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Pneumonia relevant to lung transplantation and pathogen distribution.

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Pneumonia relevant to lung transplantation and pathogen distribution.

Chin Med J (Engl). 2013 Sep;126(17):3209-14

Authors: He X, Dai HP, Chen QR, Miao JB, Sun B, Bao N, Hu B, Li H, Wu AS, Ban CJ, Ge SJ, Wang C, Hou SC

Abstract
BACKGROUND: Pneumonia is the most common cause of morbidity and mortality in lung transplant (LT) recipients. The aim of the present study was to evaluate the incidence, etiology, risk factors and prognosis of pneumonia in LT recipients.
METHODS: The LT cohort consisted of 28 recipients receiving LT in Beijing Chao-Yang Hospital from August 2005 to April 2011. Data collected included demographic data, underlying disorders, time and type of transplant, follow-up information, date of last follow-up, and patient status. A retrospective analysis was made of observational data that were prospectively collected.
RESULTS: Twenty-two patients of 28 LT recipients had 47 episodes of pneumonia throughout the study period. Thirtyeight episodes of pneumonia in 19 recipients occurred post-LT with a median follow-up of 257.5 days (1-2104 days), the incidence of pneumonia was 192.4 episodes per 100 LT/year and its median time of onset was 100.5 days (0-946 days) post-transplantation. Bacteria, virus and fungi accounted for 62%, 16% and 15% of the microbial pathogens, respectively. The most frequent were Pseudomonas aeruginosa (20%), cytomegalovirus (CMV) (15%), and Aspergillus fumigatus (10%). A total of 29% (11/38) of pneumonias occurred in the first month post-LT, and then the incidence decreased gradually. The incidence of CMV pneumonia was 25% (7/28) with a median time of 97 days (10-971 days). More than one bacterial infection and CMV infection were independent risk factors for aspergillus infection. The incidence of pulmonary tuberculosis (TB) was 18% (5/28), and the history of TB was a risk factor for TB relapse. There were 58% (7/12) of recipients who died of infection, and 71% (5/7) of these died in the first year after LT.
CONCLUSIONS: Pneumonia is still a major cause of morbidity and mortality in LT recipients. The most frequent microorganisms were Pseudomonas aeruginosa, CMV, and Aspergillus fumigates. The incidence of CMV pneumonia decreases with a delayed median time of onset. More than one incidence of bacterial infection and CMV infection are independent risk factors for aspergillus infection. LT recipients are at high risk for TB, and the history of TB is a risk factor for TB relapse.

PMID: 24033938 [PubMed - in process]

Including the smoking epidemic in internationally coherent mortality projections.

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Including the smoking epidemic in internationally coherent mortality projections.

Demography. 2013 Aug;50(4):1341-62

Authors: Janssen F, van Wissen LJ, Kunst AE

Abstract
We present a new mortality projection methodology that distinguishes smoking- and non-smoking-related mortality and takes into account mortality trends of the opposite sex and in other countries. We evaluate to what extent future projections of life expectancy at birth (e 0) for the Netherlands up to 2040 are affected by the application of these components. All-cause mortality and non-smoking-related mortality for the years 1970-2006 are projected by the Lee-Carter and Li-Lee methodologies. Smoking-related mortality is projected according to assumptions on future smoking-attributable mortality. Projecting all-cause mortality in the Netherlands, using the Lee-Carter model, leads to high gains in e 0 (4.1 for males; 4.4 for females) and divergence between the sexes. Coherent projections, which include the mortality experience of the other 21 sex- and country-specific populations, result in much higher gains for males (6.4) and females (5.7), and convergence. The separate projection of smoking and non-smoking-related mortality produces a steady increase in e 0 for males (4.8) and a nonlinear trend for females, with lower gains in e 0 in the short run, resulting in temporary sex convergence. The latter effect is also found in coherent projections. Our methodology provides more robust projections, especially thanks to the distinction between smoking- and non-smoking-related mortality.

PMID: 23325722 [PubMed - indexed for MEDLINE]

Dysfunctional endothelial cells directly stimulate cancer inflammation and metastasis.

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Dysfunctional endothelial cells directly stimulate cancer inflammation and metastasis.

Int J Cancer. 2013 Sep 15;133(6):1334-44

Authors: Franses JW, Drosu NC, Gibson WJ, Chitalia VC, Edelman ER

Abstract
Although the influence of context-dependent endothelial cell (EC) regulation of vascular disease and repair is well-established, the privileged roles ECs play as paracrine regulators of tumor progression has only recently become appreciated. We hypothesized that if the same endothelial physiology governs vascular and cancer biology then EC control in cancer should follow endothelial regulation of vascular health. Healthy ECs promote vascular repair and inhibit tumor invasiveness and metastasis. Dysfunctional ECs have the opposite effects in vascular disease, and we now ask if dysfunctionally activated ECs will promote cancer cell inflammatory signaling and aggressive properties. Indeed, while factors released from quiescent ECs induce balanced inflammatory signaling, correlating with decreased proliferation and invasiveness, factors released from dysfunctional ECs robustly activated NF-κB and STAT3 signaling within cancer cells, correlating with increased in vitro invasiveness and decreased proliferation and survival. Furthermore, matrix-embedded dysfunctional ECs stimulated intratumoral pro-inflammatory signaling and spontaneous metastasis, while simultaneously slowing primary tumor growth, when implanted adjacent to Lewis lung carcinoma tumors. These studies may broaden our appreciation of the roles of endothelial function and dysfunction, increase understanding and control of the tumor microenvironment, and facilitate optimization of anti-angiogenic and vascular-modifying therapies in cancer and other diseases.

PMID: 23463345 [PubMed - indexed for MEDLINE]

Bronchial responsiveness in patients with restrictive spirometry.

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Bronchial responsiveness in patients with restrictive spirometry.

Biomed Res Int. 2013;2013:498205

Authors: Keddissi JI, Elya MK, Farooq SU, Youness HA, Jones KR, Awab A, Kinasewitz GT

Abstract
Background. Improvement in PFT after bronchodilators is characteristic of obstructive airway diseases such as COPD. However, improvement in patients with restrictive pattern is occasionally seen. We aim to determine the clinical significance of a bronchodilator responsive restrictive defect. Methods. Patients with restrictive spirometry and a bronchodilator study were identified at the University of Oklahoma and Oklahoma City VAMC between September 2003 and December 2009. Restriction was defined as a decreased FVC and FEV1, with normal FEV1/FVC. Responsiveness to bronchodilators was defined as an improvement in FEV1 and/or FVC of at least 12% and 200 mL. Patients with lung volume measurements had their clinical and radiographic records reviewed. Results. Twenty-one patients were included in the study. Most were current or ex-smokers, with most being on bronchodilators. The average FVC and FEV1 were 65 ± 11% and 62 ± 10% of the predicted, respectively. Most patients (66%) had a normal TLC, averaging 90 ± 16% of the predicted. RV, RV/TLC, and the TLC-VA values strongly suggested an obstructive defect. Conclusions. Reversible restrictive pattern on spirometry appears to be a variant of obstructive lung disease in which early airway closure results in air trapping and low FVC. In symptomatic patients, a therapeutic trial of bronchodilators may be beneficial.

PMID: 24024196 [PubMed - in process]

Comparison of Clinical Characteristics in Patients with Obesity Hypoventilation Syndrome and Obese Obstructive Sleep Apnea Syndrome: A Case-Control Study.

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Comparison of Clinical Characteristics in Patients with Obesity Hypoventilation Syndrome and Obese Obstructive Sleep Apnea Syndrome: A Case-Control Study.

Clin Respir J. 2013 Sep 13;

Authors: Basoglu OK, Tasbakan MS

Abstract
INTRODUCTION: Obesity hypoventilation syndrome (OHS) can be overlooked unless clinicians have a high index of suspicion. The present case-control study aimed to compare characteristics of patients with OHS and obese obstructive sleep apnea syndrome (OSAS), and to identify determinants of hypercapnia in OSAS patients.
METHODS: Demographic and anthropometric features, pulmonary function tests, blood gas analysis and sleep parameters of 59 OHS patients were compared to 295 body mass index-matched OSAS patients.
RESULTS: The rate of hypertension (67.8% vs. 53.2%, respectively, p=0.027) was higher in OHS than OSAS group. In OHS patients, FVC (%) (p<0.0001), FEV1 (%) (p=0.001), and PaO2 (p<0.0001) were lower, whereas PaCO2 and HCO3 levels were increased (p<0.0001). Daytime sleepiness was more frequent (89.8% vs. 68.5%, respectively, p=0.002) and Epworth sleepiness scores were higher (14.0 vs. 11.9, respectively, p=0.021) in OHS than OSAS patients. In polysomnography, lowest and mean SpO2 were decreased, and sleep time with SpO2 <90% was increased in patients with OHS (p<0.0001). Multivariate analysis showed that hypercapnia was associated independently with HCO3 (p<0.0001) and daytime SaO2 (p=0.003). Besides, HCO3 level ≥27 mEq/L had a sensitivity of 88.1% and specificity of 73.1 %, and SaO2 ≤95% had a sensitivity of 64.4% and specificity of 73.9 % for identifying OHS.
CONCLUSION: It was shown that OHS patients have increased rate of hypertension, daytime sleepiness and HCO3 , and decreased lung functions and PaO2 levels than OSAS patients. The present results support that elevated bicarbonate levels and decreased oxygen saturations in obese OSAS patients should prompt clinicians to predict OHS.

PMID: 24028180 [PubMed - as supplied by publisher]

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