Muscular weakness in the mdx mouse.

mdx mice are believed to be virtually free from neuromuscular symptoms, despite the presence of a degenerative/regenerative process that involves all skeletal muscles. We analyzed both the spontaneous motility and treadmill motor activity of mdx mice aged 15 days to 6 months. Our results indicate that there is an early period, between the end of the second and up to the fifth week of life, when mdx mice experience extreme weakness. After this critical period, both spontaneous motility and endurance of mdx mice, although lower than those of controls, do not show statistically significant differences up to 6 months of age. We also carried out a detailed histological analysis of proximal and distal muscle groups in mdx mice during this early critical motility period. The occurrence of extensive necrosis followed by regeneration and involving proximal muscles before distal ones was documented in mice as young as 16-17 days of age and reached a peak at day 18. We conclude that dystrophin deficiency induces muscle degeneration and significant weakness in mdx mice, but only in an early period. Later on, during development, mdx mice adapt to the lack of this protein and do not show detectable in vivo functional muscle impairment up to 6 months of age

Genetic and clinical characteristics of skeletal and cardiac muscle in patients with lamin A/C gene mutations

Alterations of the lamin A/C (LMNA) gene are associated with different clinical entities, including disorders that affect skeletal and cardiac muscle, peripheral nerves, metabolism, bones, and disorders that cause premature aging. In this article we review the clinical and genetic characteristics of cardiac and skeletal muscle diseases related to alterations in the LMNA gene. There is no single explanation of how LMNA gene alterations may cause these disorders; however, important goals have been achieved in understanding the pathogenic effects of LMNA gene mutations on cardiac and skeletal muscle

LncRNA colon cancer-associated transcript 1 (CCAT1) in ovarian cancer

We read the study published by Lai et al1 with great interest. The complex nature of neoplastic transformation has an enormous impact at various moments of the cancer diagnostics and therapy protocols. Sophisticated individualized therapeutic approaches, supported by an increasing use of tumorspecific molecular tests, are now available2,3. In particular, more details are necessary among molecular differences of primary lesion and its metastases, because these are frequently responsible for the failure of systemic therapy4-6. In this contest, the study published by Lai and Cheng represent an interesting approach in order to study the molecular mechanism of metastasis and proliferation in ovarian cancer (OC). In OC, more than in other types of tumors, morphologic diagnosis is no more sufficient to obtain a qualified therapeutic decision; therefore, the use of new molecular markers is mandatory to improve the clinical management of this type of cancer7. The authors of this study, for the first time, observed that the LncRNA colon cancer-associated transcript 1 (CCAT1) promotes OC proliferation and metastasis