Serum levels of vitamin D metabolites and the subsequent risk of colon and rectal cancer in Finnish men

Experimental and human epidemiologic data suggest a protective rolefor vitamin D in large bowel cancer. To investigate this association, weconducted a nested case-control study within a Finnish clinical trial cohort.Cases (n = 146) were participants diagnosed with primary adenocarcinoma ofthe large bowel. Controls were matched (2:1) to cases on age, date ofbaseline blood draw, and study clinic. Prediagnostic serum levels of thevitamin D metabolites, 25-hydroxyvitamin D (25-OH D), and1,25-dihydroxyvitamin D (1,25-DIOHD) were used as primary exposure measures.The baseline geometric-mean serum level of 25-OH D was 11.6 percent lower incases than in controls (12.2 cf 13.8 ug/l, P = 0.01) while serum levels of1,25-DIOH D did not differ by case-control status. No association was seenbetween serum levels of 1,25-DIOH D and large bowel cancer risk. However, theestimated relative risk (RR) of large bowel cancer decreased with increasinglevel of serum 25-OH D and the associa tion was more pronounced for rectalcancer (55 cases; RR by quartile = 1.00, 0.93, 0.77, 0.37; trend P = 0.06).Neither exclusion of early cases nor multivariate adjustment for potentialconfounders materially altered these estimates. There was no evidence ofeffect modification by level of 1,25-dihydroxyvitamin D or with other knownrisk-factors for large bowel cancer.     

Does body size contribute to sensitivity of bone tumor induction by radionuclide exposure?

Investigation of a possible increase in sensitivity to occurrence of radionuclide-induced skeletal malignancy with increasing body size was analyzed among 358 beagles injected as young adults with either 226Ra or monomeric 239Pu and maintained for their lifespans. Corresponding analyses were performed for about 240 other beagles injected as young adults with 90Sr, 228Ra, or 228Th. Body masses at the time of injection ranged between about 5.6 and 16 kg. Logistic regression analysis using body mass and cumulative skeletal radiation dose as the independent variables indicated that there could not be established a dependency of tumor occurrence upon body mass, although skeletal dose was found to be significantly correlated with occurrence of bone cancer. Regression analysis indicated that for any dosage group there could not be established a correlation between body mass and skeletal dose. Each dosage group having similar injected kBq kg(-1) for each nuclide was divided into 2 subgroups of equal size, one containing the less massive dogs and the other containing the more massive dogs. These subgroups within a roughly uniform value of skeletal dose-rate were compared by Fisher's Exact Test, and the less massive subgroups were combined within each nuclide for an additional, separate analysis against the combined more massive subgroups using the same method. In only one instance (the dosage group given 3607 kBq 90Sr kg(-1)) was there indicated a substantially greater tumor occurrence among dogs in the more massive subgroup (p = 0.061). However, for the group given 0.382 kBq 239Pu kg(-1) there was indicated a significant difference between subgroups, but the effect was exactly opposite to that found for the highest level 90Sr dogs in that the less massive subgroup had a higher relative tumor occurrence than the most massive (p = 0.042). For all groups with a p-value < 0.10, a possible correlation was investigated between survival and body mass at injection (since bone tumor occurrence might be a function of longevity), but a significant relationship could not be determined. No significant differences could be established between the combined more massive and the combined less massive subgroups for any radionuclide. We conclude that, for the conditions in our experiment, relative size within a species does not contribute importantly to the sensitivity (lifetime occurrence) for induction of skeletal malignancy.     

Use of a computerised maternity information system to improve clinical effectiveness: thromboprophylaxis at caesarean section

An audit of the introduction of a protocol for thromboprophylaxis at caesarean section revealed over treatment of low risk women and the under treatment of high risk women. A routine computer generated risk assessment profile was introduced as part of a maternity information system. Reaudit showed a significant improvement in adherence to the thromboprophylaxis protocol in all risk groups.     

High-resolution sonography of the abnormal cranial suture

Objective. The purpose of this investigation is to elucidate the sonographic features of abnormal major cranial sutures. Materials and methods. Eight excised synostosed suture specimens were evaluated. The high-resolution sonographic appearance was correlated with the histological section, plain radiographs, CT and MRI. Diastatic and molded sutures were also evaluated with sonography and compared with the normal cranial suture appearance. Results. Synostosed sutures demonstrated one or more of the following features: (a) loss of echo-poor fibrous gap between bony plates (five sagittal and coronal synostoses); (b) irregular thickened inner sutural margin (three lambdoid synostoses); (c) loss of bevelled edge (one lambdoid synostosis); (d) asymmetric anterior fontanelle (one coronal synostosis). Cranial molding results in an overlap of echogenic bony plates. Sutural width (the distance between bony plates) is increased in cases of elevated intracranial pressure. Conclusion. Sonography is an inexpensive, radiation-free modality which can confirm synostosis versus molding versus an underlying intracranial lesion as a cause of plagiocephaly. The high-resolution sonographic images also provide a relatively easy means to assess sutural width and may provide information in regard to increased intracranial pressure. Received: 24 March 1997 Accepted: 25 September 1997     

Split calvarial graft cranioplasty for the prevention of headache after retrosigmoid resection of acoustic neuromas

Objective: This study describes the technique and efficacy of split calvarial graft cranioplasty for the reconstruction of retrosigmoid/suboccipital defects following surgery for acoustic neuromas. Study Design: A prospective study of the technique of split calvarial graft cranioplasty, its postoperative healing, and incidence of postoperative headache. Methods: The technique requires splitting of the craniotomy bone flap into outer and inner table bone grafts. The combination of both bony grafts allows the coverage of a wider area of posterior fossa dura. This technique was used in 18 patients. All patients were followed for a minimum of 6 months. Eleven of 18 patients were followed for 1 year or longer. Four patients had three-dimensional computed tomography of their skull and area of split calvarial bone graft. Results: One of 18 patients had a persistent disabling headache at 1 year postoperatively. A natural contour of the retrosigmoid area was achieved in all patients. Three-dimensional computed tomography scan, obtained 6 months postoperatively, showed total coverage of the retrosigmoid area and fusion of the bone flap to the surrounding skull. Conclusion: The technique of split calvarial grafting of posterior fossa defects is a feasible, safe, and effective way of separating the nuchal musculature and posterior fossa dura. The technique also allows the restoration of the contour and bony covering of the retrosigmoid area. The technique is a simple alternative to other types of cranioplasties aimed at reducing the incidence of postoperative headache in patients with acoustic neuromas. Laryngoscope, 108:1450–1452, 1998     

Genotypic analysis of tumor suppressor genes PTEN/MMAC1 and p53 in head and neck squamous cell carcinomas

Objectives: Tumor suppressor gene mutations in both p53 and PTEN/MMAC1 genomic DNA have been detected in many types of cancer. The purpose of this study was to investigate the presence and importance of PTEN/MMAC1 mutations in squamous cell carcinomas. Methods: Exons of each gene were amplified after polymerase chain reaction (PCR) using genomic DNA derived from cell lines of squamous cell carcinoma of the head and neck (SCCHN) and snap-frozen biopsy specimens from primary established head and neck tumors. The amplified and purified DNA was then sequenced directly. Result: As anticipated, point mutations of the p53 gene were found in 80% of cell lines examined. A single base mutation in codon 151 was found in six of 10 cell lines studied. PTEN/MMAC1 gene mutations were found in neither the cell lines tested nor the tumor biopsy samples. Conclusion: This study, as well as a large volume of data, confirms that mutations of the p53 gene are frequent events in head and neck cancer cell lines. Although PTEN/MMAC1 gene mutations have been found in a variety of carcinomas, this gene was not found to be mutated in SCCHN cell lines or in primary squamous cell carcinomas of the head and neck. This information is useful for further studies of mutations in these cell lines. Laryngoscope, 108:1553–1556, 1998     

An early onset muscular dystrophy with diaphragmatic involvement, early respiratory failure and secondary alpha2 laminin deficiency unlinked to the LAMA2 locus on 6q22.

We present four subjects from one family and one subject (with an affected sibling who had died) from a second, unrelated family, with early onset, Duchenne-like, muscular dystrophy who presented with proximal girdle weakness, calf and generalized muscle hypertrophy, selective wasting of the sternomastoid muscles, rigidity of the spine and contractures of the tendo Achilles. Intellect was normal. Serum creatine kinase was grossly elevated and the muscle biopsies showed a dystrophic picture. All five subjects have developed early respiratory failure due to severe diaphragmatic involvement; two have already died aged 4 and 7 years of age and the remaining three are dependent on night time ventilation. There has been very little deterioration over time in the skeletal muscle function, and the survivors remain ambulant, the oldest being 11 years. Immunocytochemical studies of the muscle biopsy showed a normal pattern for dystrophin and the dystrophin-associated glycoproteins, but a reduction of the laminin alpha2 chain of merosin. Magnetic resonance imaging of the brain was normal. The disease did not link to the LAMA2 locus for laminin alpha2 on chromosome 6q, so that these families seem to represent a new form of autosomal recessive muscular dystrophy with a secondary merosin deficiency. The primary protein deficiency has not yet been identified.