Staging and prognostic factors in carcinoma of the base of the tongue.

During the period 1966-1985, 66 patients were submitted for curative treatment of a carcinoma of the base of the tongue in the Netherlands Cancer Institute. Treatment consisted of radiotherapy (59 patients), surgery and post-operative radiotherapy (4 patients) and surgery alone (3 patients). Patients were staged according to the UICC (1982) and UICC (1987)/AJCC (1988) criteria. Regrouping by the latter system caused enlargement of the N2-group and of stage IV. The crude 5-year survival was 22%, the 5-year tumour control was 36% and the locoregional control was 47%. The most important prognostic factors for the tumour-free interval are the T-category (P = 0.01) and stage grouping (UICC 1982) (P = 0.022). The same factors predict the locoregional control (P = 0.005 and 0.02 respectively). Crude survival is lower in smokers, and in patients in poor general condition (P = 0.04 and 0.007 respectively).     

The ubiquitin ligase Rnf6 regulates local LIM kinase 1 levels in axonal growth cones

LIM kinase 1 (LIMK1) controls important cellular functions such as morphogenesis, cell motility, tumor cell metastasis, development of neuronal projections, and growth cone actin dynamics. We have investigated the role of the RING finger protein Rnf6 during neuronal development and detected high Rnf6 protein levels in developing axonal projections of motor and DRG neurons during mouse embryogenesis as well as cultured hippocampal neurons. RNAi-mediated knock-down experiments in primary hippocampal neurons identified Rnf6 as a regulator of axon outgrowth. Consistent with a role in axonal growth, we found that Rnf6 binds to, polyubiquitinates, and targets LIMK1 for proteasomal degradation in growth cones of primary hippocampal neurons. Rnf6 is functionally linked to LIMK1 during the development of axons, as the changes in axon outgrowth induced by up- or down-regulation of Rnf6 levels can be restored by modulation of LIMK1 expression. Thus, these results assign a specific role for Rnf6 in the control of cellular LIMK1 concentrations and indicate a new function for the ubiquitin/proteasome system in regulating local growth cone actin dynamics.     

Preoperative embolization in surgical treatment of a primary hemangiopericytoma of the rib: a case report

Primary hemangiopericytoma of the rib is extremely rare and only a few cases have been reported. A 62-yr-old man presented with an aching chest pain and dyspnea. Thoracic computed tomography revealed a homogenous mass expanding the right seventh rib. A diagnosis of hemangiopericytoma was established by percutaneous needle biopsy. Preoperative embolization of the feeding vessels of the tumor was performed in order to prevent perioperative bleeding. There was no significant bleeding during the surgery, where complete resection of the tumor with 7th to 9th ribs with a surgical margin of 5 cm was performed. Postoperative course was uneventful and there has been no recurrence for thirteen months. To our knowledge, there has been no report to apply a preoperative embolization of a primary hemangiopericytoma of the rib.     

Fourteen novel OPA1 mutations in autosomal dominant optic atrophy including two de novo mutations in sporadic optic atrophy

The OPA1 gene, encoding a dynamin-related GTPase that plays a role in mitochondrial biogenesis, is implicated in most cases of autosomal dominant optic atrophy (ADOA). Sixty-nine pathogenic OPA1 mutations have been reported so far. Most of these are truncating mutations located in the GTPase domain coding region (exons 8-16) and at the 3'-end (exons 27-28). We screened 44 patients with typical ADOA using PCR-sequencing. We also tested 20 sporadic cases of bilateral optic atrophy compatible with ADOA. Of the 18 OPA1 mutations found, 14 have never been previously reported. The novel mutations include one nonsense mutation, 3 missense mutations, 6 deletions, one insertion and 3 exon-skipping mutations. Two of these are de novo mutations, which were found in 2 patients with sporadic optic atrophy. The recurrent c.2708_2711delTTAG mutation was found in 2 patients with a severe congenital presentation of the disease. These results suggest that screening for OPA1 gene mutations may be useful for patients with optic atrophy who have no affected relatives, or when the presentation of the disease is atypical as in the case of early onset optic atrophy.     

Byssinosis in carpet weavers exposed to wool contaminated with endotoxin

All the 303 full time day workers in a carpet weaving factory were submitted to a physical examination, chest radiography, and vitalograph test, and answered a respiratory questionnaire. Fifty four healthy non-exposed subjects served as controls. Dust concentrations and concentrations of bacterial endotoxin were measured. Of the 303 workers, 259 (85.5%) had airway symptoms and 62 (20.5%) had maximum mid-expiratory flow (MMF) values of less than 60% compared with 9.2% of the controls. The symptoms in 68 workers (22%) were compatible with byssinosis and 36 of these workers underwent vitalography before starting work and after four hours work on Mondays when significant reductions of their FEV1 and MMF were found. Twenty one of these 36 workers were tested on Tuesday and no differences in these measurements were found between measurements before work started and four hours later. The airborne dust concentrations in the factory were high and bacterial endotoxin was found. These findings suggest that a large number of workers in this carpet weaving factory suffer from a disease indistinguishable from byssinosis even though wool is used almost exclusively, the only cotton being the warp. The finding of endotoxin together with the absence of cotton confirms the theory that "byssinosis" is due to bacterial endotoxin rather than to cotton per se.     

Residential exposure to magnetic fields: an empirical examination of alternative measurement strategies

OBJECTIVES: To investigate the impact of measuring a single home then imputing information from another home among subjects who lived in two homes in a subset of the National Cancer Institute/Children's Cancer Group (NCI/CCG) investigation of residential exposure to magnetic fields and risk of childhood leukaemia. METHODS: Each subject's summary time weighted average (TWA) exposure was derived from measurements of two homes, weighted by the fraction of the reference period lived in the residence. The three cost efficient field work strategies examined were measuring: (a) the longer lived in home; (b) the currently lived in home; and (c) the former lived in home. Two different methods were used for imputing the missing values: (a) control mean imputation, (b) status specific mean imputation. The subject's summary exposure to magnetic fields estimated with each approach was compared with the subject's TWA calculated from measurements in both homes. The association between estimated exposure to magnetic fields and the risk of leukaemia under different approaches was examined with unconditional logistic regression analysis. RESULTS: The Pearson correlation coefficient between the two measurements within subjects was 0.31 (p < 10(-4), indicating a lack of independence of measurements. Differences were found between mean exposures in current and former homes of cases, and between longer and shorter lived in homes of controls. All methods with measurements from one of the homes in conjunction with imputation of measurements for the second home led to marked attenuation of risk estimates at the highest exposure category, particularly when measurements from current homes were used and those from former homes were imputed. CONCLUSION: Results argue against attempting to estimate lifetime magnetic field exposure from imputed values derived from current residences to fill in gaps caused by unmeasured residences previously lived in.