No evidence of enhanced oxidant production in blood obtained from patients with obstructive sleep apnea

<p>Abstract</p> <p>Background</p> <p>Obstructive sleep apnea syndrome (OSAS) is a recognized risk factor for cardiovascular morbidity and mortality, perhaps due to causative exacerbations of systemic oxidative stress. Putative oxidative stress related to numerous episodes of intermittent hypoxia, may be an oxidants chief driving force in OSAS patients.</p> <p>Methods</p> <p>We assessed the resting and n-formyl-methionyl-leucyl-phenylalanine (fMLP)- induced whole blood chemiluminescence (as a measure of oxidant production by polymorphonuclear leukocytes and monocytes), ferric reducing ability of plasma (FRAP) and H₂O₂generation in the whole blood of 27 untreated OSAS patients, 22 subjects after a night of CPAP therapy and 11 controls without OSAS. All of them were matched to age, BMI (body mass index) and smoking habits. All parameters were measured before and after polysomnography-controlled sleep, individual results were obtained as a mean from duplicated experiments.</p> <p>Results</p> <p>No significant differences were distinguished between evening and morning blood chemiluminescence, H₂O₂activity and FRAP within and between all three study groups.</p> <p>For instance patients with untreated OSAS had similar morning and evening resting whole blood chemiluminescence (2.3 +/- 2.2 vs. 2.4 +/- 2.2 [aU·10^-4phagocytes]), total light emission after stimulation with fMLP (1790 +/- 1371 vs. 1939 +/- 1532 [aU·s·10^-4phagocytes]), as well as FRAP after 3 min. plasma incubation (602 +/- 202 vs. 671 +/- 221 [uM]). Although, in the subgroup of 11 patients with severe OSAS (apnea/hypopnea index 58 +/- 18/h and oxygen desaturation index 55 +/- 19/h), the morning vs. evening resting chemiluminescence and total light emission after stimulation with fMLP observed a propensity to elevate 2.5 +/- 2.7 vs. 1.9 +/- 1.8 [aU·10^-4phagocytes] and 1778 +/- 1442 vs. 1503 +/- 1391 [aU·s·10^-4phagocytes], respectively, these did not attain statistical significance (p > 0.05).</p> <p>Conclusion</p> <p>Our investigation exposed no evidence in the overproduction of oxidants via circulating phagocytes, once considered a culprit in the oxidative stress of OSAS patients.</p

Original paper<br>The Abbott LCx-MTB assay is more sensitive than culture for detection of Mycobacterium tuberculosis in respiratory specimens

Background: In countries with a high incidence of tuberculosis quick, reliable and cost effective testing for this disease is mandatory. With the introduction of new methods based on detection of amplificated DNA fragment (Abbott LCx Mycobacterium tuberculosis assay) re-evaluation of the diagnostic panel (smear, culture and BACTEC versus LCx) is needed. We conducted a prospective study comparing clinical usefulness of these tests in detecting Mycobacterium tuberculosis in respiratory specimens from four clinical settings mandating transfer of respiratory specimens. Material and methods: Respiratory specimens (320 sputum specimens and 54 bronchoalveolar lavage fluid specimens) collected from 374 patients under investigation for tuberculosis at the four clinical centers were divided into 2 portions. One portion was used for standard staining and cultures (auramine-fluorochrome and Ziehl-Neelsen staining, culture on Loevenstein-Jensen medium and in BACTEC Middlebrook 12B vials) and the second one was investigated for presence of Mycobacterium tuberculosis with LCx -MTB assay.Results: In patients with a final diagnosis of tuberculosis we found LCx test more sensitive than culture and bacterioscopy (93.3% versus 81.3%; p<0.01 and 41.0%; p<0.001, respectively); while there was no difference in specificity and negative predictive value between LCx and culture.Conclusions: LCx test is an effective diagnostic tool in the setting of the central laboratory to cooperate with different, distant, clinical centers for detection of Mycobacterium tuberculosis in respiratory specimens from subjects belonging to a population with a high incidence of tuberculosis

Original article Is Hsp27 a marker of myocardial ischaemia?

Background: Heat shock protein (Hsp) 27 expression in cardiomyocytes increases in response to ischaemia. The extracellular release of Hsp27 from cardiomyocytes is proportional to its intracellular levels. Aim: To assess the influence of significant coronary artery disease (CAD), which by definition results in chronic myocardial ischaemia, on blood serum levels of Hsp27. Methods: Blood serum levels of Hsp27 in 62 patients with at least 50% lumen diameter narrowing in at least one main epicardial coronary artery on angiography and in 21 controls with normal coronaries were measured. Results: Patients with CAD tended to have higher serum level of Hsp27 than controls [0.463 (0.158-0.809) vs. 0.184 (0.099-0.337) ng/ml, p = 0.084]. Serum Hsp27 level in patients with CAD affecting more than a single vessel was significantly increased [0.529 (0.192-1.004) ng/ml] compared with controls (p = 0.035) and with one artery narrowed [0.276 (0.087-0.549) ng/ml, p = 0.041]. No correlation between Hsp27 serum levels and severity of coronary narrowings assessed by Gensini score was found (r = 0.21, p = 0.11). Conclusions: Serum level of Hsp27 seems to be a potential marker of myocardial ischaemia caused by advanced 2- or 3-vessel CAD.Wstęp: Ekspresja białka szoku cieplnego Hsp27 wzrasta w kardiomiocytach poddanych niedokrwieniu. Wiadomo, że wzrost ekspresji wewnątrzkomórkowej Hsp27 powoduje jego zwiększone uwalnianie z komórki do płynów ustrojowych. Cel: Ocena wpływu istotnej choroby wieńcowej (ChW), która z definicji wiąże się z przewlekłym niedokrwieniem miokardium, na stężenie Hsp27 w krwi obwodowej. Metody: Przy użyciu komercyjnie dostępnego testu ELISA (Calbiochem, Stany Zjednoczone) zmierzono stężenie Hsp27 w surowicy krwi obwodowej 62 pacjentów z potwierdzoną koronarograficznie przynajmniej 50-procentową stenozą w przynajmniej jednej tętnicy nasierdziowej i w surowicy 21 osób z prawidłowymi tętnicami wieńcowymi w badaniu angiograficznym. Kryteriami wykluczającymi z udziału w badaniu były: 1) niekontrolowana cukrzyca (glikemia na czczo lub glikemia przygodna w trakcie hospitalizacji przekraczająca odpowiednio 140 mg% lub 200 mg% albo HbA1c > 7,5%); 2) niekontrolowane nadciśnienie tętnicze (> 160/90 mmHg w więcej niż 50% pomiarów w ciągu poprzedzającego miesiąca); 3) przewlekła niewydolność krążenia w klasie wg NYHA wyższej niż I lub/i frakcja wyrzutowa lewej komory w aktualnym badaniu echokardiograficznym < 40%; 4) hemodynamicznie istotna zastawkowa wada serca; 5) ostre zakażenie w ciągu poprzedzających 3 tygodni; 6) przewlekła choroba zapalna w wywiadzie (m.in. przewlekła obturacyjna choroba płuc &#8211; POChP, choroby reumatologiczne); 7) niedokrwistość (Hb < 11 g%); 8) choroba nowotworowa; 9) udar niedokrwienny w wywiadzie lub inne zespoły niedokrwienne, poza ChW. Wyniki: Stężenie Hsp27 w surowicy krwi obwodowej pacjentów z istotną ChW wykazywało jedynie tendencję do wyższych wartości w porównaniu ze stężeniem w krwi osób z prawidłowymi tętnicami wieńcowymi [0,463 (0,158&#8211;0,809) vs 0,184 (0,099&#8211;0,337) ng/ml, odpowiednio; p = 0,084]. Stężenie Hsp27 było natomiast wyższe w surowicy pacjentów z 2- i 3-naczyniową ChW [0,529 (0,192&#8211;1,004) ng/ml] w porównaniu z osobami bez zmian w tętnicach wieńcowych (p = 0,035) i w porównaniu z pacjentami z jedno-naczyniową ChW [0,276 (0,087&#8211;0,549) ng/ml, p = 0,041]. Stężenie Hsp27 w surowicy nie wykazywało korelacji z ciężkością ChW ocenianą na podstawie skali Gensiniego (r = 0,21, p = 0,11). Wnioski: Stężenie Hsp27 w surowicy krwi obwodowej może świadczyć o rozległym niedokrwieniu miokardium i zaawansowanej ChW

Body mass index is negatively associated with telomere length: a collaborative cross-sectional meta-analysis of 87 observational studies

Background: Even before the onset of age-related diseases, obesity might be a contributing factor to the cumulative burden of oxidative stress and chronic inflammation throughout the life course. Obesity may therefore contribute to accelerated shortening of telomeres. Consequently, obese persons are more likely to have shorter telomeres, but the association between body mass index (BMI) and leukocyte telomere length (TL) might differ across the life span and between ethnicities and sexes. Objective: A collaborative cross-sectionalmeta-analysis of observational studies was conducted to investigate the associations between BMI and TL across the life span. Design: Eighty-seven distinct study samples were included in the meta-analysis capturing data from 146,114 individuals. Studyspecific age- and sex-adjusted regression coefficients were combined by using a random-effects model in which absolute [base pairs (bp)] and relative telomere to single-copy gene ratio (T/S ratio) TLs were regressed against BMI. Stratified analysis was performed by 3 age categories ("young": 18-60 y; "middle": 61-75 y; and "old": >75 y), sex, and ethnicity. Results: Each unit increase in BMI corresponded to a-3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI:-10.03,-5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10 -3 unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10 -3 , -1.01 × 10 -3 ) difference in ageand sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10 -3 unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10 -3 , -1.25 × 10 -3 ). The associations were predominantly for the white pooled population. No sex differences were observed. Conclusions: A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL arewarranted