tbuckley/cabot-search huggingface dataset:
Fatal Cardiac Tamponade-Reply
Authors: William B. Guiney
Journal: JAMA (1983)

In Reply.—  We appreciate Dr Parsa's comments on the pathogenesis of perforation with venous catheterization and indwelling catheters. His impressive personal series without vessel perforation is admirable.  We are grateful to Dr Merrill for pointing out that not all guide wires employed in the Seldinger technique are flexible at both ends. Their report of venous perforation during insertion of a dialysis catheter is instructive in the potential hazards of central venous catheterization.  As we state in our article, perforation may occur during catheter insertion or at some later time. Clinical alertness to the possibility of perforation is, therefore, necessary during the entire period of use of central venous catheters.
PNEUMOCOCCUS INVASION OF THE THROAT, FOLLOWED BY PLEUROPNEUMONIA AND APPENDICITIS: OPERATION AND RECOVERY
Authors: Wm. E. Peacock
Journal: BMJ (1909)

Once the appendix has gained the position described, ths veins in the meso-appendix are kinked, but it is pro- bzb1e that the artery with its firmer walls is not.This quickly produces a condition of congestion in the appendix, which the small veins passing directly from the appendix to the caecum, although they are not obstructed, are inadequate to relieve.When this condition once occurs all chance of spontaneous recovery is passed.What appears at the operation to be a tight constriction at the base of the appendix is really only the line of demarcation
Antisense to LOX-1 Inhibits Oxidized LDL–Mediated Upregulation of Monocyte Chemoattractant Protein-1 and Monocyte Adhesion to Human Coronary Artery Endothelial Cells
Authors: Dayuan Li, Jawahar L. Mehta
Journal: Circulation (2000)

Background —We have recently demonstrated a lectin-like receptor for oxidized (ox)-LDL (LOX-1) in human coronary artery endothelial cells (HCAECs). This receptor is upregulated by ox-LDL. The present study examined the significance of LOX-1 in monocyte adhesion to HCAECs and endothelial injury in response to ox-LDL. Methods and Results —HCAECs were incubated in the presence of antisense oligodeoxynucleotides to the 5′-coding sequence of the human LOX-1 gene (0.5 μm/L). Basal LOX-1 mRNA and protein were suppressed by antisense LOX-1. Ox-LDL–mediated upregulation of LOX-1 was also suppressed by antisense LOX-1. Incubation of HCAECs with ox-LDL (40 μg/mL) for 24 hours markedly increased monocyte chemoattractant protein-1 (MCP-1) mRNA and protein expression as well as monocyte adhesion to HCAECs ( P &lt;0.01). After 48 hours of preincubation of HCAECs with antisense LOX-1, ox-LDL–mediated upregulation of MCP-1 and monocyte adhesion to HCAECs both were suppressed ( P &lt;0.01), whereas sense LOX-1 had no effect. Whereas antisense or sense LOX-1 alone (both 0.5 nmol/L) did not injure the cells, antisense LOX-1, but not sense LOX-1, reduced ox-LDL–mediated HCAEC injury, determined as LDH release ( P &lt;0.01). Activation of mitogen-activated protein kinase (MAPK) may play a critical role in signal transduction in ox-LDL–mediated alteration in MCP-1 expression, since antisense LOX-1, but not the sense LOX-1, completely inhibited the ox-LDL–induced MAPK activation. Conclusions —These observations with the first use of a specific antisense to human LOX-1 mRNA suggest that LOX-1 is a key factor in ox-LDL–mediated monocyte adhesion to HCAECs.
Letter: Diabetic diarrhoea.
Authors: T S Low-Beer
Journal: BMJ (1973)

Lung Cancer and Smoking SIR,-It seems that cigarette smokers adjust the number of cigarettes smokzd to obtain a predetermined dose of nicotine (Dr.M. A. H. Russell and others, 1 December, p. 512).Would it not be much safer (no tar), and much cleaner for non-smokers in the vicinity, to market nicotine inhalers, similar to those used by asthmatics?The price of these could be adjusted so that the Govern- ment need not lose revenue.The nicotine addicts would presumably not be at risk from bronchogenic carcinoma and chronic bronchitis, and there would be no carbon monoxide to contribute to atheroma forma- tion.-Iam, etc.,
318 THE HEPATITIS C VIRUS ENHANCES ACTIVATION OF THE EGF-RECEPTOR AND AKT-ACTIVITY BY NS3/4A-MEDIATED CLEAVAGE OF THE T-CELL PROTEIN TYROSINE PHOSPHATASE
Authors: E. Brenndörfer, J. Karthe, L. Frelin, P. Cebula, A. Erhardt, H. Hengel, R. Bartenschlager, M. Sällberg, D. Häussinger, J. Bode
Journal: Journal of Hepatology (2009)
Endocrine aspects of liver disease.
Authors: R M Jenkins
Journal: BMJ (1980)

The table gives correlation coefficients between wet and dry bulb temperatures and systolic and diastolic blood pressure.A normal Blood pressure and ambient temperature: correlation coefficients between wet and dry bulb ambient temperatures and systolic and diastolic blood pressure (phase V) in 2178 males aged 40-65 at work in west central Scotland Age Systolic Diastolic (y) No Wet Dry Wet Dry 40-44 100 0.
Acute and long term respiratory damage following inhalation of ammonia.
Authors: D Leduc, P Gris, P Lheureux, P A Gevenois, P De Vuyst, J C Yernault
Journal: Thorax (1992)

A lifelong non-smoker who was the victim of a massive accidental exposure to anhydrous ammonia gas was followed up for 10 years. In the acute phase the patient presented with severe tracheobronchitis and respiratory failure, caused by very severe burns of the respiratory mucosa. After some improvement he was left with severe and fixed airways obstruction. Isotope studies of mucociliary clearance, computed tomography, and bronchography showed mild bronchiectasis. It is concluded that acute exposure to high concentrations of ammonia may lead to acute respiratory injury but also to long term impairment of respiratory function.
Prostaglandin E<sub>2</sub>in the expired breath condensate of patients with asthma
Authors: K. Kostikas, G. Papatheodorou, K. Psathakis, P. Panagou, S. Loukides
Journal: European Respiratory Journal (2003)

Inhaled prostaglandin (PG)E 2 has been found to cause bronchodilation in asthmatics, although it does not have bronchodilative effects in normal subjects. The aim of this study was to investigate the levels of PGE 2 in the expired breath condensate of patients with asthma, the possible contribution of smoking habit to its levels and the possible relationship between PGE 2 and the degree of bronchial hyperresponsiveness, as assessed by the provocation dose of histamine causing a 20% fall in forced expiratory volume in one second (FEV 1 ) (PD 20 ). A total of 30 mild asthmatics (15 smokers, all steroid-naive, FEV 1 88±6 (%±sd)) and 20 healthy control subjects (10 smokers) were studied. Histamine challenge testing was performed in all subjects and the PD 20 was determined. The results showed that asthmatic smokers had significantly higher values of PGE 2 compared to asthmatic nonsmokers and control subjects (40±21 versus 14.5±4.5 versus 11.7±3 pg·mL −1 , respectively). Further analysis showed that PGE 2 levels were significantly higher in asthmatic smokers compared to smoker and nonsmoker controls (40±21 versus 11.6±2 versus 11.7±4 pg·mL −1 , respectively). No significant difference was observed between asthmatic nonsmokers and both control smokers and control nonsmokers. No significant correlation was found between PGE 2 levels and PD 20 in all groups of asthmatics, irrespective of smoking habit. In conclusion, the elevation of prostaglandin E 2 in the expired breath condensate of patients with asthma is mainly attributed to smoking habit and prostaglandin E 2 levels do not predict the degree of bronchial hyperresponsiveness.
SOME NOTES ON THE EFFECTIVENESS OF THE VENEREAL DISEASE PROGRAM
Authors: H. G. IRVINE
Journal: JAMA (1922)

Four years ago it was my privilege to present a paper<sup>1</sup>before the Surgeon General's Conference in Washington outlining a state program against venereal diseases. This program was based very largely on work done in California, the first state to organize and finance a bureau of venereal diseases, and in Minnesota, where the work was organized some months later. This program included medical work, such as epidemiologic investigation of cases, organization of clinics, distribution of arsphenamin and the reporting of cases; laboratory work, such as Wassermann tests, examination of smears for gonococci, and dark field examinations for spirochetes; social service work, such as investigation of sources of infection, the rounding up of delinquent patients and in some cases stimulation of law enforcement against prostitution, and rehabilitation of delinquents; and educational work with both the laity and the medical profession in a variety of ways. Within a comparatively short period
Interleukin-5 Induces CD34<sup>+</sup>Eosinophil Progenitor Mobilization and Eosinophil CCR3 Expression in Asthma
Authors: ROBERT G. STIRLING, ELIZABETH L. J. VAN RENSEN, PETER J. BARNES, K. FAN CHUNG
Journal: American Journal of Respiratory and Critical Care Medicine (2001)

Asthma is characterized by the accumulation of activated T cells and eosinophils within the airway. Eosinophils derive from CD34+ bone marrow progenitor cells under the influence of hematopoietic growth factors, subsequently migrating to the airways under the cooperative influence of interleukin (IL)-5 and chemokines, including eotaxin. We compared the relative effects of systemic versus local IL-5 on progenitor-cell mobilization and mature eosinophil phenotype by using flow cytometry, following the administration of intravenous (2 μ g) or inhaled (15 μ g) IL-5 to nine patients with mild asthma. Intravenous IL-5 induced a rapid reduction in circulating eosinophil counts followed by prolonged blood eosinophilia. Both intravenous (p < 0.002) and inhaled (p < 0.05) IL-5 significantly increased CD34+/CD45+ lymphoblastoid eosinophil progenitors. Intravenous IL-5 increased mature eosinophil CCR3 expression from a baseline mean fluorescence intensity (MFI) of 658 ± 51.7 to 995 ± 93.2 at 24 h (p < 0.05), but had no effect on interleukin-5 receptor subunit α or CD11b expression. Lymphocyte CCR3 MFI was increased by intravenous IL-5 from 38.5 ± 13.6 at baseline to 73.6 ± 14.3 at 24 h (p < 0.05). Systemic IL-5 increased circulating eosinophil progenitors, suggesting a key role for systemic IL-5 in eosinophil mobilization. Further, IL-5 causes terminal maturation of the eosinophil by increasing CCR3 expression, potentially affecting CCR3-dependent chemotaxis by eosinophils and lymphocytes.
Chlamydial Pneumonia and Asthma: A Potentially Important Relationship
Authors: Roger C. Bone
Journal: JAMA (1991)

In this issue of<i>JAMA</i>, Hahn et al<sup>1</sup>document an interesting relationship between chlamydial pneumonia and asthma in adults using a matched comparison method. These investigators found that patients with serologically confirmed<i>Chlamydia pneumoniae</i>infection (antibody titers greater than 1:64) were much more likely to develop bronchial asthma subsequent to their chlamydial infection than were seronegative patients (antibody titers less than 1:16). Nearly 30% of the<i>Chlamydia</i>-exposed (seropositive) patients were later diagnosed as having asthmatic bronchitis, whereas only 7% of unexposed (seronegative) patients received the same diagnosis in the 6-month period after their respiratory illness. The context for this finding is a trend toward increasing incidence, morbidity, and mortality attributable to asthma— despite advances in diagnosis and treatment. During the 1980s, statistics relating to asthma showed distinct increases in mortality in the United States and in most industrialized countries.<sup>2,3</sup>Furthermore, a recent article demonstrated
Hepatitis B-virus (HBV) markers in serum and liver tissue of HBsAg carriers after liver transplantation and treatment with anti-HBs-hyperimmune globulin
Authors: U. Hopf, B. Möller, R. Steffen, W.O. Bechstein, G. Blumhardt, P. Neuhaus, D. Huhn
Journal: Journal of Hepatology (1989)
A commensal bacterial product elicits and modulates migratory capacity of CD39<sup>+</sup>CD4 T regulatory subsets in the suppression of neuroinflammation
Authors: Yan Wang, Sakhina Begum-Haque, Kiel M Telesford, Javier Ochoa-Repáraz, Marc Christy, Eli J Kasper, Dennis L Kasper, Simon C Robson, Lloyd H Kasper
Journal: Gut Microbes (2014)

Tolerance established by host-commensal interactions regulates host immunity at both local mucosal and systemic levels. The intestinal commensal strain Bacteroides fragilis elicits immune tolerance, at least in part, via the expression capsular polysaccharide A (PSA). How such niche-specific commensal microbial elements regulate extra-intestinal immune responses, as in the brain, remains largely unknown. We have recently shown that oral treatment with PSA suppresses neuro-inflammation elicited during experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. This protection is dependent upon the expansion of immune-regulatory CD4 T cells (Treg) expressing CD39, an ectonucleotidase. Here, we further show that CD39 modulation of purinergic signals enhances migratory phenotypes of both total CD4 T cells and Foxp3+ CD4 Tregs at central nervous system (CNS) lymphoid-draining sites in EAE in vivo and promotes their migration in vitro. These changes are noted during PSA treatment, which leads to heightened accumulation of CD39+ CD4 Tregs in the CNS. Deficiency of CD39 abrogates accumulation of Treg during EAE, and is accompanied by elevated Th1/Th17 signals in the CNS and in gut-associated lymphoid tissues. Our results demonstrate that immune-modulatory commensal bacterial products impact the migratory patterns of CD4 Treg during CNS autoimmunity via the regulation of CD39. These observations provide clues as to how intestinal commensal microbiome is able to modulate Treg functions and impact host immunity in the distal site.
Therapeutic Efficacy of Oral Charcoal in Congenital Erythropoietic Porphyria
Authors: Neville R. Pimstone, Shobha N. Gandhi, Sudhir K. Mukerji
Journal: New England Journal of Medicine (1987)

GüNTHER'S disease, or congenital erythropoietic porphyria, is a rare autosomal recessive disorder of heme biosynthesis characteristically associated with diminished uroporphyrinogen III cosynthetase activity.1 , 2 Disfiguring photomutilation starts in childhood. Avoidance of sunlight has been the only sure way to prevent or retard photosensitivity. The treatments that have been tried have had limited success. A partial benefit after splenectomy has been reported,3 but there is little evidence of specific, long-term improvement.4 5 6 Haining and colleagues first reported suppression of bone marrow release of porphyrins by induced polycythemia,7 supporting the notion that disease activity can be modulated by diminishing porphyrin overproduction at the source . . .
New gene associated with Alzheimer's disease
Authors: D. Josefson
Journal: BMJ (1998)

Researchers have uncovered intriguing new insights into the aetiology of the most common form of Alzheimer's disease.

Most of those who succumb to Alzheimer's disease have the late onset form, and develop symptomsafter the age of 60. Yet much of what is known about the disease relates to the less common, earlyonset type, which only accounts for 10% of cases. The two new studies elucidate the complexity of late onset Alzheimer's disease (Nature Genetics 1998;19:321-2 and 357-360).

Pathologically, Alzheimer's disease is characterised by the accumulation of neurofibrillary tangles and protein plaques of s amyloid in the brain. These protein deposits are thought to disrupt cellular function and may themselves be byproducts of dying neurons. In brains without Alzheimer'sdisease, the amount of amyloid plaque is minimal.

Scientists at the Massachusetts …
Enhancing Diabetes Care in a Low-Income, High-Risk Population
Authors: M. J. Friedrich
Journal: JAMA (2000)

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Understanding the molecular and cellular basis of therapeutic stem and progenitor cell transplantation for tissue revascularization
Authors: I SPYRIDOPOULOS
Journal: Cardiovascular Research (2004)

See also article by Li et al.  [6]  (pages 64–72) in this issue. 

The primary goal of therapy for patients with acute myocardial infarction is rapid revascularization of ischemic tissue. Since thrombolytic therapy or catheter-based intervention can only accomplish so much initially, new strategies are desirable to salvage already injured tissue and restore organ function. A decade ago, several researchers developed and refined the concept of therapeutic angiogenesis by gene therapy, either through the application of cDNA-encoding plasmids or by local injection of the desired protein [1]. Shortcomings of this approach included the lack of precise targeting, fading activity over time, or even clinical complications such as enhancement of rhythm disorders by injuring the electrical conduction system, i.e., when using intramyocardial transfer of DNA plasmids.

Over the past years, it has become clear that bone marrow contains vascular progenitor cells that can mobilize to ischemic sites and facilitate neoangiogenesis from preexisting endothelium. Adult bone marrow is a reservoir of tissue-specific stem and progenitor cells. Angiocompetent hematopoietic cells (hemangioblasts) consist of endothelial progenitor cells (EPCs) and hematopoietic stem cells … 

*Tel.: +49 69 6301 7387, +49 69 6301 5749; fax: +49 69 6301 6546. Email address: spyridopoulos{at}em.uni-frankfurt.de
β <sub>2</sub> -Adrenergic Receptor Stimulation Improves Endothelial Progenitor Cell–Mediated Ischemic Neoangiogenesis
Authors: Gennaro Galasso, Roberta De Rosa, Michele Ciccarelli, Daniela Sorriento, Carmine Del Giudice, Teresa Strisciuglio, Chiara De Biase, Rossella Luciano, Raffaele Piccolo, Adele Pierri, Giuseppe Di Gioia, Nella Prevete, Bruno Trimarco, Federico Piscione, Guido Iaccarino
Journal: Circulation Research (2013)

Endothelial progenitor cells (EPCs) are present in the systemic circulation and home to sites of ischemic injury where they promote neoangiogenesis. β2-Adrenergic receptor (β2AR) plays a critical role in vascular tone regulation and neoangiogenesis.We aimed to evaluate the role of β2AR on EPCs' function.We firstly performed in vitro analysis showing the expression of β2AR on EPCs. Stimulation of wild-type EPCs with β-agonist isoproterenol induced a significant increase of Flk-1 expression on EPCs as assessed by fluorescence-activated cell sorter. Moreover, β2AR stimulation induced a significant increase of cell proliferation, improved the EPCs migratory activity, and enhanced the EPCs' ability to promote endothelial cell network formation in vitro. Then, we performed in vivo studies in animals model of hindlimb ischemia. Consistent with our in vitro results, in vivo EPCs' treatment resulted in an improvement of impaired angiogenic phenotype in β2AR KO mice after induction of ischemia, whereas no significant amelioration was observed when β2AR knock out (KO) EPCs were injected. Indeed, wild-type-derived EPCs' injection resulted in a significantly higher blood flow restoration in ischemic hindlimb and higher capillaries density at histological analysis as compared with not treated or β2AR KO EPC-treated mice.The present study provides the first evidence that EPCs express a functional β2AR. Moreover, β2AR stimulation results in EPCs proliferation, migration, and differentiation, enhancing their angiogenic ability, both in vitro and in vivo, leading to an improved response to ischemic injury in animal models of hindlimb ischemia.
Mechanism of Control of Hemorrhage from Duodenal Ulcer by Gastric Hypothermia
Authors: Henry Sosin
Journal: JAMA (1963)

LOCAL GASTRIC HYPOTHERMIA has been employed successfully for control of massive upper gastrointestinal hemorrhage in a variety of pathological conditions. The beneficial effects derived from this form of management in massive, uncontrolled hemorrhage from duodenal ulcer have been especially gratifying. Bleeding gastric lesions also have responded to this form of therapy, but less uniformly. 1   Previous experiments have shown that local gastric hypothermia results in a 66% decrease in gastric blood flow. 2,3 Marked decreases in the rate of gastric secretion and in the digestive activity of the gastric juice secreted also have been observed. 2,4-6   Despite accumulating knowledge, the mechanism of control and arrest of hemorrhage from ulcers of the duodenum remains obscure. Gastric secretion and the digestive activity of the juice are markedly inhibited at all temperatures below 30 C (86 F), but temperatures of 8 to 10 C (46.4 to 50 F) are required for
Abstract 3198: Growth factors protect intestinal stem cells from radiation-induced apoptosis by suppressing PUMA through the PI3K/AKT/p53 axis
Authors: Wei Qiu, Brian Leibowitz, Lin Zhang, Jian Yu
Journal: Cancer Research (2010)

Abstract Gastrointestinal toxicity is the primary limiting factor in abdominal and pelvic radiotherapy, but has no effective treatment currently. We recently showed a critical role of the BH3-only protein PUMA in acute radiation-induced GI damage and GI syndrome in mice. Growth factors such as IGF-I and bFGF have been shown to protect against radiation-induced intestinal injury, though the underlying mechanisms remain to be identified. We report here the suppression of PUMA through the PI3K/AKT/p53 axis in the intestinal stem cells (ISCs) as a novel molecular mechanism of growth factor-mediated intestinal radioprotection. IGF-I or bFGF impaired radiation-induced apoptosis, and the expression of PUMA and p53 in the crypt cells and intestinal stem cells. Using colonic epithelial cells that undergo PUMA-dependent and radiation-induced apoptosis, we found that a PI3K inhibitor, dominant-negative PI3K, or Mdm2 antagonist restored the induction of PUMA, p53 and apoptosis in the presence of growth factors. In contrast, overexpression of AKT suppressed the induction of PUMA and p53 by radiation. Furthermore, inhibiting PI3K or activating p53 abrogated growth factor-mediated suppression of apoptosis and PUMA expression in the intestinal crypts and stem cells following radiation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3198.