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OBJECTIVE: To report a superior sagittal sinus thrombosis occurring as a rare complication of neck dissection, and to present a review of published literature. CASE REPORT: A 42-year-old man underwent an elective neck dissection for a tumour stage 2, node stage 2b, tonsillar squamous cell carcinoma, prior to chemoradiotherapy. During surgery, the right internal jugular vein was sacrificed as part of the resection, as tumour was adherent to it. Two weeks after surgery, the patient was readmitted with seizures. Subsequent computed tomography and magnetic resonance venography confirmed a superior sagittal sinus thrombosis. The patient was subsequently anticoagulated and underwent radiotherapy without further complication. A review of pre-operative imaging indicated a dominant internal jugular vein, ligation of which may have been a factor in the subsequent sagittal sinus thrombosis. CONCLUSION: Superior sagittal sinus thrombosis following neck dissection is a rare occurrence, with little reported in the literature. Dominant internal jugular vein anatomy may be evident on pre-operative imaging. An awareness of this complication may be helpful to surgeons contemplating sacrifice of the internal jugular vein.

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This report details a rapid method for screening the entire p53 coding region (exons 2-11). This method, based on the non-isotopic RNase cleavage assay, uses novel primer sequences and an adaptation of the MutationScreener method. A mutation in 20% of the sample was easily detectable by this method, whereas mutations below 50% were undetectable using the original method. Alterations to the wild-type p53 mRNA sequence were found in nine of the 130 patients with low grade lymphoproliferative disorders screened, and this was confirmed by DNA sequencing in eight of eight samples. The method is a simple and reliable technique for screening for p53 mutations.

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Samples from 51 chronic lymphocytic leukaemia (CLL) patients (42 typical, nine atypical) were assessed for in vitro response to fludarabine and cladribine (2-CdA) using the flow cytometric terminal deoxynucleotidyl transferase (TdT) assay. No difference was demonstrated between the in vitro response of typical and atypical CLL and previous treatment did not result in a more apoptosis resistant phenotype. The assay could not distinguish those patients who required subsequent treatment from those whose disease remained stable, and universal cross-resistance/sensitivity to the two purine analogues was demonstrated. The assay's potential for use in the rapid assessment of in vivo response to purine analogue therapy in CLL was limited; correctly predicting the clinical outcome of 10/12 patients to treatment but failing to predict progression in two p53 deficient patients. The level of bcl-2 in the clonal lymphocytes did not influence the in vitro, spontaneous or drug-induced, apoptosis.

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131 patients with lymphoproliferative disorders were classified as having typical Chromic Lymphocytic Leukaemia [CLL], atypical CLL, Chromic Lymphocytic Leukaemia/Prolymphocytic Leukaemia [CLL/PL] or Non-Hodgkin's Lymphoma [NHL] using immunophenotyping and morphology. The incidence of trisomy 12 (+12) in each of the groups was ascertained using fluorescent in situ hybridization. Trisomy 12 was found to be rare in the typical CLL group (<3%) and more common in the atypical CLL (22%), CLL/PL (40%) and NHL (43%) categories. The low incidence of +12 in the typical CLL group is most likely due to our adherence to strict inclusion criteria to ensure other similar lymphoproliferative disorders, with a high incidence of +12, were excluded. This approach leads to more homogeneous disease categories and consequently may help to resolve issues such as the impact on survival of +12 in CLL.

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The existence of subpopulations of clonal lymphocytes in patients with low grade lymphoproliferative disorders, with regard to both cell size and bcl-2 protein concentration is reported. Flow cytometric analysis showed that the lymphocytes with higher levels of bcl-2 corresponded to a subset of larger lymphocytes. Statistical analysis suggested that the increased concentration of bcl-2 was not accounted for by the increase in cell size and it is possible that these cells form a functionally distinct component of the clonal proliferation. One patient, analysed in greater detail during treatment with a purine analogue, showed the subpopulations to exhibit a differential sensitivity to chemotherapy.

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We report a case of acute myeloid leukaemia (AML), FAB classification M2, associated with tetrasomy 8. This chromosomal aberration was detected using conventional cytogenetics and flourescent in-situ hybridization (FISH). Using FISH, the pre-treatment cells with tetrasomy 8 were disomic for chromosome 7. A small number of tetrasomy 8 cells were found post-treatment, but these were tetrasomic for chromosome 7. The significance of this is considered, and the literature regarding tetrasomy 8 in acute myeloid leukaemia is reviewed.

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The enzyme Terminal Deoxynucleotidyl Transferase (TdT) is a DNA polymerase which can be used to label DNA strand breaks by the incorporation of a labelled nucleotide followed by a fluorescent detection step. The amount of label incorporated can then be assessed by flow cytometry. The mechanism of action of TdT, however, will allow the addition of varying numbers of nucleotides to the free 3' termini produced by DNA strand breaks. The substitution of Digoxigenin (DIG) labelled dideoxy-nucleotides for labelled deoxy-nucleotides in the TdT assay will limit the addition of label to a DNA break to a single nucleotide, thus ensuring a direct relationship between an increase in DNA strand breaks and an increase in fluorescence. We have used this adaptation of the TdT Assay to evaluate DNA damage incurred in lymphocytes, from patients with Chronic Lymphocytic Leukaemia (CLL), on exposure to UV irradiation and apoptosis-inducing drugs, fludarabine and 2-Chloro-2'-deoxyadenosine (2-CdA). This technique may give a good indication of the susceptibility of CLL patients to apoptosis inducing drugs, and hence an indication of the likely response to these therapies.

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The transforming growth factor beta s (TGF-beta s) are a group of multifunctional growth factors which inhibit cell cycle progression in many cell types. The TGF-beta-induced cell cycle arrest has been partially attributed to the regulatory effects of TGF-beta on both the levels and the activities of the G1 cyclins and their kinase partners. The activities of these kinases are negatively regulated by a number of small proteins, p21 (WAF1, Cip1), p27Kip1, p16, and p15INK4B, that physically associate with cyclins, cyclin-dependent kinases, or cyclin-Cdk complexes. p21 has been previously shown to be transcriptionally induced by DNA damage through p53 as a mediator. We demonstrate that TGF-beta also causes a rapid transcriptional induction of p21, suggesting that p21 can respond to both intracellular and extracellular signals for cell cycle arrest. In contrast to DNA damage, however, induction of p21 by TGF-beta is not dependent on wild-type p53. The cell line studied in these experiments, HaCaT, contains two mutant alleles of p53, which are unable to activate transcription from the p21 promoter when overexpressed. In addition, TGF-beta and p53 act through distinct elements in the p21 promoter. Taken together, these findings suggest that TGF-beta can induce p21 through a p53-independent pathway. Previous findings have implicated p27Kip1 and p15INK2B as effectors mediating the TGF-beta growth inhibitory effect. These results demonstrate that a single extracellular antiproliferative signal, TGF-beta, can act through multiple signaling pathways to elicit a growth arrest response.

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Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor, thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand. Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated by a single receptor complex consisting of R4 and the type II receptor.

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Transforming growth factor beta (TGF-beta) is a multifunctional factor that regulates many aspects of cellular functions. TGF-beta signals through a heteromeric complex of the type I and type II TGF-beta receptors. However, the molecular mechanism of signal transduction by this receptor complex remains unresolved. The type II receptor belongs to a transmembrane receptor serine-threonine kinase family. A new member of this receptor family (R4) was identified and shown to be a functional TGF-beta type I receptor on the basis of its ability to restore a TGF-beta-induced gene response in mutant cell lines lacking endogenous type I receptor. Both ligand binding and signaling of the R4 protein were dependent on the presence of a functional type II receptor. The type I receptor has an intrinsic serine-threonine kinase activity, which was essential for signal transduction.

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Cells obtained from the blood or bone marrow of patients with haematological malignancies can both be stained with fluorescent labelled monoclonal antibodies to determine an immunophenotype and permeabilized with 30% ethanol then stained with propidium iodide for simultaneous DNA analysis. In the technique described here, no evidence of selective depletion of the malignant cell population was demonstrated and decreases in the mean fluorescence intensity of the surface markers were insufficient to affect the sensitivity of flow cytometric analysis. The combined method is simple and robust enough to allow incorporation of DNA analysis into routine immunophenotyping of leukaemia and lymphoma cells.

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Films made from cationic surfactants and well-retained redox catalysts were investigated. Full loading of metal phthalocyaninetetrasulfonates (MPcTS4-) into water-insoluble dialkyldimethylammonium surfactants by ion exchange from aqueous solutions yielded coatings on electrodes that retain these catalyst ions for 1-2 weeks in electrolyte solutions. In contrast, partly loaded films lost most MPcTS4- ions in a few hours. All films showed gel-to-liquid crystal phase transitions at temperatures characteristic of surfactant bilayers. Cross-sectional views by SEM showed layers of 0.1-0.2 micron, as well as some disordered regions. Each larger layer is probably made up of stacks of many molecular bilayers. Retention of MPcTS4- ions seems related to their dimerization. Dimers of MPcTS4- associated with ammonium head groups may crosslink adjacent surfactant bilayers. The MPcTS4- ions that enhance stability in these films are also good redox catalysts.

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Traumatic anterior perineal hip dislocation with an associated fracture of the femoral head is a rare entity. A 26-year-old man injured in a motorcycle accident was treated by closed reduction of the dislocation within three hours after admission. However, several reports of patients with anterior hip dislocation with associated femoral head fractures were treated nonoperatively and had unfavorable results when treatment failed to achieve anatomical position of the fragments. Consequently, this patient was treated by open reduction and internal fixation of the fractured fragment. Follow-up examination three and one-half years after the operation showed painless functional range of hip motion with only minimal discomfort after prolonged exertion.

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A case report of pneumonia secondary to aspiration of povidone-iodine, which was used as an oral preoperative antiseptic, is presented. Associated morbidity is described, along with suggested preventive measures.

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