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1.
Bratisl Lek Listy ; 121(4): 259-262, 2020.
Article in English | MEDLINE | ID: mdl-32356439

ABSTRACT

BACKGROUND: Triggering receptor expressed on myeloid cells 1 (TREM-1) is secreted by phagocytes in adipose tissue and it also upregulates the expression of genes involved in the inflammatory response and atherosclerotic conditions. This study was aimed to investigate the serum TREM-1 levels in overweight patients. METHODS: Twenty-eight subjects in the overweight group (OG) and 20 age-matched healthy subjects in the control group (CG) (BMI 27.6±1.2 vs 23.1±2.17 kg/m2, respectively, p<0.001) were included in the study. The serum sTREM-1 level was measured by ELISA. The homeostasis model assessment score (HOMA-IR) was also calculated. RESULTS: The mean TREM-1 levels were significantly higher in OG than in CG (407.3±323.7 vs 150.3±152.7 pg/mL, respectively, p<0.001). The HOMA-IR score was also significantly higher in OG than in CG (3.42±3.63 vs 2.77±1.61, respectively). A positive correlation was detected between TREM-1 and BMI (r=0.318, p=0.028). CONCLUSIONS: This study mainly demonstrated that a high serum TREM-1 level might be an early inflammatory marker in overweight patients. We found that TREM-1 might be associated with BMI in overweight patients regardless of insulin resistance (Tab. 1, Ref. 21). Text in PDF www.elis.sk.


Subject(s)
Inflammation/blood , Overweight/blood , Triggering Receptor Expressed on Myeloid Cells-1/blood , Biomarkers/blood , Case-Control Studies , Humans , Insulin Resistance
2.
Bratisl Lek Listy ; 116(12): 746-50, 2015.
Article in English | MEDLINE | ID: mdl-26924146

ABSTRACT

BACKGROUND: Sugammadex is primarily excreted via renal route. We investigated effects of low and high doses of sugammadex (16 mg/kg versus 96 mg/kg) on renal tissue samples of streptozotocin-induced diabetic rats. MATERIAL AND METHODS: Twenty-four Wistar albino rats were divided into 4 groups. Group C (control - 0.9 % NaCl), Group DC (diabetes control; 55 mg/kg streptozotocin, IP, only), Group DR-16S (diabetes-rocuronium - 16 mg sugammadex, IV.) and Group DR-96S (diabetes- rocuronium - 96 mg sugammadex, IV). Renal tissue histopathological evaluation and antioxidant status (measurements of MDA levels and NO activities) were studied. RESULTS: Significantly higher levels of all inflammation parameters (inflammation, degeneration/necrosis, tubular dilatation, tubular cell degeneration, dilatation in Bowman's space, tubular hyaline casts, and lymphocyte infiltration) were found in the 96 mg/kg sugammadex group. Higher MDA tissue levels and lower NO activity were found in the 96 mg/kg sugammadex group. DISCUSSION: We can conclude that high-dose (96 mg/kg) sugammadex administration resulted in significant renal tissue damage in diabetic rats. As a consequence, low doses of sugammadex have to be preferred in diabetic patients (Tab. 2, Fig. 4, Ref. 26).

3.
Parasitology ; 122(Pt 2): 169-73, 2001 Feb.
Article in English | MEDLINE | ID: mdl-11272647

ABSTRACT

It is generally accepted that free-living stages of parasitic helminths are dependent on aerobic degradation of endogenous energy sources for their energy generation. This concept, however, is not the result of extensive experimental evidence, but originated mainly intuitively as oxygen is widely available in their habitat and these stages generally have a small size. Schistosoma mansoni, the sole parasitic helminth whose energy metabolism has been studied throughout its life-cycle indeed has aerobically functioning free-living stages. However, large differences exist in energy metabolism between adult stages of distinct parasitic helminths, and caution should be taken in predicting that all free-living stages of all parasitic helminths have the same, aerobic energy metabolism. Hence, this report studied the energy metabolism of Fasciola hepatica miracidia and demonstrated that F. hepatica miracidia are also dependent on aerobic degradation of their endogenous glycogen stores by glycolysis and on Krebs cycle activity for energy generation. However, in contrast to S. mansoni, F. hepatica miracidia cannot function anaerobically, as inhibition of the respiratory chain blocked motility and carbohydrate degradation, and finally resulted in death of the miracidia. Therefore, this report demonstrated that differences exist between miracidia of distinct species, in pre-adaptation of their energy metabolism to the occasional hypoxic conditions within their next host.


Subject(s)
Energy Metabolism , Fasciola hepatica/physiology , Glycogen/metabolism , Oxygen Consumption , Animals , Carbohydrate Metabolism , Fascioliasis/veterinary , Life Cycle Stages , Liver/parasitology , Sheep , Sheep Diseases/parasitology
4.
Eur J Gastroenterol Hepatol ; 10(1): 11-3, 1998 Jan.
Article in English | MEDLINE | ID: mdl-9512947

ABSTRACT

OBJECTIVE: The effects of dopamine infusion on portal blood flow were examined in 12 cirrhotic patients (seven men, five women) in a Child-B group. METHODS: Dopamine was administered as an intravenous infusion (2 micrograms kg-1 min-1). RESULTS: At 0, 30 and 60 min, portal blood flow, left ventricular systolic and diastolic functions were evaluated using the pulsed doppler method. No significant difference was found between heart rate, blood pressure and parameters demonstrating left ventricular systolic and diastolic functions before and after dopamine infusions. Portal blood flow decreased significantly at 30 and 60 min. Portal blood flow fell from 1802 +/- 88 to 1339 +/- 50 ml min-1 (P < 0.001) at 30 min and to 1121 +/- 60 ml min-1 (P < 0.001) at 60 min. CONCLUSION: The reducing effects of dopamine on portal blood flow in cirrhotic patients were demonstrated by the pulsed doppler method, which is a noninvasive test.


Subject(s)
Dopamine/pharmacology , Liver Circulation/drug effects , Liver Cirrhosis/physiopathology , Portal System/drug effects , Adult , Aged , Dopamine/administration & dosage , Female , Hemodynamics/drug effects , Humans , Infusions, Intravenous , Liver Cirrhosis/diagnostic imaging , Male , Middle Aged , Portal System/diagnostic imaging , Ultrasonography , Ventricular Function, Left
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