scholarly journals Club Cell protein: a candidate diagnostic biomarker of Pseudomonas aeruginosa nosocomial pneumonia

Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P218
Author(s):  
V Moroz ◽  
A Kuzovlev ◽  
S Polovnikov
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Nosocomial Pneumonia ◽  
Protein A ◽  
Cell Protein ◽  
Diagnostic Biomarker ◽  
Club Cell

Nosocomial Pneumonia: An Update on Early Diagnosis and Prevention

2020 ◽  
Vol 15 (4) ◽  
pp. 251-259
Author(s):  
Artem Kuzovlev ◽  
Aslan Shabanov ◽  
Andrey Grechko
Keyword(s):  
Critical Care ◽  
Early Diagnosis ◽  
Nosocomial Pneumonia ◽  
Molecular Biomarkers ◽  
Surfactant Proteins ◽  
Cell Protein ◽  
Evidence Based ◽  
Effective Prevention ◽  
Promising Direction ◽  
Club Cell

Nosocomial pneumonia and nosocomial tracheobronchitis present a significant problem of anesthesiology and critical care medicine. This review presents the results of our own research on the usefulness of new molecular biomarkers in the early diagnosis of nosocomial pneumonia, as well as modern principles for its prevention. A promising direction for the early diagnosis of nosocomial pneumonia and its complications is the study of new molecular biomarkers, in particular, Club cell protein and surfactant proteins. Effective prevention of nosocomial pneumonia should be based on a complex of modern evidence-based methods.

scholarly journals Clara Cell Protein (Club Cell Protein) is a New Diagnostic Molecular Candidate Biomarker in Nosocomial Pneumonia

2014 ◽  
Vol 10 (6) ◽  
pp. 6
Author(s):  
V. V. Moroz ◽  
A. M. Golubev ◽  
A. N. Kuzovlev ◽  
A. K. Shabanov ◽  
V. M. Pisarev
Keyword(s):  
Nosocomial Pneumonia ◽  
Clara Cell ◽  
Cell Protein ◽  
Clara Cell Protein ◽  
Club Cell

scholarly journals Exercise-mitigated gender-based differences in aging: From genetic alterations to heart performance

2020 ◽  
Author(s):  
Denise Börzsei ◽  
Daniel Priksz ◽  
Renáta Szabó ◽  
Mariann Bombicz ◽  
Zoltán Karácsonyi ◽  
...  
Keyword(s):  
Heart Function ◽  
Protein A ◽  
Genetic Alterations ◽  
Functional Adaptation ◽  
Voluntary Exercise ◽  
Female Rats ◽  
Cell Protein ◽  
Calcium Balance ◽  
Male And Female Rats ◽  
Heart Performance

The prevalence of cardiovascular diseases dramatically increases with age, therefore striving to maintain a physiological heart function became particularly important. We aimed to study the voluntary exercise evoked cardioprotective effects in aged male and female rats, from genetic alterations to changes in heart performance. We divided 20-month-old female and male Wistar rats to control and running groups. After the 12-week-long experimental period, echocardiographic measurements were performed. Afterwards, hearts were either removed for biochemical measurements or mounted into a Langendorff-perfusion system to detect infarct size. The following genes and their proteins were analyzed from heart: catechol-O-methyltransferase (Comt), endothelin-1 (Esm1), Purkinje cell protein-4 (Pcp4), and osteoglycin (Ogn). Recreational exercise caused functional improvements; however, changes were more prominent in males. Cardiac expression of Comt and Ogn were reduced as a result of exercise in aged males, while Pcp4 and Esm1 showed a marked overexpression, along with a markedly improved diastolic function. The key result of this study is that exercise enhanced the expression of the Pcp4 gene and protein, a recently described regulator of calcium balance in cardiomyocytes, and suppressed Comt and Ogn gene expression, that has been associated with impaired cardiac function. In addition, as a result of exercise, a significant improvement was observed in the size of infarct elicited by left anterior descending coronary artery occlusion. Our results clearly show that age and sex-dependent changes were both apparent in key proteins linked to cardiovascular physiology. Exercise-moderated fundamental genetic alterations may have contributed to the functional adaptation of the heart.

Nebulized imipenem to control nosocomial pneumonia caused by Pseudomonas aeruginosa

2008 ◽  
Vol 23 (1) ◽  
pp. 148-150 ◽  
Author(s):  
M. Radhakrishnan ◽  
A. Jaganath ◽  
G.S. Umamaheswara Rao ◽  
H.B.Veena Kumari
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Nosocomial Pneumonia

Identification of pilin pools in the membranes of Pseudomonas aeruginosa

1982 ◽  
Vol 152 (2) ◽  
pp. 687-691
Author(s):  
T H Watts ◽  
E A Worobec ◽  
W Paranchych
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Gel Electrophoresis ◽  
Type Strain ◽  
Wild Type Strain ◽  
Polyacrylamide Gel Electrophoresis ◽  
Protein A ◽  
Sodium Dodecyl ◽  
Wild Type ◽  
Outer Membranes

The proteins of purified inner and outer membranes obtained from Pseudomonas aeruginosa strains PAK and PAK/2Pfs were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, and treated with antiserum raised against pure pili. Bound antipilus antibodies were visualized by reaction with 125I-labeled protein A from Staphylococcus aureus. The results showed that there are pools of pilin in both the inner and outer membranes of P. aeruginosa and that the pool size in the multipiliated strain is comparable with that of the wild-type strain.

scholarly journals Recombinant club cell protein 16 (CC16) ameliorates cigarette smoke‑induced lung inflammation in a murine disease model of COPD

2018 ◽  
Author(s):  
Min Pang ◽  
Hong‑Yan Liu ◽  
Ting Li ◽  
Dan Wang ◽  
Xiao‑Yun Hu ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Disease Model ◽  
Cell Protein ◽  
Club Cell

scholarly journals Club cell protein 16 and cytokeratin fragment 21-1 as early predictors of pulmonary complications in polytraumatized patients with severe chest trauma

PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175303 ◽  
Author(s):  
Lukas L. Negrin ◽  
Gabriel Halat ◽  
Stephan Kettner ◽  
Markus Gregori ◽  
Robin Ristl ◽  
...  
Keyword(s):  
Chest Trauma ◽  
Pulmonary Complications ◽  
Cell Protein ◽  
Club Cell ◽  
Early Predictors

scholarly journals Emphysema and extrapulmonary tissue loss in COPD: a multi-organ loss of tissue phenotype

2018 ◽  
Vol 51 (2) ◽  
pp. 1702146 ◽  
Author(s):  
Bartolome R. Celli ◽  
Nicholas Locantore ◽  
Ruth Tal-Singer ◽  
John Riley ◽  
Bruce Miller ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Forced Expiratory Volume ◽  
Fat Free Mass ◽  
Tissue Loss ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Club Cell ◽  
Body Compartments

We tested whether emphysema progression accompanies enhanced tissue loss in other body compartments in 1817 patients from the ECLIPSE chronic obstructive pulmonary disease (COPD) cohort.Clinical and selected systemic biomarker measurements were compared in subjects grouped by quantitative tomography scan emphysema quartiles using the percentage of low attenuation area (LAA%). Lowest and highest quartile patients had amino-acid metabolomic profiles. We related LAA% to 3 years decline in lung function (forced expiratory volume in 1 s (FEV1)), body mass index (BMI), fat-free mass index (FFMI) and exacerbations, hospitalisations and mortality rates.Participants with more baseline emphysema had lower FEV1, BMI and FFMI, worse functional capacity, and less cardiovascular disease but more osteoporosis. Systemic C-reactive protein and interleukin-6 levels were similar among groups, but club cell protein 16 was higher and interleukin-8, surfactant protein D and soluble receptor for advanced glycation end product were lower with more emphysema. Metabolomics differed between extreme emphysema quartiles. Patients with more emphysema had accelerated FEV1, BMI and FFMI decline and more exacerbations, hospitalisations and mortality.COPD patients with more emphysema undergo excessive loss of pulmonary and extrapulmonary tissue, which is probably related to abnormal tissue maintenance. Because of worse clinical outcomes, we propose this subgroup be named the multi-organ loss of tissue (MOLT) COPD phenotype.

scholarly journals Pneumoproteins in Offshore Drill Floor Workers

2019 ◽  
Vol 16 (3) ◽  
pp. 300 ◽  
Author(s):  
Niels E. Kirkhus ◽  
Bente Ulvestad ◽  
Lars Barregard ◽  
Øivind Skare ◽  
Raymond Olsen ◽  
...  
Keyword(s):  
Strong Association ◽  
Surfactant Protein ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Drilling Mud ◽  
Air Concentration ◽  
Work Period ◽  
Club Cell ◽  
Before And After ◽  
Oil Mist

The aim was to assess pneumoproteins and a certain biomarker of systemic inflammation in drill floor workers exposed to airborne contaminants generated during drilling offshore, taking into consideration serum biomarkers of smoking, such as nicotine (S-Nico) and cotinine. Blood samples of club cell protein 16 (CC-16), surfactant protein D (SP-D) and C-reactive protein (CRP) were collected before and after a 14-day work period from 65 drill floor workers and 65 referents. Air samples of oil mist, drilling mud components and elemental carbon were collected in person. The drill floor workers were exposed to a median air concentration of 0.18 mg/m3 of oil mist and 0.14 mg/m3 of airborne mud particles. There were no differences in the concentrations of CC-16 and SP-D across the 14-day work period and no difference between drill floor workers and referents at baseline after adjusting for differences in sampling time and smoking. CRP decreased across the work period. There was a strong association between the CC-16 concentrations and the time of sampling. Current smokers with S-Nico > detection limit (DL) had a statistically significantly lower CC-16 concentration, while smokers with S-Nico <DL had CC-16 concentrations similar to that of the non-smokers. Fourteen days of work offshore had no effect on serum pneumoprotein and CRP concentrations. However, the time of blood sampling was observed to have a strong effect on the measured concentrations of CC-16. The effect of current smoking on the CC-16 concentrations appears to be dependent on the S-Nico concentrations.

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