Risk factors for injury in Olympic-style competition taekwondo: a systematic review.

AIM: The aim of this review was to systematically collate and qualitatively evaluate the epidemiologic data on risk factors related to injuries in taekwondo athletes. METHODS: Electronic searches of relevant literature were carried out in the AusportMed, CINAHL, PubMed, Scopus, and SPORTDiscus databases. A study was included if: 1) it was a prospective experimental or observational investigation; 2) it contained data on Olympic-style taekwondo athletes; and 3) it contained data on risk factors for injuries. All eligible studies were assessed by two independent reviewers. RESULTS: Sixteen studies were deemed eligible for inclusion, of which a total of nine unique data sets were identified. Six potential risk factors were found to have been prospectively investigated to date, of which only three were shown to be associated with the occurrence of injury. The available data indicated that competing in heavier weight divisions was associated with increased overall injury incidence rates. In addition, adolescent athletes and athletes lacking blocking skills were both found to be associated with increased occurrence of concussion injuries. CONCLUSION: There is a paucity of identified risk factors for injury in taekwondo. Future epidemiologic research should consider a wider range of potential risk factors, in particular modifiable risk factors, and translate ascertained factors into practical preventive efforts.

Effect of probenecid on 5-hydroxyindoleacetic acid in cisternal cerebrospinal fluid of rats with portacaval anastomosis.

Portal-systemic encephalopathy (PSE) is characterized by a neuropsychiatric disorder progressing through personality changes, to stupor and coma. Previous studies have revealed alterations of serotonin and of its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in brain tissue and CSF in experimental (rat) and human PSE. Increased brain 5-HIAA concentrations could result from its decreased removal rather than to increased serotonin metabolism. In order to evaluate this possibility, CSF 5-HIAA concentrations were measured using an indwelling cisterna magna catheter technique at various times following end-to-side portacaval anastomosis in rats (the most widely used animal model of PSE) treated with probenecid, a competitive inhibitor that blocks the active transport of acid metabolites out of the brain and CSF. Following portacaval anastomosis and probenecid treatment, CSF concentrations of 5-HIAA were increased to a greater extent than in sham-operated controls. When data were expressed as per-cent baseline values, the relative increase of CSF 5-HIAA in portacaval shunted rats following probenecid treatment was not significantly different from sham-operated controls. These findings confirm that increased 5-HIAA in the CNS in experimental PSE results from increased 5HT metabolism or turnover and that the probenecidsensitive acid metabolite carrier is intact in PSE.

Regional alterations of dopamine and its metabolites in rat brain following portacaval anastomosis.

Hyperammonemia and changes in brain monoamine metabolism have been proposed to contribute to the pathogenesis of the neuropsychiatric symptoms characteristic of human portal-systemic encephalopathy (PSE) resulting from chronic liver disease. Portacaval anastomosis (PCA) in the rat leads to sustained hyperammonemia and mild encephalopathy. In order to evaluate the role of dopamine (DA) metabolism in PSE, levels of DA and its metabolites were measured by HPLC with electrochemical detection in brain regions of rats with PCA at various stages of encephalopathy precipitated by ammonium acetate administration. Following ammonium acetate administration, rats with PCA rapidly develop severe neurological signs of encephalopathy progressing through loss of righting reflex to coma; sham-operated control animals administered ammonium acetate showed no such neurological deterioration. Concentrations of the DA metabolites DOPAC and HVA as well as [DA metabolites]/[DA] ratios, an indirect measure of DA turnover in brain, were increased in caudate-putamen, in cingulate and pyriform entorhinal cortices as well as in raphe nucleus and locus coeruleus. Increased DA metabolites, however, did not worsen at coma stages of PSE. Increased DA turnover thus appears to relate to early neuropsychiatric and extrapyramidal symptoms of PSE.

Densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand 3H-PK11195 are increased in brain 24 hours following portacaval anastomosis.

Quantitative receptor autoradiography was used to measure the densities of binding sites for the "peripheral-type" benzodiazepine receptor ligand 3H-PK11195 in regions of the rat brain 1, 3, 7 and 28 days following portacaval anastomosis (PCA) and in sham-operated control animals. The results demonstrate that densities of 3H-PK11195 binding sites were significantly increased in the cerebral cortex (by 40%, p < 0.05) as early as 24 hours following PCA. In the thalamus significant increases in densities of 3H-PK11195 binding sites were seen 3 days after PCA, whereas in brain regions such as the striatum and cerebellum, significant increases in 3H-PK11195 binding sites were not evident until 7 days following PCA. By 28 days following PCA increased densities of 3H-PK11195 binding sites were well established and widespread throughout the brain. Previous studies demonstrate early increases of brain ammonia following PCA. PTBRs or their endogenous ligands could play an important role in the early astrocytic response (mitochondrial proliferation, swelling) to ammonia following PCA.

Monitoring of neurotransmitter amino acids by means of an indwelling cisterna magna catheter: a comparison of two rodent models of fulminant liver failure.

Alterations of brain and cerebrospinal fluid amino acids have consistently been described in human and experimental fulminant liver failure. To evaluate the significance of such changes in the pathogenesis of hepatic encephalopathy in fulminant liver failure, brain and cerebrospinal fluid amino acids (glutamate, aspartate, GABA, glycine, taurine) were measured at various stages during the development of neurological dysfunction in rats after hepatic devascularization or thioacetamide treatment to induce acute liver failure. To facilitate repetitive removal of cerebrospinal fluid, a technique employing long-term implantation of cisterna magna catheters in conscious, freely moving rats was developed. Brain but not cerebrospinal fluid concentrations of the excitatory amino acids glutamate and aspartate were reduced in both animal models of fulminant liver failure in parallel with deterioration of neurological status. Brain and cerebrospinal fluid GABA levels were not significantly altered. Cerebrospinal fluid glycine levels were increased two to three times in parallel with increasing brain glycine content in the devascularized rat but were unchanged in thioacetamide-induced liver failure, suggesting distinct pathophysiological mechanisms in these two experimental situations. On the other hand, onset of coma in both animal models of fulminant liver failure was accompanied by significantly increased cerebrospinal fluid taurine levels. We suggest that such changes result from taurine release from astrocytes in brain into the extracellular fluid; this is consistent with taurine's role in the regulation of intracellular osmolarity in brain. Sequential measurements of amino acids in the cerebrospinal fluid of small rodents with indwelling cisterna magna catheters adds a useful new approach for exploring the neurobiology of hepatic encephalopathy in fulminant liver failure.

Intracellular pH rises and astrocytes swell after portacaval anastomosis in rats.

The basis for astrocytic swelling after the early period after portacaval anastomosis (PCA) is poorly defined. In other eukaryotic cells intracellular pH (pHi) and volume are determined, in part, by the same general mechanisms, yet how astrocytic pHi varies with enlargement of these cells after PCA is unknown. Therefore, direct measurements of pHi in astrocytes were made and compared with pericapillary astrocytic area as determined from electron micrographs in rats 5-8 days after PCA. Astrocytic area (n = 14 measurements for each group) was found to be significantly (P less than 0.0009) greater in PCA animals (n = 3) than in sham-operated control animals. (n = 3). Double-barrel pH-sensitive microelectrodes were used to measure pHi in neocortical cells defined by electrophysiological criteria to be astrocytic. Astrocytes (n = 25) from PCA animals (n = 5) had a resting membrane potential of 72 +/- 5 mV (mean +/- SD) and an pHi of 7.11 +/- 0.11 while comparable cells (n = 12) from sham-operated controls (n = 2) had a membrane potential of 81 +/- 6 mV and an pHi of 7.00 +/- 0.10. Astrocytes from PCA animals were significantly more depolarized (P less than 0.001) and alkaline (P less than 0.009), at a time when they were also significantly larger than those from sham-operated controls. Astrocytes are known to become more alkaline when they are activated by brief depolarizing stimuli. However, this is the first demonstration that such an interrelationship can also exist for steady-state conditions of these cells.(ABSTRACT TRUNCATED AT 250 WORDS)

An alternative to property rights in human tissue.

A three-tiered legal structure of the substances constitutive of human beings can accommodate property rights in new products created by the investment of labor in human tissue.

Effect of ammonia on brain serotonin metabolism in relation to function in the portacaval shunted rat.

Four weeks following portacaval anastomosis (PCA) in the rat, severe liver atrophy, sustained hyperammonemia, and increased plasma and brain tryptophan are observed. Administration of ammonium acetate (NH4Ac) to rats with PCA precipitates severe signs of hepatic encephalopathy (HE) (loss of righting reflex progressing to loss of consciousness and ultimately deep coma). To evaluate the relationship between the deterioration of neurological status in HE and serotonin (5-HT) metabolism, the levels of 5-HT, its precursor 5-hydroxytryptophan, and its major metabolite 5-hydroxy-indole-3-acetic acid (5-HIAA) were measured by HPLC with ion-pairing and electrochemical detection in three well-defined areas of the cerebral cortex: anterior cingulate, piriform and entorhinal, and frontoparietal; as well as in the caudate-putamen, the raphe nuclei, and the locus ceruleus in rats with PCA at different stages of HE, before and after injection of NH4Ac, as well as in sham-operated controls. The results demonstrate increased 5-HIAA/5-HT ratios after PCA and NH4Ac loading, suggesting increased 5-HT turnover in the brains of these animals. However, these changes do not appear to be related to the precipitation of coma as no significant difference in 5-HT turnover was observed between precoma and coma stages of HE. Increased 5-HT turnover in brain of shunted rats may be related to early symptoms of HE such as altered sleep patterns and disorders of motor coordination.

Hybridization between fructose diphosphate aldolase subunits derived from diverse biological systems: anomolous hybridization behavior of some aldolase subunit types.

In the present studies we investigated the abilities of fructose diphosphate aldolase subunits derived from diverse biological sources to form stable heterotetramers with each other in vitro. Aldolase C subunits isolated from chicken brain readily "hybridized" with aldolase subunits derived from lobster muscle and wheat germ following reversible acid dissociation of mixtures of these enzymes; however, appreciable amounts of stable heterotetramers containing chicken C subunits and aldolase subunits isolated from two other invertebrates (Ascaris and squid) were not produced under the same conditions. In contrast to the situation with chicken C subunits, aldolase B subunits isolated from rat liver did not "hybridize" appreciably with lobster muscle or wheat germ aldolase subunits. The present observations are not consistent with the hypothesis that the abilities of different aldolase subunit types to form heterotetramers in vitro is governed solely by the evolutionary relationships which exist between the organisms from which the enzymes are derived.

Specific, limited tryptic modification of wheat-germ fructose-bisphosphate aldolase subunits: destruction of catalytic activity but not of ability to establish precise subunit-subunit recognition.

We have been using the glycolytic enzyme fructose-bisphosphate aldolase (D-fructose-1,6-bisphosphate D-glyceraldehyde-3-phosphate lyase, EC 4.1.2.13) as a model system to investigate the assembly of oligomeric enzymes. In the present work, we investigate the effect of specific, limited tryptic modification on the properties of aldolase isolated from wheat germ. The wheat-germ enzyme was selected, since several aldolases isolated from animal sources were not readily susceptible to the specific tryptic modification seen with this plant enzyme. We will show that: Low levels of trypsin cause a first-order inactivation of wheat-germ aldolase activity which is associated with a fairly specific cleavage of the enzyme which reduces its subunit molecular weight from 41000 to 39000. The proteolytic modification is greatly inhibited in the presence of the aldolase substrate, fructose bisphosphate. The intact and modified enzymes appear to have similar surface changes, as judged by their behavior during electrophoresis in polyacrylamide gels under non-denaturing conditions. The modified aldolase is not specifically eluted from phosphocellulose columns by fructose bisphosphate under the conditions used in the affinity chromatographic isolation of the intact enzyme, suggesting that the modified enzyme may no longer be able to bind substrate. Although enzymatically inactive, the modified aldolase subunits are able to refold and reassociate into tetrameric combinations following unfolding of the subunits by treatment at low pH; thus, this specific proteolytic modification does not interfere with the ability of wheat-germ aldolase subunits to refold and to establish precise subunit-subunit recognition in vitro.