tbuckley/cabot-search huggingface dataset:
Circulating Activated Endothelial Cells in Sickle Cell Anemia
Authors: Anna Solovey, Yi Lin, Paul Browne, Stephana Choong, Elizabeth Wayner, Robert P. Hebbel
Journal: New England Journal of Medicine (1997)

The vascular wall participates in the pathogenesis of sickle cell disease. To determine whether the endothelium is activated in this disease, we studied the number, origin, and surface phenotype of circulating endothelial cells in patients with sickle cell anemia.
Diagnostic Import of QRS Notching in High-Frequency Electrocardiograms of Living Subjects with Heart Disease
Authors: NANCY C. FLOWERS, LEO G. HORAN
Journal: Circulation (1971)

In a 10-month period 92 patients have been studied for the occurrence of high-frequency notching in orthogonal electrocardiographic leads X, Y, and Z obtained by high-frequency, high-speed techniques. The same patients were studied radiographically with barium, with routine electrocardiograms, hemodynamically at cardiac catheterization and, in many instances, with left ventricular angiograms. Sixty-nine patients had not had cardiac surgery prior to recording and had normal duration of ventricular activation. These patients were placed into groups which included those with no ventricular enlargement, isolated right ventricular enlargement, isolated left ventricular enlargement, and biventricular enlargement. The patients with no ventricular enlargement had a mean of 2.9 notches and never exceeded a total notch count of 6. Those with single ventricular enlargement had a mean of between 5 and 6, while those with biventricular enlargement frequently exceeded 6 notches and had a mean of 8.6. The differences were statistically significant. We concluded, then, that notch count correlates well with the dynamic evidence of ventricular enlargement in a living population. Since the effect is additive, biventricular enlargement elevates the counts sufficiently to remove the overlap with normal seen in groups with univentricular enlargement.
Number and activity of inflammatory cells in bronchoalveolar lavage fluid in asthma and their relation to airway responsiveness.
Authors: C Kelly, C Ward, C S Stenton, G Bird, D J Hendrick, E H Walters
Journal: Thorax (1988)

Bronchial responsiveness to inhaled methacholine was measured four to six days before fibreoptic bronchoscopy in 22 asthmatic patients (10 smokers) and 20 control subjects (12 smokers). The asthmatic patients had a baseline FEV1 greater than 60% predicted and a PD20FEV1 (provocative dose of methacholine causing a 20% fall in FEV1) of 0.006-3.7 mg. The 20 control subjects had normal pulmonary function and a PD20FEV1 above the maximum cumulative dose of methacholine of 6.4 mg. Bronchoalveolar lavage of a middle lobe segment (lingula in four subjects) was performed with three sequential 60 ml aliquots of sterile saline. Cellular metabolic activity was stimulated with latex in aliquots of resuspended cells, and measured by means of luminol enhanced chemiluminescence to assess neutrophil activity and lucigenin enhanced chemiluminescence to assess macrophage activity. Mean absolute total cell counts were similar in the asthmatic and control groups but there were differences in differential cell counts, with a significant increase in eosinophil (p less than 0.05) and lymphocyte (p less than 0.005) counts in asthma. PD20FEV1 was negatively correlated with percentage neutrophil counts (p less than 0.005). Luminol enhanced chemiluminescence/1000 neutrophils was increased about twofold in asthmatic subjects (p less than 0.001), but was not correlated with PD20FEV1 Lucigenin enhanced chemiluminescence/1000 macrophages was increased nearly fourfold in asthmatic patients (p less than 0.001) and showed a negative correlation with PD20FEV1 (p less than 0.01). The macrophage count was increased twofold in current smokers in both groups, but other cell numbers were not altered significantly. Smoking did not affect cellular metabolic activity in either group. This study supports the idea that an inflammatory process is present in the airways of those with asthma, and suggests a relation between bronchial responsiveness and both neutrophil numbers and macrophage activity.
Prevalence of HNPCC in a Series of Consecutive Patients on the First Endoscopic Diagnosis of Colorectal Cancer: A Multicenter Study
Authors: None Riegler, None Savastano, None Selvaggi, None Ciociano, None Martino, None Riccio, None Iorio, None Ponti, None Carratú, None the Italian Collaborative Group:, None Borgheresi, None de Filippo, None Rossi, None Tempesta, None de Palma, None Catanzano, None Russo, None Bianco, None Piscitelli, None di Carlo, None Baldi, None Avagliano, None Guardascione, None Petrelli, None di Giorgio, None de Luca, None d'Avenia, None Cattaneo, None Montanaroi, None Maisto, None Parente, None Vincenti, None Saffiotti, None di Cesare, None Bozzi, None Beatrice
Journal: Endoscopy (1999)

Hereditary non-polyposis colorectal cancer (HNPCC) is a neoplastic syndrome transmitted as an autosomal dominant trait, and is also known as “Lynch syndrome” and “cancer family syndrome.” Recently, four genes responsible for HNPCC were isolated in the majority of the families studied (hMSH2, hMLH1, hPMS1, hPMS2) and germline mutations were reported in HNPCC patients [1] [2] [3] [4].
C-Reactive Protein Levels, Haplotypes, and the Risk of Incident Chronic Obstructive Pulmonary Disease
Authors: Yannick M.T.A. van Durme, Katia M.C. Verhamme, Albert-Jan L.H.J. Aarnoudse, Geert R. Van Pottelberge, Albert Hofman, Jacqueline C.M. Witteman, Guy F. Joos, Guy G. Brusselle, Bruno H.C. Stricker
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Chronic obstructive pulmonary disease (COPD) is characterized by substantial chronic inflammation in the pulmonary compartment as well as in the systemic circulation.To investigate potentially causal association, we examined whether serum levels of high-sensitivity C-reactive protein (hsCRP) and variations in the CRP gene are associated with the risk of developing COPD.This study is part of the Rotterdam Study, a prospective population-based cohort study among subjects aged 55 years or older. At baseline, 6,836 subjects without COPD had a blood sample available for assessment of hsCRP serum levels and haplotypes of the CRP gene. We analyzed the association between hsCRP levels, CRP gene haplotypes, and incident COPD with Cox proportional hazard models, adjusted for age, sex, and other confounders.High levels of hsCRP (>3 mg/L) were associated with a significantly increased risk of incident COPD (hazard ratio [HR], 1.7; 95% confidence interval [CI], 1.16-2.49) compared with persons with low levels (<1 mg/L). The risk remained increased after adjusting for potential confounders and introducing a latency period of 3 years. The risk was most pronounced in former smokers (HR, 2.2; 95% CI, 1.12-3.74). hsCRP was not a risk factor in never smokers. No CRP single nucleotide polymorphism or haplotype was associated with a significantly increased or decreased COPD risk.Increased hsCRP levels are predictive for the occurrence of COPD in smokers. However, haplotypes of the CRP gene, which influence hsCRP levels, are not associated with an altered risk of developing COPD.
Chronic THC intake modifies fundamental cerebellar functions
Authors: Nephi Stella
Journal: Journal of Clinical Investigation (2013)

Delta9-tetrahydrocannabinol (THC), the principal bioactive component in the Cannabis plant, is truly a captivating drug. Acute and chronic THC intake produces a spectrum of biological effects ranging from transient psychotropic effects to prolonged medicinal benefits, many of which have been fostered for centuries by our society. In the July 2013 issue of the JCI, Cutando et al. combined mouse genetics with classic mouse behavioral analysis to deepen our understanding of the physiological consequence of subchronic THC intake on eyeblink reflexes, a fundamental neuronal adaptive response, revealing that this regimen leads to downregulation of the cannabinoid CB1 receptor (referred to as CB1 in the Cutando et al. article) in cerebellar stress fibers and the activation of microglia, raising provocative new questions about the safety profile of regimented THC intake.
AN ABSTRACT OF PAPER ON CHRONIC CATARRHAL LARYNGITIS.Read by Title in the Section of Laryngology and Otology, at the Forty-second Annual Meeting of the American Medical Association, held at Washington, D. C., May, 1891.
Authors: MARION THRASHER
Journal: JAMA (1891)

Chronic catarrhal laryngitis is a continuous passive inflammation of the laryngeal mucous membrane. Its etiology is multifarious. The most influential causes are nasal stenosis, liquor drinking, tobacco smoking, vitiated air, and an intemperate use of the vocal organs. Nasal stenosis necessitates mouth breathing—an abnormal respiration, by which we have carried into the laryngeal cavity an air pregnant with dust, that soon begets an inflammatory process. Chronic alcoholism produces an abnormal activity of the mucous glands of the mouth and fauces, which, during sleep, drops depraved excretions into the larynx, thereby producing a permanent inflammation. Tobacco smoking causes to be deposited daily in the air passages the liquid alkaloid nicotina, which produces partial paralysis of the vasomotor nerves of this locality, and a resultant permanent injury to the mucous texture. Vitiated air, in illy ventilated apartments, is one of the commonest causes of chronic laryngitis. Air reeking with noxious vapors poisons
ANTIBODY SYNTHESIS AT THE CELLULAR LEVEL
Authors: Hans Wigzell
Journal: The Journal of Experimental Medicine (1966)

The specific suppressing activity of passively administered antibody on 7S antibody synthesis against sheep and chicken red blood cells has been investigated at the cellular level using the indirect hemolytic agar-plaque technique. 7S antibody production was found to be sensitive to antibody-induced suppression. No inhibitory effect of transferred antibody was seen until 48 to 72 hr after administration. This indicates that the action of antibody is not by direct suppression of synthesis of already committed cells but rather by removal from the system of the stimulus for maintenance of 7S synthesis. The sensitivity of the 7S system to inhibition decreases with time after immunization but significant specific suppression could still be obtained if transfer of antibody was delayed until 40 days after immunization. The present findings emphasize the role of antibody as a feedback factor during a substantial postpeak period of 7S antibody synthesis and suggest an important role of antigen in stabilizing the 7S antibody production.
On the change of cardiac action potential with age: a study in dogs
Authors: H. BOSKER, A. J DRAKE-HOLLAND, H. E D J T. KEURS, M. I M NOBLE, J. E PASSINGHAM, J. R PEPPER, M. J MAIN, R. B WANLESS
Journal: Cardiovascular Research (1985)

Journal Article On the change of cardiac action potential with age: a study in dogs Get access HANS BOSKER, HANS BOSKER 1Department of Experimental Cardiology, University of Leiden, The Netherlands Search for other works by this author on: Oxford Academic PubMed Google Scholar ANGELA J DRAKE-HOLLAND, ANGELA J DRAKE-HOLLAND * 2Department of Medicine I and Cardiothoracic Surgery, St George's Hospital, London SW17 ORE *Address for correspondence: Dr A J Drake-Holland, Department of Medicine 1, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE. Search for other works by this author on: Oxford Academic PubMed Google Scholar HENK E D J TER KEURS, HENK E D J TER KEURS 1Department of Experimental Cardiology, University of Leiden, The Netherlands Search for other works by this author on: Oxford Academic PubMed Google Scholar MARK I M NOBLE, MARK I M NOBLE 3King Edward VIIHospital, Midhurst, Sussex GU29OBL Search for other works by this author on: Oxford Academic PubMed Google Scholar JANE E PASSINGHAM, JANE E PASSINGHAM 4Department of Cardiac Medicine, Cardiothoracic Institute, Midhurst, Sussex GU29OBL Search for other works by this author on: Oxford Academic PubMed Google Scholar JOHN R PEPPER, JOHN R PEPPER 2Department of Medicine I and Cardiothoracic Surgery, St George's Hospital, London SW17 ORE Search for other works by this author on: Oxford Academic PubMed Google Scholar MARK J MAIN, MARK J MAIN 2Department of Medicine I and Cardiothoracic Surgery, St George's Hospital, London SW17 ORE Search for other works by this author on: Oxford Academic PubMed Google Scholar RICHARD B WANLESS RICHARD B WANLESS 4Department of Cardiac Medicine, Cardiothoracic Institute, Midhurst, Sussex GU29OBL Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 19, Issue 11, November 1985, Pages 674–678, https://doi.org/10.1093/cvr/19.11.674 Published: 01 November 1985
951. Evaluation of HSV-Mediated Alzheimer Gene Therapy Vectors Using Novel Alzheimer Mouse Model: Applications of siRNA and Neprilysin Vectors to Adjust the Metabolic Imbalance of Aâ in Alzheimer's Disease
Authors: Chang-Sook Hong, James R. Goss, William F. Goins, Joseph C. Glorioso
Journal: Molecular Therapy (2005)

Alzheimer's disease (AD) is the most common type of dementia occurring in mid- to late-life, affecting more than 4 million individuals in the United States alone. The amyloid--protein (A), which is generated from the amyloid precursor protein (APP) by - and -secretase cleavage, is a major component of pathological plaques that accumulate in AD brains. The majority of AD patients develop the disease due to over-secretion or faulty clearance of A peptide. Thus down-regulation of the expression of A or stimulation of the A clearance process may ameliorate or potentially cure the devastating disease. As we previously have presented, we have developed replication-defective HSV-mediated gene therapy vectors to favorably adjust the metabolic imbalance of A. The first vector (QAPPi), which carries an siRNA expression cassette targeting APP gene under control of human H1 RNA polymerase III promoter, significantly lowered APP protein level compared to controls in MOI-dependent manner in vitro. The second vector (QNep), which carries Neprilysin, potent A degrading protease, produced a five fold decrease on A secretion compared to cells infected with an isogenic control virus. These results support the hypothesis that HSV-mediated APP-siRNA or Neprilysin expression may reduce A levels in vivo. To test this hypothesis in vivo, we have developed a novel in vivo mouse model using a lentivirus delivering a familial AD mutant form of APP gene (Swedish mutation). The targeted viral delivery system for modeling neurodegenerative diseases has several advantages over germline transgenic mice such as temporal control of transgene expression to avoid any developmental effect and to study aging effect, spatial control of transgene expression to target brain region associated with specific disease, and ability to deliver several transgenes. We are currently investigating the in vivo efficacy of the QAPPi and QNep vectors in the APP lentivirus model.
Routine primary repair vs two-stage repair of tetralogy of Fallot.
Authors: J W Kirklin, E H Blackstone, A D Pacifico, R N Brown, L M Bargeron
Journal: Circulation (1979)

Fifteen of 194 patients (7.7%) with tetralogy of Fallot operated upon since January 1, 1972 under a protocol of routine primary repair despite young age died in-hospital. Most deaths were from low cardiac output. Young age and smallness of size increased the risk of operation. No deaths occurred among patients older than 4 years. High hematocrit was also a risk factor. Transannular patching has an independent effect in increasing risk. The post-repair ratio of peak pressure in the right ventricle to that in the left did not exert an independent effect. To project current risks of a two-stage approach, we determined that five of 158 patients (3.2%) died in-hospital after secondary intracardiac repair after a previous Blalock-Taussig or Waterston anastomosis between 1967--1978. Using these data and those we have published on the risk of shunting, we project that except in very small babies, the risks of hospital death of a two-stage approach are not less than those of primary repair done without a transannular patch, except when body surface area is less than about 0.35 m2. When a transannular patch is used in the primary repair, the two-stage approach is projected to be safer when the child has a body surface area of about 0.48 m2 or smaller.
Abstract 2950: Deletion of TRADD sensitizes oxidative stress-induced necrotic cell death.
Authors: Ki-Bang Koo, Da-gyum Lee, Ji-Yoon Oh, Yun-Sun Lee, You-Sun Kim
Journal: Cancer Research (2013)

Abstract TNF Receptor-Associated Death Domain (TRADD) is an essential mediator of TNF receptor-1-mediated TNF signaling and is responsible for recruitment of other effector proteins. Recruitment of these adaptor proteins leads to the activation of MAP kinases and NF-kB, as well as cell death. it is well known that aspect of ROS biological effects is their regulatory roles on cell death to function as direct activator cell death or as second messengers in the cell death processes. ROS may initiate cell death processes through affecting various signaling cascade. Several studies on the oxidative stress-induced cell death has shown that some of the key TNF signaling molecules serve as the molecular targets of ROS in cell death. However, there is no report concerning whether TRADD has a function in oxidative stress-induced cell death. The availability of TRADD deficiency mice let us investigate the physiological functions of TRADD on oxidative stress-induce cell death. In this study, we found that TRADD deficiency renders cells more susceptible to oxidative stress-induced cell death through the persistent activation of JNK. Citation Format: Ki-Bang Koo, Da-gyum Lee, Ji-Yoon Oh, Yun-Sun Lee, You-Sun Kim. Deletion of TRADD sensitizes oxidative stress-induced necrotic cell death. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2950. doi:10.1158/1538-7445.AM2013-2950
Salvage Chemotherapy with ABVD in MOPP-Resistant Hodgkin's Disease
Authors: Armando Santoro, Valeria Bonfante, Gianni Bonadonna
Journal: Annals of Internal Medicine (1982)

Fifty-five consecutive patients with advanced recurrent Hodgkin's disease resistant to MOPP chemotherapy (mechlorethamine, vincristine, procarbazine, and prednisone) were given ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, and dacarbazine). In 54 patients evaluable for response, complete remission after pathologic restaging was seen in 59% and partial remission in 13%. Fifteen of 29 patients (52%) showing disease progression during primary MOPP treatment achieved complete remission after ABVD. The median time to complete response was 3 months. The median duration for complete remission was 17 months, and 38% of patients who attained complete remission have remained alive and continuously disease free at 5 years from start of ABVD treatment. The median survival of complete responders was more than 60 months. Toxic manifestations were moderate, aside from pronounced vomiting in more than half of patients. These results indicate that ABVD is an effective salvage regimen for MOPP-resistant Hodgkin's disease.
Lack of Efficacy of Haemophilus b Polysaccharide Vaccine in Minnesota
Authors: Michael T. Osterholm, Joan H. Rambeck, Karen E. White, Jean L. Jacobs, Lynne M. Pierson, James D. Neaton, Craig W. Hedberg, Kristine L. MacDonald, Dan M. Granoff
Journal: JAMA (1988)

We evaluated the efficacy of Haemophilus b polysaccharide vaccine in children in Minnesota using a case-control study. The vaccine became available in Minnesota in August 1985. During the subsequent 28 months, 88 cases of invasive H influenzae type b disease were identified in children 24 to 71 months of age, the group targeted for vaccination. Of the 88 cases, 36 (41%) occurred in vaccinated children. Fifty-eight (33%) of 176 controls were vaccinated during a similar period. The vaccine's protective efficacy for children with any history of vaccination was -58% (95% confidence interval = -204% to 18%). The vaccine's protective efficacy for children who were most likely to be protected by vaccination was -55% (95% confidence interval = -238% to 29%). Our results indicate that vaccination with Haemophilus b polysaccharide vaccine had no effect in preventing H influenzae type b disease in Minnesota children.
Laryngeal Muscle Activities with Cerebral Hypoxia–Ischemia in Newborn Lambs
Authors: Alastair A. Hutchison, David J. Burchfield, John A. Wozniak, Sondra J. Mohrman
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

This study tested the hypotheses that (1) acute cerebral hypoxia–ischemia changes laryngeal adductor, laryngeal abductor, and diaphragmatic activities, resulting in central apnea with laryngeal closure; and (2) these laryngeal muscle activities act to maintain absolute lung volume. The respiratory pattern was determined in three asphyxiated, awake preterm lambs after cesarean section birth and in 12 awake, term lambs, with normal lung function, after induction of acute cerebral hypoxia–ischemia by occlusion of the brachiocephalic artery. Electrocorticogram activity, flow, volume, electromyograms of laryngeal abductor and adductor muscles and diaphragm, and, in the term lambs, trans-upper airway pressure and carotid blood flow were recorded. With either preterm birth asphyxia or induced acute cerebral hypoxia–ischemia, minute ventilation initially increased, and then hypopnea occurred. During the hypopnea, laryngeal adductor activity was prominent, accompanied by an increased upper airway pressure and a maintained/raised absolute lung volume. Thus, when acute hypoxia–ischemia limited to the upper body is induced in lambs with normal lung function, expiratory laryngeal adduction with closure of the upper airway occurs and likely functions to aid autoresuscitation.
TEN Is TEN, but Is SSSS?-Reply
Authors: Alexander K. C. Leung
Journal: JAMA (1985)

<h3>In Reply.—</h3> I still must insist that there are two types of TEN, namely, the SSSS and the drug-induced type. My statement is supported by many authors of various medical journals and textbooks.<sup>1-5</sup> I do agree with Dr Arnold that SSSS and drug-induced TEN have different causes, different pathogeneses, different pathological lesions, different treatments, and different prognoses. The reason why I did not elaborate on this previously was because of the limitation of space and because it is well recognized. But TEN is TEN no matter what the cause. To draw an analogy, there are two types of diabetes mellitus: the juvenile onset type and the maturity (adult) onset type. They, too, have different etiologies, pathogeneses, treatments, and prognoses. Despite this, they are still called diabetes mellitus.
DIFFICULT DEFECATION IN INFANTS.
Authors: THOS. CHAS. MARTIN
Journal: JAMA (1898)

ual looseness of his conduct with women.He made no attempt to conceal his amused incredulity when I charged this vice with being largely responsible for his nasal discomfort, but he agreed nevertheless to give virtue a month's trial.Not to rob this remedy of any possible credit, all other treatment was for the time suspended.