacerbation had occurred four years before admission and had responded to an 11-month course of oral prednisolone.She had never taken methotrexate.Twenty-six months before admission she had presented with symptoms and signs of right and left ventricular failure and had been found to have a blood pressure of 200/120 mm Hg.Treatment-She had responded rapidly to treatment with methyldopa, 1 5 g/day, frusemide 40 mg,/day, and digoxin 0 25 mg day.Four months later an acute generalised eczematous reaction had occurred.All drugs had been stopped for three weeks but the rash had persisted and her heart failure rapidly become more severe.Treatment had been restarted with the same drugs in the same doses.The rash had responded rapidly to topical fluocin- onide, and she had left hospital much improved 11 days later.She had taken the methyldopa, frusemide, and digoxin regularly during the next 21 months, and had remained reasonably well and active until the onset of jaundice.