tbuckley/cabot-search huggingface dataset:
β3-adrenergic receptor activation increases human atrial tissue contractility and stimulates the L-type Ca2+ current
Authors: V. Arvydas Skeberdis, Vida Gendvilieneη, Danguoleη Zablockaiteη, Rimantas Treinys, Regina Macχianskieneη, Andrius Bogdelis, Jonas Jurevicχius, Rodolphe Fischmeister
Journal: Journal of Clinical Investigation (2008)

β3-adrenergic receptor (β3-AR) activation produces a negative inotropic effect in human ventricles. Here we explored the role of β3-AR in the human atrium. Unexpectedly, β3-AR activation increased human atrial tissue contractility and stimulated the L-type Ca2+ channel current (ICa,L) in isolated human atrial myocytes (HAMs). Right atrial tissue specimens were obtained from 57 patients undergoing heart surgery for congenital defects, coronary artery diseases, valve replacement, or heart transplantation. The ICa,L and isometric contraction were recorded using a whole-cell patch-clamp technique and a mechanoelectrical force transducer. Two selective β3-AR agonists, SR58611 and BRL37344, and a β3-AR partial agonist, CGP12177, stimulated ICa,L in HAMs with nanomolar potency and a 60%–90% efficacy compared with isoprenaline. The β3-AR agonists also increased contractility but with a much lower efficacy (~10%) than isoprenaline. The β3-AR antagonist L-748,337, β1-/β2-AR antagonist nadolol, and β1-/β2-/β3-AR antagonist bupranolol were used to confirm the involvement of β3-ARs (and not β1-/β2-ARs) in these effects. The β3-AR effects involved the cAMP/PKA pathway, since the PKA inhibitor H89 blocked ICa,L stimulation and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) strongly increased the positive inotropic effect. Therefore, unlike in ventricular tissue, β3-ARs are positively coupled to L-type Ca2+ channels and contractility in human atrial tissues through a cAMP-dependent pathway.
The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias.
Authors: H Garan, B A McGovern, V J Canzanello, J McCauley, M Bodvarsson, J T Harrington, N E Madias, J B Newell, J N Ruskin
Journal: Circulation (1988)

The effect of potassium ion (K+) depletion on postmyocardial infarction ventricular arrhythmias was investigated in 32 dogs: 12 control animals, 10 animals that ate a diet extremely low in K+ for 15 days, and 10 others that, in addition to dietary K+ deprivation, received 50 mg of hydrochlorothiazide four times. The experimental myocardial infarction was created by proximal left anterior descending coronary artery ligation. In a subgroup of 24 animals selected for relatively uniform size of myocardial infarction (14% to 22% of left ventricular mass), eight animals with mean cumulative K+ balance of -4.01 +/- 2.19 meq/kg developed spontaneous ventricular fibrillation within 4 to 17 min of coronary ligation, whereas 16 animals with a mean cumulative K+ balance of -0.11 +/- 1.82 meq/kg didn't. By univariate analysis cumulative K+ deficit (p = .001) and plasma K+ concentration (p = .039) correlated significantly with spontaneous ventricular fibrillation. Multivariate analysis of the entire population of 32 animals identified cumulative K+ deficit and size of myocardial infarction as the only independent predictors of ventricular fibrillation. Cumulative K+ deficit was also an independent predictor of ventricular fibrillation induced by programmed cardiac stimulation in the conscious state 1 day after myocardial infarction.
Granulocytic sarcoma of the ovary in patients with acute myelogenous leukemia
Authors: Kou Yamamoto, Hideki Akiyama, Tamotsu Maruyama, Hisashi Sakamaki, Yasusuke Onozawa, Kenji Kawaguchi
Journal: American Journal of Hematology (1991)

Abstract Two cases of granulocytic sarcoma of the ovary found at the time of relapse of acute myelogenous leukemia (AML) are presented. Almost 5 years after the initial diagnosis of AML, both cases presented ovarian tumors which were discovered to be myeloblastoma of the ovary on laparotomy in one case and at the time of autopsy in the other. Evidence of hematological relapse followed the presentation of the ovarian tumor within a month. Both patients were treated with surgery and/or chemotherapy.
Surgical Considerations in the Management of Supravalvular Aortic Stenosis
Authors: HARRIS B. SHUMACKER, ISIDORE MANDELBAUM
Journal: Circulation (1965)

Nine cases of surgically treated supravalvular aortic stenosis have been presented. The pertinent literature has been reviewed. It is concluded that this anomaly can be managed satisfactorily by insertion of a large patch graft into an aortic incision placed across the stenotic area and extended well beyond it in both directions. Total cardiopulmonary bypass is utilized. Left ventricular decompression and coronary arterial perfusion are valuable adjuvants. The risk of operation appears to be small and the results rewarding.
INACTIVATION OF ENDOTOXIN BY A HUMORAL COMPONENT. VII. ENZYMATIC DEGRADATION OF ENDOTOXIN BY BLOOD PLASMA*
Authors: Willis R. Keene, Maurice Landy, Murray J. Shear
Journal: Journal of Clinical Investigation (1961)

The pathogenesis of the febrile response that follows the intravenous injection of bacterial endotoxin has been the subject of extensive investigations. In the course of these studies it became evident that blood serum contains factors which, when interacted in vitro with endotoxin, may either enhance or inactivate the fever-producing effects. LeQuire demonstrated that a brief period of interaction between serum and endotoxin results in augmentation of pyrogenicity (3). Others have confirmed this observation and have, in addition, defined some of the conditions necessary for demonstrating the pyrogen-enhancing effect of serum (4-8). In seeking to explain the termination of endotoxin fever, Hegemann postulated that this was effected by components of serum capable of detoxifying endotoxin. He demonstrated the presence of such agents in serum by incubating endotoxin and serum for prolonged periods at physiological temperature (9-12). However, these experiments did not provide evidence that this effect of serum was operative in the termination of endotoxin fever. The observations of LeQuire and of Hegemann were confirmed by Cluff and Bennett (8), who clearly distinguished the two effects of serum by demonstrating that pyrogen augmentation was not dependent upon the time or temperature of incuba-
An Established Porcine Model for Animate Training in Diagnostic and Therapeutic ERCP
Authors: M. D. Noar
Journal: Endoscopy (1995)

Traditionally, training in ERCP has consisted of texts and atlases, videotape presentations, didactic presentations, and li~e demonstrations. Recenlly, attempts have been made to develop simulators to provide additional practical experience. Simulators may actually be able to provide significant psychomotor conditioning and shorten the learning curve; however. current s imulators stiU fall short of true real·time realistic simulation, and provide only a .limited variety of clinical situations (8-12).
Mutations in CBL occur frequently in juvenile myelomonocytic leukemia
Authors: Mignon L. Loh, Debbie S. Sakai, Christian Flotho, Michelle Kang, Manfred Fliegauf, Sophie Archambeault, Charles G. Mullighan, Leslie Chen, Eva Bergstraesser, Carlos E. Bueso-Ramos, Peter D. Emanuel, Henrik Hasle, Jean-Pierre Issa, Marry M. van den Heuvel-Eibrink, Franco Locatelli, Jan Starý, Monica Trebo, Marcin Wlodarski, Marco Zecca, Kevin M. Shannon, Charlotte M. Niemeyer
Journal: Blood (2009)
Induction of labour using prostaglandin E2 pessaries.
Authors: J Shepherd, J M Pearce, C D Sims
Journal: BMJ (1979)

The routine method of induction at Queen Charlotte9s Maternity Hospital is now by the use of prostaglandin E2 pessaries. The first 502 consecutive patients thus induced are presented: the caesarean section rate for a failed induction with an unfavourable cervix has fallen to 2%. The prostaglandin E2 pessary is highly efficient and acceptable for all cases in which a simple amniotomy will not suffice.
Can determination of the proliferative capacity of the nontumor portion predict the risk of tumor recurrence in the liver remnant after resection of human hepatocellular carcinoma?
Authors: Jen-Hwey Chiu, Li-Hwa Wu, Hwa-Li Kao, Hwey-May Chang, Shyh-Haw Tsay, Che-Chuan Loong, Gar-Yang Cha, Wing-Yu Lui
Journal: Hepatology (1993)

To test the hypothesis that increased proliferative capacity of cells in a liver remnant is a risk factor for tumor recurrence in patients who have undergone liver resection for hepatocellular carcinoma, DNA flow-cytometric measurement and cell-cycle analysis of the nontumor parts of resected hepatocellular carcinomas (tumor size < 5 cm) were performed. The disease-free survival rates 1, 2, 3 and 4 yr after surgery were 64%, 58%, 43%, and 36%, respectively. Proliferative capacity (fractions of synthetic, postsynthetic and mitotic phases) of the nontumor parts, irrespective of liver pathology, was higher than that of normal liver and statistically lower than that of tumor parts from resected hepatocellular carcinoma specimens. Livers with chronic active hepatitis (+) and with hepatocyte dysplasia (-) had significantly lower proliferative activity than did those with chronic active hepatitis (-) and with hepatocyte dysplasia (+), respectively [corrected]. We saw no significant difference in proliferative capacity between patients with and without cirrhosis. Disease-free-survival analysis showed that the presence of liver pathology (hepatitis B infection, cirrhosis, chronic active hepatitis and hepatocyte dysplasia) was not the factor linked to tumor recurrence in the liver remnant and that a marked increase in proliferative capacity (> or = 18%), regardless of liver pathology, was the risk factor linked to tumor recurrence after liver resection. We conclude that there is some degree of increased proliferative capacity in the nontumor parts of resected hepatocellular carcinomas and that a marked increase in the proliferative capacity (> or = 18%) of the nontumor part is a significant risk factor in predicting tumor recurrence in the liver remnant after liver resection.
Synergistic regulation of human megakaryocyte development.
Authors: M W Long, R J Hutchinson, L L Gragowski, C H Heffner, S G Emerson
Journal: Journal of Clinical Investigation (1988)

Little information exists concerning differing levels of regulation occurring during human megakaryocyte development. We hypothesize that megakaryocytic proliferation and maturation is controlled by two, synergistic regulatory factors. One, megakaryocyte colony-stimulating activity, is an obligate requirement for colony formation and drives the development of relatively immature cells. Megakaryocyte colony-stimulating activity is a functional component of the human recombinant proteins, interleukin 3 or GM-CSF. Human recombinant growth factors, interleukin 1, interleukin 6, or crythropoietin, do not effect megakaryocyte development either alone or in combination with interleukin 3. Full maturation requires a second synergistic activity which increases megakaryocyte number, size, and cytoplasmic and antigenic content. In culture, this synergistic regulator augments maturation by increasing the number of colonies, colony cellularity, and size. In suspension cultures, this cofactor increases megakaryocyte cytoplasmic and antigenic content, and shifts the morphological distribution from immature to mature megakaryocytes. Finally, this activity also increases the number of antigen positive megakaryocytes, either by stimulating proliferation or conversion of antigen-negative to antigen-positive cells. Comparative studies of megakaryocytic regulation suggests that this in vitro regulator mimicks some of the known effects of thrombopoietin in vivo.
Reduction in mortality from breast cancer
Authors: Elsebeth Lynge, Anne Helene Olsen
Journal: BMJ (2005)

Reduction in mortality from breast cancerDecrease with screening was marked in younger age group Editor-Based on a complicated statistical model, Olsen et al reported that the breast cancer mortality in Copenhagen dropped by 25% for women aged 50-79 when comparing mortality in the screening period (1991-2001) with a pre-screening period (1981-91) and claimed that this decrease was caused by screening. 1According to Statistics Denmark, 217 breast cancer deaths occurred in Copenhagen in the age group 35-54 years in the period 1981-90 and 196 deaths in 1991-2000. 2By comparing these data with those in the article by Olsen et al we calculate that less than 5% of the breast cancer mortality in this age group is caused by tumours diagnosed after age 50 years when women were invited to screening.The number of exposure years increased from about 484 000 to about 538 000.This gives a significant 19% (age adjusted) reduction in breast cancer mortality in the age group 35-54 years.No reduction at all occurred in the age group 55-79. 2Our estimates are based on raw and complete data.In contrast, the estimates in the paper by Olsen et al are sensitive to exclusion of data and model choice.In Copenhagen a drop in breast cancer mortality may reflect a higher fertility quotient due to non-Western immigration, fewer nulliparous women, and other non-screening related factors.It is therefore strange that no causal note was made by Olsen et al on the marked decrease in the breast cancer mortality in the age group 35-54 years.
THE METABOLISM OF THE ISCHEMIC KIDNEY
Authors: Sigwin B. Raska
Journal: The Journal of Experimental Medicine (1943)

The consumption of oxygen by slices of kidney tissue of dogs made hypertensive by the Goldblatt technique was studied manometrically. The respiration of the ischemic kidney tissue was found to be much less than that of the normal kidney. Further, a marked reduction in oxidizing ability, as measured by the oxygen uptake and ammonia formation in the presence of the added amines and amino acids, tyramine, isoamylamine, dl-alanine, and l-aspartic acid, was observed. Extracts of the kidneys were made and tested for amine oxidase, amino acid oxidase, and polyphenol oxidase activity by measuring the increased oxygen consumption and ammonia formation in the presence of the substrates listed above with the addition of l-epinephrine, histamine, and dl- and l-dihydroxyphenylalanine. The preparations from ischemic kidneys of dogs and rabbits showed much lower activity. Animals with varying degrees of constriction of the renal arteries and therefore varying degrees of renal ischemia were prepared and studied. The results with these animals suggested a direct relationship between the degree of renal ischemia and the decrease in oxidizing power of the tissue. The product of the enzymic oxidation of tyramine was identified as p-hydroxyphenylacetaldehyde by isolation as the dinitrophenylhydrazone of p-hydroxyphenylacetaldehyde.
P2-174: ERCC1 and Beta Tubulin III (BTUB) isoform expression by Immunofluorescence (IF) may correlate with survival after combined modality therapy (CMT) for stage III NSCLC
Authors: Martin J. Edelman, King Kwong, Mohan Suntharalingam, Ming Tan, Steve Lesko, Paul Ts’o
Journal: Journal of Thoracic Oncology (2007)
Expression and methylation of CASP8 in neuroblastoma: Identification of a promoter region
Authors: Barbara Banelli, Ida Casciano, Michela Croce, Angela Di Vinci, Ilaria Gelvi, Gabriella Pagnan, Chiara Brignole, Giorgio Allemanni, Silvano Ferrini, Mirco Ponzoni, Massimo Romani
Journal: Nature Medicine (2002)
Mesenchymal Cell Transplantation and Myocardial Remodeling After Myocardial Infarction
Authors: Jennifer A. Dixon, Robert C. Gorman, Robert E. Stroud, Shenikqua Bouges, Hamamoto Hirotsugu, Joseph H. Gorman, Timothy P. Martens, Silviu Itescu, Michael D. Schuster, Theodore Plappert, Martin G. St John-Sutton, Francis G. Spinale
Journal: Circulation (2009)

Targeted delivery of mesenchymal precursor cells (MPCs) can modify left ventricular (LV) cellular and extracellular remodeling after myocardial infarction (MI). However, whether and to what degree LV remodeling may be affected by MPC injection post-MI, and whether these effects are concentration-dependent, remain unknown.Allogeneic MPCs were expanded from sheep bone marrow, and direct intramyocardial injection was performed within the borderzone region 1 hour after MI induction (coronary ligation) in sheep at the following concentrations: 25x10(6) (25 M, n=7), 75x10(6) (75 M, n=7), 225x10(6) (225 M, n=10), 450x10(6) (450 M, n=8), and MPC free media only (MI Only, n=14). LV end diastolic volume increased in all groups but was attenuated in the 25 and 75 M groups. Collagen content within the borderzone region was increased in the MI Only, 225, and 450 M groups, whereas plasma ICTP, an index of collagen degradation, was highest in the 25 M group. Within the borderzone region matrix metalloproteinases (MMPs) and MMP tissue inhibitors (TIMPs) also changed in a MPC concentration-dependent manner. For example, borderzone levels of MMP-9 were highest in the 25 M group when compared to the MI Only and other MPC treatment group values.MPC injection altered collagen dynamics, MMP, and TIMP levels in a concentration-dependent manner, and thereby influenced indices of post-MI LV remodeling. However, the greatest effects with respect to post-MI remodeling were identified at lower MPC concentrations, thus suggesting a therapeutic threshold exists for this particular cell therapy.
Role of the Fas/FasL pathway in combination therapy with interferon-α and fluorouracil against hepatocellular carcinoma in vitro
Authors: Masato Nakamura, Hiroaki Nagano, Masato Sakon, Tameyoshi Yamamoto, Hideo Ota, Hiroshi Wada, Bazarragchaa Damdinsuren, Takehiro Noda, Shigeru Marubashi, Atsushi Miyamoto, Yutaka Takeda, Koji Umeshita, Shoji Nakamori, Keizo Dono, Morito Monden
Journal: Journal of Hepatology (2006)
Progress in Neuropathology
Authors: Martin R. Krigman
Journal: JAMA (1972)

<i>Progress in Neuropathology</i>is a newly initiated series envisioned by the editor as a medium for presenting new, provocative, or evolving problems in neuropathology. Although this initial volume is not a neuropathology textbook, many of the topics will be incorporated into future textbooks. The volume is highly recommended to the reader interested in following the developments and future directions of neuropathology. The judicious selection of the topics and the prominence of the contributors have resulted in a collection of 12 informative and stimulating papers. The contributions include reviews, case studies with clinicopathologic correlations, and reports of experimental studies. Structure as well as basic chemical and functional processes are considered, so that each paper is a complete and thorough presentation. The topics range from a review of the role and use of electron microscopy in neuropathology to a consideration of the vascular injury of the central nervous system lesions of systemic
Pituitary hormone receptors and tumorigenesis
Authors: Anat Ben-Shlomo, Shlomo Melmed
Journal: Nature reviews. Cancer (2007)

We read with interest the Review 'G-protein-coupled receptors and cancer' by Dorsam and Gutkind published in Nature Reviews Cancer 1 .In table 1 the authors state inaccurately that thyrotropin secreting hormone (TSH) and adrenocorticotropin hormone (ACTH) receptors (TSHR and ACTHR, respectively) cause pituitary tumours.The pituitary gland secretes six polypeptide hormones -ACTH, TSH, growth hormone (GH), gonadotropins (follicle stimulating hormone (FSH) and luteinizing hormone (LH)) and prolactin.These trophic hormones act at their respective target glands (adrenals, thyroid, cartilage, gonads and breast) to regulate peripheral hormone secretion and glandular growth and differentiation 2 .TSH is secreted by the pituitary and signals through the TSHR at the thyroid gland to induce thyroid hormone synthesis.Several naturally occurring mutations are found in the TSHR 3-5 .Activating, somatic TSHR mutations cause toxic thyroid adenomas 6 , and activating, germline TSHR mutations can cause hereditary toxic thyroid hyperplasia 7 and familial gestational hyperthyroiditis 8 .Inactivating, germline TSHR mutations can cause partial or complete resistance to TSH 9,10 or isolated central hypothyroidism 11 .No TSHR mutation is yet known to cause pituitary tumours; moreover, TSHR mutations are unlikely do so, as TSH is secreted by the pituitary and acts at the periphery.ACTH is secreted by the pituitary gland and acts peripherally at the ACTHR (currently known as melanocortin 2 receptor (MC2R 3 )) in the adrenal glands to induce adrenal steroid synthesis.An inactivating, germline mutation in MC2R was shown to cause familial glucocorticoid deficiency in 25% of patients with this disease 12 .A deletion of MC2R was found in two very aggressive undifferentiated adrenocortical tumours 13 .Adrenal tumours have not been found to harbour gain-of-function mutations of MC2R 3,14,15 .No MC2R mutation is known to cause pituitary tumours.
Myocardial reperfusion in acute experimental ischemia. Beneficial effects of prior treatment with steroids.
Authors: P L da Luz, J S Forrester, H L Wyatt, G A Diamond, M Chag, H J Swan
Journal: Circulation (1976)

To test the hypothesis that prior steroid administration may enhance the mechanical and metabolic response to myocardial reperfusion, regional myocardial function (Hg-in-silastic length gauges), transmyocardial lactate balance and K+ difference were measured in 12 control and 13 treated (30 mg/kg methyl-prednisolone, 30 to 60 min postocclusion) dogs. At three hours of ischemia, systolic shortening in the ischemic segment was greater in treated dogs (40.6% vs. 12%, P less than 0.05), while both lactate balance and K+ arteriovenous difference became positive. Lactate balance and K+ difference remained negative in the untreated animals. After three hours of occlusion and one hour of reperfusion, recovery of shortening was significantly greater in the treated animals (75.9 vs. 31.6%, P less than 0.05). In addition, while lactate balance remained negative among the control dogs, it further improved in the treated dogs. Thus, steroid administration during experimental coronary occlusion impedes the progression of ischemia and is additive to reperfusion in reversing ischemic dysfunction.
Patients Who Know Best-Reply
Authors: Lourdes C. Corman
Journal: JAMA (1987)

<h3>In Reply.—</h3> Ms Kendall makes a very pertinent and, unfortunately, true observation that we physicians as a group are more likely to ignore the complaints of women (not just young women) than complaints from men and to consider women's complaints to be psychological.<sup>1</sup> I think there are several reasons that can account for this tendency. Sometimes the complaints are not familiar to the physician, as illustrated by the patients I described. The physician, instead of accepting them at face value while awaiting confirmatory reports, deals with his or her ignorance by assuming the patient must be in error in describing the symptoms. Some physicians have not had adequate psychiatric training and tend to think of psychopathology or somatizing syndromes as diagnoses that can only be made when all possible organic diseases have been ruled out. On the contrary, symptoms and signs of emotional or cognitive dysfunction are either present
Altered Intestinal Function in Patients With Chronic Heart Failure
Authors: Anja Sandek, Juergen Bauditz, Alexander Swidsinski, Sabine Buhner, Jutta Weber-Eibel, Stephan von Haehling, Wieland Schroedl, Tim Karhausen, Wolfram Doehner, Mathias Rauchhaus, Philip Poole-Wilson, Hans-Dieter Volk, Herbert Lochs, Stefan D. Anker
Journal: Journal of the American College of Cardiology (2007)