tbuckley/cabot-search huggingface dataset:
Does climate change induce more heat stress related COPD exacerbations in metropolitan Berlin
Authors: Marc Hanisch, Baback Parandian, Uta Liebers, Matthias Grabenhorst, Melissa Jehn, Christian Witt
Journal: European Respiratory Journal (2013)

Background  There is growing evidence that climate change negatively impacts patients with COPD by increasing the risk for exacerbation requiring hospital admission during periods of high temperature and poor air quality.  In this study we evaluated the relationship between temperature, air quality and COPD related hospital admissions (COPDHA) in a mid latitude metropolitan city.  We wanted to assess if a particular subgroup of COPD patients can be identified as vulnerable to exacerbation under aggravated climate conditions.  Methods  Data was obtained from the Charite university hospital registry between August 1st – and August 31st (COPDHA and related clinical data) and superimposed onto environmental data (daily maximum temperature (Tmax), PM10, NO2 and ozone (O3) levels). Clinical and anamnestic similarities of patients suffering from exacerbation were retrospectively analysed.  Results  55 patients (GOLD II, N = 6; GOLD III, N = 15, GOLD IV, N = 34) were admitted to the emergency room (ER) for exacerbation of COPD (age = 70.4 ± 9.1years, 100% male).  On the hottest recorded day Tmax was 35.4 °C. The highest number of COPD exacerbations (N = 21) was admitted to the ER after a lag period of two days.  On this day, maximum temperature had markedly dropped (Tmax = 25.9 ± 1.1 °C). However, particle pollution was at its highest point (PM10 = 36, NO2 = 48 and O3 = 138 μg/m2. Clinical patient characteristics were: male sex, age > 65 y, BMI ≥ 23kg/m², GOLD III-IV, FEV1  Conclusion  This pilot study suggests that climate change leads to an increase in exacerbation rates on days following heat waves with rising air pollutants in mid latitude metropolitan cities in vulnerable COPD patients.
Dementia in Patients With Schizophrenia
Authors: Constantine G. Lyketsos, Matthew E. Peters
Journal: JAMA Psychiatry (2015)

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Tobacco smoke in patients with pulmonary hypertension
Authors: Stephan Keusch, Florian Hildenbrand, Tom Bollmann, Michael Halank, Matthias Held, Ralf Kaiser, Gabor Kovacs, Tobias Lange, Rudolf Speich, Silvia Ulrich Somaini
Journal: European Respiratory Journal (2013)

Background: We aimed to assess active and passive tobacco smoke exposure in a larger PH-collective and to compare it with epidemiological data from presumptively healthy subjects.  Methods: This is an international, multicenter, case-control study including patients with differently classified precapillary PH from Germany (DE), Austria (AUT) and Switzerland (CH). All patients were asked specific questions about active and second-hand tobacco smoke exposure. Presumptively healthy controls were retrieved from the Swiss Health Survey (SHS) and the SHIP-cohort (Germany).  Results: We analyzed 494 PH-patients (61.9% females) from CH (46%), DE (48%), and AUT (6%). The mean age was 57.7, BMI 26.9, and the 6 minute walking distance 372m. Patients were classified as pulmonary arterial (idiopathic (37.0%), associated (24.7%)), chronic thromboembolic (24.5%), PH in left heart disease (0.6%), miscellaneous PH (3.2%) and 8.7% had PH in chronic lung disease. Overall, tobacco smoke exposure was common in PH, 51.8% were smokers, 22.3% persistent smokers. Smoking rates were comparable in the different centers/countries. Men with pulmonary arterial hypertension were significantly more smokers compared with the Swiss control group but not with the SHIP cohort. Second-hand smoke exposure was found more frequent in women of all PH classes compared with Swiss controls.  Conclusions: Tobacco smoke exposure is common in all PH-classes, especially in men, with half of the patients being ever exposed and over a fifth of patients being persistent smokers. We found no overall difference of tobacco smoke exposure between PH-patients and controls, however, PH-woman were significantly more exposed to second-hand smoke than healthy controls.
Changes in lung function and comorbidity in patients with COPD over 4 to 10 years of follow-up
Authors: J. Fernández-Lahera, S. Rojas, M. Lerin, D. Barros, A. Mendieta, D. Romera, J. Fernández-Bujarrabal, B. Ortega, R. Alvarez-Sala
Journal: European Respiratory Journal (2013)

OBJECTIVES

To study FEV1 evolution and analyse changes in comorbidity over a 4 to 10 year period in patients diagnosed with COPD

METHODS

Retrospective study of demographic, spirometric and comorbidity variables of patients with COPD who were followed up for 4 to 10 years. We calculated the yearly change in prebronchodilator FEV1 and differences in comorbidity between the start (2001-2007) and end (2011-2012).

RESULTS

We included 65 patients (91% men, 9% women, mean age 76±8 years, BMI, 28±4 kg/m2, FEV1% 59±19%). The follow-up time was 7±3 years. Air flow limitation (GOLD): 13% level I, 47% II, 32% III and 8% IV. The mean yearly decline in FEV1 was -26±51 ml. We classified patient decline according to the yearly percentile decline in FEV1 as follows: rapid decline (

P75, 35±42 ml, 24%).

We determined (ANOVA) that age, BMI, Charlson index and dyspnea (MRC) had no significant effect on FEV1 decline.

The mean Charlson index (ChI) at the start was 1.07±1.02 (3.2±1.5 corrected for age), and the most recent mean ChI was 2.14±1.2 (5.22±1.7).

Comorbidities: HBP 51%, dyslipidemia 38%, cardiac 30%, rheumatologic 25%, neurologic 16%, DM 14%, and neoplasms 12% (increased incidence of 10%, 12%, 10%, 11%, 4%, 3%, and 5%, respectively). Others: 34% respiratory failure, 12% OSAHS, nodules or lung cancer 13%, asthma 7%. There were no significant differences in comorbidities based on the pattern of FEV1 decline.

CONCLUSION

The change in FEV1 over the course of the study was heterogeneous. We were able to distinguish three patterns: rapid, slow and no decline.

Comorbidities increased with time, with a difference of 1.07 points (1.99 corrected for age) in the Charlson index between the start and the end.
Elevated serum LOXL2 levels are associated with rapid disease progression in idiopathic pulmonary fibrosis (IPF)
Authors: Jason Chien, Lixin Shao, Susan Lyman, Joanne Adamkewicz, Victoria Smith, Thomas O'Riordan
Journal: European Respiratory Journal (2012)

Background : LOXL2, expressed in fibrotic lung, plays a crucial role in matrix remodeling and fibrogenesis. We hypothesized that elevated serum LOXL2 levels are associated with rapid IPF disease progression.   Methods : Baseline serum samples were collected prior to treatment randomization at selected U.S. clinical trial sites for ARTEMIS-IPF. LOXL2 levels were measured using proprietary anti-human-LOXL2 antibodies. Progression free survival ([PFS] lung function decline, respiratory hospitalizations [RH] and death) served as the primary endpoint.   Results : Subjects with (n=69) and without (n=423) serum samples had similar baseline IPF severity. Among subjects with detectable LOXL2 (n=67), the median LOXL2 level was 315.4pg/ml (IQR 144.5-752.4 pg/ml). Although subjects randomized to receive ambrisentan (n=49) had more severe IPF and higher LOXL2 levels than placebo treated subjects (mean 902.8pg/ml±1172 vs 294pg/ml±288, p=0.026), LOXL2 levels and IPF severity did not correlate. In multivariate analyses that included treatment assignment, 6-minute walk distance and composite physiologic index, high LOXL2 levels (>800pg/ml), in comparison to low LOXL2 levels (≤800pg/ml), were associated with increased risk for disease progression (hazard ratio [HR] 4.95, 95% confidence interval [CI] 1.52-16.18, p=0.008), lung function decline (HR 7.36, 95% CI 1.16-46.74, p=0.034, and RHs (HR 4.85, 95% CI 1.09-21.68, p=0.039).   Conclusion : High baseline serum LOXL2 levels are associated with rapid IPF progression and may reflect disease activity, not severity. Due to potential confounding effects of ambrisentan, these results need to be replicated in other IPF populations.
Flow cytometry, cellular DNA content, and prognosis in human malignancy.
Authors: D E Merkel, L G Dressler, W L McGuire
Journal: Journal of Clinical Oncology (1987)

The use of flow cytometry to analyze the cellular DNA content of human malignancies has become increasingly commonplace. The relationship between abnormalities in DNA content or proliferative characteristics and prognosis is becoming clear for a variety of malignancies in part through new techniques that permit analysis of archival material. High- and low-risk groups of patients with early breast and bladder carcinomas, non-small-cell lung cancer, and colorectal, ovarian, and cervical carcinoma can be distinguished on the basis of abnormal stemline DNA content. In several hematologic and common pediatric malignancies, the prognostic relevance of DNA content flow cytometry has been similarly established. Though the interpretation of tumor cell cycle analyses is less certain, this characteristic may also be prognostically important. However, generalizations cannot be made when applying flow cytometric DNA analysis to clinical decision making. The prognostic importance of an abnormal DNA histogram for an individual patient must be assessed on the basis of the relevant data base for that particular tumor type. The current extent of this data base for various malignancies is reviewed.
Abstract 34: A Human G109E Polymorphism in Inibitor-1 Compromises Cardiomyocyte Function and Induces Arrhythmias
Authors: Kobra Haghighi, Tracy J Pritchard, Vivek P Singh, Parthib Das, Erica L Vanderbilt, Jack Rubinstein, Evangelia G Kranias
Journal: Circulation Research (2014)

Protein phosphatase 1 (PP1) has emerged as a nodal regulator of function and survival in the heart. Indeed, the increased activity of this enzyme in failing hearts contributes to depressed SR Ca-cycling and deteriorative remodeling. PP1 is negatively regulated by endogenous inhibitor-1, which is considered a promising therapeutic target. Increases in inhibitor-1 activity and decreases in PP1 protect against ischemia/reperfusion injury, chronic isoproterenol stimulation and heart failure progression. We recently identified a polymorphism (G109E) in the inhibitor-1 gene in heart failure patients with a frequency of 6%. Expression of G109E (called mutant) in rat cardiomyocytes resulted in ~20% decreases in contractile parameters, Ca-transients and sarcoplasmic reticulum Ca-load. This depressed function was rescued by isoproterenol. Interestingly, when subjected to stress conditions (2 Hz +/- Iso), the mutant cells were more susceptible to aftercontractions. Similar findings were obtained by expression of G109E in inhibitor-1 knockout cardiomyocytes in the absence of endogenous protein. The underlying mechanisms included reduced binding of mutant to PP1, increased PP1 activity and hyper-phosphorylation of S2814 in ryanodine receptor (RyR), promoting aberrant SR Ca-release. These findings were also reflected by in vivo cardiac overexpression of G109E. Contractile and Ca-kinetic parameters were depressed by ~30% in mutant cardiomyocytes, while isoproterenol relieved these inhibitory effects. Stress conditions were associated with induction of Ca waves and aftercontractions in G109E cells. Furthermore, serial caffeine/Iso injections in vivo, elicited higher incidence of ventricular ectopy (bigeminy, trigeminy and non-sustained ventricular tachycardia) in mutant mice, whereas WTs had normal rhythm. Our findings suggest that G109E and increased PP1 may dephosphorylate the RyR and promote Ca-leak, in agreement with previous reports. Subsequently, the increased Ca-levels activate CAMK, leading to hyperphosphorylation of RyR and further increases in Ca-leak. Thus, inhibitor-1 is critical in cardiac function and represents a key control in balancing phosphatase/kinase activities to stabilize Ca-cycling in the heart.
Kinetic Response of Cultured Chinese Hamster Cells to Treatment With 4′-[(9-Acridinyl-amino] methanesulphon-m-anisidide-HCl2
Authors: Robert A. Tobey, Larry L. Deaven, Melvin S. Oka
Journal: JNCI Journal of the National Cancer Institute (1978)

4′-[(9-Acridinyl)-amino]methanesulphon-m-anisidide- HCl (MAC) (NSC-141549) was examined for effects on survival and cell-cycle progression in exponentially growing (cycling) populations of line CHO Chinese hamster cells and in isoleucine-deficient G1-arrested (noncycling) cells. Cell analysis involved flow microfluorometry, [3H]thymidine autoradiography, and cell enumeration. Noncycling cells were approximately two to four times more resistant to the toxic effects of MAC, although at high concentrations (i.e., Δ2 μg/ml), noncycling cells appeared to be as sensitive as cycling cells. Noncycling cells treated with MAC prior to return to cycle traversed through G, and S at a nearly normal rate and suffered only a slight delay (≈2 hr) in progressing through G2 and mitosis. In contrast, in cycling cell populations treated with MAC and under conditions yielding similar survival levels, the cells initially in Sand G2 were grossly delayed in their capacity for normal progression, leading to a transitory (≈8 hr) accumulation of cells in S, followed at later times by arrest in G2; a subpopulation of cells initially In G1 progressed through G1 and S at a nearly normal rate and then appeared to be delayed for only 2 hours in traversing through G2 and mitosis. A limited degree of unequal distribution of chromosome fragments to daughter cells at mitosis and a high degree of polyploidization were induced in cycling cell populations receiving MAC. Cycling cells exposed to MAC exhibited a terminal point of inhibition of traverse capacity situated 57 minutes prior to prophase. On the basis of the generally similar kinetic responses observed with MAC and adriamycin (ADR), we would expect MAC to exhibit many biochemical properties in common with ADR.
Short-term exposure to concentrated ambient particles increases airway hyperresponsiveness in normal mice
Authors: Jôse Mára Brito, Kelly Yoshizaki, Alessandra Choqueta Toledo, Beatriz Mangueira Saraiva-Romanholo, Adair Aparecida Santos Alemany, Mariangela Macchione, Paulo Hilário Nascimento Saldiva
Journal: European Respiratory Journal (2011)

Epidemiological studies show an association between short periods of exposure to air pollution with increase of hospital admissions for respiratory diseases. This study investigated if short-term exposures (1-hour) to relatively low levels of concentrated ambient fine particles (CAP) induce bronchial hyperresponsiveness and lung inflammation in mice. 45 Balb/C mice divided at two groups: 22 exposed to filtered air (FA) and 23 exposed to CAP (200 μg/m 3  divided by 24 hours = ±8 μg/m 3 ). The PM2.5 concentration inside the chamber was monitored in real time. The pulmonary responsiveness to methacholine (Mch) was obtained 30 minutes after exposure, and bronchoalveolar lavage (BALF) to verify lung inflammation, 24 hour after exposure. Lung mechanical showed significant differences between the groups on the parameters following: Penh, PEF (p 3 ), a single exposure to CAP was capable of triggering pulmonary responsiveness and the increase in the lung inflammatory infiltration.
Neuroblastoma: the Joint Center for Radiation Therapy/Dana-Farber Cancer Institute/Children's Hospital experience.
Authors: E M Rosen, J R Cassady, C N Frantz, C Kretschmar, R Levey, S E Sallan
Journal: Journal of Clinical Oncology (1984)

The treatment results for 118 patients with neuroblastoma seen at the Joint Center for Radiation Therapy/Dana-Farber Cancer Institute/Children's Hospital from 1970 to 1980 were analyzed. Patients were treated with a combination of surgery, radiation therapy, and chemotherapy depending on stage and age. Disease-free survival was excellent in all patient groups except those over one year of age with stage IV disease, a group for which currently available therapy cures only a small proportion of patients. Patients with stage III disease and older patients with stage II disease did extremely well (survival of 81% and 89%, respectively) and may have benefited from intensive treatment with all three modalities. Survival for infants (under one year) with stage IV neuroblastoma (90%) has clearly improved with intensive combination chemotherapy. With combination approaches and newer, more effective systemic regimens, a real impact on survival appears to have been made in the last decade. Better approaches will be necessary to cure more than an occasional older patient with stage IV disease.
Cardiovascular consequences of fibreoptic bronchoscopy
Authors: L Davies, R Mister, DP Spence, PM Calverley, JE Earis, MG Pearson
Journal: European Respiratory Journal (1997)

Fibreoptic bronchoscopy (FOB) is now commonly performed, and the number of elderly patients undergoing the procedure is increasing. Problems with oxygenation during FOB are well-recognised, but there are few data about its cardiovascular effects. Forty five patients (median age 65 yrs) undergoing elective FOB were studied prospectively. Patients were connected to a 12-lead computerized electrocardiographic recorder, a finger plethysmographic blood pressure (FPBP) monitor and pulse oximeter. Forty three patients were sedated with fentanyl and droperidol, and all were given 5 mL 2.5% cocaine intratracheally and xylocaine spray to the pharynx. Mean sphygmomanometric cuff blood pressure was raised initially (167/88 mmHg). Mean blood pressure recorded by FPBP rose on intratracheal injection (178/96 mmHg) and remained high throughout the procedure. Mean (SD) initial cardiac frequency was 93 (5.1) beats x min(-1) and rose to 134 (7.5) beats x min(-1) during the procedure. Four of the 45 patients showed unexpected ST segment depression of >1 mm for >1 min, and a further three developed bundle branch block. These seven patients had significantly greater tachycardia (152 vs 131 beats x min(-1)) and higher blood pressure (238/131 vs 207/109 mmHg). They were older (72 vs 61 yrs), had smoked more (63 vs 39 pack-years), but had similar lung function and similar changes in oxygen saturation. Oxygen desaturation occurred in 19 patients and this was associated with poor lung function (69 vs 84% predicted forced expiratory volume in one second), but was independent of the cardiovascular changes. Significant cardiovascular changes occur during fibreoptic bronchoscopy, with evidence of cardiac strain in 21% of patients over the age of 60 yrs.
Chronic allergen exposure enhances cholinergic neurotransmission in sensitized guinea-pigs
Authors: N Kageyama, A Igarashi, M Ichinose, M Miura, H Yamauchi, M Tomaki, J Ishikawa, Y Sasaki, K Shirato
Journal: European Respiratory Journal (1995)

Airway hyperresponsiveness in asthmatic patients may be related to cholinergic hyperresponsiveness. In this study, we examined whether chronic allergen exposure induces cholinergic hyperresponsiveness in ovalbumin (OA) sensitized guinea-pig airways. Three weeks after active sensitization, ovalbumin (0.03%, for 3 min, challenged group) or saline inhalation (control group) was repeated every day for 4 weeks. Cholinergic responses were assessed by isometric tracheal contraction after electrical field stimulation (EFS) or exogenously applied acetylcholine (ACh). The contractions were expressed as a percentage of the maximum response to ACh (10(-3) M) (AChmax). We calculated the effective frequencies producing 25% of AChmax (EF25) from frequency-response curves. EFS-induced contractile responses were significantly enhanced in the challenged group (logEF25 = 0.66 +/- 0.08 (mean +/- SEM)) compared with the control group (logEF25 = 1.12 +/- 0.16). In contrast, exogenous ACh-mediated contractile tracheal responses were almost the same in both groups. We conclude that repeated allergen inhalation causes cholinergic airway hyperresponsiveness, presumably due to the facilitation of cholinergic neurotransmission. This mechanism may be involved in the airway hyperresponsiveness in asthmatic airways.
Changes in DNA Content During In Vitro Transformation of Mouse Salivary Gland Epithelium2
Authors: John K. Cowell, Caroline B. Wigley
Journal: JNCI Journal of the National Cancer Institute (1980)

DNA content was measured in single cells in situ during the in vitro development of neoplastic transformation in epithelial cells from mouse salivary glands. The earliest change in DNA content was found in stage III of the transformation process (a preneoplastlc stage). In foci of these cells, the percentage of tetraploid (4C) cells was 30–60% compared with the starting tissue and early primary cultures, which were diploid. The stage III foci eventually gave rise to subtetraploid tumorigenic cell lines. The studies suggested that during in vitro development of neoplastic transformation in salivary gland epithelium, tetraploids were generated that then underwent a period of chromosome instability and loss. Evidence was also presented that a similar mechanism may be operating in transformation of salivary gland epithelium in vivo. A possible mechanism for transformation on the basis of chromosome imbalance was discussed.
Association of COPD stages and comorbidities in Italian general practices: The COMODHES study
Authors: Sara Maio, Sandra Baldacci, Marco Borbotti, Franca Martini, Patrizia Silvi, Giuseppe Sarno, Sonia Cerrai, Annapaola Pala, Giovanni Viegi
Journal: European Respiratory Journal (2012)

Background : Chronic obstructive pulmonary disease (COPD) represents an important and increasing burden worldwide. COPD often coexists with other diseases that may have an impact on prognosis.   Aims : to evaluate the association between different COPD severity levels and comorbidity in Italian patients of general practitioners (GP).   Methods : prospective observational study in different Italian areas. 176 GP enrolled 2288 patients with COPD diagnosis. Questionnaires were used to collect data on COPD management, health status and risk factors.  Univariate analyses were used to assess the relationship between COPD severity levels (mild, moderate, severe, very severe) and demographic characteristics (age, sex), smoking habits, comorbidities. Multinomial regression analysis was used to assess the relationship between COPD severity levels and comorbidity adjusting for demographic characteristics and smoking habits.   Results : Univariate analyses showed a significantly higher frequency of high severity levels in males, older age, ex-smokers, subjects with cardiovascular diseases, osteoporosis/skeletal muscle dysfunction, anaemia, depression and weight loss. The Multinomial regression analysis confirmed the associations between moderate severity COPD and cardiovascular disease (OR 1.30); severe COPD and cardiovascular disease (OR 1.35), osteoporosis/skeletal muscle dysfunction (OR 1.43), anaemia (OR 2.06) and weight lost (OR 2.77); very severe COPD and weight loss (OR 6.34) and depression (OR 2.50).   Conclusions : this study indicates that COPD stages are significantly associated with different kinds of comorbidities which need to be taken into account in disease management.