tbuckley/cabot-search huggingface dataset:
TRANSMISSION OF THE COMMON COLD TO VOLUNTEERS UNDER CONTROLLED CONDITIONS. IV. SPECIFIC IMMUNITY TO THE COMMON COLD*
Authors: George Gee Jackson, Harry F. Dowling
Journal: Journal of Clinical Investigation (1959)

Although the common cold is the most prevalent illness of humans, information on the antigenicity of the infectious agents and the immune response of the host to the infection has been difficult to obtain.Epidemiologic investigations have led to divergent hypotheses.The frequent repetition of colds, on the one hand, has suggested little or no immunity to reinfection.On the other hand, the diminution or disappearance of colds among isolated populations, even in an arctic climate, is compatible with the belief that persons develop im- munity to specific common cold agents (1, 2).Analysis of the influence of age upon susceptibility also is inconclusive with regard to acquired im- munity to the common cold.The frequency of common colds tends to decline with age beyond childhood (3-5), but in a survey of colds within a group of families apparent evidence of brief im- munity was observed after infection only among children (3).Transmission of the common cold to volunteers by filtered nasal secretions or nasopharyngeal washings offers the most direct approach to the problem.Several groups of investigators have shown that the common cold can be successfully transmitted to volunteers, but almost always it has been impossible to infect all of them.The inci- dence of experimental colds has been about 35 to 50 per cent (6, 7).The basis for susceptibility or resistance is not known but might be specific im- munity.In previous studies we have shown that the infectivity of filtered infectious nasal secretions can be neutralized by the globulin fraction, but not by albumin, from pooled human plasma (8).
Utility of Preload Alteration in Assessment of Left Ventricular Filling Pressure by Doppler Echocardiography: A Simultaneous Catheterization and Doppler Echocardiographic Study
Authors: David G. Hurrell, Rick A. Nishimura, Duane M. Ilstrup, Christopher P. Appleton
Journal: Journal of the American College of Cardiology (1997)
A novel ϵγδβ thalassemia of 1.4 Mb deletion found in a Japanese patient
Authors: Chiemi Furuya, Yasuhiro Yamashiro, Yukio Hattori, Minako Hino, Hiroko Nishioka, Yoshihisa Shimizu, Kozue Okano, Keizou Horibe
Journal: American Journal of Hematology (2007)

Abstract A novel large deletion, causing ϵγδβ thalassemia (here called, ϵγδβ thalassemia Jpn‐I) was discovered in a 6‐year‐old Japanese boy. He was born uneventfully, but revealed thalassemia minor after birth. The mutation was inherited from his mother. The deletion, caused by an illegitimate recombination extended from 750 kb upstream to 660 kb downstream of e‐globin gene, and removed about 1.4 Mb of DNA, the largest in ϵγδβ thalassemias. A 19‐nucleotide orphan sequence and direct repeats were present at the junction. The deletion lost several functional genes, but no relevant symptoms manifested. The breakpoints were determined by relatively simple methods. Am. J. Hematol., 2008. © 2007 Wiley‐Liss, Inc.
Bacterial Endotoxin (Lipopolysaccharide) as a Cause of Erythema Multiforme
Authors: Walter B. Shelley
Journal: JAMA (1980)

The classic iris lesions in a patient with erythema multiforme bullosum were reproduced grossly as well as microscopically by the intradermal injection of a variety of heat-killed, Gram-negative bacteria, as well as their common endotoxin, lipopolysaccharide W. In vitro exposure of the patient's blood to these antigens induced specific fibrin microclots characteristic of a hypersensitivity state. It is possible that some cases of erythema multiforme associated with a variety of respiratory, gastrointestinal, or urinary tract infections may represent a single specific delayed sensitivity reaction to the bacterial endotoxin, lipopolysaccharide. (<i>JAMA</i>243:58-60, 1980)
INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
Authors: Maurice Landy, Louis Pillemer
Journal: The Journal of Experimental Medicine (1956)

It has been shown that injection of lipopolysaccharides, derived from a variety of Gram-negative bacterial species, evokes in mice a rapidly developing rise in resistance to infection with Gram-negative pathogens. This is accompanied by an elevation in properdin titer, at times to levels 2 to 3 times the normal. The rate, magnitude, and duration of these responses are dependent on many factors, the most important of which are the quantity and timing of the lipopolysaccharide administered. The increased resistance to infection evoked in mice by lipopolysaccharides was effective against infections produced by endotoxin-bearing organisms-bacterial species highly susceptible in vitro to the bactericidal action of the properdin system. Properdin titers of mice prior to infection provide an incomplete picture of the subsequent reaction of the host to the infective agent. Following infection with Gram-negative organisms, properdin levels accurately reflect the bacteriologic course and outcome of the infection. Thus, in control animals, properdin titers progressively declined and the animals died, while in mice appropriately treated with lipopolysaccharide, properdin levels were either maintained in the normal range or increased, depending on the dose and time of administration of lipopolysaccharide; this was always accompanied by successful management of the infection. The complex nature of the alterations produced in the host by lipopolysaccharides is stressed. It is pointed out that the increase in the ability of the host to cope with Gram-negative infections may be the result of stimulation of other defense mechanisms, in addition to the properdin system.
Who's in Charge Here? — Or Alice Searches for a King in Mediland
Authors: Anne R. Somers
Journal: New England Journal of Medicine (1972)

Abstract There is no king in Mediland. Despite Alice's yearning — and she speaks for millions who seek simple solutions to complex problems — there probably never will be, as long as we remain a democracy. What is needed is a shared, multi-group, responsibility within a framework of clearly, but democratically, defined public accountability. Five groups share major responsibility — for both our current problems and their solution: consumers, doctors, hospitals, private health-insurance carriers, and the government. Within this shared responsibility, the pre-eminent role will probably go to the group demonstrating greatest capacity for leadership, which, paradoxically, may mean greatest capacity for self-discipline. The extent to which this self-discipline and leadership are realized may determine whether we achieve a creative new synthesis for medical education, health-care delivery and financing, or whether we doom ourselves to a mutually destructive stalemate.
Congenital Abnormalities in Infancy.
Authors: Arnold J. Rudolph
Journal: JAMA (1963)

The relative importance of congenital anomalies has increased considerably as the infant mortality rate from other causes has decreased. This book, therefore, will be popular among those interested in the diagnosis and management of congenital abnormalities, particularly since it contains a remarkable amount of information not readily available elsewhere. The editor notes in his preface that he has attempted  limit the scope of the book to anomalies apparent, by and large, in the first weeks of life, and the book's ten chapters are mainly by contributors with special knowledge of the newborn.  The first chapter, on incidence and etiology, by C. O. Carter, contains an excellent, concise discussion on the incidence of congenital anomalies and their environmental and genetic determination, as well as the general principles of genetic counseling. In successive chapters congenital abnormalities are described under the various organ systems. A final chapter by A. White Franklin, devoted
EXPERIMENTAL TYPE III PNEUMOCOCCUS PNEUMONIA IN MONKEYS
Authors: Thomas Francis, Edward E. Terrell
Journal: The Journal of Experimental Medicine (1934)

It has been possible by the intratracheal or intrabronchial inoculation of Type III Pneumococcus to produce in monkeys of the M. cynomolgos species an experimental pneumonia which in its clinical aspects closely resembles pneumococcus lobar pneumonia in man. The experimental disease is characterized by the development of a well localized pulmonary lesion of lobar distribution which tends to spread, the frequent occurrence of septicemia, a sustained fever, and the termination of the infection after a variable interval, in recovery or death of the animal. Wide variations in the severity of the disease in different monkeys have been noted. These variations appear to be due primarily to differences in the resistance of individual animals. The height of the septicemia accompanying the experimental pneumonia has been found to be the most valuable objective index of the probable outcome of the disease. Other factors which may influence the course and outcome of the disease are discussed.
THE BUTYRIC ACID TEST FOR SYPHILIS IN THE DIAGNOSIS OF METASYPHILITIC AND OTHER NERVOUS DISORDERS
Authors: Hideyo Noguchi, J. W. Moore
Journal: The Journal of Experimental Medicine (1909)

1. In the secondary and tertiary stages of syphilis without direct involvement of the nervous system the cerebro-spinal fluid yielded the butyric acid reaction of feeble intensity. The fluid under these conditions gave neither a positive cytodiagnosis nor the Wassermann test for syphilis. 2. The cerebro-spinal fluid of cases of hereditary syphilis showed a positive butyric reaction in about 90 per cent. and a positive Wassermann test in about 80 per cent. of the cases examined. 3. The cerebro-spinal fluid of cases of cerebral and spinal syphilis yielded the butyric acid reaction and the cytodiagnosis in every instance (100 per cent.) and gave the Wassermann reaction in from 50 to 75 per cent. of those examined. 4. The cerebro-spinal fluid from cases of general paralysis gave positive butyric acid reactions in 90 per cent., positive cell counts in 91 per cent., and positive Wassermann test in 73 per cent. of those examined. 5. The cerebro-spinal fluid from cases of tabes dorsalis gave positive butyric acid reactions and cell counts in 100 per cent. and positive Wassermann test in 53 per cent. of those examined. 6. The cerebro-spinal fluid from other forms of psychosis in which a syphilitic history was not obtained gave positive butyric acid reactions and cell count in 2.8 per cent. and Wassermann test in 13 per cent. of those examined. 7. The cerebro-spinal fluid from cases of acute inflammatory diseases of the meninges always gave a flocculent precipitate with the butyric acid reaction but never gave the Wassermann test. 8. The cerebro-spinal fluid from persons suffering from typhoid fever, pneumonia, pulmonary tuberculosis, etc., in which the meninges are not inflamed, gave neither the butyric acid nor the Wassermann test. 9. We think it justifiable to conclude that the butyric acid reaction affords a ready means of distinguishing normal from pathological cerebro-spinal fluid and will prove to be useful in routine clinical practice, especially in detecting syphilitic disease and in confirming or setting aside certain doubtful diagnoses of syphilitic or metasyphilitic lesions of the central nervous system. The reaction should commend itself as a valuable addition to the Wassermann test, the results of which it is capable of confirming and extending.
Child outpatient non-attendance may indicate welfare concerns
Authors: M. Watson
Journal: BMJ (2002)

EDITOR—Much effort has been put into reducing the high rates of non-attendance at outpatient clinics. 1 2 Currently there is a drive to improve the quality of outpatient services, which in itself will improve attendance rates. The laudable recommendations of the Clinical Standard Advisory Group approach the problem from a health perspective.3 Sharp …
Increased Blood Leukocytes in Patients with Campylobacter pylori
Authors: Tuomo Karttunen, Seppo Niemelä
Journal: Annals of Internal Medicine (1990)

Letters and Corrections1 February 1990Increased Blood Leukocytes in Patients with Campylobacter pyloriTuomo Karttunen, MD, Seppo Niemelä, MDTuomo Karttunen, MDSearch for more papers by this author, Seppo Niemelä, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-112-3-232_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:Campylobacter pylori infection is strongly associated with chronic gastritis, but its systemic effects are unknown. We have studied the relation between C. pylori-associated gastritis and peripheral leukocyte count.We studied 105 randomly chosen outpatients with dyspepsia (from 40 to 71 years of age) (1). Warthin-Starry stain was used to search for curved rods in eight biopsy specimens taken systematically from the antrum and corpus. The quantity of inflammatory cells was estimated in specimens from the antrum stained with haematoxylin and eosin, using a 4-point scale (0 = normal; 3 = heavy increase). Leukocyte counts were done on...References1. KarttunenNiemeläLehtolaHeikkiläMäentaustaRäsänen TSJJOO. Campylobacter-like organisms and gastritis: histopathology, bile reflux, and gastric fluid composition. Scand J Gastroenterol. 1987;22:478-86. CrossrefMedlineGoogle Scholar2. JonesEldridgeFoxSethiWhorwell DJAPP. Antibody to the gastric campylobacter-like organism ("Campylobacter pyloridis")-clinical correlations and distribution in the normal population. J Med Microbiol. 1986;22:57-62. CrossrefMedlineGoogle Scholar3. LangenbergRauwssHouthoff WEH. Follow-up study of individuals with untreated Campylobacter pylori-associated gastritis and of noninfected persons with non-ulcer dyspepsia. J Infect Dis. 1988;157:1245-9. CrossrefMedlineGoogle Scholar4. VirellaLopes-Virella GM. Infections and atherosclerosis. Transplant Proc. 1987;19:(Suppl 5):26-35. MedlineGoogle Scholar5. MattilaNieminenValtonen KMV. Association between dental health and myocardial infarction. Br Med J [Clin Res]. 1989;298:779-81. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBlood leukocyte differential inHelicobacter pylori infectionCould Helicobacter pylori infection increase the risk of coronary heart disease by modifying serum lipid concentrations?Helicobacter pylori induces lymphocyte activation in peripheral blood cultures 1 February 1990Volume 112, Issue 3Page: 232-232KeywordsBiopsyBloodCellsGastritisHelicobacter pyloriOutpatients Issue Published: 1 February 1990 PDF downloadLoading ...
Biliary excretion of cadmium.
Authors: C G Elinder, M Pannone
Journal: Environmental Health Perspectives (1979)

Biliary excretion of cadmium was studied in two groups of five rats which were given repeated injections of 109Cd. The first group was given a total amount of 6 mg Cd/kg which was 6 times as much as the second group. The elimination of cadmium in bile, urine, and feces was measured 4 to 5 weeks after the last injection. The relative biliary excretion of cadmium was the same in both groupetion, which was 0.001% but, less than the total fecal elimination of cadmium, which averaged 0.034% during the same time.
A 5-hydroxytryptophan-secreting carcinoid tumour
Authors: A. C. P. Campbell, A. H. Gowenlock, D. S. Platt, P. J. D. Snow
Journal: Gut (1963)

An atypical case of the malignant carcinoid syndrome, associated with multiple peptic ulcers, is described. The tumour cells were argyrophil but not argentaffin, and the tumour was found to contain 5-hydroxytryptophan (5-H.T.P.) but not 5-hydroxytryptamine (5-H.T.). This aberrant biochemical behaviour was associated with the virtual absence of 5-H.T.P.-decarboxylase from the tumour tissue. The tumour contained notable quantities of histamine.
Cardiac Resynchronization Therapy: Current State of the Art
Authors: Angelo Auricchio, William T. Abraham
Journal: Circulation (2004)

2][3][4][5][6] As noted below, CRT makes heart failure patients feel better, improves cardiac structure and function, and reduces all-cause as well as heart failure morbidity and mortality.Thus, there may be a clinical mandate for use of CRT in many patients with chronic heart failure.This notion raises important questions about the clinical application of this therapy.For example, will the availability of CRT change our current clinical approach to heart failure patients?Will it lead to new research advances?Will CRT patients also require an implantable cardioverter defibrillator (ICD) to optimize outcomes?Will the clinical benefits of these therapies justify the costs? Ventricular Dyssynchrony: A Pathophysiological Cause or Contributor to Heart FailurePatients with left ventricular (LV) systolic dysfunction and dilation, with or without clinical signs or symptoms of heart failure, frequently have ventricular conduction delays. 7In such patients, this is usually manifested as a left bundlebranch block (LBBB).This type of conduction abnormality is generally associated with delayed depolarization and contraction of the lateral LV free wall (Figure 1), whereas the interventricular septum exhibits a normal (early) contraction resulting in paradoxical septal motion.The abnormal activation sequence induced by spontaneous LBBB or by right ventricular (RV) pacing generates changes in regional ventricular loading conditions (Figure 2), possibly redistributes myocardial blood flow, 8 and creates a regional nonuniform myocardial metabolism. 9These effects of ventricular dyssynchrony might contribute to disease progression in LV systolic dysfunction patients. 10For example, studies in experimental heart failure induced by rapid ventricular pacing showed regional differences in the extent of ventricular hypertrophy with an apicobasal-and septolateral-oriented gradient. 11Moreover, experimentally induced LBBB has demonstrated a large effect on the expression of regional stress kinases and calcium-handling proteins. 12Preliminary evidence suggests that the expression of p38-MAPK (a stress kinase) is significantly elevated in the endocardium of the late-activated region, whereas phospholamban is significantly decreased. 11In addition, sarco(endo)plasmatic reticulum Ca 2ϩ -ATPase is decreased in the region of early activation. 11he meaning of such complex interactions between changes in regional loading conditions, blood flow distribution, regional myocardial metabolism, and gene and protein expression induced by an abnormal activation sequence is not fully understood.However, it is likely that these conse-
Error in Identification
Authors: Fredrick J. Stare
Journal: JAMA (1963)

<h3>To the Editor:</h3> —The following correction has been sent W. Coda Martin, MD, and his attorneys, Olson and Markey: "On page 636 of Vol 184 of<i>JAMA</i>[Special Communication: 'Boston Nutrition Society, Inc., Plaintiff vs Fredrick J. Stare, Defendant,' May 25, 1963] it states, 'Present in the courtroom for part of the trial and conferring with the plaintiff's counsel, but not appearing as a witness, were Dr. W. Coda Martin, a physician from Beverly Hills, Calif....' We have been informed that Dr. Martin was not in the courtroom and we regret this error in identification."
Pregnancy and Untreated Addisonian Pernicious Anaemia
Authors: B. K. Armstrong, R. E. Davis, J. D. Martin, H. J. Woodliff
Journal: BMJ (1968)

The case histories are given of two patients, aged 38 and 35 years, who conceived while suffering from Addisonian pernicious anaemia. The relationship of these findings to the routine use of folic acid during pregnancy is discussed.
Isolation of the Encysted Form of<i>Toxoplasma gondii</i>from Human Skeletal Muscle and Brain
Authors: Jack S. Remington, Ellen N. Cavanaugh
Journal: New England Journal of Medicine (1965)

DESPITE the high prevalence of antibodies to toxoplasma among adults in the United States1 the parasite is rarely recognized in routine histologic sections obtained at autopsy. Since antibodies are demonstrable for many years (and perhaps for life) after acute acquired toxoplasmosis2 the question arises whether the stimulus to antibody formation in these persons is persistence of live parasites or of residual antigens. The first aspect of this question can be answered by the demonstration of living organisms in the course of isolation procedures. Because cysts of toxoplasma are often distributed sparsely throughout an organ it would be necessary in such . . .
Protease-Activated Receptor-2 Activation Causes EDHF-Like Coronary Vasodilation
Authors: Peter G. McLean, Daniel Aston, David Sarkar, Amrita Ahluwalia
Journal: Circulation Research (2002)

Activation of protease-activated receptor (PAR)-2 has been proposed to be protective in myocardial ischemia/reperfusion (I/R) injury, an effect possibly related to an action on the coronary vasculature. Therefore, we investigated the effects of PAR2 activation on coronary tone in isolated perfused rat hearts and elucidated the mechanisms of any observed effects. Although having a negligible effect on ventricular contractility, the PAR2 activating peptide SLIGRL produced an endothelium-dependent coronary vasodilatation (ED 50 =3.5 nmol). Following I/R injury, the response to SLIGRL was selectively preserved, whereas the dilator response to acetylcholine was converted to constriction. Trypsin also produced a vasodilator dose-response curve that was biphasic in nature (ED 50-1 =0.36 U, ED 50-2 =38.71 U). Desensitization of PAR2 receptors indicated that the high potency phase was mediated by PAR2. Removal of the endothelium but not treatment with L-NAME (300 μmol/L), indomethacin (5 μmol/L), or oxyhemoglobin (10 μmol/L) inhibited the response to SLIGRL and trypsin. Treatment with the K + -channel blockers TEA (10 mmol/L), charybdotoxin (20 nmol/L)/apamin (100 nmol/L), or elevated potassium (20 mmol/L) significantly suppressed responses. Similarly, inhibition of lipoxygenase with nordihydroguaiaretic acid (1 μmol/L), eicosatetraynoic acid (1 μmol/L), or baicalein (10 μmol/L), desensitization of C-fibers using capsaicin (1 μmol/L, 20 minutes), or blockade of vanilloid (VR1) receptors using capsazepine (3 μmol/L) inhibited the responses. This study shows, for the first time, that PAR2 activation causes endothelium-dependent coronary vasodilation that is preserved after I/R injury and is not mediated by NO or prostanoids, but involves the release of an endothelium-derived hyperpolarizing factor (EDHF), possibly a lipoxygenase-derived eicosanoid, and activation of VR1 receptors on sensory C-fibers.