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9 záznamů v Medvik Filtry

Článek

Infekční komplikace u pacientů s akutním srdečním selháním – přehled
[Infectious complications in patients with acute heart failure – an overview]

Pařenica, Josef, 1941-
Autor Autorita Interní kardiologická klinika LF MU a FN Brno
Hanslianová, Markéta
Autor Autorita Lékařská fakulta MU, Brno Oddělení klinické mikrobiologie, FN Brno

Kardiologická revue. 2016 ; 18 (1) : 18-21.

ISSN 2336-288x
Medvik
Zdroj

Infekce je považována asi u 17 % pacientů za spouštěcí faktor, který vede k akutní dekompenzaci chronického srdečního selhání. Zároveň může infekce komplikovat hospitalizační průběh pacientů s akutním srdečním selháním, u pacientů v kardiogenním šoku je to až u 65 %. Článek podává přehled nejčastějších patogenů komunitních a nozokomiálních infekcí dýchacích a močových cest, možnosti jejich diagnostiky a léčby. Klíčová slova: akutní srdeční selhání – infekce – prokalcitonin

Infection is considered to be a trigger factor leading to acute decompensation of chronic heart failure in about 17% of hospitalised patients. Simultaneously, infection may complicate the course of hospitalisation of acute heart failure patients, and in cardiogenic shock patients this can be up to 65% of cases. The article gives an overview of the most common pathogens of community and nosocomial infections of the respiratory and urinary tract and the possibilities of their diagnosis and treatment. Keywords: acute heart failure – infection – procalcitonin

Klíčová slova
presepsin,
MeSH
akutní nemoc MeSH
algoritmy MeSH
antibakteriální látky aplikace a dávkování MeSH
antigeny CD14 krev MeSH
bakteriální pneumonie diagnóza etiologie farmakoterapie MeSH
biologické markery MeSH
infekce dýchací soustavy * diagnóza farmakoterapie komplikace MeSH
infekce močového ústrojí * diagnóza farmakoterapie komplikace MeSH
infekce spojené se zdravotní péčí diagnóza farmakoterapie komplikace MeSH
infekce získané v komunitě diagnóza farmakoterapie komplikace MeSH
kalcitonin krev MeSH
lidé MeSH
management nemoci MeSH
peptidové fragmenty krev MeSH
prokalcitonin MeSH
proteinové prekurzory krev MeSH
srdeční selhání * komplikace MeSH
ventilátorová pneumonie diagnóza etiologie farmakoterapie MeSH
Check Tag
lidé MeSH
Publikační typ
práce podpořená grantem MeSH
přehledy MeSH

Článek

Sepsis biomarkers

Clinica chimica acta. 2015 ; 440 (-) : 97-103. [pub] 20141118

Clin Chim Acta
ISSN 1873-3492
Medvik
Zdroj

Sepsis is the most frequent cause of death in non-coronary intensive care units (ICUs). In the past 10 years, progress has been made in the early identification of septic patients and in their treatment and these improvements in support and therapy mean that the mortality is gradually decreasing but it still remains unacceptably high. Leaving clinical diagnosis aside, the laboratory diagnostics represent a complex range of investigations that can place significant demands on the system given the speed of response required. There are hundreds of biomarkers which could be potentially used for diagnosis and prognosis in septic patients. The main attributes of successful markers would be high sensitivity, specificity, possibility of bed-side monitoring, and financial accessibility. Only a fraction is used in routine clinical practice because many lack sufficient sensitivity or specificity. The following review gives a short overview of the current epidemiology of sepsis, its pathogenesis and state-of-the-art knowledge on the use of specific biochemical, hematological and immunological parameters in its diagnostics. Prospective approaches towards discovery of new diagnostic biomarkers have been shortly mentioned.

MeSH
antigeny CD14 krev MeSH
biologické markery analýza krev MeSH
C-reaktivní protein analýza MeSH
cytokiny krev MeSH
fibrin-fibrinogen - produkty degradace analýza MeSH
jednotky intenzivní péče MeSH
kalcitonin krev MeSH
leukocyty metabolismus MeSH
lidé MeSH
membránové glykoproteiny krev MeSH
peptidové fragmenty krev MeSH
proteinové prekurzory krev MeSH
proteiny akutní fáze MeSH
sepse diagnóza metabolismus MeSH
syndrom systémové zánětlivé reakce diagnóza metabolismus MeSH
transportní proteiny krev MeSH
Check Tag
lidé MeSH
Publikační typ
časopisecké články MeSH
přehledy MeSH

Článek online

Presepsin jako solubilní CD 14 subtyp a prokalcitonin v prognostice mortality sepse

Drábková, Jarmila, 1934-
Autor Autorita KARIM/OCHRIP 2. LF UK a FN Motol, Praha

Referátový výběr z anesteziologie, resuscitace a intenzivní medicíny. 2014 ; 61 (3) : 49-51.

ISSN 1212-3048
Medvik
Zdroj

Článek

Rosiglitazone influences the expression of leukocyte adhesion molecules and CD14 receptor in type 2 diabetes mellitus patients

Physiological research. 2014 ; 63 (Suppl. 2) : S293-S298.

Physiol. Res. (Print)
ISSN 1802-9973
Medvik
Zdroj

Professor Schreiber celebrates his 90th birthday. 2014 ; () : S293-S298.

Medvik
Zdroj

Diabetes mellitus is associated with increased inflammatory response, which may contribute to atherosclerosis progression. Experimental results demonstrated anti-inflammatory activity of glitazones; their effect on leukocyte adhesion molecules has not been studied to date. We therefore studied the effect of rosiglitazone treatment on leukocyte surface expression of adhesion molecules in patients with type 2 diabetes mellitus and compared our results with findings in healthy subjects. 33 subjects with type 2 diabetes and 32 healthy controls were included; patients were examined at baseline and after 5 months of rosiglitazone treatment (4 mg/d). Leukocyte expression of adhesion molecules LFA-1, CD18 and ICAM-1 was quantified using flow cytometry; in addition, CD14 (lipopolysaccharide receptor) expression was analyzed as a marker of nonspecific immunity. The expression of examined molecules at baseline was higher in patients compared to controls. Despite only mild decrease in blood glucose, rosiglitazone treatment induced substantial decrease of CD18 and CD14 expression and borderline decrease of LFA-1 and ICAM-1 expression (on monocytes only). We thus observed improvement in the expression of leukocyte inflammatory markers after rosiglitazone treatment. This effect is supposed to be mediated by direct effect of rosiglitazone on PPAR-gamma receptors on leukocytes.

MeSH
antigeny CD14 krev MeSH
biologické markery krev MeSH
diabetes mellitus 2. typu krev farmakoterapie imunologie MeSH
down regulace MeSH
hypoglykemika terapeutické užití MeSH
krevní glukóza účinky léků metabolismus MeSH
lidé středního věku MeSH
lidé MeSH
mediátory zánětu krev MeSH
molekuly buněčné adheze krev MeSH
senioři MeSH
studie případů a kontrol MeSH
thiazolidindiony terapeutické užití MeSH
výsledek terapie MeSH
Check Tag
lidé středního věku MeSH
lidé MeSH
mužské pohlaví MeSH
senioři MeSH
ženské pohlaví MeSH
Publikační typ
časopisecké články MeSH
práce podpořená grantem MeSH

Článek

Postprandial inflammation is not associated with endoplasmic reticulum stress in peripheral blood mononuclear cells from healthy lean men

British Journal of Nutrition. 2014 ; 112 (4) : 573-582.

Br J Nutr
ISSN 1475-2662
Medvik
Zdroj

The consumption of lipids and simple sugars induces an inflammatory response whose exact molecular trigger remains elusive. The aims of the present study were to investigate (1) whether inflammation induced by a single high-energy, high-fat meal (HFM) is associated with endoplasmic reticulum stress (ERS) in peripheral blood mononuclear cells (PBMC) and (2) whether these inflammatory and ERS responses could be prevented by the chemical chaperone ursodeoxycholic acid (UDCA). A total of ten healthy lean men were recruited to a randomised, blind, cross-over trial. Subjects were given two doses of placebo (lactose) or UDCA before the consumption of a HFM (6151 kJ; 47·4 % lipids). Blood was collected at baseline and 4 h after the HFM challenge. Cell populations and their activation were analysed using flow cytometry, and plasma levels of inflammatory cytokines were assessed by ELISA and Luminex technology. Gene expression levels of inflammatory and ERS markers were analysed in CD14⁺ and CD14⁻ PBMC using quantitative RT-PCR. The HFM induced an increase in the mRNA expression levels of pro-inflammatory cytokines (IL-1β, 2·1-fold; IL-8, 2·4-fold; TNF-α, 1·4-fold; monocyte chemoattractant protein 1, 2·1-fold) and a decrease in the expression levels of miR181 (0·8-fold) in CD14⁺ monocytes. The HFM challenge did not up-regulate the expression of ERS markers (XBP1, HSPA5, EDEM1, DNAJC3 and ATF4) in either CD14⁺ or CD14⁻ cell populations, except for ATF3 (2·3-fold). The administration of UDCA before the consumption of the HFM did not alter the HFM-induced change in the expression levels of ERS or inflammatory markers. In conclusion, HFM-induced inflammation detectable on the level of gene expression in PBMC was not associated with the concomitant increase in the expression levels of ERS markers and could not be prevented by UDCA.

Článek

Changes associated with lenalidomide treatment in the gene expression profiles of patients with del(5q)

Clinical lymphoma, myeloma & leukemia. 2012 ; 12 (5) : 375-383.

Clin Lymphoma Myeloma Leuk
ISSN 2152-2669
Medvik
Zdroj

UNLABELLED: We used microarray profiling to investigate the direct effects of lenalidomide on gene expression in isolated CD14(+) monocytes from 6 patients with del(5q). Our data demonstrate that changes in genes involved the tumor necrosis factor (TNF) signaling pathway and the bone marrow stroma, suggesting that treatment with lenalidomide may help restore the damaged niche and suppress the TNF signaling pathway. BACKGROUND: Lenalidomide is an effective treatment for patients with del(5q) and myelodysplastic syndrome (MDS) The exact mechanism of lenalidomide function and its impact on the prognosis of patients is not known exactly. MATERIALS AND METHODS: We used gene expression profiling to study the effect of lenalidomide therapy in peripheral blood CD14(+) monocytes of 6 patients with del(5q) and MDS. RESULTS: After lenalidomide treatment, genes involved in the tumor necrosis factor (TNF) signaling pathway that were upregulated in the patients before treatment decreased to the healthy control baseline expression level. This change in gene expression, in conjunction with increased expression of repressed genes that affect the stem cell niche (ie, CXCR4 and CRTAP), may exert a positive effect on treated patients. In contrast, we found that increased expression of the ARPC1B gene may have a negative impact on the stability of patient remission. CONCLUSION: The observed changes in gene expression described here may contribute to the identification of pathways that are affected by lenalidomide, which may help to explain the effects of this drug.

Článek

Chronic immune activation in common variable immunodeficiency (CVID) is associated with elevated serum levels of soluble CD14 and CD25 but not endotoxaemia

Clinical and experimental immunology. 2012 ; 170 (3) : 321-332.

Clin Exp Immunol
ISSN 1365-2249
Medvik
Zdroj

Common variable immunodeficiency (CVID), the most frequent symptomatic immunoglobulin primary immunodeficiency, is associated with chronic T cell activation and reduced frequency of CD4(+) T cells. The underlying cause of immune activation in CVID is unknown. Microbial translocation indicated by elevated serum levels of lipopolysaccharide and soluble CD14 (sCD14) has been linked previously to systemic immune activation in human immunodeficiency virus/acquired immune deficiency syndrome (HIV-1/AIDS), alcoholic cirrhosis and other conditions. To address the mechanisms of chronic immune activation in CVID, we performed a detailed analysis of immune cell populations and serum levels of sCD14, soluble CD25 (sCD25), lipopolysaccharide and markers of liver function in 35 patients with CVID, 53 patients with selective immunoglobulin (Ig)A deficiency (IgAD) and 63 control healthy subjects. In CVID subjects, the concentration of serum sCD14 was increased significantly and correlated with the level of sCD25, C-reactive protein and the extent of T cell activation. Importantly, no increase in serum lipopolysaccharide concentration was observed in patients with CVID or IgAD. Collectively, the data presented suggest that chronic T cell activation in CVID is associated with elevated levels of sCD14 and sCD25, but not with systemic endotoxaemia, and suggest involvement of lipopolysaccharide-independent mechanisms of induction of sCD14 production.