tbuckley/cabot-search huggingface dataset:
Abstract 12440: Does Low Diastolic Blood Pressure Contribute to the Risk of Recurrent Cardiovascular Disease Events? The Framingham Heart Study
Authors: Stanley S Franklin, Sohum G Gokhale, Vincent H Chow, Nathan D Wong, Daniel Levy, Martin G Larson, Ramachandran S Vasan, Gary F Mitchell
Journal: Circulation (2014)

Background: The clinical significance of low diastolic blood pressure (DBP) as a risk for recurrent cardiovascular disease (CVD) events in persons with isolated systolic hypertension (ISH) is controversial. Methods: We examined risk for recurrent CVD events in 791 individuals (age 75 years, 47% female, mean follow-up time: 8±6 years) with DBP&lt;70 (N=225) versus 70-89 mmHg (N=566) following initial CVD events in the original and offspring cohorts of the Framingham Heart Study. Results: Recurrent CVD events occurred in 153 (68%) participants with lower DBP and 271 (48%) with higher DBP (p&lt;0.0001). Risk of recurrent CVD events in risk factor-adjusted Cox regression was higher in those with DBP&lt;70 mmHg versus DBP 70-89 mmHg in both treated [HR, 5.1 (95% CI: 3.8-6.9) p&lt;0.0001] and untreated individuals [HR, 11.7 (6.5-21.1) p&lt;0.0001] (treatment interaction: p=0.10). Individually, coronary heart disease, heart failure, and stroke recurrent events were more likely with DBP&lt;70 mmHg versus 70-89 mmHg (p&lt;0.0001). To judge the potential modifying effect of wide pulse pressure (PP) on excess risk associated with low DBP, we defined 4 binary groupings of median PP (≥ 68 verses &lt;68 mmHg) and categorical DBP (&lt;70 versus 70-89 mmHg), and found that CVD event rates were higher only in the group with wide PP and DBP&lt;70 mmHg (Chi Square = 32.6, p&lt;0.001, see Figure). Conclusions: Persons with ISH and initial CVD events have increased risk for recurrent CVD events in the presence of DBP&lt;70 mmHg versus DBP 70-89 mmHg, supporting wide PP as an important risk modifier of the adverse effect of low DBP; we postulate increased CVD risk is related to the pernicious effects of faulty microvascular function resulting from increased elastic artery stiffness in combination with low diastolic perfusion pressure.
Anterior Mediastinal Metastasis of Testicular Germ Cell Tumor: Relation to Benign Thymic Hyperplasia
Authors: K. (a) Suzuki, K. (a) Kurokawa, T. (a) Suzuki, I. (b) Yoshida, A. (b) Otaki, K. (a) lmai, H. (a) Yamanaka
Journal: European Urology (1997)
Diagnostic and Prognostic Utility Of a 26-Gene Panel For Deep-Sequencing Mutation Analysis In Myeloid Malignancies
Authors: Alexander Kohlmann, Sabrina Kuznia, Niroshan Nadarajah, Tamara Alpermann, Sandra Weissmann, Andreas Roller, Andreia Albuquerque, Wolfgang Kern, Claudia Haferlach, Susanne Schnittger, Torsten Haferlach
Journal: Blood (2013)
ALKALOSIS, A CLINICAL PROBLEM
Authors: Charles T. Way, Edward Muntwyler
Journal: Annals of Internal Medicine (1935)

Article1 January 1935ALKALOSIS, A CLINICAL PROBLEMCHARLES T. WAY, F.A.C.P., EDWARD MUNTWYLERCHARLES T. WAY, F.A.C.P.Search for more papers by this author, EDWARD MUNTWYLERSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-8-7-818 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAlkalosis is a term applied to that condition of the acid-base balance of the blood in which the concentration of the blood bicarbonate is above the normal level. It may be more broadly defined as an abnormal condition caused by the accumulation in the body of an excess of alkali or by the loss of acid. Alkalosis has been observed clinically in a number of conditions, but has, however, been most frequently encountered in cases on Sippy management or in cases with pyloric or upper intestinal obstruction accompanied by vomiting. It is not the purpose of this report to consider...References1. WHITNEY JL: Studies on acidosis. The immediate cause of death and remarks on the acidosis of nephritis, Arch. Int. Med., 1917, xx, 931. CrossrefGoogle Scholar2. CHACEMYERS AFVC: Acidosis in nephritis, Jr. Am. Med. Assoc., 1920, lxxiv, 641. CrossrefGoogle Scholar3. MARRIOTTHOWLAND WMJ: Phosphate retention as a factor in the production of acidosis in nephritis, Arch. Int. Med., 1916, xviii, 708. DENIS, W., and MINOT, A. S.: A study of phosphate retention from the standpoint of blood analysis, Arch. Int. Med., 1920, xxvi, 99. DE WESSELOW, O. L. V.: On the phosphorus and calcium of the blood in renal disease, Quart. Jr. Med., 1923, xvi, 341-362. CrossrefGoogle Scholar4. WAKEFIELD EG: Inorganic serum sulfates in renal insufficiency, Arch. Int. Med., 1929, xliv, 244. CrossrefGoogle Scholar5. PETERSWAKEMANEISENMANLEE JPAMAJC: Total acid-base equilibrium of plasma in health and disease. X. The acidosis of nephritis, Jr. Clin. Invest., 1929, vi, 517. CrossrefGoogle Scholar6. PALMERVAN SLYKE WWDD: Studies of acidosis. IX. Relation between alkali retention and alkali reserve in normal and pathological individuals, Jr. Biol. Chem., 1918, xxxii, 499-507. Google Scholar7. MYERSBOOHER VCLE: Observations on the excretion of an acid urine in alkalosis, Proc. Soc. Exper. Biol. and Med., 1925, xx, 513. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cleveland, Ohio*Read at the Chicago meeting of the American College of Physicians, April 18, 1934.From the Department of Biochemistry, School of Medicine, Western Reserve University, Cleveland, and the Division of Medicine, St. Luke's Hospital, Cleveland. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1935Volume 8, Issue 7Page: 818-824KeywordsAttentionBicarbonatesBiochemistryBloodHospital medicineVomiting Issue Published: 1 January 1935 PDF DownloadLoading ...
Telephone consultations for follow-up of interstitial lung disease: Patient satisfaction survey
Authors: Rina Adhikary, Leanne Cheyne, Paul Beirne
Journal: European Respiratory Journal (2012)

Introduction  The long-term follow-up required by Interstitial Lung Disease (ILD) patients imposes a significant burden on healthcare resources. Telephone consultations have been piloted as an alternative to some face-to-face consultations in a teaching hospital based ILD service. Patients whose next consult is anticipated to be uncomplicated (eg stable patients having interval lung function tests) are offered a phone consult with the ILD consultant.  Aims and Objectives  To assess whether ILD patients are as satisfied with a telephone consultation as with a face-to-face consult.  Methods  A postal survey was sent to 95 consecutive ILD patients who had a phone consult over a 12-month period. Patients used a 5-point score to report if, in comparison to a face-to-face consult, the phone consult was as punctual, convenient, reassuring, and afforded the same opportunity to ask questions, and facilitated the same understanding of information.  Results  52 patients (55%) posted responses (see Table 1). 67% agreed phone consults were as punctual. 78% agreed they were as convenient. 77% felt as reassured and as able to ask questions. 88% understood the information given just as easily. 80% were willing to have another phone consult.  Discussion  The majority of ILD patients selected for a telephone consultation were at least as satisfied as with a face-to-face consult. Telephone consultations are acceptable to the majority of ILD patients for at least some of their follow-up.
Insulin resistance in heart failure: differences between patients with reduced and preserved left ventricular ejection fraction
Authors: Nadja Scherbakov, Maximiliane Bauer, Anja Sandek, Tibor Szabó, Agnieszka Töpper, Ewa A. Jankowska, Jochen Springer, Stephan von Haehling, Stefan D. Anker, Mitja Lainscak, Stefan Engeli, Hans‐Dirk Düngen, Wolfram Doehner
Journal: European Journal of Heart Failure (2015)
Abstract P317: Association of Dietary Insulin Index, Insulin Load With Risk of Coronary Heart Disease Among Us Men and Women
Authors: Shanshan Li, Eric B Rimm, Frank B Hu, Laura Sampson, Mary Franz, Walter C Willett
Journal: Circulation (2015)

Introduction: Dietary insulin index and insulin load were developed to quantify the insulinogenice effects of various foods to capture the postprandial insulin response elicited by carbohydrate, protein and fat intake. However, the association between dietary insulin index, dietary insulin load with risk of coronary heart disease is unknown. Methods: Based on the Nurses’ Health Study (NHS) and the Health Professionals Follow-up Study (HPFS), two large prospective cohort studies of US women and men, we included 76,277 women and 42,689 men into our study with dietary information measured every 4 years. We excluded participants with a baseline history of cardiovascular disease, type 2 diabetes, or cancer. Multivariate Cox proportional hazard models were used, adjusting for major risk factors for coronary heart diseases. We modeled dietary insulin index and insulin load using simple update, cumulative average, continue updating and stop updating after intermediate outcomes. Results: The multivariate adjusted hazard ratio (HR) and 95% confidence intervals comparing the highest vs. the lowest quintile of dietary insulin index was 1.08 (95% CI: 0.95-1.23; p for trend=0.66) for women, and 1.07 (95% CI: 0.98-1.17; p for trend =0.02) for men. For dietary insulin load, the adjusted HR was 1.1 (95% CI: 0.97-1.25; p for trend=0.50) for women and 1.05 (95%CI: 0.96-1.14; p for trend=0.10) for men. Results were similar across different analytic methods. Conclusion: In this cohort of US women and men, we did not observe a strong positive between dietary insulin index or dietary load and risk of coronary heart diseases.
Abstract 4181: Chronic stress and beta adrenergic signaling promote angiogenesis and prostate cancer progression through suppressing the expression of Thrombospondin 1
Authors: Mohit M. Hulsurkar, Meixiang Sang, Haiping Song, Wenliang Li
Journal: Cancer Research (2015)

Abstract Several recent studies have revealed that the activation of beta adrenergic signaling induced by chronic biobehavioral stress promotes the progression of ovarian, breast and prostate cancers. Conversely, the use of hypertension medicine, beta blockers (beta adrenergic antagonists), has been found to be associated with better prognosis in several human cancers. Although the beta adrenergic signaling has been shown to be activated by chronic stress and responsible for promoting cancers, the mechanisms through which beta adrenergic signaling promotes tumor angiogenesis and cancer progression are still unclear. We found that chronic stress and activation of beta adrenergic signaling suppressed the expression of Thrombospondin 1 (TSP1) in prostate cancer cells in vitro, as well as in mouse xenograft tumors in vivo, which in turn promoted tumor angiogenesis and cancer progression. TSP1 was the first endogenous angiogenesis inhibitor to be discovered and its down-regulation is associated with increased angiogenesis. We recently demonstrated that G-protein coupled receptor kinase 3 (GRK3, ADRBK2) promotes angiogenesis and prostate cancer progression through suppressing TSP1. Interestingly, GRK3 expression is up-regulated by chronic stress and activation of beta adrenergic signaling, suggesting that GRK3 acts as a mediator for chronic stress and beta adrenergic signaling in repressing TSP1 expression. Taken together, these results suggest that beta adrenergic signaling pathway stimulates angiogenesis through GRK3 mediated suppression of TSP1. Citation Format: Mohit M. Hulsurkar, Meixiang Sang, Haiping Song, Wenliang Li. Chronic stress and beta adrenergic signaling promote angiogenesis and prostate cancer progression through suppressing the expression of Thrombospondin 1. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4181. doi:10.1158/1538-7445.AM2015-4181
Inhibition of amyloid-β plaque formation by α-synuclein
Authors: Teresa Bachhuber, Natalie Katzmarski, Joanna F McCarter, Desiree Loreth, Sabina Tahirovic, Frits Kamp, Claudia Abou-Ajram, Brigitte Nuscher, Alberto Serrano-Pozo, Alexandra Müller, Marco Prinz, Harald Steiner, Bradley T Hyman, Christian Haass, Melanie Meyer-Luehmann
Journal: Nature Medicine (2015)
Cyclin D1 regulation of mitochondrial function in breast cancer
Authors: Chenguang Wang, Mathew Casimiro, Lifeng Tian, Toshiyuki Sakamaki, Andrew Quong, Richard Pestell
Journal: Cancer Research (2007)

4472   Cyclin D1 is overexpressed in human breast cancers and is sufficient for the development of murine mammary tumors. The cyclin D1 gene encodes a regulatory subunit of the holoenzyme that phosphorylates and inactivates the pRb tumor suppressor protein to promote nuclear DNA synthesis. In addition to the ability of cyclin D1 to form a holoenzyme with cdk4/6, we and others have previously shown that cyclin D1 regulates distinct cellular functions through physical association with nuclear receptors and transcriptional coregulators. In knockdown experiments using siRNA against cyclin D1 we observed that both mitochondial size and activity were increased, this observation was validated using cyclin D1 anti-sense transgenic mice. Mammary epithelial cells obtained from cyclin D1 anti-sense transgenic mice demonstrated induction of genes governing mitochondrial function and glycolysis. Reciprocal expression of these genes was observed in mammary tumors induced by mammary gland targeted cyclin D1 overexpression. Global gene expression profiling and functional analysis of mammary epithelial cell-targeted cyclin D1 anti-sense transgenics demonstrated cyclin D1 inhibits mitochondrial activity, and aerobic glycolysis  in vivo . We further examined the mitochondrial components including mitochondrial transcriptional factor A (mtTFA) and mitochondrial nuclear respiratory factor 1 (NRF-1) that are key regulators of mitochondrial DNA synthesis and function. Cyclin D1 repressed expression of mtTFA and inhibited D-loop transcriptional activity. NRF-1, which induces nuclear-encoded mitochondrial genes, was transcriptionally repressed and its activity was inhibited by cyclin D1. Cyclin D1 levels and NRF-1 expression were inversely correlated during cell cycle progression. In addition, NRF-1- and cyclin D1-regulated genes were inversely correlated by microarray expression profiling. Cyclin D1 associated with NRF-1  in vivo  by immunoprecipitation and in mammalian two-hybrid assays. Screening for the potential phosphorylation site of NRF-1 demonstrated that cyclin D1-dependent kinase phosphorylated NRF-1 at Serine 47. In summary, in addition to regulating nuclear DNA synthesis, cyclin D1 regulates mitochondrial function  in vivo , coordinating metabolic substrate utilization within the cell.
Features of mucous membrane changes of bronchial tree at patients with COPD
Authors: Tetyana Pertseva, Igor Ivakh
Journal: European Respiratory Journal (2011)

Aim:  Research was an estimation of expressed of changes of mucous membrane of bronchial tree at patients of COPD on the different stages of pathological process.   Study population and methods:  We investigated 86 patients (pts) (53 male, mean age 62.4±4.2 yrs) with COPD. All pts were divided on three groups: I group (gr.) – 10 pts. with COPD I stage (st.); II gr. – 28 pts. with II st.; III gr. – 36 pts. with COPD III st., IV gr. – 12 pts. with COPD IV st. The state of mucous membrane of bronchial tree, degrees of atrophy of epithelium, character and amount of mucus, was estimated.   Results:  All pts had manifestations of atrophic change of bronchial tree mucous (1 and 2 degree of atrophic endobronchitis), however significant differences in pts I and II gr. (1 degree of atrophic endobronchitis) didn9t found. Endoscopic picture in pts III gr. was characterized by atrophic change (atrophic endobronchitis of 2 degree). Pts with IV st. COPD was dominated by manifestations of deforming endobronchitis against mucosal atrophy 3 st.  In pts. I and II gr. hadn9t distinctions in quantitative and qualitative description of sputum: light lucid sputum in little quantity or no. Increase of bronchoobstruction in III gr. was accompany by considerable changes character, viscosity and quantity of sputum (ample quantity rich cloudy mucus).   Conclusions:  1.Progress of COPD is characterized growth of degree and expressed of atrophy displays in the mucous membrane of bronchial tree.  2. Structural change of epithelium of mucous membrane of bronchial tree cause the change of character and amount mucus.
Restoration of fusion in children with intracranial tumors and incomitant strabismus
Authors: Benjamin Shalev, Michael X Repka
Journal: Ophthalmology (2000)

Purpose Intracranial tumors may cause eye misalignment and interruption of sensory fusion. The ocular misalignment may be permanent or may be corrected after tumor treatment with or without specific strabismus treatment. This report analyzes the binocular vision outcome of children with misaligned eyes from brain tumors who regain orthotropia. Design A retrospective noncomparative case series. Participants Twenty-three surviving children less than 18 years of age with a new heterotropia and absence of fusion associated with the development of a brain tumor. Interventions Tumor resection/radiation/chemotherapy and necessary strabismus management. Main outcome measure Stereopsis (≥ 4 of 10 circles) measured with the Randot II stereo test at near fixation. Results Fourteen children regained orthotropia either after tumor therapy, strabismus treatment, or both. Ten of these 14 children with realigned vision regained high-grade stereovision. Nine patients did not regain orthotropia and were excluded. The mean age at tumor diagnosis of the fusing group was 9.9 years (range, 3–17 years) compared with 8.5 years (range, 6–12 years) in the four realigned nonfusing patients. The mean duration of misalignment was 12 months (range, 2–51 months) for the fusing group, and 45 months (range, 14–120 months) for the nonfusing group. Conclusions Children and adolescents with brain tumor–associated eye misalignment may regain the ability to fuse if their misalignment can be corrected. An improved prognosis was noted for those patients when the misalignment had been present for a shorter duration. These data suggest that the outcome may be better for incomitant strabismus than that reported for acute comitant esotropia.
REACTIVE SPLENOMEGALY AND VARIATION OF LYMPHOID-PLASMA CELL POPULATION ASSOCIATED WITH A MOUSE PITUITARY THYROTROPIC TUMOR.
Authors: Edith E. Sproul, Raul Grinberg
Journal: Cancer Research (1964)

Summary  A transplantable thyrotropic pituitary tumor, subline L24a, which grew after 13 months of dormancy in an intact mouse was associated in its early passage with a variety of lymphoid tumors. On subsequent passage, slow growth over a 6- to 12-month period was regularly accompanied by striking splenomegaly without lymphoid or thymic neoplasia. The enlargement was due to a great increase in cells of the lymphoid series in the red pulp without loss of splenic architecture. In thyroidectomized mice plasma cells with many Russell bodies were especially numerous, and these cells were found in hypertrophied lymphoid follicles within other organs. It is suggested that the splenomegaly and, in earlier passage the lymphoid tumors, may represent an exaggerated antibody response to a tumor9s having unusual or abnormal hormonal activity. The transplanted pituitary tumors, in turn, showed severe hemorrhagic degeneration with peripheral small lymphocyte stasis in the lymphatics.
Impact of comorbidities by ACE‐27 in the revised‐IPSS for patients with myelodysplastic syndromes
Authors: Naval Daver, Kiran Naqvi, Elias Jabbour, Tapan Kadia, Courtney DiNardo, Marylou Cardenas‐Turanzas, Sherry Pierce, Khanh Thi‐Thuy Nguyen, Carlos Bueso‐Ramos, Hagop Kantarjian, Guillermo Garcia‐Manero
Journal: American Journal of Hematology (2014)

Comorbidities significantly affect the prognosis and outcomes of patients with hematological malignancies. We have previously reported the impact of comorbidities on the International Prognostic Scoring System (IPSS) score. The aim of this study was to determine whether comorbidities continued to have a significant impact when patients were reclassified according to the Revised-IPSS (IPSS-R). The medical records of 600 consecutive myelodysplastic syndrome patients who presented to MD Anderson Cancer Center between January 2002 and June 2004 were reviewed. The Adult Comorbidity Evaluation-27 (ACE-27) was used to assess the severity of comorbid conditions. Four hundred and two (67%) patients were male. Median age at presentation was 66.6 years (17-94). Mean duration of follow-up was 54 months (1-100). Five hundred and two (84%) patients died, and 54 (9%) patients underwent stem cell transplantation. Overall median survival was 16.8 months (1-100). Median survival by IPSS-R was 47, 34, 21, 16, and 6 months for patients in very low, low, intermediate, high, and very high-risk groups, respectively (P < 0.001). The ACE-27 comorbidity score significantly impacted the median survival of patients in the intermediate (P < 0.001), high (P = 0.045), and very high (P = 0.004) IPSS-R groups; but did not significantly impact the median survival in the low (P = 0.11) and very low (P = 0.49) IPSS-R groups. The ACE-27 comorbidity score significantly impacted the median survival of patients ≤65 years (P < 0.001) but did not significantly impact those >65 years (P = 0.18). Assessment of comorbidity may enhance the prognostic ability of the IPSS-R.