Fear of aids: An assessment of knowledge and attitudes of medical,nursing, and medical technology students

The reluctance of students in health professions to care for AIDS patients is partially based on the perceived risk of transmission of HIV from patient contact. We hypothesize that fear of contagion is due to lack of knowledge and deep‐rooted attitudes and emotions existing even in areas of low HIV seroprevalence. We tested this hypothesis on medical, nursing, and medical technology students. Using a questionnaire that yielded four scales, results showed only 58% of students were knowledgeable, 81% were fearful of contagion, 57% were homophobic, and 8% had death anxiety. Lack of knowledge was correlated with fear of contagion (p < .05), whereas homophobia was weakly associated (p = .08). We conclude that this perceived risk of infection is a result of lack of knowledge, disbelief of the facts, and the interplay of personal values and emotions. Alternative educational methods are needed to increase students’ knowledge and to encourage students to examine their personal feelings and attitudes.     

Experimental investigation of the character of hypnosis

A backward masking paradigm was employed to test die hypothesis that high hypnotic susceptible Ss are able to process information at a faster rate than low susceptible Ss. The critical interstimulus interval was determined for 8 high and 8 low susceptible Ss. A t-test analysis of the critical interstimulus intervals showed a significant difference between high and low susceptible Ss with the high susceptible Ss showing a lower critical interstimulus interval. Mean critical interstimulus intervals for die high (76 milliseconds) and low (98 milliseconds) susceptible groups suggested that the high susceptible Ss were an average of 22 milliseconds faster at processing information. Results were interpreted as being consistent with, and providing support for attentional theories of hypnosis.     

Cognitive impairment in survivors of out-of-hospital cardiac arrest

Background

The huge importance of rapid provision of care, especially early defibrillation, for survival of out-of-hospital cardiac arrest (OHCA) is well known. This prospective cohort study investigated cognitive functioning of OHCA survivors in relation to the time-related elements of the resuscitation.

Methods

Fifty-seven consecutive survivors, from a cohort of 308 witnessed OHCA patients with ventricular fibrillation as the initial rhythm, underwent extensive neuropsychologic examination, including tests of memory, attention, and executive functioning, 6 months after the resuscitation. Time-related aspects of the resuscitation were collected on scene. Cognitive functioning was studied in relation to the administration of cardiopulmonary resuscitation (CPR) prior to ambulance arrival, and time from collapse to start of CPR, defibrillation, and return of spontaneous circulation (ROSC).

Results

Depending of the test, between 11% and 28% of survivors were cognitively impaired, while 58% scored unimpaired for all tests. Daily life activities were limited in 19% of the patients. Patients who received CPR prior to arrival of the ambulance showed a trend towards overall better cognitive functioning and significant better immediate memory and visuomotor tracking (P = .03 and P < .01). We found a weak correlation between the time to CPR, time to defibrillation, or time to ROSC and cognitive functioning.

Conclusions

The majority of survivors of OHCA with ventricular fibrillation as the initial rhythm are cognitively unimpaired. Long delays to ROSC are compatible with good cognitive outcome. Initiation and cessation of resuscitation efforts should not be based on the duration of circulatory arrest.     

Nylon-fiber-induced neutrophil fragmentation

We have investigated the effects of mechanical elution of neutrophils from nylon-wool fiber (NWF) using the scanning electron microscope and biochemical analysis of elution fractions. We have determined that mechanical removal of neutrophils from nylon-wool fiber disrupts neutrophils adherent to nylon-wool fiber and augments release of granules, release of peripheral cytoplasmic fragments, and release of lactic dehydrogenase, a soluble cytoplasmic enzyme. Mechanical shearing of the adherent cell, and not adherence per se, causes the fragmentation. The extent of fragmentation is proportional to the NWF surface area available to neutrophils and is maximal at the temperature for optimal adherence and spreading. Agents that decrease cell spreading (n-ethylmaleimide and cold) diminish fragmentation. Cytochalasin B, an agent that destabilizes the neutrophil cortex, increases fragmentation. Fragmentation may be an important contributing cause of the abnormal morphology, function, and in vivo survival of nylon-wool-fiber procured human neutrophils. The prevention of fragmentation would appear to be necessary to insure the procurement of optimally functioning cells. Elution of NWF-adherent neutrophils in the cold might be a practical way to diminish neutrophil damage during clinical filtration leukapheresis.     

Enhancement of chemotactic factor-stimulated neutrophil oxidative metabolism by leukotriene B4

Leukotriene B4 (LTB4) is a potent primary stimulator of neutrophil chemotaxis, aggregation, and degranulation and induces superoxide production at higher concentrations. In order to determine whether LTB4 modulates neutrophil responses to oxidative stimuli, human neutrophils (PMNs) were incubated with LTB4 prior to stimulation with f-Met-Leu-Phe (fMLP, 10(-7) mol/L), opsonized zymosan (OZ, 250 micrograms/mL), or phorbol myristate acetate (PMA, 32 nmol/L). Superoxide (O2-) production by stimulated PMNs was assessed by the superoxide dismutase-inhibitable reduction of cytochrome c. LTB4 alone did not stimulate O2- production in concentrations below 10(-7) mol/L and had no effect on the O2- assay. In the concentration range of 10(-12) to 10(-8) mol/L, LTB4 did not alter O2- release induced by OZ or PMA. In contrast, LTB4-treated cells demonstrated enhanced O2- production following exposure to fMLP, and in the presence of 10 nmol/LLTB4, generated 180% +/- 41% of O-2 quantities produced by control cells (n = 23). Enhancement was LTB4 dose-dependent, was maximal in the range of 1 to 10 nmol/L LTB4, was not reversed by removal of the lipid from the medium prior to fMLP stimulation, and was not dependent on the presence of Ca++ or Mg++ in the suspending medium. Chemiluminescence of fMLP-stimulated neutrophils was increased to 323% of controls in neutrophils preincubated with 10 nmol/L LTB4. Unlike augmentation of oxidative responses to fMLP seen with other degranulating stimuli, enhancement by LTB4 was not correlated with an increase in 3H-fMLP receptor binding. These results indicate that, in addition to its primary effects on neutrophil function, LTB4 modulates PMN oxidative responses to the chemotactic peptide and, thus, may amplify the release of oxygen metabolites at inflammatory foci.     

In vivo expression of the B7 costimulatory molecule by subsets of antigen-presenting cells and the malignant cells of Hodgkin's disease

The B-lymphocyte/accessory-cell activation antigen B7 (BB1) has been shown in vitro to stimulate T-lymphocyte proliferation and cytokine production via CD28 present on the latter cells. In this study, benign lymphoid tissues, lymphomas, and extralymphoid inflammatory sites were examined immunohistochemically using anti-B7 and other relevant monoclonal antibodies. B7 was expressed by benign transformed germinal center B cells, as it was by B cells of follicular lymphomas. B7 was also expressed by a subpopulation (a mean of 31% to 65%) of macrophages and dendritic cells in a variety of lymphoid tissues. It was present in abundance on all macrophages constituting sarcoid granulomas in lymph nodes. In extralymphoid inflammation, 17% to 35% of macrophages expressed B7 only weakly. Cases of Hodgkin's disease showed expression of B7 by the majority of Reed-Sternberg cells or malignant mononuclear variants, a phenomenon that potentially contributes to the lymphocytic accumulation that is a feature of this condition. CD28+ T cells were seen in all areas where T cells were present. B7+ and CD28+ cells colocalized in, for example, lymphoid follicles, lymph node paracortex, sarcoid granulomas, and Hodgkin's disease tissue, indicating a potential for cellular interaction via these molecules at these sites.     

Normal synthesis and expression of endothelial IIb/IIIa in Glanzmann's thrombasthenia

Glanzmann's thrombasthenia is a bleeding disorder, inherited in an autosomal recessive way and characterized by an absence or deficiency of the platelet glycoprotein (GP) IIb/IIIa complex. Recently, we and others demonstrated that cultured human umbilical vein endothelial cells synthesized a membrane protein complex similar to the platelet GP IIb/IIIa complex. In this article, we demonstrate that endothelial cells isolated from the umbilical vein of a newborn with Glanzmann's thrombasthenia, as compared with normal endothelial cells, show no difference in their ability to synthesize and express this GP IIb/IIIa complex. Our results indicate that Glanzmann's thrombasthenia is not accompanied by an "endotheliopathy."     

A humanised tissue‐engineered bone model allows species‐specific breast cancer‐related bone metastasis in vivo

Bone metastases frequently occur in the advanced stages of breast cancer. At this stage, the disease is deemed incurable. To date, the mechanisms of breast cancer‐related metastasis to bone are poorly understood. This may be attributed to the lack of appropriate animal models to investigate the complex cancer cell–bone interactions. In this study, two established tissue‐engineered bone constructs (TEBCs) were applied to a breast cancer‐related metastasis model. A cylindrical medical‐grade polycaprolactone‐tricalcium phosphate scaffold produced by fused deposition modelling (scaffold 1) was compared with a tubular calcium phosphate‐coated polycaprolactone scaffold fabricated by solution electrospinning (scaffold 2) for their potential to generate ectopic humanised bone in NOD/SCID mice. While scaffold 1 was found not suitable to generate a sufficient amount of ectopic bone tissue due to poor ectopic integration, scaffold 2 showed excellent integration into the host tissue, leading to bone formation. To mimic breast cancer cell colonisation to the bone, MDA‐MB‐231, SUM1315, and MDA‐MB‐231BO breast cancer cells were cultured in polyethylene glycol‐based hydrogels and implanted adjacent to the TEBCs. Histological analysis indicated that the breast cancer cells induced an osteoclastic reaction in the TEBCs, demonstrating analogies to breast cancer‐related bone metastasis seen in patients.     

The Brief State Rumination Inventory (BSRI): Validation and Psychometric Evaluation

Depressive rumination is an emotion regulation strategy that is considered a major risk factor for depression and other emotional disorders. While well-established measures of trait rumination are available, a psychometrically sound measure of state rumination is lacking. We report on the development and validation of a new self-report measure, the Brief State Rumination Inventory (BSRI), in both Dutch and English. In Study 1, we report the results of a multi-group confirmatory factor analysis across three independent samples (n?=?155; n?=?141; n?=?199). The analysis supported the unidimensionality and measurement invariance of the 8-item BSRI. We also examined its construct validity, showing that scores on the BSRI were positively related to measures of negative affect, trait rumination, and symptoms of depression and anxiety. Scores were negatively related to adaptive emotion regulation strategies and to positive affect. In Study 2 (n?=?60), we demonstrated the measure’s sensitivity to an experimental manipulation of rumination. Taken together, these findings suggest that the BSRI is a quick-to-administer, valid, and reliable measure of state rumination.