tbuckley/cabot-search huggingface dataset:
Abstract 18000: Mitochondrial Oxidative Stress and Function compared to Lipoprotein Level, Particle Number and Size in an HIV Positive Cohort
Authors: Nisha I Parikh, Mariana Gerschenson, Todd Seto, Dominic Chow, Cecilia Shikuma
Journal: Circulation (2011)

Introduction: Dyslipidemia, arising from viral infection, antiretroviral treatment and changes in body composition, is a key metabolic abnormality believed to underlie increased CVD risk among HIV-infected subjects. Oxidative stress and mitochondrial function is linked to atherosclerosis and HIV treatment. We sought to determine the relationship between mitochondrial oxidative stress, function, and standard clinical lipid profile as well as lipoprotein subclass particle number and size among HIV-infected persons. Study Sample: HIV infected individuals, age &gt; 40 years and on stable highly activite antiretroviral therapy for &gt; 6 months. Methods: We considered the following measures: 1. mitochondrial-specific 8-oxo-deoxyguanine (8-oxo-dG) and 2. mitochondrial OXPHOS NADH dehydrogenase (Complex I) and cytochrome c oxidase (Complex IV) enzyme activity . Plasma total cholesterol, triglycerides, and HDL-C and LDL-C were directly measured. Lipoprotein subclass size and particle number were measured using proton NMR spectroscopy (LipoScience Assay). Unadjusted linear regression analysis was employed to study the association between mitochondrial and lipid parameters. A p-value of &lt;0.05 was considered significant. Results: Among 109 HIV-infected persons (mean age 52 years, 14% women, 52% White, 14% Hispanic, 9% Asian), median CD4 count was 511 cell/mm 3 , median HIV RNA was 48 copies/mm 3 (majority with undetectable virus), BMI prevalence &gt;= 25 kg/m 2 was 64%, diabetes 27%, HTN 34% and current cigarette smoking 28%. 8-oxo-deoxyguanine was associated with small HDL (umol/L) (p=0.03) and VLDL particle size (nm)(p=0.03). Complex I activity was inversely associated with VLDL &amp; chylomicron particle number (nmol/L) (p=0.01), small VLDL particles (nmol/L) (p=0.005), LDL particle (total) (nmol/L) (p=0.02), and small LDL particle (total) (nmol/L) (p=0.02). Complex IV was not associated with any lipid parameters. None of the three mitochondrial parameters studied was associated with clinical lipid profile (total cholesterol, LDL, HDL, or triglycerides). Conclusions: Mitochondria oxidative stress and function is associated with lipoprotein subclass size and number but not with clinical lipid profile among treated HIV-infected individuals.
Prevalence of sleep disordered breathing (SDB) in patients undergoing coronary artery bypass graft (CABG) surgery
Authors: Martina Mason, Danielle Horton, Clare East, Rebecca Chadwick, Ian Smith
Journal: European Respiratory Journal (2014)

Background 

The prevalence of SDB in patients undergoing cardiac surgery is unknown. SDB and coronary artery disease share some of the same risk factors and it is therefore likely that patients referred for cardiac surgery will include people with unrecognised SDB. We present preliminary data examining the prevalence of SDB in cardiac surgical population using nocturnal pulse oximetry as a diagnostic tool in the pre-operative setting.

Aims 

The aim was to assess the prevalence and the severity of SDB along with sleepiness (Epworth Sleepiness Score, ESS) in patients undergoing CABG with or without heart valve surgery at a UK tertiary cardiothoracic centre.

Methods 

Patients undergoing CABG were screened for the presence of SDB, prior to surgery, with the STOP-BANG questionnaire and overnight oximetry. Sleep apnoea was defined as a 4% oxygen desaturation index (ODI) of ≥5/hr.

Results 

275 patients were approached and 99 consented to the study. Five patients had a pre-existing diagnosis of OSA and were not included in the analysis. Of 94 patients, 44 (47%) had a new diagnosis of SDB of whom 32 (73%) had mild SDB (ODI≥5<15), 11 (25%) had moderate SDB (ODI≥15<30) and 1 (2%) had severe SDB (ODI≥30). Eight patients (18%) were recommended Continuous Positive Airway Pressure (CPAP) therapy.

View this table:

Characteristics of the participants





Conclusion 

There is a high prevalence of SDB in patients undergoing CABG. The majority do not exhibit symptoms of sleepiness but in this series 8/44 were affected by OSA severe enough to require CPAP therapy.
DNA Methylation and Somatic Mutations Converge on the Cell Cycle and Define Similar Evolutionary Histories in Brain Tumors
Authors: Tali Mazor, Aleksandr Pankov, Brett E. Johnson, Chibo Hong, Emily G. Hamilton, Robert J.A. Bell, Ivan V. Smirnov, Gerald F. Reis, Joanna J. Phillips, Michael J. Barnes, Ahmed Idbaih, Agusti Alentorn, Jenneke J. Kloezeman, Martine L.M. Lamfers, Andrew W. Bollen, Barry S. Taylor, Annette M. Molinaro, Adam B. Olshen, Susan M. Chang, Jun S. Song, Joseph F. Costello
Journal: Cancer Cell (2015)
Scintigraphic parameters in COPD patients
Authors: Tatyana Ageeva, Nikolay Krivonogov, Anna Dubodelova, Elena Mishustina, Sergey Mishustin
Journal: European Respiratory Journal (2013)

Aim: to study the ventilation-perfusion ratio (V/Q), apex-base gradient of ventilation (U/L-V) and perfusion (U/LQ) and alveolar-capillary permeability (ACP) in stage I-II COPD patients on the basis of scintigraphy data.  Materials and methods: 35 people aged 38.4 (31.5-45.3) took part in the study: patients diagnosed with COPD (25) and healthy smoking volunteers (10). The scintigraphic studies were performed by means of Omega 500 gamma camera (Technicare, USA-Germany). The subject of the research was an examination of ACP in the right (RL) and left (LL) lungs in the process of radiopharmaceutical derivation, static conditions, during the 1st, 10th and 30th min after 99mTc DTPA inhalation.  Results: COPD patients: V/Q in both RL and LL was not higher than 1.0 and amounted to 0.9 (0.7-1.2) in the RL and 0.9 (0.8-1.0) in the LL. These parameters did not differ from those of healthy volunteers (p=0.78 and p=0.55). U/L-V amounted to 0.6 (0.5-0.8) in the RL and 0.6 (0.4-0.9) in the LL. It was lower than that of healthy people (p=0.23 and 0.47). U/LQ amounted to 1.0 (0.8-1.1) in the RL and 0.9 (0.8-1.1) in the LL. This parameter was higher than that of healthy people (p=0.005, p=0.01). ACP in the RL amounted to 10.5% (10.2-10.9%) and 21.4% (19.8-22.9%) during the 10th and 30th minutes of the study, respectively; it was slowed down during the 10th and 30th minutes (p=0.002 and p=0.001). ACP in the LL amounted to 11.3% (10.1-12.5%) and 23.5% (22.3-24.8%) during the 10th and 30th minutes of the study, respectively; it was slowed down during the 10th and 30th minutes of the study (p=0.001 and p=0.001).  Conclusions: The study findings may serve as additional scintigraphic criteria for COPD diagnostics.
IgG Fc Receptors
Authors: Jeffrey V. Ravetch, Silvia Bolland
Journal: Annual Review of Immunology (2001)

Since the description of the first mouse knockout for an IgG Fc receptor seven years ago, considerable progress has been made in defining the in vivo functions of these receptors in diverse biological systems. The role of activating FcγRs in providing a critical link between ligands and effector cells in type II and type III inflammation is now well established and has led to a fundamental revision of the significance of these receptors in initiating cellular responses in host defense, in determining the efficacy of therapeutic antibodies, and in pathological autoimmune conditions. Considerable progress has been made in the last two years on the in vivo regulation of these responses, through the appreciation of the importance of balancing activation responses with inhibitory signaling. The inhibitory FcR functions in the maintenance of peripheral tolerance, in regulating the threshold of activation responses, and ultimately in terminating IgG mediated effector stimulation. The consequences of deleting the inhibitory arm of this system are thus manifested in both the afferent and efferent immune responses. The hyperresponsive state that results leads to greatly magnified effector responses by cytotoxic antibodies and immune complexes and can culminate in autoimmunity and autoimmune disease when modified by environmental or genetic factors. FcγRs offer a paradigm for the biological significance of balancing activation and inhibitory signaling in the expanding family of activation/inhibitory receptor pairs found in the immune system.
Relationship between fluorouracil systemic exposure and tumor response and patient survival.
Authors: G Milano, M C Etienne, N Renée, A Thyss, M Schneider, A Ramaioli, F Demard
Journal: Journal of Clinical Oncology (1994)

The aim of this study was to analyze the link between fluorouracil (FU) systemic exposure and tumor response and overall survival.One hundred eighty-six patients (162 men, 24 women) with head and neck cancer were studied. All received cisplatin plus FU for three cycles as first-line chemotherapy. The treatment consisted of cisplatin (100 mg/m2 intravenously [IV]) followed by a 5-day continuous venous infusion of FU (1 g/m2/d). The median follow-up duration for the 104 patients alive was 24 months. For each cycle, we calculated the area under the curve over the duration of pharmacokinetic follow-up (AUC0-105 h) for plasma FU. For each patient, we analyzed the averaged AUC0-105 h and the averaged total dose for the three cycles.The response rate was 30% complete responses (CRs), 22% partial responses (PRs) more than 75%, 25% PRs less than 75%, and 23% no response (NR). Medians for averaged AUC and dose per cycle were 27,906 ng/mL h (first through third quartile, 25,398 to 31,060) and 7,000 mg (first through third quartile, 6,200 to 7,833), respectively. The tumor response was significantly linked to tumor stage (P < .001) and to averaged AUC (P = .05), but not to averaged dose. Analysis of parameters (continuous variable) expressing FU treatment intensity showed that dose did not influence survival contrary to the AUC (P = .001). The AUC remains significant (P = .025) in a multivariate analysis including tumor stage, demonstrating that the greater the FU systemic exposure, the longer the survival.These results strengthen the interest of individual FU dose adaptation based on pharmacokinetics.
Treatment of Grass Pollen‐Induced Hay Fever with Intranasal Budesonide
Authors: H. Steensen, N. Lindqvist
Journal: Allergy (1981)

The clinical effects of intranasal budesonide (16α, 17α (22 R,S) propylmethylenedioxypre‐gana‐1‐4‐diene‐11β 21 diol‐3, 20 dione)) ‐ a new non‐halogenated glucocorticoid ‐ were evaluated in a double‐blind comparison with placebo, in patients with pronounced hay fever. Aerosolized budesonide, using a daily dosage of either 400 μg or 200 μg, showed a highly significant reduction in the nasal symptoms as compared with placebo. No significant difference could be demonstrated between the effects of 400 μg and 200 μg per day, suggesting that the lower dosage is adequate. No significant effect on the eye symptoms and no fall in plasma cortisol values were observed with either dosage. Only mild side effects were reported.
Alloantisera Reacting With Tumor Cells of Inappropriate Haplotype. I. Characterization of Target Antigens
Authors: Maria Prat, Michael J. Rogers, Ettore Appella
Journal: JNCI Journal of the National Cancer Institute (1978)

Unexpected complement-dependent cytotoxic reactions of some mouse alloantisera produced against H-2 specificities, which according to the H-2 chart are expressed only by H-2d and H-2h haplotypes, were detected against a 7,12-dimethylbenz[a]anthracene-induced leukemia in SJL/J mice (H-2s haplotype). Antibodies directed against H-2 specificities were thought to be responsible for such reactivities on the basis of the following observations: a) Absorption of the alloantisera with normal lymphoid cells from mice expressing the appropriate haplotypes (B10.D2-H-2d and C57BL/6-H-2h) specifically removed all the cytotoxicity against the leukemia cells; b) soluble H-2 molecules purified about 200-fold from spleens of A/J, BALB/c, or C57BL/6 mice fully inhibited the cytotoxic reactivities of the appropriate antisera. These cross-reacting specificities did not seem to be C-type viral structural antigens and were not tumor-specific, inasmuch as they were also expressed by two other leukemias induced by the same chemical carcinogen in the same mouse strain. Normal cells from SJL/J mice, although not a target in the direct cytotoxicity assay, were able to completely absorb the reactivity of the alloantisera against the tumor cells and therefore also expressed the antigens. The results suggest that previously undetected public specificities on H-2 molecules were reacting with these antisera and that neoplastic transformation could alter them so that they became cytotoxic targets on tumor cells.
Contribution of Inherited Mutations in the BRCA2-Interacting Protein PALB2 to Familial Breast Cancer
Authors: Silvia Casadei, Barbara M. Norquist, Tom Walsh, Sunday Stray, Jessica B. Mandell, Ming K. Lee, John A. Stamatoyannopoulos, Mary-Claire King
Journal: Cancer Research (2011)

Inherited mutations in the BRCA2-interacting protein PALB2 are known to be associated with increased risks of developing breast cancer. To evaluate the contribution of PALB2 to familial breast cancer in the United States, we sequenced the coding sequences and flanking regulatory regions of the gene from constitutional genomic DNA of 1,144 familial breast cancer patients with wild-type sequences at BRCA1 and BRCA2. Overall, 3.4% (33/972) of patients not selected by ancestry and 0% (0/172) of patients specifically of Ashkenazi Jewish ancestry were heterozygous for a nonsense, frameshift, or frameshift-associated splice mutation in PALB2. Mutations were detected in both male and female breast cancer patients. All mutations were individually rare: the 33 heterozygotes harbored 13 different mutations, 5 previously reported and 8 novel mutations. PALB2 heterozygotes were 4-fold more likely to have a male relative with breast cancer (P = 0.0003), 6-fold more likely to have a relative with pancreatic cancer (P = 0.002), and 1.3-fold more likely to have a relative with ovarian cancer (P = 0.18). Compared with their female relatives without mutations, increased risk of developing breast cancer for female PALB2 heterozygotes was 2.3-fold (95% CI: 1.5-4.2) by age 55 and 3.4-fold (95% CI: 2.4-5.9) by age 85. Loss of the wild-type PALB2 allele was observed in laser-dissected tumor specimens from heterozygous patients. Given this mutation prevalence and risk, consideration might be given to clinical testing of PALB2 by complete genomic sequencing for familial breast cancer patients with wild-type sequences at BRCA1 and BRCA2.
The ratio of inspiratory ∑Rrs to expiratory ∑Rrs measured by forced oscillation technique correlates with the parameters reflecting narrowing of small airway measured by spirometry in patients with mild to moderate COPD
Authors: Yasuhiro Yamauchi, Taisuke Jo, Yasushi Goto, Masafumi Horie, Yuu Mikami, Satoshi Noguchi, Kazutaka Takami, Tadashi Kohyama, Takahide Nagase
Journal: European Respiratory Journal (2013)

Rationale: Chronic Obstructive Pulmonary Disease (COPD) is characterized by airflow limitation caused by narrowing of small airway. Airflow limitation is defined as parameters associated with forced expiratory volume in 1 second (FEV1) by spirometry; however, parameters of respiratory impedance (Zrs) measured by forced oscillation technique (FOT) have also been known to be useful markers for evaluation of airway obstruction. Thus, we evaluated whether the parameters of Zrs by FOT correlated with the parameters reflecting small airway narrowing by spirometry.  Method: Patients with mild (n=22) and moderate (n=19) COPD were recruited at our hospital. Respiratory resistance (Rrs) and reactance (Xrs) at 4Hz to 35Hz were measured with FOT device MOSTGRAPH-01 each 0.25 seconds during tidal breathing. ΣRrs was calculated by summation of Rrs values during a respiratory cycle.  Results: Rrs at 4Hz in whole-breath did not correlate with FEV1, the ratio of FEV1 to Forced Vital Capacity, and the parameters reflecting small airway narrowing. However, the ratio of inspiratory (ins) ΣRrs to expiratory (ex) ΣRrs at 4Hz weakly correlated with FEV1 (r=0.35, p=0.03), maximal midexpiratory flow (r=0.36, p=0.03), and maximal expiratory flow at 25% of vital capacity (r=0.33, p=0.04). The ratios of ins ΣRrs to ex ΣRrs at 20Hz and 35Hz were similar to that at 4Hz.  Conclusion: The ratio of ins ΣRrs to ex ΣRrs weakly correlates with parameters reflecting small airway narrowing in COPD. Measurement of Zrs with FOT might be useful to detect impairments of small airway in early stage of COPD.
Tumorigenicity and Isoimmunizing Properties of C3H Mouse Cells Undergoing “Spontaneous” Malignant Conversion &lt;italic&gt;In Vitro&lt;/italic&gt;&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: J. Kieler, C. Radzikowski, J. Moore, K. Ulrich
Journal: JNCI Journal of the National Cancer Institute (1972)

Journal Article Tumorigenicity and Isoimmunizing Properties of C3H Mouse Cells Undergoing “Spontaneous” Malignant Conversion In Vitro Get access J. Kieler, J. Kieler The Fibiger Laboratory,52800 Lyngby, Copenhagen, Denmark Search for other works by this author on: Oxford Academic PubMed Google Scholar C. Radzikowski, C. Radzikowski The Fibiger Laboratory,52800 Lyngby, Copenhagen, Denmark Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Moore, J. Moore The Fibiger Laboratory,52800 Lyngby, Copenhagen, Denmark Search for other works by this author on: Oxford Academic PubMed Google Scholar K. Ulrich K. Ulrich The Fibiger Laboratory,52800 Lyngby, Copenhagen, Denmark Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 48, Issue 2, February 1972, Pages 393–405, https://doi.org/10.1093/jnci/48.2.393 Published: 01 February 1972 Article history Received: 23 July 1971 Accepted: 04 November 1971 Published: 01 February 1972
Ovarian Cancer Survival and Chemotherapy Dosing, Body Mass Index, and Body Surface Area
Authors: S. Percy Ivy, Jan H. Beumer
Journal: JAMA Oncology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
Beginnings of Cancer Research Centers in the United States&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: H P Rusch
Journal: JNCI Journal of the National Cancer Institute (1985)

The first center for cancer research in the United States was started in 1898, and during the first half of the present century 19 additional cancer research centers had their origins. Most of them were initiated with funds from wealthy individuals who had experienced the tragic loss of a close relative. The early years of these centers and anecdotes about some of the early directors of the centers are described.
Enhancement of Glutathione &lt;italic&gt;S&lt;/italic&gt;-Transferase Activity of the Mouse Forestomach by Inhibitors of Benzo[&lt;italic&gt;a&lt;/italic&gt;]pyrene-Induced Neoplasia of the Forestomach&lt;xref ref-type="fn" rid="fn2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn3"&gt;3&lt;/xref&gt;
Authors: Vella L. Sparnins, Lee W. Wattenberg
Journal: JNCI Journal of the National Cancer Institute (1981)

The effects of glutathione S-transferases (GST) activity and acid-soluble sulfhydryl levels of a number of compounds previously investigated for their capacity to inhibit benzo[a]pyrene (BP)-induced neoplasia of the mouse forestomach were determined. Five of the compounds studied increased the GST activity of the forestomach 78-182%. The five compounds were: p-methoxyphenol, 2-tert-butyl-4-hydroxyanisole, coumarin, alpha-angelicalactone, and benzyl isothiocyanate. With the exception of benzyl isothiocyanate. With the exception of benzyl isothiocyanate, these compounds also increased acid-soluble sulfhydryl levels, but to a lesser magnitude. All five chemicals inhibited BP-induced neoplasia of the forestomach. These data indicate that enhancement of the GST activity by an amount of about 75% or greater is associated with a reduced carcinogenic response of the forestomach to BP. The data also suggest that such enhancement might be used as a method of identifying compounds likely to inhibit BP and other carcinogens detoxified in a similar manner. Inasmuch as inhibition of the action of carcinogens may involve mechanisms other than detoxification by GST, the failure to increase GST activity substantially does not rule out the possibility of a compound being an inhibitor.
Risk of Cardiomyopathy in Younger Persons With a Family History of Death from Cardiomyopathy
Authors: Mattis F. Ranthe, Lisbeth Carstensen, Nina Øyen, Morten K. Jensen, Anna Axelsson, Jan Wohlfahrt, Mads Melbye, Henning Bundgaard, Heather A. Boyd
Journal: Circulation (2015)

Background— Recommendations for presymptomatic screening of relatives of cardiomyopathy patients are based on findings from tertiary centers. Cardiomyopathy inheritance patterns are fairly well understood, but how cardiomyopathy in younger persons (&lt;50 years) aggregates in families at the population level is unclear. In a nationwide cohort, we examined the risk of cardiomyopathy by family history of premature death (&lt;60 years) from cardiomyopathy. Methods and Results— By linking Danish national register data, we constructed a cohort of 3.9 million persons born from 1950 to 2008. We ascertained family history of premature (&lt;60 years) death from cardiomyopathy or other conditions, and cohort members were followed from 1977 to 2008 for cardiomyopathy diagnosed at &lt;50 years. We identified 3890 cardiomyopathies in 89 million person-years of follow-up. Using Poisson regression, we estimated incidence rate ratios for cardiomyopathy by family history of premature death. Premature cardiomyopathy deaths in first- and second-degree relatives were associated with 29- and 6-fold increases in the rate of cardiomyopathy, respectively. If the first-degree relative died aged &lt;35 years, the rate of cardiomyopathy increased 100-fold; given ≥2 premature deaths in first-degree relatives, the rate increased more than 400-fold. In contrast, a family history of premature death from other cardiac or noncardiac conditions increased the rate of cardiomyopathy 3-fold at most. Conclusions— A family history of premature cardiomyopathy death was associated with an increase in risk of cardiomyopathy ranging from 6- to 400-fold, depending on age, kinship, gender and number of affected family members. Our general population-based results support recommendations for presymptomatic screening of relatives of cardiomyopathy patients.