BackgroundBacterial resistance to antibiotics is increasing worldwide. Antibiotic-resistant strains can lead to serious problems regarding treatment of infection. Carbapenem antibiotics are the final treatment option for infections caused by serious and life-threatening multidrug-resistant gram-negative bacteria. Therefore, an understanding of carbapenem resistance is important for infection control. In the study described herein, the phenotypic and genotypic features of carbapenem-resistant Enterobacteriaceae strains isolated in our hospital were evaluated.MethodsIn total, 43 carbapenem-resistant strains were included in this study. Sensitivity to antibiotics was determined using the VITEK®2 system. The modified Hodge test (MHT) and metallo-β-lactamase (MBL) antimicrobial gradient test were performed for phenotypic identification. Resistance genes IMP, VIM, KPC, NDM-1, and OXA-48 were amplified by multiplex PCR.ResultsThe OXA-48 gene was detected in seven strains, and the NDM-1 gene in one strain. No resistance genes were detected in the remainder of strains. A significant correlation was observed between the MHT test and OXA-48 positivity, and between the MBL antimicrobial gradient test and positivity for resistance genes (p < 0.05).ConclusionThe finding of one NDM-1-positive isolate in this study indicates that carbapenem resistance is spreading in Turkey. Carbapenem resistance spreads rapidly and causes challenges in treatment, and results in high mortality/morbidity rates. Therefore, is necessary to determine carbapenem resistance in Enterobacteriaceae isolates and to take essential infection control precautions to avoid spread of this resistance.

Platelets have the capacity to release mediators with potent inflammatory or anaphylactic properties. Platelet factor-4 (PF4) and beta-thromboglobulin (BTG) are two of these mediators. On the other hand, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) are two important mediators of fibrinolysis. Both mediators are secreted mainly by vascular endothelium. Plasma levels of PF4, BTG, PAI-1, and tPA may show changes in chronic inflammatory diseases such as asthma. This study examined the role of thrombocytes and the function of the endothelium in asthmatic patients during an attack and during a stable phase. Eighteen patients with known allergic asthma who came to our emergency department with an asthma attack and 14 control subjects were included in the study. Blood samples were taken after starting therapy with salbutamol inhalation. Lung function tests were performed after receiving the first emergency therapy for asthma. Plasma levels of PF4, BTG, PAI-1, tPA were determined before starting steroid therapy and after receiving 1 week of steroid therapy. Plasma levels of PF4 among patients with an asthma attack were significantly higher than those of controls (150.5+/-8.92 IU/mL vs. 92.5+/-7.63 IU/mL, p<0.001). A further increase in plasma PF4 levels was detected after steroid therapy (163.5+/-9.16 IU/mL). Plasma BTG levels of patients on admission were not statistically different from those in the control group (140.4+/-6.34 IU/mL vs. 152.2+/-8.71 IU/mL). An increase was detected after therapy (171.6+/-7.27 IU/mL) and post-treatment plasma levels were statistically meaningful versus the controls. Plasma levels of tPA and PAI were statistically higher than those in controls in asthmatic patients on admission (6.01+/-2.72 vs. 5.4+/-2.3 ng/mL for tPA and 75.2+/-27.2 ng/mL vs. 32.7+/-14.3 ng/mL for PAI-1). Further increases were detected in two parameters after 1 week of therapy with steroids (tPA levels were 6.85+/-2.96 ng/mL and PAI-1 levels were 83.5+/-29.6 ng/mL). There seems to be an increased activity of platelets during an asthma attack. Elevated PAI-1 and tPA levels may also indicate the activated endothelium in asthma. Increases of plasma levels of PAI-1 and tPA after steroid therapy need further investigation because elevated PAI-1 levels enhance airway remodeling.

We investigated the vascular effects of glucagon-like peptide-1 (GLP-1) and Exendin-4 in type 2 diabetic rat aortae. Studies were performed in a normal control group (NC) (0.2 ml i.p. saline, n = 10), streptozotocin (STZ)/nicotinamide diabetic control group (DC) (a single dose of 80 mg/kg STZ i.p. injection 15 min after administration of 230 mg/kg nicotinamide i.p.), GLP-1 (GLPC) control group (1 µg/kg twice daily i.p. for 1 month, n = 10), Exendin-4 control group (EXC) (0.1 µg/kg twice daily i.p. for 1 month, n = 10), GLP-1-treated diabetic group (GLPT) (1 µg/kg twice daily i.p. for 1 month, n = 10), and Exendin-4-treated diabetic group (EXT) (0.1 µg/kg twice daily i.p. for 1 month, n = 10). One month of GLP-1 and Exendin-4 treatment significantly decreased the blood glucose levels of diabetic rats (113 ± 2 mg/dl, p < 0.001, and 117 ± 1 mg/dl, p < 0.001, respectively versus 181 ± 9 mg/dl in the DC group). Sensitivity (pD₂) and maximum response (% Max. Relax) of acetylcholine-stimulated relaxations in the DC group (pD₂: 6.73 ± 0.12 and 55 ± 6, respectively) were decreased compared with the non-diabetic NC group (pD₂: 7.41 ± 0.25, p < 0.05, and 87 ± 4, p < 0.01). Treating diabetic rats with GLP-1, pD₂ values and with Exendin-4, Max. Relax %values of aortic strips to acetylcholine returned to near non-diabetic NC values (pD₂: 7.47 ± 0.15, p < 0.05, and 87 ± 3, p < 0.01, respectively). Maximal contractile responses (E_max) to noradrenaline in aortic strips from the diabetic DC group (341 ± 27 mg tension/mg wet weight) were significantly decreased compared with the non-diabetic NC (540 ± 66 mg tension/mg wet weight, p < 0.001) and the GLPT group (490 ± 25 mg tension/mg wet weight, p < 0.05). There were no significant differences in pD₂ values of aortic strips to noradrenaline from all groups. E_max to KCl in aortic strips from the DC group (247 ± 10 mg tension/mg wet weight, p < 0.01) was significantly decreased compared with non-diabetic NC group (327 ± 26 mg tension/mg wet weight). Treating diabetic rats with GLP-1 (GLPT), E_max values of aortic strips to KCl returned to near non-diabetic NC values (271 ± 12 mg tension/mg wet weight). GLP-1 and (partially) Exendin-4 treatment could improve the increased blood glucose level and normalize the altered vascular tone in type 2 diabetic rats.

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