tbuckley/cabot-search huggingface dataset:
Abstract 17203: Increasing Age, Arterial Stiffness, and Ambulatory Blood Pressure
Authors: Marwah Abdalla, Laura DiCola, Paul Muntner, Keith M Diaz, Daichi Shimbo, Joseph E Schwartz
Journal: Circulation (2014)

Background: Ambulatory blood pressure (ABP) is associated with an increased risk of cardiovascular disease (CVD) events and mortality. Age is positively associated with higher ABP, particularly systolic ABP. The physiological basis for the association between age and ABP is incompletely understood, and no studies to our knowledge have examined the contributions of arterial stiffness to the age-ABP association. Our objective was to examine whether arterial stiffness might explain the association between increasing age and ABP.

Methods: The Masked Hypertension Study is an ongoing population study of employed adults in New York without CVD, renal failure, or treated hypertension. Clinic BP (CBP), 24-hr ABP, and carotid-femoral pulse wave velocity (PWV) were assessed in 225 participants. Three manual CBP measurements were obtained on three separate occasions (total 9 readings) over a 3-week period and averaged. ABP was assessed using a SpaceLabs 90207 monitor (Snoqualmie, WA). PWV was measured using a SphygmoCor device (AtCor, Itasca, IL).

Results: Of the 225 participants, 90 (40%) were male, 12 (5.3%) were African American, and 29 (12.9%) were Hispanic. Mean ± SD age and body mass index (BMI) were 44.4 ± 10.3 years and 26.4 ± 4.6 kg/m2, respectively. Mean ± SD systolic/diastolic CBP was 115 ± 12 /75 ± 8 mmHg and ABP was 121 ± 11 /77 ± 7 mmHg. The correlation between age and PWV was 0.44 (p<0.001), and between age and awake systolic/diastolic ABP were 0.14 (p=0.041)/0.15 (p=0.028). The positive associations of age with systolic and diastolic ABP in a sex, race/ethnicity, and BMI-adjusted model were completely attenuated after further adjusting for PWV (see Table). In contrast, PWV was significantly associated with awake systolic and diastolic ABP after multivariable adjustment.

Conclusions: The associations between age and elevated BP outside of the clinic setting may, in part, be explained by age-related increases in arterial stiffness.

   ![][1]  [1]: /embed/graphic-1.gif
Biochemical basis of inflammation in children with obstructive sleep apnea syndrome (OSAS) and in children with obesity
Authors: Melania Evangelisti, Anna Claudia Massolo, Filomena Ianniello, Maria Chiara Paolino, Marilisa Montesano, Silvia Miano, Martina Forlani, Maria Pia Villa
Journal: European Respiratory Journal (2011)

Rationale: OSAS and obesity are two risk factors that can lead to the early development of cardiovascular events. These two diseases very often coexist, and it's hard to understand the mecchanisms that characterize each one. Our aim was to determine the different pathways of these two disorders.

Methods: We evaluated 38 children (M/F=23/15; mean age: 7.68±3.78 years), divided in three groups (18 children with OSAS but non obese, 10 Obese children but without OASA, 10 controls). All children underwent blood sample test for the evaluation of CRP hs, the lipidic and metabolic aspect (Glycemia, Insulin, Cholesterol total, LDL and HDL, triglycerides, leptin, adiponectin, and resistin), the interleuchines pattern (IL-1 α e β, IL-2, IL-4, IL-6, IL-8, IL-10, IFN-γ, TNF-α, VEGF, EGF, MCP1) and the polysomnography examination.

Results: Children with OSAS and children with obesity showed higher levels of LDL-cholesterol and triglycerides compared to controls (OSAS p=0.005 and p=0.01; Obese p=0.01 and p=0.005). In the obese group leptin levels were significantly higher compared to controls and to the OSAS (p=0.00). In the OSAS groups we found significantly higher levels of IL 1 β (p=0.04) and TNF-α (p=0.05) compared to controls and obese groups.

Conclusions: OSAS and obesity have two different pathways. OSAS promotes an inflammatory pattern through the stimulation of TNF-α, wehereas obesity determines an hormonal deregulation especially of the adipokines one, as leptin.
Controversies in management: Does palliative care have a role in treatment of anorexia nervosa? We should strive to keep patients alive Palliative care does not mean giving up
Authors: C. J Williams, L. Pieri, A. Sims, L. Russon, D. Alison
Journal: BMJ (1998)

# Does palliative care have a role in treatment of anorexia nervosa? {#article-title-2} A recent report in a palliative care journal described a patient with longstanding and severe anorexia nervosa who was transferred from a psychiatric unit to a hospice, where she died. Williams and colleagues argue that patients with anorexia nervosa should be actively treated. Russon and Alison put the case for palliative care. # We should strive to keep patients alive {#article-title-3} Anorexia nervosa is defined as severe, self inflicted loss in body weight to at least 15% below that expected for the subject's sex and height. Mortality varies between 5% and 18% depending on case selection and length of follow up. A recent report described the case of a 24 year old woman who had suffered from anorexia nervosa for seven years and who was admitted for palliative care to a UK hospice in a poor physical state, received opiates, and died.1 This report concerns us for a number of reasons and raises several issues about how such cases should best be managed. The goal of treatment must always be clarified when considering palliative care. In terminal illness, the decision to withdraw active treatments and provide a supportive approach to symptom control is often appropriate. We question whether this is applicable in anorexia. Recovery is possible even in patients with longstanding severe anorexia. In a 10 year follow up of 76 severely ill women with anorexia, Eckert et al found that 18 (24%) had fully recovered, about half had a benign outcome, and only five (7%) had died.2 Ratnasuriya et al found a fairly constant rate of recovery during the first 12 years after onset of illness, with reduced likelihood of recovery after this.3 In the light of these findings, we believe that the hospice admission and treatment with opiates raises important issues about the difficulties some medical and nursing staff have in dealing with chronic … Correspondence to: Dr Russon Lynne.Russon@st-gemma.co.uk
Modern Therapy of Chronic Myeloid Leukemia
Authors: M.M. Zaharieva, G. Amudov, S.M. Konstantinov, M. L.
Journal: Leukemia (2013)

Chronic myeloid leukemia is one of the most thoroughly studied and, undoubtedly, best understood neoplasms. There are about 4000 and 5000 new cases of CML every year in the USA. CML is a hematologic stem cell malignancy that typically evolves in 3 distinct clinical stages: chronic and accelerated phases and blast crisis. The chronic phase lasts several years and is characterized by accumulation of myeloid precursors and mature cells in bone marrow, peripheral blood, and extramedullary sites. The accelerated phase lasts 4 to 6 months and is characterized by an increase in disease burden and in the frequency of progenitor/precursor cells. The blast crisis lasts a few months and is the terminal phase of chronic myelogenous leukemia, characterized by the rapid expansion of a population of myeloid or lymphoid differentiation-arrested blast cells (Calabretta and Perrotti 2004; Radich 2007).
Abstract 4417: Targeting Ras with small molecules that activate SOS-mediated nucleotide exchange
Authors: Olivia W. Rossanese, Michael C. Burns, Qi Sun, R. Nathan Daniels, DeMarco V. Camper, J. Phillip Kennedy, Jason Phan, Edward T. Olejniczak, Taekyu Lee, Alex G. Waterson, Stephen W. Fesik
Journal: Cancer Research (2014)

Abstract Aberrant activation of Ras, by mutation or constitutively active upstream kinases, occurs in nearly 30% of all human cancers, rendering Ras one of the most validated targets in cancer drug discovery. Historically, the direct inhibition of Ras with small molecules has proven extremely difficult. Here we report the discovery of compounds that bind to a unique pocket on the Ras:SOS:Ras complex, which increase the rate of SOScat-catalyzed nucleotide exchange in vitro and modulate Ras signaling pathways in cells. X-ray crystallography reveals that the molecules bind in a hydrophobic pocket in the CDC25 domain of SOS, adjacent to the Switch II region of Ras. Structure-based mutational analyses confirmed the functional relevance of this binding site and demonstrated that it is essential for compound activity. Consistent with their increased exchange activity in vitro, these molecules increase Ras-GTP levels in cells. However, the compounds inhibit ERK and AKT phosphorylation; the ERK inhibition at high concentrations is accompanied by an increase of p-ERK levels at lower compound concentrations. These molecules represent a unique tool to study the acute activation of Ras and highlight a novel pocket on SOS that may be exploited to modulate Ras signaling. Citation Format: Olivia W. Rossanese, Michael C. Burns, Qi Sun, R. Nathan Daniels, DeMarco V. Camper, J. Phillip Kennedy, Jason Phan, Edward T. Olejniczak, Taekyu Lee, Alex G. Waterson, Stephen W. Fesik. Targeting Ras with small molecules that activate SOS-mediated nucleotide exchange. [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 4417. doi:10.1158/1538-7445.AM2014-4417
Can C-reactive protein, procalcitonin and mid-regional pro-atrial natriuretic peptide measurements guide choice of in-patient or out-patient care in acute pyelonephritis? Biomarkers In Sepsis (BIS) multicentre study
Authors: Y-E. Claessens, J. Schmidt, E. Batard, S. Grabar, D. Jegou, P. Hausfater, G. Kierzek, S. Guérin, J-L. Pourriat, J-F. Dhainaut, C. Ginsburg
Journal: Clinical Microbiology and Infection (2009)
Abstract 3917: Understanding the mechanisms driving pancreatic neuroendocrine tumorigenesis
Authors: Amanda R. Wasylishen, Guillermina Lozano
Journal: Cancer Research (2014)

Abstract A recent exome sequencing study of pancreatic neuroendocrine tumors (PanNETs) provided valuable information about the genetic landscape of these cancers and for the first time implicated DAXX and ATRX loss in tumorigenesis. These interacting proteins are chaperones for the histone variant H3.3 and contribute to chromatin homeostasis and telomere maintenance. Mutually exclusive mutations in DAXX or ATRX occur in 43% of PanNETs. To understand how loss of these epigenetic regulators specifically contributes to tumorigenesis, we are developing genetically engineered mouse models of PanNETs. While a mouse with a conditional Daxx allele is publically available, subsequent sequencing and characterization revealed a mutant loxP site, which renders recombination extremely inefficient. We are, therefore, currently generating a new conditional Daxx allele, as well as using an existing conditional Atrx allele to specifically delete these genes in the endocrine pancreas. Cohorts of mice are being built and followed for developmental and tumor phenotypes. In addition, in vitro studies have also implicated a role for DAXX as a negative regulator of the p53 tumor suppressor pathway. Interestingly, p53 is rarely mutated in PanNETs. We are using a Daxx-null allele, generated using the existing conditional Daxx mouse, to investigate the relationship between DAXX and the p53 pathway in vivo. Combined, this work aims to generate and characterize mouse models which will lead to a better understanding of both the etiology of PanNETs and how loss of DAXX and ATRX contribute to tumorigenesis. Note: This abstract was not presented at the meeting. Citation Format: Amanda R. Wasylishen, Guillermina Lozano. Understanding the mechanisms driving pancreatic neuroendocrine tumorigenesis. [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 3917. doi:10.1158/1538-7445.AM2014-3917
Evidence for a second genetic locus in Carney complex
Authors: None Irvine, None Armstrong, None Bingham, None Hadden, None Nevin, None Hughes
Journal: British Journal of Dermatology (1998)

Carney complex (MIM no. 160980) is an autosomal dominant condition of lentiginosis, cutaneous and cardiac myxomas and multiple endocrine neoplasia. A locus for Carney complex has recently been mapped to chromosome 2p16. We have studied two Northern Irish families with this disorder. Linkage analysis was performed on the families using five highly informative dinucleotide repeat markers covering this area. Negative logarithm of the odds scores were obtained for all markers at all recombination fractions. We conclude that Carney complex is genetically as well as clinically heterogeneous.
<i>FADS</i> gene cluster modulates the effect of breastfeeding on asthma. Results from the GINIplus and LISAplus studies
Authors: M. Standl, S. Sausenthaler, E. Lattka, S. Koletzko, C.‐P. Bauer, H.‐E. Wichmann, A. von Berg, D. Berdel, U. Krämer, B. Schaaf, I. Lehmann, O. Herbarth, N. Klopp, B. Koletzko, J. Heinrich
Journal: Allergy (2011)

To cite this article: Standl M, Sausenthaler S, Lattka E, Koletzko S, Bauer C‐P, Wichmann H‐E, von Berg A, Berdel D, Krämer U, Schaaf B, Lehmann I, Herbarth O, Klopp N, Koletzko B, Heinrich J. FADS gene cluster modulates the effect of breastfeeding on asthma. Results from the GINIplus and LISAplus studies. Allergy 2012; 67 : 83–90. Abstract Background: The protective effect of breastfeeding (BF) on the development of asthma has been widely recognized, even if not all results have been consistent. Gene variants of the FADS gene cluster have a major impact on fatty acid composition in blood and in breast milk. Therefore, we evaluated the influence of the FADS1 FADS2 gene cluster polymorphisms on the association between BF and asthma. Methods: The analysis was based on data ( N = 2245) from two German prospective birth cohort studies. Information on asthma and BF during the first 6 months was collected using questionnaires completed by the parents. Logistic regression modelling was used to analyse the association between exclusive BF and ever having asthma stratified by genotype. Results: In the stratified analyses, BF for 3 or 4 months after birth had a protective effect for heterozygous and homozygous carriers of the minor allele (adjusted odds ratio between 0.37 (95% CI: 0.18–0.80) and 0.42 (95% CI: 0.20–0.88). Interaction terms of BF with genotype were significant and ranged from −1.17 ( P ‐value: 0.015) to −1.33 (0.0066). Moreover, heterozygous and homozygous carriers of the minor allele who were exclusively breastfed for 5 or 6 months after birth had a reduced risk of asthma [0.32 (0.18–0.57) to 0.47 (0.27–0.81)] in the stratified analyses. For individuals carrying the homozygous major allele, BF showed no significant effect on the development of asthma. Conclusions: The association between exclusive BF and asthma is modified by the genetic variants of FADS genotypes in children.
Relationship of serum cholesterol levels to atopy in the US population
Authors: M. B. Fessler, R. Jaramillo, P. W. Crockett, D. C. Zeldin
Journal: Allergy (2009)

Cholesterol promotes Th2 immunity and allergic inflammation in rodents; whether this occurs in humans is unclear. Reports of both direct and inverse associations between serum cholesterol and atopy in different populations suggest that race and/or other demographic variables may modify these relationships.To determine the relationships between levels of three serum cholesterol measures [total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), and non-HDL-C] and atopy in a sample representative of the US population.Cross-sectional study of 6854 participants aged > or =6 years from the 2005-2006 National Health and Nutrition Examination Survey.In the overall population, adjusted odds ratios (AORs) per two-standard deviation increase in TC and non-HDL-C for biochemical atopy (defined as > or =1 allergen-specific IgE to 19 allergens) were 1.17 [95% confidence interval (CI), 1.00-1.38] and 1.19 (95% CI, 1.03-1.39), respectively. Interactions by race were noted for the two relationships (interaction P = 0.004 and P = 0.009, respectively) with non-Hispanic Whites (NHWs) having direct relationships [TC: AOR 1.27 (95% CI, 1.03-1.57); non-HDL-C: AOR 1.27 (95% CI, 1.03-1.56)] and non-Hispanic Blacks (NHBs) inverse relationships [TC: AOR 0.77 (95% CI, 0.62-0.95); non-HDL-C: AOR 0.86 (95% CI, 0.69-1.08)]. The adjusted HDL-C-atopy relationship was nonsignificant for NHWs and inverse for NHBs [AOR 0.77 (95% CI, 0.61-0.96)]. Relationships were independent of body mass index and serum C-reactive protein and unmodified by corticosteroid or statin usage. Results were similar using current hay fever/allergy as the atopy outcome.There are marked inter-racial differences in the relationship between serum cholesterol and atopy in the US population.
A Comparison of the Diagnostic Value of the Wassermann, Kahn and Micro-Precipitation Tests for Syphilis
Authors: Norbert Enzer, G. V. Hallman, Eleanor A. Conway, Lois Hyslop
Journal: Annals of Internal Medicine (1931)

Article1 February 1931A Comparison of the Diagnostic Value of the Wassermann, Kahn and Micro-Precipitation Tests for SyphilisNORBERT ENZER, M.D., G. V. HALLMAN, M.Sc., ELEANOR A. CONWAY, B.A., LOIS HYSLOP, B.A.NORBERT ENZER, M.D.Search for more papers by this author, G. V. HALLMAN, M.Sc.Search for more papers by this author, ELEANOR A. CONWAY, B.A.Search for more papers by this author, LOIS HYSLOP, B.A.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-4-8-1028 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe diagnosis of syphilis by serological methods has become universal. Indeed, the tendency on the part of clinicians is to rely solely, or almost so, on the findings of the serologist. In hospital practice it is becoming common to have a serological test performed routinely on all patients. In our experience this is excellent practice, and a good axiom for adoption would be "a reliable serological test for syphilis should be performed on every new patient." In a large percentage of instances the clinical discovery of a previous syphilitic infection is well-nigh impossible, and a thoroughly reliable test will uncover...References1 KAHN RL, Serum Diagnosis of Syphilis by Precipitation, Williams and Wilkins, 1925. Google Scholar2 KLINEYOUNG BSA, A Microscopic Slide Precipitation Test for Syphilis, Jour. of the Amer. Med. Assoc., 86:928, 1926. CrossrefGoogle Scholar3 KLINEYOUNG BSAM, A Microscopic Slide Precipitation Test for Syphilis, Jour. of Lab. & Clin. Med., 12:477, 1927. Google Scholar4 KOLMER JA, Serum Diagnosis of Syphilis, Jour. of the Amer. Med. Assoc., 93: 1429, 1929. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Milwaukee Wis.*From the Laboratories of Mount Sinai Hospital, Milwaukee, Wis.**Director of Laboratories. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byKlassische Serologie der SyphilisÜber die Brauchbarkeit der Klineschen Mikroskopischen Objektträgerflockungsreaktion für die Serumdiagnose der Syphilis 1 February 1931Volume 4, Issue 8Page: 1028-1035KeywordsSyphilis ePublished: 1 December 2008 Issue Published: 1 February 1931 PDF downloadLoading ...
Understanding controlled trials: Randomisation methods in controlled trials
Authors: C. Roberts, D. Torgerson
Journal: BMJ (1998)

The main purpose of randomisation is to avoid bias by distributing the characteristics of patients that may influence outcome randomly between treatment groups so that any difference in outcome can be explained only by treatment. These characteristics might be demographic ones such age or prognostic factors such as clinical history or disease severity. For example menopausal status may influence outcome of treatment for breast cancer.

The most elementary form of randomisation is, in the case of two treatments, equivalent to allocating treatment by tossing a coin. Lists for allocating patients by simple randomisation may be constructed with tables of random numbers or random functions on pocket calculators or statistical software. Treatments may then be allocated to patients in sequence using numbered opaque envelopes containing treatment allocations or remotely by phone.

While such simple randomisation will on …
TRENDS IN CANCER DEATH RATES AND CURE RATES
Authors: E C HAMMOND
Journal: Annals of Internal Medicine (1959)

Article1 February 1959TRENDS IN CANCER DEATH RATES AND CURE RATESE. CUYLER HAMMOND, SC.D.E. CUYLER HAMMOND, SC.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-50-2-300 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe study of trends in the occurrence and management of a disease is important from three points of view: (1) it may give leads for further research on etiology, (2) it gives an indication as to whether we are on the right track in our efforts to control the disease, and (3) it gives some idea of what we may expect in the future, particularly in respect to needs for medical care and facilities. A few highlights of trends in cancer are presented, with emphasis on medical implications rather than etiology.TRENDS IN DEATH RATESThe death rate from a...Bibliography1. GerhardtHardyFerber PVB: Trends in cancer incidence, mortality, and probability in the State of New York, New York State J. Med. 57: 1387 (Apr.) 1957. MedlineGoogle Scholar2. Lombard H: Significance of statistical analysis of end results in the treatment of breast cancer, Round table discussions, Proceedings of the Second National Cancer Conference, Vol. I, March, 1952, 1954, National Cancer Society, New York, p. 107. Google Scholar3. Hammond EC: The possibility of improving cancer cure rates at the present time, Cancer 10: 581 (May-June) 1957. CrossrefGoogle Scholar4. GriswoldWilderCutlerPollack MHCSSJES: Cancer in Connecticut, 1935-1951, 1955, Connecticut State Department of Health, Hartford, Connecticut. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication May 21, 1958.Presented at the Symposium on Medical Aspects of Cancer at the Fifth International Congress of Internal Medicine, April 24, 1958.Requests for reprints should be addressed to E. Cuyler Hammond, SC.D., Director, Statistical Research Section, American Cancer Society, 521 West Fifty-seventh Street, New York 19, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHistogenesis of pancreatic carcinogenesis in the hamster: ultrastructural evidence.Simultaneous cancer of the pancreas occurring in husband and wife.The integration of chemotherapy into a combined modality approach for cancer treatmentPancreatic carcinomaCancer of the Digestive TractHormonal Treatment of Breast CancerDetection and disposal of breast cancer in pregnancy 1 February 1959Volume 50, Issue 2Page: 300-312KeywordsColorectal cancerDeath ratesEtiologyForecasting ePublished: 1 December 2008 Issue Published: 1 February 1959 PDF downloadLoading ...
The Part of Mammalian Genetics in Founding The Jackson Memorial Laboratory&lt;xref ref-type="fn" rid="fn1"&gt;1&lt;/xref&gt;
Authors: W. E. Castle
Journal: JNCI Journal of the National Cancer Institute (1954)

The Part of Mammalian Genetics in Founding The Jackson Memorial Laboratory W. E. Castle W. E. Castle University of California, Berkeley, Calif. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 15, Issue 3, December 1954, Pages 595–606, https://doi.org/10.1093/jnci/15.3.595 Published: 01 December 1954