Role of Neutrophil CD64 Index as a Screening Marker for Late-Onset Sepsis in Very Low Birth Weight Infants

<div><p>Introduction</p><p>The role of CD64 in late onset sepsis (LOS) in preterm infants has been described in several studies. Aim of this study was to investigate whether CD64 expression is increased in the days before clinical manifestation of LOS.</p><p>Methods</p><p>Patients with birth weight below 1,500g were eligible for study participation. During routine blood sampling CD64 index was determined between day of life 4 and 28. Patients were allocated to one of four groups: (1) blood-culture positive sepsis, (2) clinical sepsis, (3) symptoms of infection without biochemical evidence of infection, or (4) patients without suspected infection. Kinetics of CD64 expression were compared during a period before and after the day of infection in the respective groups.</p><p>Results</p><p>50 infants were prospectively enrolled and allocated to each group as follows: group (1) n = 7; group (2) n = 10; group (3) n = 8; and group (4) n = 25. CD64 index was elevated in 57% of patients in group (1) at least two days before infection. In contrast only 20% in the clinical sepsis group and 0% in group (3) had an elevated CD64 index in the days before infection. 10 of the 25 patients in the control group (4) presented increased CD64 index values during the study period.</p><p>Conclusions</p><p>The CD64 index might be a promising marker to detect LOS before infants demonstrate signs or symptoms of infection. However, larger prospective studies are needed to define optimal cut-off values and to investigate the role of non-infectious inflammation in this patient group.</p></div

Flow diagram of group allocation of the 50 infants enrolled in the study.

<p>During the study period (i.e. day of life 4 until day of life 28), 25 infants were evaluated for sepsis. Infants with septicemia represent the culture positive group (n = 7). Infants with clinical features of infection, a negative blood culture and antibiotic treatment for at least 5 days were allocated to the clinical sepsis group (n = 10) and infants with evaluation for sepsis who were subsequently proven not to be infected were allocated to the indeterminate group (n = 8). The control group consisted of the remaining 25 infants without sepsis evaluation.</p

Additional file 1: of The magnitude of antibiotic resistance to Helicobacter pylori in Africa and identified mutations which confer resistance to antibiotics: systematic review and meta-analysis

African countries included in the systematic search based on PubMed’s. (DOCX 25 kb

Cumulative incidence of infants with elevated CD64 index values during the observation period.

<p>A CD64 index greater than 1.86 was defined as the cut-off value for infection. Day 0 indicates the day of sepsis evaluation (i.e. day of diagnosis). The bars represent the percentage of infants with a positive CD64 index from the beginning of the observation period until the respective day. The differences between groups did not reach statistical significance.</p

Additional file 2: of The magnitude of antibiotic resistance to Helicobacter pylori in Africa and identified mutations which confer resistance to antibiotics: systematic review and meta-analysis

Academic Databases. (DOCX 26 kb

Median CD64 index values during the observation period.

<p>Median CD64 index was compared for every day during the observation period (day -4 until day +5) in the respective groups using the Mann-Whitney test. Median CD64 index was significantly higher on day +1 in the culture positive group compared to the clinical sepsis group (p <0.05; *) and significantly higher in the culture positive group compared to the indeterminate group on day +3 and day +4 (p <0.05; ‡). There was no difference in median CD64 index values between the clinical sepsis group and the indeterminate group. The dashed vertical line indicates the day of diagnosis (day 0). The numbers of samples for each data point are reported in Table 3.</p

Role of the Phosphatase PTEN in Early Vascular Remodeling

<div><p>Background</p><p>The phosphatase PTEN represents an important physiological inhibitor of phosphatidylinositol-3 kinase (PI3-K)/protein kinase B (Akt) signalling, however, the functional role of PTEN in the initial phase of angioplasty-induced vascular injury remains elusive. In the present study we sought to determine PTEN's effect on vascular smooth muscle cell (VSMC) apoptosis following acute injury <i>in vivo</i> and <i>in vitro</i>.</p> <p>Methods and Results</p><p>Immunohistochemistry indicated a faint basal expression and equal distribution of PTEN in uninjured rat carotid arteries. 12 h following balloon-injury, PTEN expression was strongly increased in apoptotic (TUNEL+) VSMC. In vitro, stimulation with serum or different growth factors or subjecting VSMC to cyclic stretch had no effect on PTEN expression, whereas stimulation with H₂O₂ robustly increased PTEN expression in a time- and dose-dependent manner. To evaluate the functional role of PTEN expression, human VSMC were transduced with WT-PTEN. Overexpression of PTEN increased the number of apoptotic VSMC (19.8%±4.4 vs. 5.6%±2.3; <i>P</i><0.001) as determined by TUNEL assay. In contrast, siRNA-mediated knock-down of PTEN attenuated the basal as well as H₂O₂-induced apoptosis of VSMC. Mechanistically, overexpression of PTEN prevented serum-induced Akt-phosphorylation, whereas siRNA-mediated knock down of PTEN augmented Akt-activation. Moreover, co-transfection of PTEN and a constitutive active Akt mutant prevented PTEN-dependent augmentation of VSMC apoptosis, indicating, that PTEN regulates VSMC apoptosis by inhibition of Akt phosphorylation/activation.</p> <p>Conclusion</p><p>By interfering with the PI3-K/Akt-dependent survival signalling, the oxidative stress-induced up regulation of PTEN in VSMC of injured arteries augments the sensitivity of VSMC to apoptotic stimuli in the early phase following vascular injury, augmenting the initial injury and cell loss of the injured vessel wall. Thus, these data add to our understanding of PTEN's role during vascular remodelling.</p> </div

Patients with rheumatoid arthritis have an altered circulatory aggrecan profile-4

From patients with Rheumatoid arthritis (RA) (lane 3) and the membrane was stained with the monoclonal antibody F-78 raised against intact bovine aggrecan, binding to G1 and G2, or with BC-3 raised against the aggrecanase-generated ARGSVI sequence. As control, plasma samples from 22 healthy individuals were used (lane 2). A standard molecular weight marker was also run to determine the size of the detected fragments (lane 1).<p><b>Copyright information:</b></p><p>Taken from "Patients with rheumatoid arthritis have an altered circulatory aggrecan profile"</p><p>http://www.biomedcentral.com/1471-2474/9/74</p><p>BMC Musculoskeletal Disorders 2008;9():74-74.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2426686.</p><p></p

Patients with rheumatoid arthritis have an altered circulatory aggrecan profile-6

, or treated with pro-inflammatory cytokines 10 ng/ml oncostatin M (OSM) in combination with 20 ng/ml tumour necrosis factor alpha (TNFα) (-◆-). The conditioned medium from four independent wells was measured for the presence of G1/G2 molecules at each collected time-point , or accumulated throughout the study-period. As negative control, explants were frozen and thawed four times in liquid nitrogen (--). The asterisks indicate significant differences (P < 0.05). For the statistical analysis, two-tailed non-parametric t tests were used.<p><b>Copyright information:</b></p><p>Taken from "Patients with rheumatoid arthritis have an altered circulatory aggrecan profile"</p><p>http://www.biomedcentral.com/1471-2474/9/74</p><p>BMC Musculoskeletal Disorders 2008;9():74-74.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2426686.</p><p></p

Patients with rheumatoid arthritis have an altered circulatory aggrecan profile-3

Thritis (RA) (N = 38) were analyzed in the G1/G2 assay. The concentrations are log-transformed data and the values are mean + SEM. The asterisks indicate significant differences (P < 0.05). For the statistical analysis, two-tailed non-parametric t-tests were used.<p><b>Copyright information:</b></p><p>Taken from "Patients with rheumatoid arthritis have an altered circulatory aggrecan profile"</p><p>http://www.biomedcentral.com/1471-2474/9/74</p><p>BMC Musculoskeletal Disorders 2008;9():74-74.</p><p>Published online 28 May 2008</p><p>PMCID:PMC2426686.</p><p></p