Production of consonants by prelinguistically deaf children with cochlear implants

Consonant production following the sensory restoration of audition was investigated in 22 prelinguistically deaf French children who received cochlear implants. Spontaneous speech productions were recorded at 6, 12, and 18 months post‐surgery and consonant inventories were derived from both glossable and non‐glossable phones using two acquisition criteria. The results showed that children initiated appropriate production of consonants after six months of implant use. Stops and labials were the most frequently produced speech sounds, whereas glides and palatals were still infrequent after 18 months. Speech accuracy also improved throughout the study. Consonant visibility appeared to influence the order of acquisition in the first months following the implantation and, as experience with auditory information increased, patterns of development tended to resemble those seen in children with normal hearing. Finally, a signed mode of communication and oral rehabilitation programs prior to implantation were better outcome predictors than age at implantation.     

Transient neutropenia increases macrophage accumulation and cell proliferation but does not improve repair following intratendinous rupture of Achilles tendon

Neutrophils are the first leukocytes to invade tendons after an acute injury. They could modulate both the inflammatory response and early repair processes through the release of reactive species, cytokines, growth factors, and proteinases. However, the exact role of these cells in damaged tendons remains unclear. We investigated their role by inducing a transient neutropenia in C57BL/6 male mice using an anti‐Ly6C/Ly6G antibody. Placebo mice received only serum. The right Achilles tendon was sectioned and sutured using the 8‐strand technique, which allowed immediate weight bearing. A significant increase in macrophage accumulation and cell proliferation was observed in tendons from neutropenic animals compared to the placebo group at days 3 and/or 7 postinjury. However, there was a reduction in cell proliferation in a group of mice depleted in macrophages, indicating that macrophages play a role in cell replication in injured tendons. Lastly, the tendons of neutropenic and placebo mice had similar collagen content and mechanical properties at days 7, 14, and/or 28 postinjury. Our findings demonstrate that neutropenia modulates macrophage accumulation and cell proliferation, but overall, a reduction in neutrophil number has no significant effect on tendon repair. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1084–1091, 2010     

Single nucleotide polymorphisms in the myostatin (MSTN) and muscle creatine kinase (CKM) genes are not associated with elite endurance performance

Maximal oxygen uptake (VO_2max) is one of the most important determinants of elite endurance performance. VO_2max is determined by a whole range of genetic and environmental factors. Single nucleotide polymorphisms (SNPs) in muscle myostatin (MSTN) and creatine kinase (CKM) genes are candidates for VO_2max and skeletal muscle performance phenotypes. Common MSTN (rs3791783, rs11681628 and rs7570532) and CKM (rs344816, rs10410448, rs432979, rs1133190, rs7260359, rs7260463 and rs4884) SNPs, selected from HapMap CEU data in order to tag the genetic variability of the proteins, were genotyped in 316 male Caucasian elite endurance athletes and 304 sedentary controls from the Genathlete study. Association with elite endurance performance was determined by logistic regression analysis. The P‐value for statistical significance was set at <0.01. None of the SNPs or haplotypes showed a significant association with elite endurance status. We conclude that common variants of MSTN and CKM genes do not play a role in attaining high‐level endurance performance in Caucasian populations.     

Silencing is Not-So Golden: A New Model for Inheritance of Lynch Syndrome

Heritable somatic methylation and inactivation of MSH2 in families with Lynch syndrome due to deletion of the 3' exons of TACSTD1
Ligtenberg et al. (2009)
Nature Genetics 41: 112–117