tbuckley/cabot-search huggingface dataset:
THE TREATMENT OF CERTAIN RESPIRATORY DISEASES BY CHLORIN
Authors: EDWARD B. VEDDER
Journal: JAMA (1925)

Since the publication of an earlier paper1on this subject, considerable additional work has been done, and many inquiries have been received, and it is believed that the observations presented here should be reported.  In the original paper, it was stated that cultures taken after exposure to chlorin remained sterile or developed only a few scattered colonies, and it was believed that hour exposures appeared sufficient practically to sterilize the tonsillar, postnasal and pharyngeal surfaces.  Undoubtedly this conclusion was at least partially erroneous, and later investigations have shown that sterility of the mucous surfaces following the therapeutic administration of chlorin cannot be expected. The error was probably due to two conditions of the experiment. In the first place, normal volunteers were used for this work; and, as relatively few bacteria were obtained in the first culture, sterility in the second culture was obtained with relative ease. Again, a higher
Severe malaria in children in Yemen: two site observational study
Authors: Abdullah Al-Taiar, Shabbar Jaffar, Ali Assabri, Molham Al-Habori, Ahmed Azazy, Nagiba Al-Mahdi, Khaled Ameen, Brian M Greenwood, Christopher J M Whitty
Journal: BMJ (2006)

<h3>Abstract</h3> <b>Objectives</b> To assess the burden of malaria on health services, describe the clinical presentation of severe malaria in children, and identify factors associated with mortality by means of a prospective observational study. <b>Setting</b> Two public hospitals in Taiz (mountain hinterland) and Hodeidah (coastal plain), Yemen. <b>Participants</b> Children aged 6 months to 10 years. <b>Results</b> Of 12 301 paediatric admissions, 2071 (17%) were for suspected severe malaria. The proportion of such admissions varied according to the season (from 1% to 40%). Falciparum malaria was confirmed in 1332 children; 808 had severe disease as defined by the World Health Organization. Main presentations were respiratory distress (322/808, 40%), severe anaemia (291/800, 37%), and cerebral malaria (60/808, 8%). Twenty two of 26 children who died had a neurological presentation. No deaths occurred in children with severe anaemia but no other signs of severity. In multivariate analysis, a Blantyre coma score ≤ 2, history of fits, female sex, and hyperlactataemia predicted mortality; severe anaemia, respiratory distress, and hyperparasitaemia were not significant predictors of mortality. <b>Conclusions</b> Severe malaria puts a high burden on health services in Yemen. Although presentation is similar to African series, some important differences exist. Case fatality is higher in girls.
USE OF SUBCUTANEOUS INJECTIONS OF OXYGEN
Authors: T. S. Kirk
Journal: BMJ (1928)

applies to an infected .herd of cattle.It is "herd treat- ment."I quote once -more words by Major Church:"' To 'the native --races,' as -Sir Frederick Lugard has said, 'civilization must mean something more, than the methods of the development syndicate or the assiduous cultivation of new wants.'....The pu-rsuit of wealth, if-it is accompanied by the careless exploitation of native races, is neither an honourable nor in the long run a profitable policy for the representatives of a great nation."DisiiXfested labour -is more profitable labouri; anid it is easier to treat a whole-heavily infected -community herd fashion, at the risk of a few deaths in uninfected persons, than to determine who are iinfected anid to treat them only.The secondand antithetic usage is an expression of the belief that every individual is.entitled to an individual
A Prudent Approach to Control of Cholesterol Levels
Authors: Stephan D. Fihn
Journal: JAMA (1987)

Concern about serum cholesterol has become a national preoccupation. Recently, this pernicious substance has received even greater attention after announcement of the recommendations of the National Cholesterol Education Program.<sup>1</sup>This initiative represents the culmination of four decades of epidemiologic research that has demonstrated a nearly monotonic relationship between elevations of the serum cholesterol level and risk of atherosclerotic heart disease. Until recently, however, it was uncertain whether lowering of the serum cholesterol level would also lower cardiac risk. The results of the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT) now confirm that in men with substantial elevations of plasma cholesterol levels, dietary and drug intervention can indeed reduce coronary morbidity and mortality.<sup>2</sup> The LRC-CPPT data, viewed as the linchpin in the cholesterol-coronary chain of evidence, have served as the catalyst for the National Cholesterol Education Program. The recommendations advise frequent screening of most adults and treatment of
Beta receptor occupancy. Assessment in the intact animal.
Authors: C J Homcy, H W Strauss, S Kopiwoda
Journal: Journal of Clinical Investigation (1980)

Organ uptake of 125I-hydroxybenzylpindolol, a potent beta adrenergic antagonist, was determined after intravenous administration. Pretreatment with the beta agonist, epinephrine, inhibited an almost identical fraction of 125I-hydroxybenzylpindolol binding as did the antagonist, propranolol. Specific beta receptor binding accounted for 50% of total uptake in the lung and demonstrated the following characteristics. The dose-response curve for propranolol inhibition of 125I-hydroxybenzylpindolol binding duplicated that reported for its physiologic action. Simultaneous serum propranolol levels as determined by a sensitive radioimmunoassay allowed an apparent dissociation rate constant approximately 7 nM to be obtained that correlated closely with the results reported from membrane binding studies. Alpha blockade had no effect and inhibition of 125I-hydroxybenzylpindolol binding by propranolol demonstrated stereospecificity. After chemical sympathectomy with reserpine or 6-OH dopamine, there was a 100% increase in receptor specific binding. Finally, a scintillation camera was employed to visually and quantitatively detect 125I-hydroxybenzylpindolol displacement from the lung during intravenous propranolol administration in the living animal. Reversal of binding was rapid and an in vivo inhibition curve was generated. Such a method provides the potential for longitudinally assessing beta receptor occupancy and apparent affinity directly in man.
An orally active ETA/ETB receptor antagonist ameliorates proteinuria and glomerular lesions in rats with proliferative nephritis
Authors: Dulcenombre Gómez-Garre, Raquel Largo, Xue-Hui Liu, Sylvia Gutierrez, M. José López-Armada, Itziar Palacios, Jesús Egido
Journal: Kidney International (1996)
Sickle cell disease and hemochromatosis
Authors: Marcel E. Conrad
Journal: American Journal of Hematology (1991)

A 50 year-old patient with sickle cell anemia was seen who had received only two units of blood during his lifetime. He had marked iron overloading, cirrhosis of the liver, arthralgia, and mild glucose intolerance. We believe the iron overloading was associated with hereditary hemochromatosis rather than sickle cell anemia because he had HLA-A3 and B7 antigens, and hepatic iron deposits were primarily in parenchymal cells rather than Kupfer cells. The coexistence of either homozygous or heterozygous hemochromatosis should be suspected in sickle cell patients with organ damage from iron overloading.
Vitamin E reduces platelet adhesion to human endothelial cells in vitro
Authors: T. Szuwart, T. Brzoska, T.A. Luger, T. Filler, E. Peuker, R. Dierichs
Journal: American Journal of Hematology (2000)

Although it has been reported that vitamin E (alpha-tocopherol) can reduce platelet adhesiveness and aggregation in vivo, the mechanism is still unknown. Therefore, the aim of the present study was to determine whether incubations of platelet-rich plasma (PRP) with vitamin E influence platelet adhesion to cultured endothelial cells. To exclude blood plasma involvement, also washed platelets were pretreated with alpha-tocopherol. Vitamin E (0.5-1.0 mM) was added to PRP or washed platelets. Endothelial cells in monolayer were incubated with thrombin-activated platelets (1 or 2 U/ml). After 1 hr of incubation, non-adhered platelets were removed and counted. Treating of PRP with alpha-tocopherol inhibited platelet adhesion to endothelial cell monolayer. This effect was dose dependent on concentrations of alpha-tocopherol and thrombin. In our experiments PRP was treated with alpha-tocopherol and endothelial cell monolayer was used as test surface. These findings agree with previous observations on the adhesivity of platelets to synthetic surfaces after dietary vitamin E in healthy volunteers. When washed platelets were incubated with alpha-tocopherol, no significant reduction of adhesion was detectable. As preincubation of washed platelets with alpha-tocopherol does not inhibit platelet adhesion, it may be supposed that the effect of vitamin E does not occur in a directly cellular mechanism. The data suggest that alpha-tocopherol may reduce platelet adhesiveness probably after incorporation by plasma lipoproteins.
Capacity after stroke.
Authors: G F Adams
Journal: BMJ (1971)

The new knowledge and clearer concepts of the pathogenesis of cerebrovascular disease and of order and disorder in the cerebral circulation acquired in recent years have improved the possibilities of treatment, which may now be considered at four stages in the evolution of a stroke: by prevention, when factors contributing to stroke-proneness may be identified and offset; by anticipation of impending stroke and the use of new techniques to locate and treat disordered regional blood flow in the cerebral circulation; by medical or surgical modi fication of progressing stroke; and by rehabilitation of completed stroke. There are two phases of the latter: the first a period of intensive care required at onset to save life and ensure survival: the second, often prolonged, being the treat ment required to obtain the best recovery possible for a disabled survivor.
Early afterdepolarizations induced in vivo by reperfusion of ischemic myocardium. A possible mechanism for reperfusion arrhythmias.
Authors: S G Priori, M Mantica, C Napolitano, P J Schwartz
Journal: Circulation (1990)

Recent studies in vitro have shown that afterdepolarizations may develop during reperfusion after hypoxia, thus suggesting that these afterdepolarizations may contribute to the genesis of reperfusion arrhythmias. We recorded monophasic action potentials (MAPs) during myocardial ischemia and reperfusion to investigate whether afterdepolarizations develop in vivo when reperfusion arrhythmias occur. In 15 anesthetized cats, 24 trials of 10 minutes of occlusion of the left anterior descending coronary artery were followed by reperfusion. In 13 of 24 (54%) trials, afterdepolarizations developed at the moment of reperfusion, with a mean amplitude of 2.4 +/- 1.1 mV (13 +/- 8% of MAP amplitude). When cycle length was either increased by vagal stimulation or decreased by atrial pacing, early afterdepolarization (EAD) amplitude was modified, according to what has been described for EAD in vitro, with a positive linear correlation between cycle length and EAD amplitude (r = 0.91, p less than 0.0001). The occurrence of EAD was not related to rapid changes in left ventricular pressure. In the eight of 13 (62%) cases in which EAD development was associated with reperfusion arrhythmias, the coupling interval of the EAD and of premature ventricular contractions showed a significant correlation (r = 0.86, p less than 0.0001). However, in five of 13 (38%) cases, occurrence of reperfusion arrhythmias was not accompanied by the presence of EAD on the MAP recording. In two animals, a 2:1 block of EAD conduction was observed, and this was reflected on the intracavitary electrocardiogram as T wave alternans. Thus, EADs occur frequently after reperfusion in vivo, with a time course that parallels the onset of reperfusion arrhythmias. This finding further supports the role of triggered activity in the genesis of reperfusion arrhythmias in vivo.
Male gender predisposes to development of endotoxic shock in the rat
Authors: G Losonczy
Journal: Cardiovascular Research (2000)

Objective: After intravenous (i.v.) injection of lipopolysaccharide (LPS) macrophages release nitric oxide (NO) due to the expression of the inducible NO synthase (iNOS). After LPS NO is abundantly produced also in the cardiovascular system and may contribute to the development of hypotension and shock. Since the immune response, the synthesis of NO and the regulation of blood pressure (BP) differ between males and females, in the present study the effect of LPS on BP, renal function, the plasma and urinary concentration of the metabolites of NO as well as the splenic and aortic expression of the iNOS gene were compared between male and female rats. Methods: BP and renal function were measured in anesthetized rats following the i.v. injection of LPS (E. coli, 4 mg/kg). The NO2− and NO3− (metabolites of NO=NOx) concentration was measured by the Griess reaction. The iNOS gene expression was studied by RT-PCR. Results: Four hours after LPS, BP of males (n=9) was reduced by 63±12 mmHg versus 10±4 in females (n=7, P<0.005). Aminoguanidine, a selective inhibitor of iNOS, prevented the reduction of BP in males. The plasma concentration of NOx (PNOx, μM) was lower in hypotensive males (128±20) than in normotensive females (235±29, P<0.005). Males also exhibited lower urinary NOx excretion (UNOxV) after LPS (P<0.001 vs. females). Prior castration of males provided protection against hypotension (fall of BP: −4±4 mmHg, n=6, P<0.02 versus males) and resulted in higher PNOx as well as UNOxV (both P<0.001 versus males and not different from females). Prior ovariectomy (n=5) had no influence on the hemodynamic and NOx response to LPS. Male rats displayed enhanced aortic iNOS/beta-actin ratio relative to females after LPS (n=3 in each group, P<0.05). Conclusions: (1) Male gender may sensitize to LPS-induced shock and (2) sensitivity of males to endotoxin is associated with an attenuated, not exaggerated total rate of NO synthesis.
Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery.
Authors: A Williams, D Heath, J M Kay, P Smith
Journal: Thorax (1977)

Exposure to acute hypoxia (barometric pressure 263 mmHg) for 8 hours did not lead to increased numbers of mast cells in the lungs of rats. In contrast, in adult rats kept for 35 days at a barometric pressure of 380 mmHg there was a proliferation of mast cells around the pulmonary blood vessels and in the alveolar septa. This hyperplasia of lung mast cells in response to chronic hypoxia was reversible on removal of the hypoxic stimulus. There was a correlation between the logarithm of the perivascular lung mast cell density (defined in the paper) and the logarithm of the right ventricular weight. There was no increase in the mast cells in the carotid bodies of the hypoxic rats. Young male, old male, young female, and old female rats which had been subjected for 39 days to a barometric pressure of 380 mmHg showed a proliferation of mast cells around the pulmonary blood vessels and in the alveolar walls. This response was greatest in the adult animals and independent of their sex. In the age and sex experiment there was a correlation between the perivascular lung mast cell density and the medial thickness of the muscular pulmonary arteries. Since mast cell hyperplasia has been reported as preceding right ventricular hypertrophy, it is conceivable that mast cell proliferation in the lung may be a defence mechanism to limit the severity of hypoxic pulmonary hypertension rather than to mediate it.
MYD88 L265P is a marker highly characteristic of, but not restricted to, Waldenström’s macroglobulinemia
Authors: C Jiménez, E Sebastián, M C Chillón, P Giraldo, J Mariano Hernández, F Escalante, T J González-López, C Aguilera, A G de Coca, I Murillo, M Alcoceba, A Balanzategui, M E Sarasquete, R Corral, L A Marín, B Paiva, E M Ocio, N C Gutiérrez, M González, J F San Miguel, R García-Sanz
Journal: Leukemia (2013)
Abstract 4558: Synergistic effect of alcohol and estradiol in breast cancer
Authors: Ajeet Singh, Arulkumaran Shanmugam, Shilpi Rajoria, Andrea George, Robert Suriano
Journal: Cancer Research (2011)

Abstract Breast cancer is the most common malignancy and the second leading cause of death among women in the United States. In addition to the various risks associated with breast cancer development, an interesting epidemiological observation exists, which is an increase in breast cancer incidence with increased alcohol consumption. Post-menopausal women on estrogen replacement therapy are at an even greater risk suggesting a synergistic interplay between estrogen and alcohol. Since the risk of alcohol for breast cancer can be partly attributed to circulating estrogens, the alcohol-estrogen axis, currently understudied at the biological level, is a viable breast cancer etiological agent. The precise cellular and biochemical mechanism for the role of the estrogen- alcohol axis in breast cancer progression is poorly understood. To investigate this, an in-vitro study was performed using 4T1 breast cancer cell line. The breast cancer cells were treated with alcohol (0.5%), estradiol (E2, 10-8 M) and with combination of alcohol and E2. Alcohol and E2 treatment modulates activation of cell surface receptors, specifically the epidermal growth factor receptor 2 (Erb2), which subsequently affects signaling through downstream pathways, such as Akt and mTOR. Akt/mTOR pathways are related to tumor development, and are target for any therapeutic agent. Alcohol, E2 and the combination treatments elicited a significant stimulation of estrogen receptor (ERα), Erb2, Akt and mTOR in 4T1 breast cancer cells. Accordingly, our data suggest that ERα, Erb2, Akt and mTOR may serve as key regulators that are involved in alcohol induced breast cancer progression. Thus the present study reveals the key pathways for alcohol-mediated promotion of cancer that could be targeted for therapy or prevention of alcohol-related cancers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4558. doi:10.1158/1538-7445.AM2011-4558
A CURRENT EVALUATION OF THE ANTICONVULSANT DRUGS
Authors: RUSSELL N. DEJONG
Journal: American Journal of Psychiatry (1949)

Definite advances have been made in the treatment of epilepsy during recent years. The bromides, then phenobarbital, and finally dilantin have in this order been found to be increasingly effective. Research on some of the newer hydantoin derivatives has given even more hope in the control of grand mal attacks. The ketogenic diet, glutamic acid, and finally tridione have been found to be helpful in the treatment of petit mal seizures, and tridione also in the alleviation of psychomotor attacks. The therapeutic approach depends, of course, upon the underlying etiology and upon the type of attack from which the patient is suffering. Epilepsy, or the convulsive state, must not be regarded as a disease entity. The etiology differs in individual cases, and although grand mal, petit mal, psychomotor, and other varieties of attacks may occur in the same patient, each may be a manifestation of a different type of pathologic physiology. There may be a variability in symptoms from time to time; there may be no clear-cut distinction between one type of attack and another; there may be formes frustes which cannot be classified. The essential criteria should be not only an adequate description of the seizures and, if possible, observation of them, but also an electroencephalographic recording and an evaluation of the patient's personality and psychologic state. Specific therapies are now available for individual types of attacks and for specific abnormalities of the cerebral rhythm. The various anticonvulsants often have a definite synergistic effect, and a combination of 2 or more of them may be more helpful than any one alone; such combinations may be tried when individual drugs, used singly, do not control attacks. In a mixed type of epilepsy one may use phenobarbital, dilantin or Mesantoin with tridione. One must bear in mind, however, that the use of the anticonvulsant drugs does not constitute the sole treatment of epilepsy. The underlying etiologic factors must be determined, if possible, and in addition to drugs one often must use physical measures, diet, mental hygiene, and occasionally surgery. By knowing the mode of action of all the possible therapeutic agents, and by a careful, detailed study of each patient, the physician can, in most instances, control the symptoms of disease and return the patient to a useful life.
Bronchial Lability and Responsiveness in School Children Born Very Preterm
Authors: ANNA S. PELKONEN, ARJA L. HAKULINEN, MARKKU TURPEINEN
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

We evaluated bronchial lability and responsiveness in 29 prematurely born children (birth weight < 1,250 g) 8 to 14 yr of age, 12 with histories of bronchopulmonary dysplasia (BPD). Flow-volume spirometry, a bronchodilator test, and histamine challenge at the office and home monitoring of peak expiratory flow (PEF) values twice daily for 4 wk with and without a β2-agonist were performed with a novel device, the Vitalograph Data Storage Spirometer. The spirometric values at the office and the results of home monitoring were compared with those for a control group of children born at term. All spirometric values except FEV1/FVC were significantly lower in the BPD group than in the non-BPD group (p < 0.0001). Ten children (83%) in the BPD group and four (24%) in the non-BPD group had subnormal spirometric values at the office, indicating bronchial obstruction. Of the children with obstruction, 79% reported respiratory symptoms during the preceding year, and 57% had increased diurnal PEF variation and/or responded to administration of a β2-agonist during home monitoring or at the office. The BPD children were significantly more responsive to histamine than the non-BPD children (p = 0.002). All spirometric values were significantly lower in both preterm groups than in the control group born at full term (p < 0.01). In conclusion, regardless of BPD, bronchial obstruction, bronchial lability, and increased bronchial responsiveness are common in prematurely born children of school age.