Content validity of the Rodeo-SCAT.

The purpose of this study was to establish the content validity of the Rodeo SCAT for the sport of rodeo and bull riding. The study design was comprised of expert consensus and content validation. A modified Ebel procedure was employed to content validate the rodeo SCAT. Content validation using this method includes experts agreeing on the importance of each item that comprises the rodeo SCAT. This 3-stage process involved: 1) face validation by a local committee: 2) initial expert consensus measurement via distance; and 3) a face-to-face discussion for items that did not originally achieve 80% consensus of the group. Experts were chosen from the Canadian Professional Rodeo Sport Medicine Team (Canada) and the Justin Sports Medicine Team (USA). 27 out of a total possible 68 items achieved 80% consensus in the second stage. In the third stage, 4 of the 68 items were removed with consensus from the expert group. All remaining items achieved 80% consensus for inclusion. In summary, the rodeo SCAT is content valid and thus, appropriate for use in the sport of rodeo context or environment.

Prevalence of food allergy in Taiwan: a questionnaire-based survey.

AIM: Food allergy is common in children and adults, and could be potentially fatal in minor groups. It is important for physicians to identify the prevalence of food allergies and to recognise common food allergens to make precise diagnosis and choose correct therapeutic approaches. METHODS: We used a nationwide, cross-sectional, random questionnaire-based survey to estimate the self-reported and expert-screened prevalence of food allergies and to identify the common food allergens in Taiwan. In this study, the perceptional diagnosis of food allergies was screened by physicians according to descriptions of convincing symptoms and medical recordings; in the meantime, non-allergic adverse reactions to foods, including food intolerance or food avoidance, were clarified. RESULTS: A total of 30 018 individuals who met the inclusion criteria was evaluated, and 6.95% of them were diagnosed as victims of food allergies. The prevalence was 3.44% in children under 3 years of age, 7.65% in children aged 4-18 years and 6.40% in adults respectively. About 77.33% of the food allergy population had experienced recurrent allergic attacks. Systemic reactions happened about 4.89% in food allergies group. The most commonly reported food allergen in Taiwan is seafood, including shrimp, crab, fish and mollusc. In addition, mango, milk, peanuts and eggs were also important food allergens in the general population; while milk, shellfish, peanuts and eggs were common in children. CONCLUSIONS: Less than 10% of the Taiwan population suffers from food allergy with different allergic symptoms to variable food allergens in different age groups.

PYCNOGENOL chewing gum minimizes gingival bleeding and plaque formation.

PYCNOGENOL is an antioxidant phytochemical shown to have antiinflammatory activity in both the in vitro and in vivo models. This study compared the effects of chewing gums with and without PYCNOGENOL on gingival bleeding and plaque formation in 40 human subjects. In this double-blind study, subjects were assigned randomly to receive either control gums without PYCNOGENOL or experimental gums containng 5 mg PYCNOGENOL. Subjects used chewing gums for 14 days. Gingival bleeding and plaque scores were taken before and after the experiment. PYCNOGENOL chewing gums significantly reduced gingival bleeding, while no changes were noted in bleeding indexes in control subjects who used regular chewing gums. Subjects using regular control gums had significant increases of dental plaque accumulation during the two-week period. No increases in plaque accumulation were noted in subjects using PYCNOGENOL chewing gums. The data of this study suggest that the use of Pycnogenol chewing gums can minimize gingival bleeding and plaque accumulation.

Pycnogenol protects neurons from amyloid-beta peptide-induced apoptosis.

Neuronal apoptosis is one of the pathological features of Alzheimer's disease (AD). Morphological pathology reveals that neuronal apoptosis is associated with senile plaques containing amyloid-beta peptide (Abeta) in AD brains. Reactive oxygen species (ROS) has been proposed to be involved in the apoptotic mechanism of Abeta-mediated neurotoxicity. In the present study, using a rat pheochromocytoma (PC12) cell line, we investigated the effect of Pycnogenol (PYC), a potent antioxidant and ROS scavenger, on Abeta(25-35)-induced apoptosis and ROS generation. We used vitamin E, a known antioxidant agent, to verify the effect of PYC. Abeta(25-35)-induced apoptosis in PC12 cells was demonstrated by: (1) a dose-dependent loss of cell viability; (2) a time- and dose-dependent increase in the apoptotic cells; (3) an induction of DNA fragmentation; and (4) an increase in caspase-3 activity and cleavage of poly (ADP-ribose) polymerase (PARP). Our data showed that a significant increase in ROS formation preceded apoptotic events after PC12 cells were exposed to Abeta(25-35). We further found that PYC not only suppressed the generation of ROS but also attenuated caspase-3 activation, DNA fragmentation, PARP cleavage, and eventually protected against Abeta-induced apoptosis. Vitamin E also suppressed cell death and caspase-3 activation induced by Abeta(25-35). Taken together, these results suggest that ROS may be involved in Abeta-induced apoptosis in PC12 cells. They further suggest that PYC can reduce apoptosis, possibly by decreasing free radical generation in PC12 cells.

Herpes zoster during varicella.

A 4-year-old boy had varicella infection. Two days later vesicular lesions clustered within the left 10th thoracic dermatome. Varicella-zoster virus IgM antibody in serum was positive. He was diagnosed with varicella infection combined with herpes zoster. This is the first case report in the medical literature.

S-allyl cysteine reduces oxidant load in cells involved in the atherogenic process.

Oxidation of low-density lipoprotein (LDL) and activation of the pleiotropic transcription factor nuclear factor kappa B (NF-kappaB), are often the chemical and molecular alterations associated with the development of the atherosclerotic lesion. We have reported previously on the antioxidant properties of a garlic compound, S-allyl cysteine (SAC), and its ability to inhibit damage caused by oxidative stress in bovine endothelial cells. In this study, the antioxidant effects of SAC were further determined, using several in vitro assay systems. First, we determined the effect of SAC on Cu2+-induced oxidation of LDL. Varying concentrations of SAC were co-incubated with a standardized Cu2+/LDL solution, and LDL-oxidation was then ascertained by determining the formation of thiobarbituric acid reactive substances (TBARS). SAC inhibited LDL-oxidation at an optimum concentration of 1 mM. In another experiment, we determined the effects of SAC on oxidized-LDL (ox-LDL) activation of J774 murine macrophages and human umbilical vein endothelial cells (HUVEC). Cells were grown on 96-well plates, preincubated with SAC at 37 degrees C and 5% CO2 for 24 h, washed, and exposed to ox-LDL for 24 h. Levels of hydrogen peroxide (H2O2) were determined by a fluorometric assay. In both cell lines, SAC exhibited dose-dependent inhibition of H2O2 formation. We also studied the effects of SAC on NF-kappaB activation in HUVEC using tumor necrosis factor-a (TNF-alpha) or H2O2 as stimulators. Cells were grown in 75 cm2 flasks at 37 degrees C and 5% CO2 and were preincubated with SAC 24 h before stimulation with TNF-alpha or H2O2. Nuclear extracts were then prepared and NF-kappaB activation was determined using an electrophoretic mobility shift assay with a 32P-labeled probe. SAC exhibited dose-dependent inhibition of NF-kappaB activation. Our data suggest that SAC may act via antioxidant mechanisms to inhibit the atherogenic process.

Suppression of LDL oxidation by garlic.

It has been known for several decades that hypercholesterolemia is a major risk factor for atherosclerosis and that lowering of cholesterol can significantly reduce risk for cardiovascular diseases. More recently, oxidation of LDL has been recognized as playing an important role in the initiation and progression of atherosclerosis. Oxidized LDL, but not native LDL, promotes vascular dysfunction by exerting direct cytotoxicity toward endothelial cells, by increasing chemotactic properties for monocytes, by transforming macrophages to foam cells via scavenger-receptors and by enhancing the proliferation of various cell types, e.g., endothelial cells, monocytes and smooth muscle cells; all of these events are recognized as contributing to atherogenesis. In this paper, experimental evidence is presented that shows that several garlic compounds can effectively suppress LDL oxidation in vitro. Short-term supplementation of garlic in human subjects has demonstrated an increased resistance of LDL to oxidation. These data suggest that suppressed LDL oxidation may be one of the powerful mechanisms accounting for the antiatherosclerotic properties of garlic.

Garlic compounds minimize intracellular oxidative stress and inhibit nuclear factor-kappa b activation.

Oxidative modification of LDL has been recognized as playing an important role in the initiation and progression of atherosclerosis. In this study, we determined the effects of aged garlic extract (AGE) and its major compound, S-allylcysteine (SAC), on oxidized LDL (Ox-LDL)-induced injury in endothelial cells (EC). Lactate dehydrogenase (LDH) release as an index of membrane damage, methylthiazol tetrazoium (MTT) assay for cell viability and thiobarbituric acid reactive substances (TBARS) indicating lipid peroxidation were measured. Ox-LDL caused an increase of LDH release, loss of cell viability and TBARS formation. Both AGE and SAC prevented all of these changes. To elucidate the mechanism, effects of AGE or SAC on intracellular glutathione (GSH) level in EC, and release of peroxide from EC and macrophages (M Phi) were determined. Ox-LDL depleted intracellular GSH and increased release of peroxides. Both AGE and SAC inhibited these changes. Effects of SAC on hydrogen peroxide (H(2)O(2)) or tumor necrosis factor (TNF)-alpha-induced nuclear factor (NF)-kappa B activation were determined. Pretreatment of EC with SAC inhibited NF-kappa B activation. We demonstrated that both AGE and SAC can protect EC from Ox-LDL-induced injury by preventing intracellular GSH depletion in EC and by minimizing release of peroxides from EC and M Phi. SAC also inhibited H(2)O(2)- or TNF-alpha-induced NF-kappa B activation. Our data suggest that AGE and its main compound, SAC, may be useful for prevention of atherosclerosis.

Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells.

The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B) participates in the control of gene expression of many modulators of inflammatory and immune responses, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). The heightened expression of these adhesion molecules has been reported to play a critical role in atherosclerosis, inflammation, ischemic vascular disorders, diabetes, and cancer metastasis. In the present study, we investigated the effect of pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated human umbilical vein endothelial cells (HUVECs). Gel-shift analysis of HUVEC demonstrated that pretreatment with pycnogenol exhibited a concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa B. Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was dose-dependently reduced by pycnogenol. TNF-alpha significantly increased the release of superoxide anion and hydrogen peroxide from HUVECs. Pycnogenol dose-dependently inhibited their release. The ability of pycnogenol to inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that this phytochemical may play an important role in halting or preventing the atherogenic process.

Pycnogenol protects vascular endothelial cells from beta-amyloid-induced injury.

The neuropathological hallmarks of Alzheimer's disease (AD) are senile plaques, cerebrovascular beta-amyloidosis, neurofibrillary tangles, and selective neuronal loss. Beta-amyloid (Abeta) has been shown to cause vascular damage mediated by generation of reactive oxygen species and this damage is considered an early event in the development of AD. In this study, we determined the effect of pyenogenol, a potent antioxidant phytochemical, on Abeta-induced cellular injury. Pulmonary artery endothelial cells (PAEC) were exposed to Abeta for 24 h. Cell injury was assessed by measuring cell viability with methylthiazol tetrazolium (MTT) assay, and by determining the release of intracellular lactate dehydrogenase (LDH). Lipid peroxidation products of PAEC were determined by measuring thiobarbituric acid-reactive substances (TBARS). Exposure of PAEC to Abeta resulted in a decrease in cell viability, an increase of LDH release indicating membrane damage, and an elevated level of TBARS. Preincubation of PAEC with pycnogenol significantly minimized these changes. This study demonstrated that pycnogenol can protect vascular endothelial cells from Abeta-induced injury. The data suggest that pycnogenol may be useful for the prevention and/or treatment of vascular or neurodegenerative diseases associated with Abeta toxicity.

Crude protein content and amino acid composition in Taiwanese human milk.

Breast milk provides the essential nutrients for infants in readily available form. The content of nitrogen in human milk is of great importance because it relates to the growth of infants in the early stage, and the composition of nitrogenated compounds varies according to the lactational stage. Three-hundred-and-three human milk specimens were obtained from 240 healthy mothers living in two different districts in Taiwan, and 264 specimens were used for the analysis. The crude protein content, total and free amino acid compositions as well as urea content were evaluated using pooled milk samples according to different lactational stages and geographical location. The crude protein content decreased sharply from colostrum (2.51 g/100 mL) to mature milk (1.25 g/100 mL). Total amino acids account for 80-85% of the crude protein throughout the whole lactation period. Crude protein also contained 30 to 35 mg/ 100 mL urea and 41 to 48 mg/ 100 mL free amino acids as non-protein nitrogen components. The ratio of essential to non-essential amino acids remained constant throughout the lactation period in spite of a decline in amino acid content. The amino acid composition per 1 g of nitrogen varied during the lactation period. The differences of these lactational changing patterns of individual amino acids were probably reflected by variation of the protein composition during lactation. The sum of free amino acid content ranged from 43 to 50 mg/100 mL in Taipei and 40 to 45 mg/100 ml, in Kaohsiung. Although the variations of free amino acids during the lactation period differed among amino acids, glutamic acid predominated in mature milk while phosphoethanolamine was predominant in colostrum.

Ginkgo biloba inhibits hydrogen peroxide-induced activation of nuclear factor kappa B in vascular endothelial cells.

The present study determined the effects of Ginkgo biloba extract (GBE) on the activation of nuclear factor kappa B (NF-kappaB) and the level of hydrogen peroxide (H2O2) in bovine pulmonary artery endothelial cells (PAEC). H2O2 showed a concentration-dependent activation of NF-kappaB. GBE demonstrated a concentration-dependent suppression of NF-kappaB activated by H2O2. GBE directly scavenged H2O2 in a cell-free system; it also decreased H2O2 levels in PAEC. These results suggest that the inhibitory effect of GBE on H2O2-induced NF-kappaB activation may be caused by its scavenging and suppression of H2O2. Our experiments demonstrate that GBE can inhibit NF-kappaB activation induced by H2O2 and may thus be effective for the prevention or treatment of atherosclerosis and other disorders related to NF-kappaB activation.

Aged garlic extract attenuates intracellular oxidative stress.

Oxidation of low density lipoprotein (LDL) has been recognized as playing an important role in the initiation and progression of atherosclerosis. We recently reported that aged garlic extract (AGE) inhibited LDL oxidation and minimized oxidized LDL-induced cell injury. In this study, the antioxidant effects of AGE were further examined using bovine pulmonary artery endothelial cells (PAEC) and murine macrophages. Lactate dehydrogenase (LDH) release, as an index of membrane injury, and intracellular glutathione (GSH) levels were determined. Oxidized LDL (Ox-LDL) caused an increase of LDH release and depletion of GSH. Pretreatment with AGE prevented these changes. AGE exhibited an inhibition of Ox-LDL-induced peroxides in PAEC. AGE suppressed peroxides in murine Macrophage (J774 cells) dose-dependently. The J774 cells were also incubated with AGE, interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) and nitric oxide (NO) production was measured. AGE inhibited NO production in J774 cells. In a cell free system, AGE was shown to scavenge H2O2 dose-dependently. Our data demonstrate that AGE can protect the endothelial cells from oxidized LDL-induced injury by preventing depletion of intracellular GSH and by removing peroxides. AGE also reduces levels of NO and peroxides in macrophages. These data suggest that AGE is a useful protective agent against cytotoxicity associated with Ox-LDL and NO, and it may thus be useful for the prevention of atherosclerosis and cardiovascular diseases.

S-allylcysteine attenuates oxidative stress in endothelial cells.

Oxidation of low-density lipoprotein (LDL) has been recognized as playing an important role in the initiation and progression of atherosclerosis. We recently reported that S-allylcysteine (SAC), one of the major compounds in the aged garlic extract (AGE), inhibited LDL oxidation and minimized oxidized LDL-induced cell injury. In this study, the antioxidant effects of SAC were further determined using several in vitro assay systems. Pulmonary artery endothelial cells (PAECs) were preincubated with SAC at 37 degrees C and 5% CO2 for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Lactate dehydrogenase (LDH) release, as an index of membrane injury, and intracellular glutathione (GSH) level were determined. Oxidized LDL caused an increase of LDH release and depletion of GSH. Pretreatment with SAC prevented these changes. Peroxides were measured directly in 24-well plates using a fluorometric assay. SAC dose-dependently inhibited oxidized LDL-induced release of peroxides in PAEC. In a cell-free system, SAC was shown to scavenge hydrogen peroxide. Our data demonstrate that SAC can protect endothelial cells from oxidized LDL-induced injury by removing peroxides and preventing the intracellular GSH depletion and suggest that this compound may be useful for the prevention of atherosclerosis.

Antioxidant effects of fructosyl arginine, a Maillard reaction product in aged garlic extract.

The amino-carbonyl (Maillard) reaction of amino acids with sugars is a nonenzymatic browning reaction that takes place during the processing, cooking, and storage of foods. Maillard reaction products (MRPs) have been shown to possess interesting chemical and biological properties including antimutagenic and antioxidant activity. In this study, we determined the antioxidant effects of fructosyl arginine (Fru-Arg), a MRP in aged garlic extract. Low density lipoprotein (LDL) was incubated with Cu(2+) at 37 degrees C and 5% CO(2) for 24 hours, which resulted in an increase of thiobarbituric acid reactive substances (TBARS) indicating lipid peroxidation. Coincubation of Cu(2+) with Fru-Arg and LDL resulted in a significant inhibition of TBARS formation. Pulmonary artery endothelial cells (PAEC) were exposed to 0.1 mg/mL oxidized LDL (Ox-LDL) at 37 degrees C and 5% CO(2) for 24 hours. Lactate dehydrogenase (LDH) release, as an index of cell membrane damage, and TBARS were measured. Ox-LDL caused an increase of LDH release and TBARS formation. Pretreatment of PAEC with Fru-Arg inhibited these changes. Murine macrophages were incubated with Ox-LDL, and the release of peroxides was measured using a fluorometric assay. Ox-LDL caused an increased release of peroxides. Coincubation of macrophages with Fru-Arg and Ox-LDL inhibited the release of peroxides dose-dependently. In a cell free system, Fru-Arg was shown to scavenge hydrogen peroxide. These data suggest that Fru-Arg is a potent antioxidant, and thus may be useful for the prevention of atherosclerosis and other disorders associated with oxidative stress.

Fructus corni attenuates oxidative stress in macrophages and endothelial cells.

The antioxidant effect of a Chinese medicinal herb, Fructus corni extract (FCE), was investigated using models of oxidative stress in macrophages and vascular endothelial cells. Murine macrophages (J774) were incubated with FCE at 37 degrees C and 5% CO2 for 1 hr. Oxidative burst was triggered by zymosan and measured with a fluorescent probe. FCE exhibited a concentration- dependent suppression of oxidative burst. Confluent monolayers of bovine pulmonary artery endothelial cells (PAEC) were preincubated with FCE for 20 hrs, washed, and then exposed to an organic oxidant t-butyl hydroperoxide (tBHP) for 2 hrs. Cell viability was assessed by methylthiazol tetrazolium (MTT) assay, and cell injury by the release of intracellular lactate dehydrogenase (LDH). Lipid peroxidation products of PAEC were determined by measuring thiobarbituric acid-reactive substances (TBARS). Exposure of PAEC to tBHP resulted in decreased cell viability, increased LDH release, and elevated TBARS. Preincubation of PAEC with FCE significantly reversed these changes. Our results demonstrated that FCE can protect vascular endothelial cells from oxidant injury. The data thus suggest that Fructus corni may be useful for the prevention and/or treatment of disorders associated with oxidative damage.

Pycnogenol enhances immune and haemopoietic functions in senescence-accelerated mice.

Pycnogenol (procyanidin extracted from Pinus maritima) has been shown to be a potent free radical scavenger and an antioxidant phytochemical. The effects of pycnogenol on immune and haemopoietic dysfunction in senescence-accelerated mice (SAM), as a murine model of accelerated ageing, were determined. SAMP8, a strain of senile-prone mice, exhibit learning and memory deficits, immunodeficiency and dysfunction of the haemopoietic system. Oral feeding with pycnogenol for 2 months significantly improved their T- and B-cell function. Pycnogenol also augmented the proliferative capacity of haemopoietic progenitors of bone marrow in SAMP8. These data suggest that pycnogenol may be useful for either retardation or restoration of parameters associated with ageing.

Fructus corni enhances endothelial cell antioxidant defenses.

1. The present study determined the effects of Fructus corni extract (FCE) on the levels of hydrogen peroxide (H2O2) and superoxide anion (O2-), on the glutathione (GSH) redox cycle and on the activities of antioxidant enzymes in bovine pulmonary artery endothelial cells (PAECs). 2. Confluent monolayers of PAECs were incubated with FCE, and oxidative stress was triggered by hypoxanthine and xanthine oxidase (to induce H2O2) or H2O2 (to induce O2-). 3. FCE exhibited a concentration-dependent suppression of H2O2 and O2-. 4. It modulated the GSH redox cycle by increasing the intracellular GSH content, the activities of GSH peroxidase and GSH disulfide reductase, and by decreasing the intracellular level of GSH disulfide. 5. It also increased the activities of superoxide dismutase and catalase. 6. These results demonstrate that FCE can promote a protective antioxidant defense state by affecting some important enzymatic and nonenzymatic oxidant-scavenging systems and may thus be useful for the prevention or treatment of disorders associated with oxidative damage.

Inactivation of bacteriophage lambda, Escherichia coli, and Candida albicans by ozone.

The effects of ozone (O3) on three types of microbes were studied. Test suspensions were exposed to 600 ppm O3 at room temperature. Control experiments were performed under identical conditions using oxygen gas. Bacteriophage lambda was completely inactivated at 10 min while Escherichia coli and Candida albicans were only inactivated by factors of 10(5) and 10(4) respectively at 40 min. Exposure of a mixed microbial suspension to O3 for 5 min resulted in 100% killing of bacteriophages while the viability of E. coli remained unchanged. Various body fluids containing phages were exposed to O3. Compared to buffered solution, the decrease in phage titers was significantly slower in whole blood, plasma, and albumin. Both E. coli and C. albicans had increased production of thiobarbituric-acid-reactive substances with increased O3 exposure. 3H-labelled amino acids were incorporated into E. coli. O3 treatment resulted in a loss of radioactivity, indicating leakage of cytoplasmic contents. The data indicate that microbes are inactivated by O3 at different rates, possibly related to differential membrane permeability. The milieu in which microbes are present determines the effectiveness and outcome of O3 treatment.

Holocord intramedullary spinal cord astrocytoma: report of one case.

Intramedullary spinal cord astrocytoma in infants is relatively uncommon. Its occurrence is usually confined to the cervical and cervicothoracic regions. In this paper, we report on the case of a 4-month old male infant with low grade holocord intramedullary spinal cord astrocytoma. He had developed progressive weakness of the lower extremities over a month period. Neurological examination revealed flaccid paraplegia as well as complete loss of all modalities of sensation below the T10 level. MRI revealed a large intramedullary mass which was found to be an intramedullary astrocytoma at surgery. This case report presents the clinical features, radiographic findings, and treatment and outcome for this patient together with a review of relevant literature.