The development of an accredited bowel-management course

Bowel management--particularly digital rectal examination (DRE) and the manual removal of faeces--has been a contentious issue for some time. In the past few years this has been brought to the fore by a number of cases of professional misconduct by nurses.     

Cognitive status and development in the oldest old: a longitudinal analysis from the Heidelberg Centenarian Study

In the present study, we investigated cognitive status, cognitive development and the effect of mortality on cognitive changes in very old age. Analyzing data from the population-based Heidelberg Centenarian Study, results revealed that centenarians differed quite strongly in their cognitive capacities. While about half of the population showed moderate to severe cognitive impairment, one quarter was found to be cognitively intact. Moreover, analyzing cognitive change over a period of 1.5 years, centenarians' cognitive performance was revealed to be rather stable. Finally, only a small effect of mortality on cognitive status and changes was detected, supporting a recent hypothesis that the terminal decline or drop in cognitive functioning decreases in very old age.     

Allogenic blood transfusion does not predispose to infection after cardiac surgery

Background

Many retrospective studies report increased postoperative infection after allogenic blood transfusion. To investigate this phenomenon, we prospectively studied 232 patients undergoing cardiac surgery.

Methods

Patients were screened daily for evidence of culture positive infections. Wounds were examined daily and defined on the ASEPSIS score. Chest radiographs and white cell counts and differentials were recorded on days 1, 2, and 4. The use of blood products was monitored blindly and independently. Patients were grouped according to transfusion status and compared using χ² or Fisher's test. Logistic regression analyses were performed to identify predictors of transfusion and infection.

Results

Of 232 patients, 116 (50%) received blood product transfusion. Patients receiving blood had lower preoperative hemoglobin, were older, with a greater proportion of urgent/emergency or revision surgery, and were higher risk. Despite this, there were no differences in the frequency of chest infection (20% versus 15%, p = 0.38), urinary infection (3.5% versus 5.3%, p = 0 0.75), wound infection (3.5% versus 8.0%, p = 0.16), or overall infection (28% versus 30%, p = 0.89) comparing the transfused versus untransfused groups. There was no evidence to suggest that administration of blood products was associated with infection (odds ratio 0.92, p = 0.77).

Conclusions

The administration of blood per se did not lead to increased postoperative infection. Clinicians should reconsider withholding blood transfusion in patients solely owing to concerns of predisposition to infection.     

An initial experience: using helical CT imaging to detect obscure gastrointestinal bleeding

Obscure gastrointestinal (GI) bleeding is a common but frustrating disease for clinicians because of its elusive nature despite extensive work-up. We evaluate the role of helical computed tomography (CT) imaging using rapid infusion of intravenous contrast and water as oral contrast in the work-up of patients who are actively bleeding. Helical CT may be a useful noninvasive, alternative study to consider when routine work-up fails to determine the cause of active GI bleeding. Our preliminary study shows that helical CT was able to identify a wide variety of causes of obscure GI bleeding.     

Caspase-1 is not required for type 1 diabetes in the NOD mouse

Interleukin (IL)-1 beta and IL-18 are two cytokines associated with the immunopathogenesis of diabetes in NOD mice. Both of these cytokines are cleaved by caspase-1 to their biologically active forms. IL-1 is a proinflammatory cytokine linked to beta-cell damage, and IL-18 stimulates production of interferon (IFN)gamma in synergy with IL-12. To examine the effects produced by caspase-1 deficiency on diabetes development in NOD/Lt mice, a disrupted Casp1 gene was introduced by a speed congenic technique. Casp1(-/-) bone marrow-derived macrophages stimulated with lipopolysaccharide produced no detectable IL-18, fourfold lower IL-1 beta, and 20-30% less IL-1 alpha than macrophages from wild-type Casp1(+/+) or Casp1(+/-) controls. Unexpectedly, despite reduced IL-1 and IL-18, there was no change in the rate of diabetes or in total incidence as compared with that in wild-type NOD mice. IL-1 reportedly makes an important pathological contribution in the multidose streptozotocin model of diabetes; however, there was no difference in sensitivity to streptozotocin between NOD mice and NOD.Casp1(-/-) mice at 40 mg/kg body wt or at 25 mg/kg body wt dosage levels. These findings show that caspase-1 processing of IL-1 beta and IL-18 is not absolutely required for mediation of spontaneous or chemically induced diabetes pathogenesis in the NOD mouse.     

Activation of Syk in neutrophils by antineutrophil cytoplasm antibodies occurs via Fcgamma receptors and CD18

Antineutrophil cytoplasm antibodies (ANCA) activate TNF-alpha-primed neutrophils to undergo a respiratory burst. The intracellular signals that mediate activation have not been studied extensively but could increase the understanding of the pathogenesis small vessel vasculitis. It was demonstrated that ANCA-IgG induced phosphorylation of the tyrosine kinase Syk in TNF-alpha-primed neutrophils from healthy donors. Syk was not phosphorylated in response to ANCA F(ab')(2). Furthermore, Syk phosphorylation was attenuated by blockade of both low-affinity Fcgamma receptors and CD18. Similarly, low-affinity Fcgamma receptor blockade reduced ANCA-induced superoxide production. In patient-derived neutrophils, the high-affinity Fcgamma receptor FcgammaRI was also demonstrated to be involved in ANCA-induced superoxide production. However, Syk phosphorylation was not attenuated by blockade of the FcgammaRI, present on neutrophils from vasculitis patients. The tyrosine kinase inhibitor 4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine inhibited the ANCA-induced respiratory burst and Syk phosphorylation, suggesting that Src kinases lie upstream of Syk activation but downstream of ANCA engagement of Fcgamma receptors. Piceatannol, another tyrosine kinase inhibitor, also inhibited ANCA-induced Syk phosphorylation and the ANCA-stimulated respiratory burst, supporting the proposed functional role for Syk in ANCA signaling. ANCA-induced phosphorylation of Cbl and intracellular calcium transients, potential downstream mediators of Syk activation, were also blocked by tyrosine kinase inhibitors. While it has previously been shown that pertussis toxin diminishes the ANCA-induced respiratory burst, indicating heterotrimeric G protein involvement, Syk phosphorylation and calcium transients were unaffected by pertussis toxin. Collectively, these data show that Syk phosphorylation is induced during ANCA-triggered neutrophil activation.