Fracturas vertebrales: evaluación, diagnóstico y tratamiento: Revisión del tema / Vertebral fractures: evaluation, diagnosis and treatment: Review

Las fracturas vertebrales son una de las fracturas más comunes relacionadas a la fragilidad ósea y son causa de morbilidad importante. Sin embargo la epidemiología de las fracturas vertebrales difiere de las fracturas osteoporóticas en otros sitios esqueléticos, ya que solo una tercera parte de las fracturas vertebrales son reconocidas clínicamente y detectadas al realizar una metodología de imagen apropiada, ya que un alto porcentaje presenta FV asintomáticas, las cuales no son detectadas hasta realizar una radiografía simple de columna dorso-lumbar. Por otro lado la identificación de una fractura vertebral como aguda o crónica, benigna o maligna, hace que el médico tratante presente diferentes estrategias terapéuticas. El objetivo de este artículo de revisión es dar al lector información sobre la epidemiología, los costos, los tipos de fracturas vertebrales, que ocurre con las fracturas vertebrales en las enfermedades reumatológicas, como realizar una evaluación radiográfica de las fracturas vertebrales, la identificación acorde a las diferentes metodologías por imagen, y como es el tratamiento adecuado de las mismas.

Vertebral fractures are one of the most common fractures associated with skeletal fragility and can cause as much morbidity. However, the epidemiology of vertebral fractures differs from that of osteoporotic fractures at other skeletal sites in important ways, largely because only one-third of vertebral fractures are recognized clinically at the time of their occurrence and they require lateral spine imaging to be recognized. In otherwise the identification of vertebral fractures as acute or chronic, benign or malignant, is important for the physician to apply the more appropriate treatment. The objective of this paper is review points as epidemiology, cost, types of vertebral fractures, what happens in rheumatological diseases, the importance of different imaging technique, and review the more appropriate treatment.

Can prosody aid the automatic classification of dialog acts in conversational speech?

Identifying whether an utterance is a statement, question, greeting, and so forth is integral to effective automatic understanding of natural dialog. Little is known, however, about how such dialog acts (DAs) can be automatically classified in truly natural conversation. This study asks whether current approaches, which use mainly word information, could be improved by adding prosodic information. The study is based on more than 1000 conversations from the Switchboard corpus. DAs were hand-annotated, and prosodic features (duration, pause, F0, energy, and speaking rate) were automatically extracted for each DA. In training, decision trees based on these features were inferred; trees were then applied to unseen test data to evaluate performance. Performance was evaluated for prosody models alone, and after combining the prosody models with word information--either from true words or from the output of an automatic speech recognizer. For an overall classification task, as well as three subtasks, prosody made significant contributions to classification. Feature-specific analyses further revealed that although canonical features (such as F0 for questions) were important, less obvious features could compensate if canonical features were removed. Finally, in each task, integrating the prosodic model with a DA-specific statistical language model improved performance over that of the language model alone, especially for the case of recognized words. Results suggest that DAs are redundantly marked in natural conversation, and that a variety of automatically extractable prosodic features could aid dialog processing in speech applications.

Decreased TET2 gene expression during chronic myeloid leukemia progression.

Recently it has been demonstrated that ten-eleven-translocation-2 (TET2) gene alterations may represent a crucial event in the pathogenesis of various myeloid malignancies. To date, the loss of TET2 function has been solely ascribed to mutations in the gene coding region. In this study, we report a chronic myeloid leukemia (CML) case showing a TET2 single copy partial deletion associated to a t(4;6;11) rearrangement, appearing during the progression of the disease and responsible for a decreased TET2 gene expression. A putative role for TET2 haploinsufficiency in this patient's CML progression is discussed.

Genomic segmental duplications on the basis of the t(9;22) rearrangement in chronic myeloid leukemia.

A crucial role of segmental duplications (SDs) of the human genome has been shown in chromosomal rearrangements associated with several genomic disorders. Limited knowledge is yet available on the molecular processes resulting in chromosomal rearrangements in tumors. The t(9;22)(q34;q11) rearrangement causing the 5'BCR/3'ABL gene formation has been detected in more than 90% of cases with chronic myeloid leukemia (CML). In 10-18% of patients with CML, genomic deletions were detected on der(9) chromosome next to translocation breakpoints. The molecular mechanism triggering the t(9;22) and deletions on der(9) is still speculative. Here we report a molecular cytogenetic analysis of a large series of patients with CML with der(9) deletions, revealing an evident breakpoint clustering in two regions located proximally to ABL and distally to BCR, containing an interchromosomal duplication block (SD_9/22). The deletions breakpoints distribution appeared to be strictly related to the distance from the SD_9/22. Moreover, bioinformatic analyses of the regions surrounding the SD_9/22 revealed a high Alu frequency and a poor gene density, reflecting genomic instability and susceptibility to rearrangements. On the basis of our results, we propose a three-step model for t(9;22) formation consisting of alignment of chromosomes 9 and 22 mediated by SD_9/22, spontaneous chromosome breakages and misjoining of DNA broken ends.