Telomere shortening and chromosomal instability are believed to play an important role in the development of myeloid neoplasia. So far, published data are only available on the average telomere length in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML), but not on the telomere length of individual chromosomes. We used a new technique, telomere/centromere-fluorescence in situ hybridization (T/C-FISH), which combines fluorescence R-banding and FISH using a probe against the telomere repeats to measure the telomere length of each chromosome arm in 78 patients with MDS. In line with the previous results, patients with MDS showed significantly shorter telomeres than those of healthy controls. Telomere lengths did not differ significantly between distinct morphological subtypes of MDS. However, there was a significant difference in telomere length between patients with an isolated monosomy 7 and patients with a normal karyotype (P < 0.05). Notably, patients with an isolated monosomy 7 showed significantly longer telomeres than patients with a normal karyotype in many chromosome arms, among them 7p and 7q. Neo-telomeres were found in two patients with a complex karyotype, in one case at the fusion site of a dic(14;20). Normal and aberrant metaphases of the same patient did not differ in telomere length, thus indicating to telomere shortening as a basic mechanism affecting all hematopoietic cells in patients with MDS. In some MDS subtypes, like MDS with isolated monosomy 7, telomeres may be stabilized and even increase in length because of the activation of telomerase or alternative mechanisms.

Total hip replacement (THR) and total knee arthroplasty (TKA) carry a high risk of postoperative venous thromboembolism (VTE); therefore, anticoagulation prophylaxis is recommended in these patients. Unfortunately, there are no guidelines about VTE prophylaxis in patients with hemophilia who underwent these high-risk surgeries. To determine whether these patients have high risk of VTE, we conducted a retrospective study on patients with hemophilia who underwent elective THR/TKA at our institute from 2004 to 2012. Postoperatively, we collected information on duration and method of factor VIII/IX infusion, VTE-prophylaxis, and complications. There were 23 patients with hemophilia, 18 (78%) with hemophilia A and 5 (22%) with hemophilia B, who underwent high-risk surgeries (39% THR and 61% TKA). The VTE prophylaxis included sequential compression device, 12 (52%), and prophylactic enoxaparin, 1 (4%). Ten (43%) patients did not receive VTE prophylaxis. At 1-year follow-up, we did not find any evidence of clinical VTE in our patients. Better risk stratification is needed to identify patients who would benefit from pharmacological prophylaxis.

Schools of education must prepare teachers to meet the myriad needs of the diverse learners in today' s classrooms. Ms. Holm and Ms. Horn discuss the essential components of a preparation program that will equip teachers to know and understand who their students are and how they learn.

The etiology of multisomatoform disorder (MSD) is largely unknown, but genetic disposition may be one of several risk factors. As pain is a major component of MSD, and polymorphisms in the catechol-O-methyltransferase (COMT) gene are associated with COMT enzymatic activity and pain sensitivity, we assumed that COMT polymorphisms could be associated with MSD. One hundred and forty-nine patients with MSD and 149 age- and sex-matched healthy controls participated in this study. The inclusion criteria for MSD were in accordance with the structured clinical interview of the diagnostic and statistical manual of mental disorders IV. DNA from MSD patients and controls was genotyped for six single-nucleotide polymorphisms (SNPs) within the COMT locus by polymerase chain reaction and restriction enzyme analysis. The distribution of COMT SNP alleles, genotypes, and haplotypes was compared between patients and controls. None of the investigated SNPs, including the functionally relevant common SNP in codon 158 (Val158Met), showed a statistically significant allelic, genotypic, or haplotypic association with MSD. We conclude that COMT polymorphisms on their own do not seem to play a relevant role as major genetic risk factors for MSD.

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