Therapy of posterior and posterolateral knee instability

The natural course after posterior cruciate ligament (PCL) tear is a slow process of degeneration starting in the medial compartment. Functional disability is mainly present in those instabilities that are combined with posterolateral insufficiency. The surgical treatment at present mainly addresses these combined types of posterior-posterolateral instability. It is generally agreed that suture of the torn PCL alone is insufficient and augmentation with autologous structures, such as the patellar ligament, are mandatory. Synthetic augmentation to facilitate after treatment is another adjunct. Because of the difficulty of precise tibial tunnel placement a two-stage procedure is advocated, an anterior approach with the patient supine being used for femoral graft placement. If a posterior approach with the patient prone is used, a straight posterior incision is made between the two heads of the gastrocnemius and the neuromuscular bundle. With this approach the tibial bone block is placed in a trough. The accuracy of graft placement and the immediate functional aftertreatment facilitated by the use of osseous fixation of a synthetic augmentation device at both ends have made better results of surgical reconstruction of the PCL possible.     

Predictors of brief smoking intervention in a midwifery setting

The aims of this study were: to assess current practice in smoking cessation interventions by midwives and to examine the relationship between the use of smoking intervention, practitioner characteristics and organizational factors. A mail-out survey was sent to a random sample of 500 midwives. The response rate was 85% (n = 425). The results indicated that most midwives used minimal interventions (advice and education) for at least some of their clients. However, the more skilled and more time-intensive forms of intervention such as counselling about methods to quit, negotiating a quit date and follow-up were infrequently utilized. Moreover, participants estimated that half their smoking clients were not offered any advice about smoking. Organizational factors such as: hospital policy for smoking intervention, type of hospital, size of hospital, cohesion of staff and work pressure predicted the use of smoking interventions. Self-reported ability to intervene for smoking and the level of assessment undertaken were practitioner characteristics which predicted the use of smoking interventions. The barriers that inhibit the use of smoking intervention by midwives are discussed and methods for change canvassed.     

Noradrenaline contractions of human prostate mediated by alpha 1A-(alpha 1c-) adrenoceptor subtype

1. The subtype of alpha 1-adrenoceptor mediating contractions of human prostate to noradrenaline was characterized by use of a range of competitive and non-competitive antagonists. 2. Contractions of the prostate to either noradrenaline (pD2 5.5), phenylephrine (pD2 5.1) or methoxamine (pD2 4.4) were unaltered by the presence of neuronal and extraneuronal uptake blockers. Noradrenaline was about 3 and 10 times more potent than phenylephrine and methoxamine respectively. Phenylephrine and methoxamine were partial agonists. 3. Pretreatment with the alkylating agent, chlorethylclonidine (10(-4M) shifted the noradrenaline concentration-contraction curve about 3 fold to the right and depressed the maximum response by 31%. This shift is 100 fold less than that previously shown to be produced by chlorethylclonidine under the same conditions on alpha 1B-adrenoceptor-mediated contractions. 4. Cumulative concentration-contraction curves for noradrenaline were competitively antagonized by WB 4101 (pA2 9.0), 5-methyl-urapidil (pA2 8.6), phentolamine (pA2 7.6), benoxathian (pA2 8.5), spiperone (pA2 7.3), indoramin (pA2 8.2) and BMY 7378 (pA2 6.6). These values correlated best with published pKi values for their displacement of [3H]-prazosin binding on membranes expressing cloned alpha 1c-adrenoceptors and poorly with values from cloned alpha 1b- and alpha 1d-adrenoceptors. 5. The good correlation between the functional data on the prostate and the binding data on the expressed alpha 1c-subtype clone for the affinities of the competitive antagonists suggests that they are the same subtype. As the expressed alpha 1c-adrenoceptor clone corresponds to the alpha 1A-adrenoceptor expressed in tissues, contraction of the human prostate to noradrenaline is therefore mediated by an alpha 1A-adrenoceptor.     

Circulating activated endothelial cells in sickle cell anemia

BACKGROUND: The vascular wall participates in the pathogenesis of sickle cell disease. To determine whether the endothelium is activated in this disease, we studied the number, origin, and surface phenotype of circulating endothelial cells in patients with sickle cell anemia. METHODS: We used immunohistochemical examination of buffy-coat smears to enumerate circulating endothelial cells, and we evaluated the surface phenotype by applying preparations of circulating endothelial cells. An immunofluorescence microscopy panel of antibodies was used, including a specific anti-endothelial-cell antibody, P1H12. RESULTS: Mean (+/-SD) numbers of circulating endothelial cells in normal blood donors, patients with sickle cell trait, and patients with hemolytic anemias not due to hemoglobin S were 2.6+/-1.6, 3.0+/-2.6, and 2.0+/-0.8 per milliliter of whole blood, respectively. Patients with sickle cell anemia who presented with acute painful episodes had 22.8+/-18.2 circulating endothelial cells per milliliter of blood (P<0.001 for the comparison with normal donors), and patients with no such events within one month before or after blood sampling had 13.2+/-11.8 circulating endothelial cells per milliliter of blood (P=0.002 for the comparison with normal donors and P=0.019 for the comparison with patients with acute events). Serial observations of three patients showed a tendency toward higher levels of circulating endothelial cells at the onset of acute painful crises. The average viability of circulating endothelial cells was 66+/-30 percent. In patients with sickle cell anemia, regardless of clinical status, the circulating endothelial cells were predominantly microvascular in origin (CD36-positive), and most of the cells expressed four markers of endothelial-cell activation: intercellular adhesion molecule 1, vascular-cell adhesion molecule 1, E-selectin, and P-selectin. CONCLUSIONS: Our studies suggest that the vascular endothelium is activated in patients with sickle cell anemia, regardless of the patients' clinical status. Adhesion proteins on activated endothelial cells may have a role in the vascular pathology of sickle cell disease.     

Effects of hippocampal and parietal cortex lesions on memory for egocentric distance and spatial location information in rats

To assess the working memory system for egocentric distance and place information, delayed matching-to-sample (DMTS) go/no-go tasks were run for each rat. To assess the reference memory system, and to serve as a control for nonmemory deficits, successive discrimination go/no-go tasks were then conducted using the same rats. Rats with hippocampal, but not parietal cortex, lesions were impaired relative to controls in the working memory (DMTS) task for both egocentric distance and place information, although the deficit observed in the working memory task for egocentric distance information by rats with hippocampal lesions was mild. Neither hippocampal nor parietal cortex lesioned rats were impaired relative to controls in the reference memory (successive discrimination) task for either cue. The hippocampus appears to be involved in working memory for egocentric distance and in spatial location information, whereas the parietal cortex is not.     

An Epstein-Barr virus-associated superantigen

More than 90% of adults are latently infected with Epstein-Barr virus (EBV), the causative agent of infectious mononucleosis, a self-limiting lymphoproliferative disease characterized by extensive T cell activation. Reactivation of this herpesvirus during immunosuppression is often associated with oncogenesis. These considerations led us to analyze the early events that occur after exposure of the immune system to EBV. Strong major histocompatibility complex (MHC) class II-dependent but not MHC-restricted, T cell proliferation was observed in vitro in response to autologous, lytically infected EBV-transformed B cells. By measuring the appearance of the early activation marker CD69 on individual T cell V beta subsets, we could demonstrate selective activation of human V beta 13- T cells. This was confirmed with murine T cell hybridomas expressing various human BV genes. While EBV- Burkitt's lymphoma cells were nonstimulatory, they induced V beta-restricted T cell activation after EBV infection. EBV specific activation was also demonstrated in cord blood cells, excluding a recall-antigen response. Thus, all of the characteristics of a superantigen-stimulated response are seen, indicating that induction of the EBV lytic cycle is associated with the expression of a superantigen in B cells. A model is presented proposing a role for the superantigen in infection, latency, and oncogenesis.