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Chronic intestinal failure patients (CIF) require a central venous access device (CVAD) to administer parenteral nutrition. Most serious complication related to a CVAD is a central line-associated bloodstream infection (CLABSI). The golden standard to diagnose a CLABSI are blood cultures, however, they may require 1–5 days before getting a result. Droplet digital polymerase chain reaction (ddPCR) for the detection of pathogen 16S/28S rRNA is a novel culture-independent molecular technique that has been developed to enhance and expedite infection diagnostics within two and a half hours. In this study, we prospectively compared ddPCR with blood cultures to detect pathogens in whole blood.

Both the initial trauma and the subsequent hemodynamic instability may contribute to intestinal damage, which is of great importance in (immunological) posttrauma complications. This study assesses intestinal damage using the biomarker intestinal Fatty Acid Binding Protein (iFABP) in trauma patients during the first days of their hospital admission and the risk factors involved. Plasma iFABP levels were measured in blood samples obtained from adult multiple trauma patients (n = 93) at the trauma scene by the Helicopter Emergency Medical Services, at arrival at the emergency department (ED), and at days 1, 3, 5, 7, 10, and 14 after trauma and related to injury severity and hemodynamic parameters. Plasma iFABP concentrations showed highest levels immediately after trauma at time points Helicopter Emergency Medical Services and ED. Nonsurvivors demonstrated higher iFABP levels at the ED compared with survivors. Furthermore, iFABP values at the ED correlated with Injury Severity Scores, and patients suffering from abdominal trauma demonstrated significantly higher iFABP concentrations in comparison with patients with other types of trauma or healthy controls. Also, patients presenting with a mean arterial pressure (MAP) less than 70 mmHg at the ED demonstrated significantly higher plasma iFABP concentrations in comparison with patients with a normal (70–99 mmHg) or high (>100 mmHg) MAP or healthy controls. Finally, patients with a low hemoglobin (Hb) (<80 of reference value) displayed significantly higher iFABP concentrations in comparison with patients with a normal Hb or healthy controls. Plasma iFABP levels, indicative of intestinal injury, are increased immediately after trauma in patients with abdominal trauma, low MAP, or low Hb and are related to the severity of the trauma. As intestinal injury is suggested to be related to late complications, such as multiorgan dysfunction syndrome or sepsis in trauma patients, strategies to prevent intestinal damage after trauma could be of benefit to these patients.

TGF is known to inhibit many of the immune cell functions including T cell proliferation and IL2 production. The mechanism of such TGFmediated inhibition of T cell functions is poorly understood. The present study examined the effects of TGF on the activation of protein tyrosine kinases PTK P56lck, P59fyn, and Zap70, and protein tyrosine phosphatases PTP SHP1 and SHP2. A balance between the actions of PTK and PTP is critical for appropriate T cell activation. These studies were carried out using nylon woolpurified splenic T cells from healthy SpragueDawley rats. Results from these studies showed that incubation of T cells with TGF inhibited the activation of P56lck, P59fyn, and Zap70. The decrease in these three protein tyrosine kinases was accompanied by an increase in the activation of the protein tyrosine phosphatase SHP1. There was no change in the phosphorylation of SHP2 with and without pretreatment of T cells with TGF. The decrease in P56lck, P59fynkinase activity, and Zap70 phosphorylation was prevented when T cells were stimulated with antiCD3 in the presence of pervanadate, an inhibitor of PTP. These results suggested that TGFmediated inhibition of P56lck, P59fyn, and Zap70 is likely due to an upregulation of protein tyrosine phosphatases such as SHP1.

The present study evaluated burninduced vascular permeability alterations of rat small intestine in vivoand assessed the effect of neutrophil depletion in burninjured rats on the altered intestinal microvascular permeability. 125IIabeled bovine serum albumin 125IBSA was injected intravenously, and its leakage from circulation into the intestinal tissue was determined by measuring tissue counts of 125IBSA. Compared with sham, vascular albumin permeability increased 1.7fold on day 1 postburn and 3.0fold on day 3 postburn in ileum. In the jejunum, albumin permeability increased 1.8 and 2.5fold on day 1 and day 3 postburn, respectively. Intestinal tissue edema, determined as increases in tissue water contents, was noted in both intestinal segments on day 1 postburn no further increase in edema was found on day 3 postburn. Neutrophil depletion before burn injury prevented the vascular leakage of albumin and edema in the ileum and jejunum on day 1 postburn. On day 3 postburn, the effect of prior neutrophil depletion on vascular permeability was less marked, and edema formation was not affected at all. These findings indicate that an absence of neutrophils prevents the loss of intestinal vascular barrier properties only in the initial periods after burns.