Attitudes of College Football Officials Regarding NCAA Mouthguard Regulations and Player Compliance

The National Collegiate Athletic Association (NCAA) mandates the use of brightly colored, intraoral mouth- guards by football players to reduce the frequency and severity of craniofacial and intraoral morbidity and mortality, and to enhance the ability of officials to observe player compliance. The purpose of this 12-question mail survey was to determine the attitudes of on-Held game officials regarding current NCAA mouthguard regulations and patterns of utilization by college football players. The sample consisted of all 50 Big East Football Conference officials; a response rate of 100 percent was achieved. Only 42 percent of the officials reported observing all players in compliance, and quarterbacks were identified by others as the least compliant group (52%). The majority (88%) indicated that the 1990 rule for brightly colored mouthguards had been beneficial to them in determining player compliance, and 52 percent reported that this rule had resulted in more frequent use by these athletes. Nearly all officials (96%) indicated that they would issue a warning for noncompliance to the player or coach, rather than charging a timeout for a violation as prescribed by NCAA regulations. The majority (70%) believe current enforcement is appropriate, but expressed the opinion that coaches should be held more accountable for player compliance.     

Identification of cathepsin C mutations in ethnically diverse papillon-Lefèvre syndrome patients

INTRODUCTION—Papillon-Lefèvre syndrome (PLS) is an autosomal recessive disorder characterised by palmoplantar keratoderma and severe, early onset periodontitis, which results from deficiency of cathepsin C activity secondary to mutations in the cathepsin C gene. To date, 13 different cathepsin C mutations have been reported in PLS patients, all of which are homozygous for a given mutation, reflecting consanguinity.
AIM—To evaluate the generality of cathepsin C mutations in PLS, we studied an ethnically diverse group of 20 unrelated families.
METHODS—Mutations were identified by direct automated sequencing of genomic DNA amplified for exonic regions and associated splice site junctions of the cathepsin C gene. Long range PCR was performed to determine the genomic structure of the cathepsin C gene.
RESULTS—The cathepsin C gene spans over 46 kb, with six introns ranging in size from 1.6 to 22.4 kb. Eleven novel mutations and four previously reported mutations were identified in affected subjects from 14 families. Missense mutations were most common (9/15), followed by nonsense mutations (3/15), insertions (2/15), and deletions (1/15). Among these 14 probands, two were compound heterozygotes. Affected subjects with transgressions of the dermal lesions onto the knees or elbows or both had mutations in both the pro- and mature regions of the enzyme, although most were in the mature region.
CONCLUSION—Mutations in the mature region of cathepsin C were more likely to be associated with the transgressions of the dermatological lesions, although the results were not statistically significant. A comprehensive list of all cathepsin C mutations described to date, representing 25 mutations from 32 families with PLS and related conditions, is also presented.


Keywords: cathepsin C; genetics; severe early onset periodontitis; hyperkeratosis     

Localisation of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation

Prepubertal periodontitis (PPP) is a rare and rapidly progressive disease of young children that results in destruction of the periodontal support of the primary dentition. The condition may occur as part of a recognised syndrome or may occur as an isolated finding. Both autosomal dominant and recessive forms of Mendelian transmission have been reported for PPP. We report a consanguineous Jordanian family with four members affected by PPP in two nuclear sibships. The parents of the affected subjects are first cousins. We have localised a gene of major effect for PPP in this kindred (Zmax=3.55 for D11S901 at θ=0.00) to a 14 cM genetic interval on chromosome 11q14 flanked by D11S916 and D11S1367. This PPP candidate interval overlaps the region of chromosome 11q14 that contains the cathepsin C gene responsible for Papillon-Lefèvre and Haim-Munk syndromes. Sequence analysis of the cathepsin C gene from PPP affected subjects from this Jordanian family indicated that all were homozygous for a missense mutation (1040A→G) that changes a tyrosine to a cysteine. All four parents were heterozygous carriers of this Tyr347Cys cathepsin C mutation. None of the family members who were heterozygous carriers for this mutation showed any clinical findings of PPP. None of the 50 controls tested were found to have this Tyr347Cys mutation. This is the first reported gene mutation for non-syndromic periodontitis and shows that non-syndromic PPP is an allelic variant of the type IV palmoplantar ectodermal dysplasias.


Keywords: prepubertal periodontitis; periodontal disease; cathepsin C; linkage     

To die or not to die for neurons in ischemia,traumatic brain injury and epilepsy: a review on the stress-activated signaling pathways and apoptotic pathways

After a severe episode of ischemia, traumatic brain injury (TBI) or epilepsy, it is typical to find necrotic cell death within the injury core. In addition, a substantial number of neurons in regions surrounding the injury core have been observed to die via the programmed cell death (PCD) pathways due to secondary effects derived from the various types of insults. Apart from the cell loss in the injury core, cell death in regions surrounding the injury core may also contribute to significant losses in neurological functions. In fact, it is the injured neurons in these regions around the injury core that treatments are targeting to preserve. In this review, we present our cumulated understanding of stress-activated signaling pathways and apoptotic pathways in the research areas of ischemic injury, TBI and epilepsy and that gathered from concerted research efforts in oncology and other diseases. However, it is obvious that our understanding of these pathways in the context of acute brain injury is at its infancy stage and merits further investigation. Hopefully, this added research effort will provide a more detailed knowledge from which better therapeutic strategies can be developed to treat these acute brain injuries.     

A microsatellite-based,physically anchored linkage map for the gray,short-tailed Opossum (<Emphasis Type="Italic">Monodelphis domestica</Emphasis>)

The genome of the gray, short-tailed opossum, Monodelphis domestica, will be the first of any marsupial to be fully sequenced. The utility of this sequence will be greatly enhanced by construction and integration of detailed genetic and physical maps. Therefore, it is important to verify the unusual recombinational characteristics that were suggested by the ‘first-generation’ M. domestica linkage map; specifically, very low levels of recombination and severely reduced female recombination, both of which are contrary to patterns in other vertebrates. We constructed a new linkage map based on a different genetic cross, using a new and much larger set of map markers, and physically anchored and oriented the linkage groups onto chromosomes via fluorescence in-situ hybridization mapping. This map includes 150 loci in eight autosomal linkage groups corresponding to the eight autosome pairs, and spans 86–89% of the autosomal genome. The sex-averaged autosomal map covers 715 cM, with a full-length estimate of 866 cM; the shortest full-length linkage map reported for any vertebrate. The sex-specific maps confirmed severely reduced female recombination in all linkage groups, and an overall F/M map ratio =  0.54. These results greatly extend earlier findings, and provide an improved microsatellite-based linkage map for this species. Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Production and characterization of murine models of classic and intermediate maple syrup urine disease

Background  

Maple Syrup Urine Disease (MSUD) is an inborn error of metabolism caused by a deficiency of branched-chain keto acid dehydrogenase. MSUD has several clinical phenotypes depending on the degree of enzyme deficiency. Current treatments are not satisfactory and require new approaches to combat this disease. A major hurdle in developing new treatments has been the lack of a suitable animal model.     

Development of dopamine innervation and turning behavior in dopamine-depleted infant rats receiving unilateral nigral transplants

Three-day-old rats were bilaterally dopamine-depleted with 6-hydroxydopamine and 3 days later cell suspensions derived from the dopamine-rich ventral mesencephalic area were injected into the right rostral striatum. The transplants rapidly developed a substantial innervation of one striatum, so that by 15 days after transplantation (21 days of age) animals rotated away from the reinnervated side in response to amphetamine. The amount of turning correlated with the extent of innervation of the striatum as determined by tyrosine hydroxylase immunocytochemistry. By 25 days post-transplantation (31 days of age), animals turned in response to stress as well as amphetamine, although this later-developing phenomenon was not associated with any significant change in the extent of dopamine innervation.

A second group of animals was bilaterally dopamine-depleted at 3 days of age, but transplantation with nigral cell suspensions was delayed until maturity. Partial reinnervation of the rostral striatum occurred with this delayed transplant paradigm, and turning to both amphetamine and stress commenced at 15 days post-transplantation. In contrast to animals receiving transplants shortly after lesioning, these animals began to turn spontaneously at about 20 days post-transplantation. The serotonin hyper-innervation that occurs following dopamine depletion in infancy was not altered by dopamine transplants made at either time.

Results from both groups of transplant animals suggest that dopamine-rich transplants can provide substantial innervation that exerts some functional control over the striatum. This occurs despite the fact that neonatally dopamine-depleted rats, unlike adult-lesioned animals, survive quite well in the absence of striatal dopamine. However, the degree of incorporation into existing circuitry, and the types of regulation that result, may vary considerably depending on the age at which the tissue is transplanted.     

Four-color flow cytometric analysis of peripheral blood donor cell chimerism

Passenger leukocytes have been demonstrated to play significant roles in initiating and also regulating immune reactions after organ transplantation. Reliable techniques to detect donor leukocytes in recipients after organ transplantation are essential to analyze the role, function, and behavior of these leukocytes. In this report we describe a simple, reliable method to detect donor cells with low frequencies using peripheral blood samples. Detection of small numbers of major histocompatibility complex (MHC) mismatched cells was first studied using four-color flow cytometry in artificially created cell mixtures. By selecting the CD45(+) population and simultaneous staining with several leukocyte lineage markers (CD3, CD4, CD8, CD56, and CD19), MHC-mismatched leukocytes were consistently detected in cell suspensions prepared from directly stained whole blood samples with a threshold sensitivity as low as 0.1%-0.2%. When the fresh peripheral blood mononuclear cells were separated by conventional Ficoll gradient purification, similar, but slightly lower levels of donor cells were detected. Blood samples obtained 1-5 months after liver, kidney, and intestine transplants revealed that the kind of organ allograft influenced levels and lineage pattern of the circulating donor cells. This procedure provided a simple and reliable method in determining early chimerism in transplant recipients. However, the detection of MHC-mismatched leukocytes of all lineages was much lower when frozen peripheral blood mononuclear cells were used.     

Vaccinia virus stimulates the growth of vesicular stomatitis virus at the level of protein synthesis in mouse L cells

Coinfection with vaccinia virus increases the growth of vesicular stomatitis virus (VSV) in mouse L cells by 10- to 20-fold. Although vaccinia has no significant effect on RNA synthesis by VSV, VSV protein synthesis is dramatically stimulated by double infection. The enhancement of VSV growth is correlated with the ability of vaccinia to inhibit the VSV-mediated damage to the host translational machinery. Coinfection with vaccinia fails to stimulate the growth of a VSV mutant which is deficient in its ability to shut off protein synthesis during infection.