Nurses' Reactions to Difficult Patients

The purpose of this study was to determine whom nurses identify as difficult patients and how nurses might react to them emotionally and behaviorally. Participants (N = 73) responded to a self-report questionnaire that contained hypothetical situations involving difficult patients. Frustration and anger were the most common reactions. The traits or behaviors that nurses reported as belonging to the most difficult patients were characteristics that are potentially modifiable. In the majority of cases the nurses' reports of their reactions were classic fight/flight responses.     

Rat Cytomegalovirus Infection Interferes with Anti-CD4 mAb-(RIB 5/2) Mediated Tolerance and Induces Chronic Allograft Damage

In order to assess the role of heterologous immunity on tolerance induction (TI) by signal 1 modification, the influence of rat cytomegalovirus infection (RCMVI) on TI by a non-depleting monoclonal anti-CD4 mAb (monoclonal antibody) (RIB 5/2) in a rat kidney transplant (KTx) model was investigated. Orthotopic rat KTx (Dark Agouty (DA)-->Lewis (LEW)) was performed after TI with RIB 5/2 [10 mg/kg body weight (BW); day -1, 0, 1, 2, 3; i.p. (intraperitoneal route)]. RCMVI (5x10E5 Plaque forming units [PFU] i.p.) was simultaneously conducted to KTx, 50 days after KTx, and 14 days before and after KTx. RIB 5/2 induced robust allograft tolerance even across the high-responder strain barrier. RCMVI broke RIB 5/2-induced tolerance regardless of the time of RCMVI but did not induce acute graft failure during the 120 days follow-up. RCMVI induced a significant chronic deterioration of allograft function (p<0.01) and enhanced morphological signs of chronic allograft damage (p<0.05). Cellular infiltrates and major histo-compatibility complex (MHC)-expression were more pronounced (p<0.05) in the infected groups. RCMVI induced not only RCMV-specific T-cell response but also enhanced the frequency of alloreactive T cells. RCMV interferes with anti-CD4 mAb-induced tolerance and leads to chronic allograft damage. The data we presented suggest a potentially important role of viral infections and their prophylaxis in clinical TI protocols.     

Multi-phase approach to eradicate enzootic mouse coronavirus infection.

Infections with mouse coronavirus (also known as mouse hepatitis virus, MHV) are common and prompt concern because the adverse research effects of infection have been well documented. The animal facility we describe had contained an enzootic infection of mouse coronavirus for more than a decade. Eradication of the virus had been tried with limited success in the past. With an increase in the populations of immune-compromised and transgenic animals elsewhere in the facility, eradication of the virus became a high priority. The affected animals were in multiple breeding colonies comprising more than 4000 mice representing more than 50 site-specific strains, lines, and sublines. A task force designed to ensure representation of all interested parties developed a multi-phase approach which included (a) culling of nonessential animals, (b) cessation of breeding, (c) testing and culling of individual animals, and (d) cross-fostering to clean dams. To date, all of the strains, lines, and sublines manipulated through this multi-phase eradication approach continue to test negative for mouse coronavirus. This multi-phase approach may be useful for other institutions attempting to eradicate mouse coronavirus.     

The autoinhibitory feedback control of acetylcholine release in human neocortex tissue.

Slices of human neocortex prelabelled with [3H]choline were superfused and stimulated electrically (3 Hz, 2 ms, 24 mA) in order to investigate the autoreceptor-mediated modulation of acetylcholine (ACh) release. The concentration-response curve of the muscarinic agonist oxotremorine (pKd = 6.76 +/- 0.06), which was equipotent to ACh, was shifted to the right in a parallel manner by atropine (pA2 = 8.56 +/- 0.11), as evaluated by non-linear regression analysis. Calculation of the biophase concentration of ACh showed that no ACh could be assumed to be present under these conditions, whereas following inhibition of the acetylcholinesterase by physostigmine (0.1 microM) a biophase concentration of 10(-6.89 +/- 0.11) M was estimated. The depression of ACh release due to physostigmine and tacrine, another anticholinesterase, was antagonized by atropine. When the autoinhibition was operative atropine and the M2 subtype specific muscarinic antagonists, AF-DX 116 and methoctramine, significantly increased the release of ACh whereas the 'facilitatory' effects of the M1 and M3-specific drugs, pirenzepine and hexahydrosiladifenidol, were not significant. Although different disinhibitory effects of the subtype-specific antagonists were found, they did, however, not show a pattern which would allow a clear characterisation of the subtype of muscarinic receptor associated with the autoreceptor. The release of ACh from neocortex tissue of the (non-demented) neurosurgical patients decreased with their age. This finding is consistent with the hypothesis that the normal aging process resembles a delayed and attenuated disease process of senile dementia of Alzheimer's type.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bone density ligand, Sclerostin, directly interacts with LRP5 but not LRP5G171V to modulate Wnt activity.

We compared and contrasted the mechanism of action for the cysteine knot protein subfamily, Wise and Sost (Sclerostin). Our data suggest that functional interactions between Sost or Wise and LRP5/LRP6 have the potential to regulate bone deposition by modulating the Wnt pathway. INTRODUCTION: The human disease sclerosteosis exhibits an increase in bone mass thought to be caused by hyperactive osteoblasts. Sclerostin, SOST, the gene affected in this disease, has been postulated to exert its activity by functioning as a BMP antagonist. However, recent evidence indicates that SOST is highly related to Wise, which can also modulate the Wnt pathway by binding to LRP5 and LRP6. MATERIALS AND METHODS: For this study, we used cell culture to test the BMP and Wnt activity function of both Wise and Sost. In addition, we used Xenopus in vivo Wnt assays along with Xenopus in vitro Wnt assays to support our cell culture results. Epitope tagged cell supernatants containing either Sost or soluble mutant or wildtype LRP5/LRP6 were used for immunoprecipitation. Sost immunoprecipitation results were confirmed in vivo using cell culture. Finally, to support our in vitro data, we co-localized Sost, Wise, LRP5, and LRP6 in mouse long bone sections. Results: In this study, we report in vitro and in vivo evidence to show that Sost physically interacts with Lrp5 and Lrp6 and inhibits the canonical Wnt signaling pathway. Furthermore, using in vitro and in vivo assays, we showed that a variant of LRP5 (LRP5(G171V)) known to cause the human high bone mass (HBM) trait and a homologous change in LRP6 (LRP6(G158V)) abolished protein interactions with Sost. We used variants of Sost amino acids to further identify the contact points between Sost and LRP6. In Xenopus and mammalian cell culture assays, we showed that SOST is able to attenuate Wnt signaling and that this attenuation can be rescued by the addition of alpha-Sost antibodies or by the introduction of single amino acid substitution that alter its binding to LRP6. Sost differs from Wise in that it is unable to stimulate Wnt signaling. Using immunohistochemistry, we found that Sost and Wise are co-localized to osteoblasts, along with LRP5 and LRP6. CONCLUSIONS: Our data suggest that functional interactions between Sost or Wise and LRPs have the potential to regulate bone deposition by modulating Wnt signaling.     

The use of amorphous silicon flat panels as detector in neutron imaging.

A first test for neutron detection with a flat panel device based on the amorphous silicon technology is described in this report. The most important parameters defining the performance for neutron imaging are described. The first findings are encouraging for further improvements.     

Short Bowel Syndrome After Continence-Preserving Procedures

The short bowel syndrome (SBS) can result from a variety of conditions, including postoperative complications and malignancy. Continence-preserving operations are generally performed for either ulcerative colitis (UC) or familial polyposis (FAP). These procedures can be associated with high morbidity and the potential for future malignancy. Our aim was to determine the causes and consequences of SBS in patients undergoing these procedures. Twenty-four patients (12 men and 12 women) 18 to 64 years of age were identified with SBS after continence-preserving procedures. Eighteen had pelvic procedures, and six had continent ileostomies. All SBS patients had a proximal ostomy. Remnant length measured <60 cm in five patients, 60–120 cm in ten patients, and >120 cm in nine patients. Overall 13 patients required long-term PN. Four FAP patients with desmoid tumors died. One patient with UC underwent intestinal transplant and expired. Follow-up ranges from 6 to 192 months. Overall 14 patients had UC, nine had FAP, and one had functional disease. Eight patients with an initial diagnosis of UC had subsequent Crohn’s disease necessitating further resection and pouch excision. Eight patients (five with UC, two FAP, and one with functional disease) had postoperative complications, including obstruction or mesenteric ischemia requiring resections. One UC patient developed adenocarcinoma in a continent ileostomy. Seven of the nine FAP patients required resection for desmoid tumors. Six of these underwent resection alone. Three died at 10, 11, and 13 months after SBS from liver failure and sepsis while awaiting transplant. One patient has recurrent desmoid at 30 months, another is alive and well at 48 months, and the other patient, who was not a transplant candidate, died from an unrelated cardiac operation at 23 months. A single patient underwent resection with simultaneous multivisceral transplantation. SBS can develop after continence-preserving procedures. This occurs with inflammatory bowel disease when unsuspected Crohn’s disease is present or complications occur. SBS related to desmoid tumors has a poor prognosis in patients undergoing resection alone. A more aggressive approach to intestinal transplantation in these patients may be warranted.     

Limitations of CT during PET/CT.

Our aim was to determine the diagnostic limitations of low-dose, unenhanced CT scans performed for anatomic reference and attenuation correction during PET/CT. METHODS: The Radiology Information System at our oncologic hospital was queried during the 9-mo period from July 2002 to April 2003 for patients with PET/CT scans and diagnostic enhanced CT within 2 wk of each other. One radiologist interpreted the CT portion of the PET/CT (CT(p)) unaware of the PET results and the associated enhanced diagnostic CT (CT(d)). A medical student compared this interpretation with the official report of the CT(d) and listed all discrepancies between reports. A separate radiologist compared CT(p) and CT(d) images and classified true discrepant findings as due to lack of intravenous contrast, arm-position artifact, lack of enteric contrast, low milliamperage (mA), and quality of lung images. RESULTS: Among 100 patients, the most common malignancies were lymphoma (n = 37), cancer of the colorectum (n = 31), and esophageal cancer (n = 15). Among 194 true discrepancies in which findings were missed at CT(p), causes were as follows: (a) lack of intravenous contrast (128/194, 66%), (b) arm-down artifact (17/194, 9%), (c) quality of lung images (26/194, 13%), (d) lack of enteric contrast (15/194, 8%), and (e) low mA (8/194, 4%). Discrepancies were seen most commonly in detecting lymphadenopathy and visceral metastases. CONCLUSION: Most missed findings on the unenhanced CT portion of the PET/CT scans were due to technical factors that could be altered. Discrepant findings would have led to altered management in only 2 patients, suggesting a role for limited repeat imaging to reduce radiation and use of valuable resources.