tbuckley/cabot-search huggingface dataset:
Inactivation of kallikrein in human plasma.
Authors: F van der Graaf, J A Koedam, B N Bouma
Journal: Journal of Clinical Investigation (1983)

Human plasma kallikrein is inactivated by plasma protease inhibitors. This study was designed to determine the nature of these protease inhibitors and to assess their relative importance in the inactivation of kallikrein. Therefore, the kinetics of kallikrein inactivation and the formation of kallikrein inhibitor complexes were studied in normal plasma and in plasma depleted of either alpha 2-macroglobulin (alpha 2M), C1 inhibitor, or antithrombin (AT III). Prekallikrein was activated by incubation of plasma with dextran sulfate at 4 degrees C. After maximal activation, kallikrein was inactivated at 37 degrees C. Inhibition of kallikrein amidolytic activity in AT III-deficient plasma closely paralleled the inactivation rate of kallikrein in normal plasma. The inactivation rate of kallikrein in alpha 2M-deficient plasma was slightly decreased compared with normal plasma, but in contrast to normal, C1 inhibitor-deficient, and AT III-deficient plasma, no kallikrein amidolytic activity remained after inactivation that was resistant to inhibition by soybean trypsin inhibitor. Suppression of kallikrein activity in C1 inhibitor-deficient plasma was markedly decreased, and this was even more pronounced in plasma deficient in both C1 inhibitor and alpha 2M. The pseudo first-order rate constants for kallikrein inactivation in normal, AT III-deficient, alpha 2M-deficient, C1 inhibitor-deficient plasma, and plasma deficient in both alpha 2M and C1 inhibitor, were 0.68, 0.60, 0.43, 0.07, and 0.016 min-1, respectively. Sodium dodecyl sulfate gradient polyacrylamide slab gel electrophoresis showed that during inactivation of kallikrein in plasma, high-Mr complexes were formed with Mr at 400,000-1,000,000, 185,000, and 125,000-135,000, which were identified as complexes of 125I-kallikrein with alpha 2M, C1 inhibitor, and AT III, respectively. In addition, the presence of an unidentified kallikrein-inhibitor complex was observed in AT III-deficient plasma. 52% of the 125I-kallikrein was associated with C1-inhibitor, 35% with alpha 2M, and 13% with AT III and another protease inhibitor. A similar distribution of 125I-kallikrein was observed when the 125I-kallikrein inhibitor complexes were removed from plasma by immunoadsorption with insolubilized anti-C1 inhibitor, anti-alpha 2M, or anti-AT III antibodies. These results suggest that only covalent complexes are formed between kallikrein and its inhibitors in plasma. As a function of time, 125I-kallikrein formed complexes with C1 inhibitor at a higher rate than with alpha 2M. No difference was observed between the inactivation rate of kallikrein in high-Mr kininogen-deficient plasma and that in high-Mr kininogen-deficient plasma reconstituted with high-Mr kininogen; this suggests that high-Mr kininogen does not protect kallikrein from inactivation in the plasma milieu. These results have quantitatively demonstrated the major roles of C1 inhibitor and alpha 2M in the inactivation of kallikrein in plasma.
Textbook of Respiratory Medicine, vols 1 &amp;amp; 2
Authors: Edward D. Sivak
Journal: JAMA (1995)

The task of reviewing the second edition of the<i>Textbook of Respiratory Medicine</i>is rather ominous if one considers that it has two volumes, 2739 pages, 141 authors, and 102 chapters. The organization of the text follows a standard format of anatomy and physiology, clinical symptoms, diagnostic evaluation, and discussions of specific disease entities. Each chapter is introduced with a block outline, which is extremely useful to the incidental reader who uses the text for quick reference for specific details about specific diseases. Beyond such use, however, one must determine the worth of these volumes. Interested parties include resident physicians, busy practitioners, seasoned clinicians, and, in the most inclusive sense, perpetual students of respiratory medicine. In the past two months, I have recommended the section on pulmonary function testing to several medical residents who were seeking detailed explanation of the methods by which lung function is assessed in the modern
Recurrent Syncopal Attacks from Bradycardia
Authors: J. K. Wagstaff
Journal: BMJ (1951)

JOURNAIIt is, I hope, obvious that nothing that I have said can be construed as an argument against finding out and recording these conditions in children-that is, against routine medical inspections.My argument is that the interpretations should not be at fault.In fact, interpreting these universal imperfections is one of the most difficult tasks that can be required of a doctor, and for this reason should, in school-children, be left to doctors and not to teachers and nurses, as suggested by Professor Moncrieff (1950).
Cutaneous manifestations of paraproteinaemia. Part II
Authors: R. Russell Jones
Journal: British Journal of Dermatology (1981)

Journal Article Cutaneous manifestations of paraproteinaemia. Part II Get access R. Russell Jones R. Russell Jones St John's Hospital for Diseases of the Skin, London WC2 Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 104, Issue 2, 1 February 1981, Pages 209–220, https://doi.org/10.1111/j.1365-2133.1981.tb00048.x Published: 01 February 1981
A comparison of the acute and long-term hemodynamic effects of ventricular inhibited and atrial synchronous ventricular inhibited pacing.
Authors: I Kruse, K Arnman, T B Conradson, L Rydén
Journal: Circulation (1982)

Sixteen patients treated with a noninvasively programmable pacemaker were examined after a prolonged period of ventricular inhibited (VVI) and atrial synchronous ventricular inhibited (VDD) pacing. Maximal working capacity was determined by bicycle ergometry. Atrial and ventricular rates, brachial artery cuff pressure and breathing rate were determined at rest and during exercise. There was a mean increase in working capacity of 24% with VDD compared with VVI pacing (p less than 0.001). Thirteen of the patients were catheterized. During VDD pacing, cardiac output was significantly higher, particularly during exercise (+/- 32%) due to the capability of heart rate increase and despite a substantial compensatory stroke volume increase during VVI pacing. Arteriovenous oxygen difference was much higher during VVI pacing, reaching 164 +/- 14 ml/l during the highest work load, while the corresponding level during VDD pacing was 140 +/- 14 ml/l (p less than 0.001). During exercise, arterial blood lactate was significantly higher during VVI than during VDD pacing. Heart size was significantly smaller, 568 +/- 98 vs 530 +/- 96 ml/m2 BSA (p less than 0.05), during VDD pacing a questionnaire was completed by the patients to evaluate subjective symptoms and pacemaker preference. This part of the study favored the VDD mode of pacing. The conclusion of this study is that VDD pacing is superior to VVI pacing.
A RANDOMIZED COMPARISON OF SECOND-GENERATION ZOTAROLIMUS-ELUTING RESOLUTE STENTS VERSUS EVEROLIMUS-ELUTING XIENCE V STENTS IN REAL-WORLD PATIENTS: 4-YEAR LONG-TERM CLINICAL OUTCOMES OF LISA-ERX TRIAL
Authors: Yisik Kim, Jei Keon Chae, Ji Young Yoon, Soo Kyeong Song, Lae Young Jung, Sun Hwa Lee, Sang Rok Lee, Kyoung Seok Lee, Jae Ki Ko
Journal: Journal of the American College of Cardiology (2015)
Acute metabolic alkalosis perpetuating hypercarbia. A role for acetazolamide in chronic obstructive pulmonary disease
Authors: P. D. Miller
Journal: JAMA (1977)

METABOLIC alkalosis leads to hypercarbia (increased Pco<sub>2</sub>). The increase in the blood Pco<sub>2</sub>owing to alveolar hypoventilation is the respiratory compensation for metabolic alkalosis as the ventilatory drive is blunted by the elevated Hco<sub>3</sub><sup>-</sup>levels.<sup>1</sup>Hypercarbia induced by a metabolic alkalosis is of no clinical consequence in most normal persons, since the rise in Pco<sub>2</sub>rarely exceeds 10 mm Hg, but it can lead to severe carbon dioxide narcosis in those with chronic obstructive pulmonary disease (COPD) who already are severely hypoxic and hypercarbic. Metabolic alkalosis owing to diureticinduced intravascular volume, chloride, or potassium depletion<sup>2</sup>usually requires more than 24 hours to be generated.<sup>2,3</sup>Because of this, metabolic alkalosis as the cause for persistent hypercarbia in subjects with COPD is generally not considered in the first few hours after hospitalization. In patients with decompensated COPD with hypercarbia and congestive heart failure (CHF), rapid
TLR9-mediated siRNA delivery for targeting of normal and malignant human hematopoietic cells in vivo
Authors: Qifang Zhang, Dewan Md Sakib Hossain, Sergey Nechaev, Anna Kozlowska, Wang Zhang, Yong Liu, Claudia M. Kowolik, Piotr Swiderski, John J. Rossi, Stephen Forman, Sumanta Pal, Ravi Bhatia, Andrew Raubitschek, Hua Yu, Marcin Kortylewski
Journal: Blood (2013)
Frequency and Clinical Implications of Fluid Dynamically Significant Diffuse Coronary Artery Disease Manifest as Graded, Longitudinal, Base-to-Apex Myocardial Perfusion Abnormalities by Noninvasive Positron Emission Tomography
Authors: K. Lance Gould, Yuko Nakagawa, Keiichi Nakagawa, Stefano Sdringola, Mary Jane Hess, Mary Haynie, Neal Parker, Nizar Mullani, Richard Kirkeeide
Journal: Circulation (2000)

Diffuse coronary atherosclerosis is the substrate for plaque rupture and coronary events. Therefore, in patients with mild arteriographic coronary artery disease without significant segmental dipyridamole-induced myocardial perfusion defects, we tested the hypothesis that fluid dynamically significant diffuse coronary artery narrowing is frequently manifest as a graded, longitudinal, base-to-apex myocardial perfusion abnormality by noninvasive PET.In this study, 1001 patients with documented coronary artery disease by coronary arteriography showing any visible coronary artery narrowing underwent rest-dipyridamole PET perfusion imaging. Quantitative severity of dipyridamole-induced, circumscribed, segmental PET perfusion defects was objectively measured by automated software as the minimum quadrant average relative activity indicating localized flow limiting stenoses. Quantitative severity of the graded, longitudinal, base-to-apex myocardial perfusion gradient indicating fluid dynamic effects of diffuse coronary artery narrowing was objectively measured by automated software as the spatial slope of relative activity along the cardiac longitudinal axis.In patients with mild arteriographic disease without statistically significant dipyridamole-induced segmental myocardial perfusion defects caused by flow-limiting stenoses compared with normal control subjects, there was a graded, longitudinal, base-to-apex myocardial perfusion gradient significantly different from normal control subjects (P=0. 001) that was also observed for moderate to severe dipyridamole-induced segmental perfusion defects (P=0.0001), indicating diffuse disease underlying segmental perfusion defects; 43% of patients with or without segmental perfusion defects demonstrated graded, longitudinal, base-to-apex perfusion abnormalities beyond +/-2 SD of normal control subjects, indicating diffuse coronary arterial narrowing by noninvasive PET perfusion imaging.
Abstract 850: Sirt1-mediated suppression of cell death in breast cancer.
Authors: Jeffrey B. Mortenson, Vajira K. Weerasekara, Josh Andersen
Journal: Cancer Research (2013)

Abstract Several lines of evidence suggest that protein lysine acetylation pathways are deregulated in cancer (1). Moreover, deacetylase inhibitors are emerging as important anti-tumor therapeutics, suggesting that the forced reprogramming of protein-lysine acetylation is toxic to tumor cells. In this study we show that Sirt1, an NAD+-dependent Sirtuin deacetylase that promotes cancer cell survival, is aberrantly mislocalized to the cytoplasm of breast tumor cells. Moreover, the depletion of cytosolic Sirt1 by siRNA sensitizes breast tumor cells to paclitaxel-induced death. Previously, we developed a biotin-switch proteomics approach to identify cytosolic Sirt1 substrates (2). This approach yielded a variety of substrates with roles in metabolism, survival, and oxidative stress signaling. Our current work focuses on three of the proteins identified as Sirt1 substrates: SOD1, DJ-1, and 14-3-3z. SOD1 and DJ-1 both suppress oxidative stress-induced death, and high levels of 14-3-3z expression suppress chemotherapy-induced apoptosis and correlate with negative patient outcomes in breast cancer. Our preliminary results suggest that acetylation of DJ-1 and SOD1 suppress their anti-oxidant functions, while acetylation of 14-3-3z disrupts its binding to pro-survival proteins. Taken together, our data support a model in which cytosolic Sirt1 activates multiple pathways that work together to promote tumor cell survival. Citation Format: Jeffrey B. Mortenson, Vajira K. Weerasekara, Josh Andersen. Sirt1-mediated suppression of cell death in breast cancer. [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 850. doi:10.1158/1538-7445.AM2013-850
Ageing and hair cycles
Authors: M. COURTOIS, G. LOUSSOUARN, C. HOURSEAU, J.F GROLLIER
Journal: British Journal of Dermatology (1995)

The phototrichogram is a non-invasive technique by which, on the same precise area of the scalp, each individual hair may be identified, and its current growth phase established. This technique was used to study the duration of hair cycles in 10 male subjects, balding and non-balding, by observations at monthly intervals over a period of 8-14 years. The accumulated data served to characterize the effects of ageing in these subjects: a reduction in the duration of hair growth and in the diameter of hair shafts, most evident in the thickest hairs, and a prolongation of the interval separating the loss of a hair in telogen and the emergence of a replacement hair in anagen. These various aspects of ageing of scalp hair contribute to its progressive overall impoverishment. They resemble those observed in the course of male-pattern balding, although their development is less marked.
A competitive manifesto
Authors: R. Hans Phaf, Gezinus Wolters
Journal: Behavioral and Brain Sciences (2000)

The distinction made by Page between localist and distributed representations seems confounded by the distinction between competitive and associative learning. His manifesto can also be read as a plea for competitive learning. The power of competitive models can even be extended further, by simulating similarity effects in forced-choice perceptual identification (Ratcliff &amp; McKoon 1997) that have defied explanation by most memory models.
Letter: The Karen Ann Quilan case
Authors: D. J. Horan
Journal: JAMA (1976)

<h3>To the Editor.—</h3> It is somewhat surprising to see a thinker of the stature of Richard A. McCormick, SJ, compound the confusion that already exists about the Karen Ann Quinlan case. The tone of his editorial (234:1057, 1975) indicates that something occurred in her case that has very reprehensible overtones for the medical profession. For example, he speaks about the fear of malpractice, outmoded homicide laws, and intrusion into the patient-family-doctor relationship, all of which, he says, forebode great catastrophes for the medical profession. It is not clear what aspect of the case he is relying on to support this parade of horrors, but the opinion written by Judge Muir does not substantiate Fr McCormick's thesis. Father McCormick complains that the case did not belong in the courts in the first place. With this I would agree, with one caveat, which<i>supports</i>and enhances that relationship. In his 50-page opinion,
MicroRNAs and epigenetics in human breast cancer.
Authors: K Miyamoto, T Ushijima
Journal: Cancer Research (2009)

Abstract Abstract #4051 MicroRNAs (miRNAs), which regulate gene expression at the post-transcriptional level, are suggested to play important roles in carcinogenesis. To clarify the miRNAs dysregulation and the relation to epigenetic mechanisms in human breast cancer, we analyzed a breast cancer cell line, MDA-MB-468 that has previously been used for the genome-wide epigenetic analysis: methylation-sensitive-representational difference analysis (MS-RDA). Normal human mammary epithelial cells (HMEC) were compared with MDA-MB-468. The global expression profile (471 miRNAs) of these samples was examined using 3D-Gene Human miRNA oligo chip (Toray, Tokyo, Japan). We identified 4 miRNAs (0.8%), hsa-miR-200a, hsa-miR-429, hsa-miR-652 and hsa-miR-200b, which were expressed at ten-times higher levels in cancer cells and, conversely, 12 miRNAs (2.5%), hsa-miR-137, hsa-miR-138, hsa-miR-34b, hsa-miR-34c, hsa-miR-374, hsa-miR-376a, hsa-miR-422b, hsa-miR-452, hsa-miR-520e, hsa-miR-455, hsa-miR-554 and hsa-miR-574 that were silenced in the cancer cells. Expression analyses using other breast cancer cells (MCF-7, YMB-1-E, T-47D, MDA-MB-231) revealed a significant overexpression of 4 miRNAs, hsa-miR-200a, hsa-miR-429, hsa-miR-652 and hsa-miR-200b and frequent silencing of 5 miRNAs, hsa-miR-138, hsa-miR-34c, hsa-miR-376a, hsa-miR-452, and hsa-miR-455 in breast cancer cells. As for epigenetic mechanisms, overexpressed miRNAs were found to target silenced genes in the MDA-MB-468 cell line, and treatment of MDA-MB-468 with a demethylating agent, 5-aza-2'-deoxycytidine, restored the expression of 5 miRNAs, hsa-miR-137, hsa-miR-374, hsa-miR-520e, hsa-miR-554 and hsa-miR-574. Our results show the existence of a novel miRNA signature in breast cancer, suggesting that epigenetic mechanisms may be involved in the regulation of miRNA expression. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 4051.
Immunoglobulin heavy chain switch region gene polymorphisms in glomerulonephritis
Authors: Richard H. Moore, Graham A. Hitman, Renato A. Sinico, Jukka Mustonen, Julia Medcraft, Ekundayo Y. Lucas, Nicholas T. Richards, Michael C. Venning, John Cunningham, Frank P. Marsh, Giuseppe D'Amico
Journal: Kidney International (1990)
Abstract LB-64: Immune modulatory effects of mesenchymal stem cells on regulatory T cells in mouse glioma model
Authors: Kyung-Sub Moon, Derek A. Wainwright, Irina V. Balyasnikova, Chung Kwon Kim, Yoo Seung Ko, Kyung Keun Kim, Maciej S. Lesniak
Journal: Cancer Research (2014)

Abstract Objective: Although mesenchymal stem cells (MSCs) have been investigated as a vector in stem cell-based therapy for malignant glioma, there has been a debate about the exact role of MSCs in tumor microenvironment. From an immunnological aspect, MSCs have been reported to inhibit T cell proliferation and to increase CD4+FoxP3+ regulatory T cells (Tregs). They also have been investigated as a potent immune suppressor in several clinical situations including autoimmune diseases. However, whether MSCs have an immune modulatory effect on Tregs in malignant gliomas or not has not been established. Materials &amp; methods: The author explored the impact of MSCs on freshly sorted CD4+ T cells or already activated Tregs in vitro to determine whether MSCs have different influences on naive T cells and Tregs. Furthermore, using orthotropic mouse glioma model, the author investigated MSC's effect on Tregs during tumor progression. Results: The authors observed that MSCs decreased Treg conversion from naive T cells and Treg proliferation, without affecting the proportion of natural / induced Treg [nTreg; CD4+FoxP3+Helios+ / iTreg; CD4+FoxP3+Helios-]. When co-cultured with already activated Tregs, however, MSCs did not affect Treg induction and proliferation, but decreased the proportion of iTreg. With an intracranially implanted GL261 cell-based orthotropic mouse model, co-injection of MSCs with tumor cell implantation slightly increased Treg recruit into the tumor and decreased the proportion of iTreg. When MSCs were injected after glioma formation, there was no significant effect of MSCs on Treg recruit and phenotypic changes. Furthermore, there was a lower level of cytokine expressions including TGF-β, INF-γ, IL-2, and IL-1β in Tregs cocultured with MSCs than that in solely cultured Tregs. Increased gene expression of IL-6, CCL17, and TGF-β, or decreased gene expression of CCL2 in MSCs may be relevant to the phenotypic changes of cocultured Tregs. Conclusions: This study demonstrates that MSCs mainly inhibit iTreg, leading to a relative increase of the proportion of nTregs in mouse glioma model, possibly throughIL-6 signaling pathway. With a better understanding for critical factors and immunological consequences for the altered Treg phenotype in glioma, future experiments will be needed to elucidate the immunological impact of MSCs on Tregs in malignant glioma. Citation Format: Kyung-Sub Moon, Derek A. Wainwright, Irina V. Balyasnikova, Chung Kwon Kim, Yoo Seung Ko, Kyung Keun Kim, Maciej S. Lesniak. Immune modulatory effects of mesenchymal stem cells on regulatory T cells in mouse glioma model. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-64. doi:10.1158/1538-7445.AM2014-LB-64
Pityriasis rubra pilaris: clinical features and natural history in a study of 93 patients
Authors: W.A.D. Griffiths
Journal: British Journal of Dermatology (1977)

Journal Article Pityriasis rubra pilaris: clinical features and natural history in a study of 93 patients Get access W.A.D. Griffiths W.A.D. Griffiths Department of Dermatology, University of Liverpool Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 97, Issue s15, 1 December 1977, Page 18, https://doi.org/10.1111/j.1365-2133.1977.tb14302.x Published: 01 December 1977
THE TOXIC FACTORS IN EXPERIMENTAL TRAUMATIC SHOCK. III. SHOCK ACCOMPANYING MUSCLE ISCHEMIA AND LOSS OF VASCULAR FLUID 1
Authors: S. S. Kety, I. T. Nathanson, A. L. Nutt, A. Pope, P. C. Zamecnik, J. C. Aub, A. M. Brues
Journal: Journal of Clinical Investigation (1945)
Recording Cross-Culturally Useful Psychiatric Interview Data : Experience from Brazil
Authors: EUGENE B. BRODY
Journal: American Journal of Psychiatry (1966)

Standardized systems of observing and recording are necessary in order to conduct cross-cultural psychiatric studies. The author presents interview data on the behavior of lower-class psychiatric patients in Rio de Janeiro recorded with the use of a specially designed instrument, the Initial Interview Inventory: Cross-Cultural schedule, and concludes that this inventory possesses a degree of validity in the recording of cross-culturally useful psychiatric interview data.
The Molecular Basis of Cancer
Authors: John Gutheil
Journal: JAMA (1996)

The science of molecular biology has been responsible for a dramatic change in our understanding of cancer. This understanding has led to improvements in the ability to diagnose and treat certain malignancies. Unfortunately, despite these advances in patient care, molecular biology remains an elusive and perplexing topic for many physicians. While a minority are able to stay abreast of advances in the field of molecular biology, this often requires a rather manic reading of the literature and a keen eye for new and significant information. Oncology was one of the first fields to benefit from advances in molecular biology and undoubtedly will benefit from additional advances in the future. For these reasons, it is important that each practitioner of oncology have at least a general understanding of the molecular mechanisms at work in the clinic. An alternative to an exhaustive reading of the literature is a well-written textbook. The textbook