tbuckley/cabot-search huggingface dataset:
INCIDENCE AND SPECIFICITY OF THE ANTIBODY FOR A DISTINCTIVE CONSTITUENT OF THE BROWN-PEARCE TUMOR
Authors: Ian MacKenzie, John G. Kidd
Journal: The Journal of Experimental Medicine (1945)

A detailed study has been made of an antibody which appears in the blood of certain rabbits implanted with the Brown-Pearce carcinoma or injected with extracts of it and which reacts specifically in vitro in mixture with a distinctive sedimentable constituent of the Brown-Pearce tumor cell. The observations as a whole seem to indicate that this constituent of the Brown-Pearce tumor differs notably from certain other sedimentable substances which can be extracted from various rabbit tissues and identified by serological means. The implications of the findings are discussed.
Warfarin Effect Enhanced By Disulfiram (Antabuse)
Authors: Emil Rothstein
Journal: JAMA (1972)

<h3>To the Editor.—</h3> Disulfiram (Antabuse) and warfarin sodium (Coumadin) both act upon, or within, the liver cell. Disulfiram competes with nadide (nicotinamide adenine dinucleotide) for the active centers of the enzyme, aldehyde dehydrogenase, and also decreases the oxygen consumption and the xanthine oxidase, succinoxidase, and catalase activity of liver homogenates.<sup>1</sup>Warfarin inhibits enzyme systems in the liver cells that synthesize prothrombin.<sup>1</sup> A review of the literature reveals only one case report,<sup>2</sup>also from this institution, describing the combined use of these two drugs. A second case of disulfiram's potentiation of warfarin is now reported. <h3>Report of a Case.—</h3> A 52-year-old man had rheumatic aortic insufficiency dating back at least to 1959. He had severe congestive failure. An aortic valve implant was performed Aug 23, 1966, with marked improvement in his cardiac reserve. Digitalis and warfarin were prescribed for him indefinitely. In July 1970 he developed a period
P03 The diagnostic value of transient elastography compared to clinical acumen, laboratory tests and ultrasound? Is there added value?
Authors: G. E. Dolman, A. Ferguson, S. Harris, A. M. Zaitoun, M. James, S. D. Ryder, G. P. Aithal, I. N. Guha
Journal: Gut (2011)

<h3>Introduction</h3> The diagnostic performance of transient elastography (TE), and other non-invasive biomarkers of fibrosis, is assessed by direct comparison with liver biopsy. However clinical acumen, laboratory tests and ultrasonography are utilised for the assessment of fibrosis in clinical practice. <h3>Aim</h3> The aim of this study was to assess the incremental value of elastography compared to routine diagnostic tools. <h3>Method</h3> We included consecutive patients with both fibroscan and biopsy data. Patients with decompensated cirrhosis or suboptimal fibroscan readings were excluded (success rate &lt;60% or IQR/median &gt;0.21). Four consultant/attending hepatologists (who were blinded to TE and biopsy results) were asked to assess the severity of fibrosis on the basis of anonymised clinical data. Simple laboratory tests (eg, full blood count, liver function tests and clotting) and ultrasonography for each case were then given to the clinicians to assess the incremental increase in diagnostic performance. One independent pathologist formally assessed the degree of fibrosis on biopsy, which was the reference standard. Receiver Operating Characteristics (ROC) curves were calculated for (1) clinical acumen (2) clinical acumen + laboratory tests + ultrasonography and (3) TE, for the prediction of significant fibrosis (greater or equal to F2) and cirrhosis. <h3>Results</h3> 130 patients were enrolled in the study with paired data and a biopsy deemed adequate for staging. The cohort (65% male; mean age 46 years) was of mixed aetiology (15% ALD, 48% chronic viral hepatitis, 24% NAFLD, 24% other). The average biopsy length was 23 mm with 16 portal tracts. The median TE reading was 6.3 (median IQR 0.8 and 100% success rate). <h3>Conclusion</h3> There appears to be little additional benefit in AUC performance of transient elastography to diagnose cirrhosis compared to clinical acumen and routinely available tests. There is however incremental diagnostic benefit for the assessment of significant fibrosis. The baseline performance of simple diagnostic tools, which will vary depending on the stage of fibrosis, needs to be accounted for when assessing liver biomarker performance.
Synergistic Antitumor Activity of Anti-CD25 Recombinant Immunotoxin LMB-2 with Chemotherapy
Authors: Rajat Singh, Yujian Zhang, Ira Pastan, Robert J. Kreitman
Journal: Clinical Cancer Research (2011)

Abstract Purpose: Although anti-CD25 recombinant immunotoxin LMB-2 is effective against CD25+ hairy cell leukemia, activity against more aggressive diseases such as adult T-cell leukemia (ATL) is limited by rapid disease progression between treatment cycles. Our goal was to determine in vivo whether rapid growth of CD25+ tumor is associated with high levels of tumor interstitial soluble CD25 (sCD25) and whether chemotherapy can reduce tumor sCD25 and synergize with LMB-2. Experimental Design: Tumor xenografts expressing human CD25 were grown in mice, which were then treated with LMB-2 and chemotherapy either alone or in combination, and sCD25 level and antitumor activity were measured. Results: CD25+ human xenografts growing rapidly in nude mice had intratumoral sCD25 at levels that were between 21- and 2,200 (median 118)-fold higher than in serum, indicating that interstitial sCD25 interacts with LMB-2 in tumors. Intratumoral sCD25 levels were in the range 21 to 157 (median 54) ng/mL without treatment and 0.95 to 6.1 (median 2.6) ng/mL (P &amp;lt; 0.0001) 1 day after gemcitabine administration. CD25+ xenografts that were too large to regress with LMB-2 alone were minimally responsive to gemcitabine alone but completely regressed with the combination. Ex vivo, different ratios of gemcitabine and LMB-2 were cytotoxic to the CD25+ tumor cells in an additive, but not synergistic, manner. Conclusions: Gemcitabine is synergistic with LMB-2 in vivo unrelated to improved cytotoxicity. Synergism, therefore, appears to be related to improved distribution of LMB-2 to CD25+ tumors, and is preceded by decreased sCD25 within the tumor because of chemotherapy. To test the concept of combined treatment clinically, patients with relapsed/refractory ATL are being treated with fludarabine plus cyclophosphamide before LMB-2. Clin Cancer Res; 18(1); 152–60. ©2011 AACR.
Raynaud's Disease and Primary Pulmonary Hypertension
Authors: GUILLERMO C. CELORIA, GILBERT H. FRIEDELL, SHELDON C. SOMMERS
Journal: Circulation (1960)

A case of Raynaud's disease with autopsy is reported in which the clinical picture was dominated by pulmonary hypertension apparently unassociated with any significant pulmonary parenchymal disease. Microscopically cellular intimal proliferation of small pulmonary muscular arteries and arterioles was the most characteristic lesion. In several proximal medium-sized muscular arteries there was necrotizing arteritis with thrombus formation. Similar vascular lesions were not found in other organs, although generalized arteriosclerosis and arteriolosclerosis were present. The pulmonary vascular changes are thought to represent a local exacerbation of generalized vascular disease, but a specific etiology was not apparent.
Functional magnetic resonance imaging of synesthesia: activation of V4/V8 by spoken words
Authors: J. A. Nunn, L. J. Gregory, M. Brammer, S. C. R. Williams, D. M. Parslow, M. J. Morgan, R. G. Morris, E. T. Bullmore, S. Baron-Cohen, J. A. Gray
Journal: Nature Neuroscience (2002)
Parathyroid Hormone-Related Protein as a Prohormone: Posttranslational Processing and Receptor Interactions*
Authors: JOHN J. ORLOFF, DAPHNE REDDY, ANNE E. DE PAPP, KAI H. YANG, NEIL E. SOIFER, ANDREW F. STEWART
Journal: Endocrine Reviews (1994)

PARATHYROID hormone-related protein (PTHrP) bioactivity was identified in 1983 in tumors associated with humoral hypercalcemia of malignancy (HHM). The N-terminal amino acid and complementary DNA (cDNA) sequences were identified in 1987. The search for the causative agent of HHM was fueled by the frequency with which HHM occurs, by the severe complications of hypercalcemia (coma, renal failure, death), and by the identification in clinical and laboratory studies of a novel calcium-regulating hormone that could be postulated as the cause of HHM. It was expected at the time that this search would lead to the purification of the responsible "humor," and that that "humor," when identified, would prove to have some normal physiological role. It was not anticipated that the "humor" would prove to be produced by almost every type of cell in the body at some stage of development, or that the search for the novel "humor" would lead to the identification of an unusually large, complicated, and interesting family of peptide hormones.
Scientific truth and perceived truth about sexual human nature: Implications for therapists
Authors: Joseph A. Buckhalt, Erica J. Gannon
Journal: Behavioral and Brain Sciences (2000)

Therapists and their patients must deal with the negative sequelae of short term mating strategies. Implications for therapy of Gangestad &amp; Simpson's strategic pluralism theory are compared with those of Buss's sexual strategies theory and Eagly's social role theory. Naive theories held by therapists and patients, as well as prevailing societal views, are posited as influential in determining the course and outcome of therapy.
Too early to introduce colorectal screening, say specialists
Authors: A. Ferriman
Journal: BMJ (2000)

Mass screening for colorectal cancer should not be introduced before the results of ongoing clinical trials because of the lack of diagnostic facilities for the investigation of symptoms, a statement from colorectal specialists said this week.

The statement, issued jointly by the British Society of Gastroenterology (BSG), the Royal College of Physicians (RCP) and the Association of Coloproctology of Great Britain and Ireland, concedes that evidence shows that some form of screening …
Clinical Remarks on Pseudo-Peritonitis and Epilepsy in Hysteria
Authors: J. S. Bristowe
Journal: BMJ (1890)

THE paper which I am about to read this evening will be devoted mainly to the narratives of two cases which came into the hos- pital within a few days of one another, which presented so many points in common that, even up to the time of their dismissal, I regarded them as being cases of the same kind, but of which later developments proved, I think, pretty clearly that while my dia- gnosis with respect to one was correct, my diagnosis with respect to the other was altogether erroneous.I propose, in the first instance, to give an account of each case during its first sojourn in the hospital; in the second instance, to trace the subsequent history of each; and, in the third instance, to discuss the phenomena of the case in respect of which I was mistaken.E. W., a married woman, aged 28, was admitted under my care on November 10th, 1888.Though supposed to be delicate, her only serious illness previous to the present one, was apparently the result of a miscarriage three years ago.The symptoms she presented then were much like those of the present illness, were attributed by her medical attendant to inflammation of the womb, and kept her confined to bed for nine months.A year later she was delivered of a still-born child at term.-.Her present illness came on suddenly three days before admis- sion, with general pain and tenderness in the abdomen, and was attributed by her husband to her having had to get up frequently in the night to attend upon him on account of an accident from the results of which he was suffering.She had 'complained of pain and tenderness in the belly ever since, with sickness and diarrheea, and some difficulty in micturition.The catamenia ap- peared on the day of admission.She was a fairly well-nourished woman, with an expression of great distress, complaining of pain and tendernfess in the belly, and difficulty in passing water.She lay on her back with her knees drawn up, breathing irregularly and shallowly at the rate of eighteen in the minute, and with the intercostal muscles only.The tongue was dry and coated, and there were sordes on the teeth and lips.Her abdomen was somewhat swollen, tense, and with rigid parietes, and very tender.The pain occupied no particular spot, the tenderness was general.Th6re was no dull area or evidence of tumour, and no sign of the presence of fluid.The
Thrombotic thrombocytopenic purpura after influenza vaccination.
Authors: R C Brown, T E Blecher, E A French, P J Toghill
Journal: BMJ (1973)

Miss Round.2We await the estimations of vitamin D levels to be completed on random samples from children in our survey.Maybe we shall be shown to be wrong, but in view of the marked difference between the heights and weights of our treated children and the control groups and the correlation of vitaniin D levels with serum alkaline phosphatase found in Asians by Dr. O'Riordan and his colleagues3 we doubt it.A full report on the effects of treatment and on alkaline phos- phatase levels will be submitted for publication shortly.-Weare, etc.,-
A susceptibility locus for Parkinson's disease maps to chromosome 2p13
Authors: Thomas Gasser, Bertram Müller-Myhsok, Zbigniew K. Wszolek, Ralph Oehlmann, Donald B. Calne, Vincenzo Bonifati, Benjamin Bereznai, Edito Fabrizio, Peter Vieregge, Rolf D. Horstmann
Journal: Nature Genetics (1998)
Treatment of Meprobamate Withdrawal Syndrome
Authors: B. Florian Sørensen
Journal: JAMA (1963)

I can approve of the statement in "Death After Withdrawal of Meprobamate" that "similar clinical courses may occur in the terminal stages of fatal withdrawal of barbiturates and meprobamate." The authors recommend that in case of abuse meprobamate be withdrawn slowly, and if convulsions occur they recommend that dosage be increased and then again reduced over a longer period. Most psychiatrists in Denmark would do otherwise. According to our experience symptoms arising after abrupt withdrawal of short-acting barbiturates or of meprobamate are best treated with phenobarbital, 0.1-0.3 gm, given three times a day for two or three days. After this period phenobarbital is slowly withdrawn.
Function of oleic acid on epidermal barrier and calcium influx into keratinocytes is associated with<i>N</i>-methyl d-aspartate-type glutamate receptors
Authors: Y. Katsuta, T. Iida, K. Hasegawa, S. Inomata, M. Denda
Journal: British Journal of Dermatology (2008)

Background Unsaturated fatty acids from sebum affect calcium dynamics in epidermal keratinocytes, disrupt the barrier function and induce abnormal keratinization. However, the mechanisms of these effects have not been clarified. Objectives To investigate the function of unsaturated fatty acids in epidermis. Methods Antagonists of calcium channel receptors were applied to mouse skin together with oleic acid. Measurements were made of transepidermal water loss (TEWL), and hyperproliferation was assessed. The effects of the antagonists on calcium influx into cultured normal human keratinocytes and on cytokine production were also evaluated. Results N‐methyl‐d‐aspartate (NMDA) receptor antagonists such as MK801 and D‐AP5 specifically inhibited the increase in TEWL caused by oleic acid, and suppressed keratinocyte hyperproliferation. These compounds also inhibited the increase in the intracellular concentration of calcium ions induced by oleic acid. MK801 suppressed the production of interleukin‐1α by keratinocytes induced by oleic acid. Conclusions Unsaturated fatty acids such as oleic acid might function via NMDA receptors.
Phasic mitral blood flow and regional left ventricular dimensions: possible mechanism of active assist to ventricular filling.
Authors: B G Bertha, J D Folts
Journal: Circulation (1986)

Postsystolic myocardial segment shortening (PSS) has been observed in dogs and humans by means of ultrasonic crystals but has never been studied specifically. In this study, both subendocardial and subepicardial regional function in the basal circumflex and midventricular anterior myocardium (LAD) was studied during late systole and early diastole with ultrasonic crystals. Fifteen open-chest dogs were instrumented with electrocardiographic leads; Millar catheters for measurement of left ventricular pressure, left ventricular dP/dt, and aortic blood pressure; flow probes for determination of aortic and mitral blood flow; and subendocardial and subepicardial crystal pairs to measure subendocardial segment length shortening velocity (dL/dt). Crystal pairs were placed in the subendocardial left oblique mode and the extreme subendocardial right oblique mode (-50 and +50 degrees from equator) in the lateral basal (circumflex, n = 9) and anterior midventricular myocardium (LAD, n = 6). Subendocardial segments showed PSS averaging 34 +/- 7% of the total shortening distance in the circumflex bed and 21 +/- 2% in the LAD bed (p = NS). The rate of subendocardial segment shortening during PSS increased 273 +/- 42.6% (p less than .05) relative to the rate of segment shortening during ejection in the circumflex bed and 126 +/- 40% (p less than .05) in the LAD bed (p = NS). The most rapid diastolic increase in subendocardial length (peak +dL/dt) occurred immediately after subendocardial PSS. Subendocardial diastolic peak +dL/dt occurred after the onset of mitral inflow during the acceleration limb of the rapid ventricular filling phase. Overlying subepicardial segments began lengthening 82 +/- 12 msec before onset of subendocardial segment lengthening in the circumflex bed and 63 +/- 9 msec before subendocardial lengthening in the LAD bed (p less than .05), indicating that the subepicardial segment had begun to lengthen while subendocardial segment shortening continued after end-systole. Onset of early segmental subepicardial lengthening varied with respect to the point of end-systole. Early segmental subepicardial lengthening with subendocardial PSS may be a mechanism by which the rapid filling phase of the left ventricle is actively potentiated by storing potential energy released as early diastolic elastic recoil.
Cardioprotective effect of metoprolol and enalapril in doxorubicin‐treated lymphoma patients: A prospective, parallel‐group, randomized, controlled study with 36‐month follow‐up
Authors: Peter Georgakopoulos, Paraskevi Roussou, Evangellos Matsakas, Apostolos Karavidas, Nick Anagnostopoulos, Theodoros Marinakis, Athanasios Galanopoulos, Fotis Georgiakodis, Stelios Zimeras, Michael Kyriakidis, Apostolos Ahimastos
Journal: American Journal of Hematology (2010)

Anthracyclines have contributed to a marked increase in survival in different types of cancer [1,2]. Unfortunately, they are associated with dose-dependent cardiotoxicity and heart failure (HF) [3–8]. Change to a weekly dosage schedule with slow infusions has been tested, a strategy that requires more frequent hospital visits and increased storage resources[7,9]. Liposomal anthracycline formulations with reduced drug exposure and lower plasma concentrations may still be cardiotoxic at higher cumulative doses [10]. Beta-blockers and angiotensin converting enzyme(ACE) inhibitors have been shown to reduce anthracycline-induced cardiotoxicity,but have not been tested in long-term prospective, randomized,controlled studies with well defined cardiotoxicity criteria and careful cardiac function monitoring [11–16]. We investigated doxorubicin-induced clinical or subclinical cardiotoxicity in lymphoma patients after concomitant prophylactic therapy with metoprolol or enalapril or no concomitant treatment. We examined whether cardiotoxicity was related to the treatment or any other variable. We found that HF was less frequent under concomitant treatment than no treatment, especially in the metoprolol group, but the differences were not significant. No association was found between the presence of cardiotoxicity and concomitant treatment or other variable apart of age that had a significant impact. The marginal benefit seen with metoprolol should be investigated further.
Vagal modulation of the rate-dependent properties of the atrioventricular node.
Authors: M Nayebpour, M Talajic, C Villemaire, S Nattel
Journal: Circulation Research (1990)

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.
Attack of the Killer Tomatoes-Reply
Authors: Cynthia J. Schmeichel
Journal: JAMA (1991)

<h3>In Reply.</h3> —The Council on Scientific Affairs' article, "Biotechnology and the American Agricultural Industry," was designed to provide information on the safety of individual, genetically modified foods, not to endorse or assert the safety of any particular food or technology. The introduction of the<i>Bacillus thuringiensis</i>var<i>kurstaki</i>(Btk) transgene into plants for purposes of pest control and the effects of the toxin on herbivorous insects is clearly described. Two parameters will require continued monitoring to ensure that human safety requirements are met: (1) the concentration of the toxin in the transgenic plant; and (2) structural changes unique to the transgene-encoded toxin protein. Current studies are directed to promoting expression of the toxin gene during those stages of the plant life cycle that are most susceptible to insect damage. The goal of transgenic plant technology is not specifically to increase toxin expression in the edible fruits of plants, but to