Nerve-responsive troponin I slow promoter does not respond to unloading.

We examined the regulation of the troponin I slow (TnIs) promoter during skeletal muscle unloading-induced protein isoform transition, by using a transgenic mouse line harboring the -4,200 to +12 base pairs region of the human TnIs promoter. Eighteen female transgenic mice ( approximately 30 g body mass) were randomly divided into two groups: weight-bearing (WB) controls (n = 9) and hindlimb unloaded (HU; n = 9). The HU mice were tail suspended for 7 days. Body mass was unchanged in the WB group but was reduced (-6%; P < 0.05) after the HU treatment. Absolute soleus muscle mass (-25%) and soleus mass relative to body mass (-16%) were both lower (P < 0.05) in the HU group compared with the WB mice. Northern blot analyses indicate that 7 days of HU result in a 64% decrease (P < 0.05) in the abundance of endogenous TnIs mRNA (microg/mg muscle) in the mouse soleus. Furthermore, there is a trend for the abundance of the fast troponin I mRNA to be increased (+34%). Analysis of transgenic chloramphenicol acetyltransferase activity in the soleus muscle revealed no difference (P > 0.05) between WB and HU groups. We conclude that additional elements are necessary for the TnIs gene to respond to an unloading-induced, slow-to-fast isoform transition stimulus.

Spinal injury at the level of the third and fourth cervical vertebrae from football.

Acute traumatic lesions of the spine at the third and fourth cervical levels without associated fracture are not common. The eight lesions in this report occurred as a result of injuries sustained during tackle football. They included acute intervertebral disc herniation, anterior subluxation of the third cervical vertebra on the fourth, unilateral dislocation of the joint between the articular processes, and bilateral dislocation of the joints between the articular processes. The mechanism of injury was the use of the top or crown of the helmet as the primary point of contact in a high-impact collision when blocking, tackling, or head-butting. To avoid a seemingly inevitable increase in the incidence of these lesions occurring from tackle football, coaches and officials will have to modify the current techniques of blocking tackling, and head-butting.

National Operating Committee on Standards for Athletic Equipment football helmet certification program.

Wayne State University, Department of Neurosurgery, was contracted in 1971 by NOCSAE to develop voluntary standards for football helmets. Preliminary tests of representative football helmets on cadavers and the Z-90 metal head form showed that a more realistic head model was necessary before it was possible to understand helmet performance. A synthetic model was developed which approached human cadaver performance and at the same time was more rugged and repeatable than a cadaver head. A test method was devised and a human tolerance limit of 1500 Severity Index based on resultant CG head accelerations was adopted as the performance standard. All new football helmets available for use in high school and college football have now been certified by the NOCSAE standard and the wearing of such helmets is mandatory for college players in 1978 and high schools in 1980. By means of design or material changes, certified helmets on the NOCSAE tests are performing at a Severity Index of 1/2 those posted by prestandard models, on the average. Experience with the equipment at a helmet reconditiong plant shows that 25% of precertified helmets being received are rejected and 84% of the remainder are testing on the front location (most critical) above a Severity Index of 1450, and should be replaced as soon as possible with certified helmets.

An Assessment of Compressive Neck Loads Under Injury-Producing Conditions.

Injury reference curves for axial compressive forces on the neck were derived from impact tests of a spring-loaded tackling block on football helmets. Results suggest that helmets, especially those with resilient liners, reduce these forces.

Transcription occurs in pulses in muscle fibers.

We report a novel mechanism of gene regulation in skeletal muscle fibers. Within an individual myofiber nucleus, not all muscle loci are transcriptionally active at a given time and loci are regulated independently. This phenomenon is particularly remarkable because the nuclei within a myofiber share a common cytoplasm. Both endogenous muscle-specific and housekeeping genes and transgenes are regulated in this manner. Therefore, despite the uniform protein composition of the contractile apparatus along the length of the fiber, the loci that encode this structure are not transcribed continuously. The total number of active loci for a particular gene is dynamic, changing during fetal development, regeneration, and in the adult, and potentially reflects the growth status of the fiber. The data reveal that transcription in particular stages of muscle fiber maturation occurs in pulses and is defined by a stochastic mechanism.