Kinesiology tape does not promote vertical jumping performance: A deceptive crossover trial.

BACKGROUND: Kinesiology tape (KINTAPE) is one of the most common adhesive therapeutic tapes. Apart from clinical applications, KINTAPE claims to be able to enhance functional performance by muscle activity facilitation. However, emerging evidence suggests that the isokinetic muscle strength remains similar when the placebo effect is eliminated. OBJECTIVES: In view of the weak relationship between functional performance and isokinetic muscle strength, this study investigated the true effects of KINTAPE on functional performance. DESIGN: Deceptive, randomized, and crossover trial. METHOD: Sixty four experienced volleyball players performed vertical jumping test under three taping conditions: true facilitative KINTAPE, sham KINTAPE, and no KINTAPE. Under the pretense of applying adhesive muscle sensors, KINTAPE was applied to their quadriceps and gastrocnemius in the first two conditions. Mean maximum jump height and peak jump power were averaged from three attempts. Within-subject comparisons were conducted by repeated measure ANOVA. RESULTS: Out of 64 participants, 30 of them were successfully deceived and they were ignorant about KINTAPE. No significant differences were found in both maximum jump height (η(2) = 0.001; p = 0.241) and peak jump power (η(2) = 0.001; p = 0.134) between three taping conditions. CONCLUSIONS: The results showed that KINTAPE did not facilitate muscle performance by generating higher jumping power or yielding a better jumping performance. These findings reinforce that previously reported muscle facilitatory effects or functional enhancement using KINTAPE may be attributed to placebo effects.

Kinesiology tape does not facilitate muscle performance: A deceptive controlled trial.

Kinesiology tape (KinTape) is a therapeutic tape without much understanding of its mechanism. KinTape claims to increase cutaneous stimulation, which facilitates motor unit firing, and consequently improves functional performance; however these, benefits could be due to placebo effects. This study investigated the true effects of KinTape by a deceptive, randomized, and controlled trial. Thirty healthy participants performed isokinetic testing of three taping conditions: true facilitative KinTape, sham KinTape, and no KinTape. The participants were blindfolded during the evaluation. Under the pretense of applying adhesive muscle sensors, KinTape was applied to their quadriceps in the first two conditions. Normalized peak torque, normalized total work, and time to peak torque were measured at two angular speeds (60°/s and 180°/s) and analyzed with one-way repeated measures ANOVA. Participants were successfully deceived and they were ignorant about KinTape. No significant differences were found between normalized peak torque, normalized total work, and time to peak torque at 60°/s or 180°/s (p = 0.31-0.99) between three taping conditions. The results showed that KinTape did not facilitate muscle performance in generating higher peak torque, yielding a greater total work, or inducing an earlier onset of peak torque. These findings suggest that previously reported muscle facilitatory effects using KinTape may be attributed to placebo effects.

Cannabinoid receptor type 1 antagonist, AM251, attenuates mechanical allodynia and thermal hyperalgesia after burn injury.

BACKGROUND: Burn injury causes nociceptive behaviors, and inflammation-related pathologic pain can lead to glial cell activation. This study tested the hypothesis that burn injury activates glial cells, and cannabinoid receptor 1 (CB1R) antagonist, AM251, will decrease burn pain. METHODS: Anesthetized rats received 0.75-cm third-degree burn on dorsal hind paw. Vehicle or AM251 30 µg intrathecally (older rats, n=6 per group) or, either vehicle, 0.1 or 1.0 mg/kg intraperitoneally (younger rats, n=6 per group), started immediate postburn, was administered for 7 days. Mechanical allodynia and thermal hyperalgesia were tested on ventral paw for 14 days. Microglial and astroglial activity was assessed by immunocytochemistry. RESULTS: Allodynia, observed on burn side from day 1 to 14, was significantly (P<0.05) attenuated by intrathecal and intraperitoneal AM251 (1 mg/kg) starting from 3 to 14 days. Hyperalgesia, observed from day 3 to 12, was completely (P<0.05) reversed by intrathecal and intraperitoneal AM251 (1 mg/kg). AM251 0.1 mg/kg had no effect. Microglial activity (n=3 per time point) increased (P<0.05) 18.5±7.5 and 12.3±1.6 (mean±SD) fold at 7 and 14 days, respectively. Astroglial activity (n=4 per time point) increased 2.9±0.3 fold at day 7 only. Glial activities were unaltered by AM251. CONCLUSIONS: AM251 inhibited nociceptive behaviors after burn even beyond 7-day period of administration. Although many studies have documented the utility of CB1R agonists, this study indicates that endogenous cannabinoids may have an unexpected pronociceptive effect during development of burn pain, explaining why CB1R antagonist, AM251, improves nociceptive behaviors. The decreased nociception with AM251 without altering glial activity indicates that AM251 acts further downstream of activated glial cells.

Self-reported antibiotic allergy incidence and prevalence: age and sex effects.

BACKGROUND: Data on the prevalence and incidence of adverse reactions to antibiotics in outpatient populations are rare. These events are commonly called "allergy" when noted in the medical record. OBJECTIVES: Determine the prevalence and incidence of allergy, as recorded in the medical record, to the most commonly used antibiotic classes in a large outpatient population using health care in the United States during 2007. METHODS: Data for drug allergy and antibiotic use were extracted from the electronic health records of 411,543 patients cared for by Kaiser Permanente in San Diego County who had at least one outpatient visit during 2007. Outpatient antibiotic utilization data was obtained for each year between 1995 and 2007. Penicillins, sulfas, cephalosporins, tetracyclines, macrolides, and quinolones were the classes of antibiotics evaluated. RESULTS: Antibiotics account for a majority of drug allergy entries. Antibiotic classes with higher historical use have higher allergy prevalence. Female patients use more antibiotics than males, and have higher allergy prevalence rates for all classes of antibiotics. There is a steady increase in antibiotic allergy prevalence with aging for both sexes. Females have higher allergy incidence rates for all classes of antibiotics. Antibiotic allergy incidence in female patients is highest for sulfas, 3.4%, compared with 1%-1.5% for all other classes of antibiotics. Antibiotic allergy incidence in males also is highest for sulfas, 2.2%, compared with 1.1% for penicillins and 0.5%-0.6% for all other classes of antibiotics. CONCLUSIONS: Female sex, use, and increasing age are the primary factors that account for higher antibiotic allergy prevalence. Antibiotic allergy incidence is highest with sulfa class antibiotics.

Association of tumor necrosis factor-alpha-238G>A and apolipoprotein E2 polymorphisms with intracranial hemorrhage after brain arteriovenous malformation treatment.

OBJECTIVE: We previously reported specific genotypes of polymorphisms in two genes, tumor necrosis factor-alpha (TNF-alpha-238G > A) and Apolipoprotein E (ApoE e2), as independent predictors of new intracranial hemorrhage (ICH) in the natural course of untreated brain arteriovenous malformations. We hypothesized that the risk of posttreatment ICH would also be greater in patients with brain arteriovenous malformations with these genotypes. METHODS: Two hundred fifteen patients undergoing brain arteriovenous malformation treatment (embolization, arteriovenous malformation resection, radiosurgery, or any combination of these) were genotyped and followed longitudinally. Association of genotype with new symptomatic ICH after initiation of treatment was assessed using Cox proportional hazards adjusted for treatment type, demographics, and established ICH risk factors censored at the time of the last follow-up evaluation or death. RESULTS: The cohort was 48% male and 55% Caucasian, and 52% had an ICH before the initiation of treatment; the mean age +/- standard deviation was 36.6 +/- 17.2 years. Posttreatment ICH occurred in 34 (16%) patients with a median follow-up period of 1.9 years (interquartile range, 1.6 yr). After adjustment, the risk of posttreatment ICH was greater for TNF-alpha-238 AG genotype (hazard ratio [HR], 3.5; 95% confidence interval [CI], 1.3-9.8; P = 0.016) and ApoE e2 (HR, 3.2; 95% CI, 1.0-9.7; P = 0.042). Similar trends for the TNF-alpha-238 AG genotype were seen in surgery (HR, 4.2; 95% CI, 0.6-28.8; P = 0.14) and radiosurgery subsets (HR, 3.8; 95% CI, 0.7-19.4; P = 0.11). An effect of ApoE e2 was seen in radiosurgery subsets (HR, 10.9; 95% CI, 1.3-93.7; P = 0.030), but not in surgery subsets (HR, 1.4; 95% CI, 0.3-7.4; P = 0.67). CONCLUSION: Despite a variety of different mechanisms for posttreatment hemorrhage, these data suggest that the TNF-alpha and ApoE genotypes may contribute common phenotypes of enhanced vascular instability that increase the risk of hemorrhagic outcome.

Racial/Ethnic differences in longitudinal risk of intracranial hemorrhage in brain arteriovenous malformation patients.

BACKGROUND AND PURPOSE: Race/ethnicity is associated with overall incidence of intracranial hemorrhage (ICH), but its impact in patients with brain arteriovenous malformation is unknown. We evaluated whether race/ethnicity was a risk factor for ICH in the natural course in a large, multiethnic cohort of patients with brain arteriovenous malformation followed longitudinally. METHODS: Data were collected prospectively for patients with brain arteriovenous malformation evaluated at the University of California, San Francisco (n=436) and retrospectively through databases and chart review in the 20 hospitals of the Kaiser Permanente Medical Care Program (n=1028). Multivariate Cox regression was performed to assess the influence of race/ethnicity on subsequent ICH, adjusting for risk factors. Cases were censored at first treatment, loss to follow-up, or death. RESULTS: Average follow up was 4.7+/-8.0 years for Kaiser Permanente Medical Care Program patients and 2.8+/-7.3 years for University of California, San Francisco patients with no difference in time to ICH between cohorts (log rank P=0.57). The annualized 5-year ICH rate was 2.1% (3.7% for ruptured at presentation; 1.4% for unruptured). Initial ICH presentation (hazard ratio: 3.0, 95% CI: 1.9 to 4.9, P<0.001) and Hispanic race/ethnicity (hazard ratio: 1.9, 95% CI: 1.1 to 3.3, P=0.02) were independent predictors of ICH, adjusting for age, gender, cohort, and a cohort-age interaction. The ICH risk for Hispanics versus whites increased to 3.1 (95% CI: 1.3 to 7.4, P=0.013) after further adjusting for arteriovenous malformation size and deep venous drainage in a subset of cases with complete data. Similar trends were observed for blacks (hazard ratio: 2.1, 95% CI: 0.9 to 4.8, P=0.09) and Asians (hazard ratio: 2.4, 95% CI: 0.8 to 7.1, P=0.11), although nonsignificant. CONCLUSIONS: This study reports the first description of race/ethnic differences in brain arteriovenous malformation, with Hispanics at an increased risk of subsequent ICH compared with whites.

MMP-9 expression is associated with leukocytic but not endothelial markers in brain arteriovenous malformations.

Brain arteriovenous malformations (BAVM) have high matrix metalloproteinase-9 (MMP-9) expression, the source of which is unclear. We hypothesized MMP-9 production might be due to inflammation in BAVM. Compared to control brain tissues (n = 5), BAVM tissue (n = 139) had a higher expression (by ELISA) of myeloperoxidase (MPO) (193 +/- 189 vs. 6 +/- 3, ng/mg, P < .001), MMP-9 (28 +/- 32 vs. 0.7 +/- 0.6, ng/mg, P < .001), and IL-6 (102 +/- 218 vs. 0.1 +/- 0.1, pg/mg, P < .001), but not eNOS (114 +/- 87 vs. 65 +/- 9, pg/mg, P = .09). MMP-9 expression in BAVM highly correlated with myeloperoxidase (R2 = .76, P < .001), as well as with IL-6 (R2 = .32, P < .001). In contrast, MMP-9 in BAVM poorly correlated with the endothelial marker, eNOS (R2 = .03, P = .05), and CD31 (R2 = .004, P = .57). Compared to non-embolized patients (n = 46), patients with pre-operative embolization (n = 93) had higher levels of myeloperoxidase (236 +/- 205 vs. 106 +/- 108, ng/mg, P < .001) and MMP-9 (33 +/- 35 vs. 16 +/- 20, ng/mg, P < .001), however the correlation between MMP-9 and myeloperoxidase was equally strong for both groups (R2 = .69, n = 93, P < .001, for both). MMP-9 expression correlated with the lipocalin-MMP-9 complex, suggesting neutrophils as the MMP-9 source. MPO co-localized with majority of MMP-9 signal by immunohistochemistry. Our data suggest that inflammation is a prominent feature of BAVM lesional phenotype, and neutrophils appear to be a major source of MMP-9 in these lesions.

Apolipoprotein E epsilon 2 is associated with new hemorrhage risk in brain arteriovenous malformations.

OBJECTIVE: Patients with brain arteriovenous malformation (AVM) are at life-threatening risk of intracranial hemorrhage (ICH). Identification of genetic variants associated with increased new ICH risk would facilitate risk stratification and guide therapeutic intervention. METHODS: Brain AVM patients evaluated at University of California, San Francisco or Kaiser Permanente Northern California were followed longitudinally. Primary outcome was new ICH after diagnosis; censoring events were any AVM treatment or last follow-up examination. The association of ApoE epsilon2 and epsilon4 genotype with new ICH was evaluated by Kaplan-Meier survival analysis and further characterized via a Cox proportional hazards model. RESULTS: We genotyped 284 brain AVM patients (50% women; 57% Caucasian; median follow-up time, 0.3 yr) including 18 patients with a history of new ICH). ApoE epsilon2, but not ApoE epsilon4 genotype, was associated with new ICH (P = 0.0052). ApoE epsilon2 carriers had fivefold increased risk of new ICH (hazard ratio, 5.09; 95% confidence interval, 1.46-17.7; P = 0.010; Cox proportional hazards model adjusting for race/ethnicity and clinical presentation). Subset analysis in the largest homogenous ethnic subcohort (Caucasians) confirmed the increased risk of new ICH in ApoE epsilon2 carriers (hazard ratio, 8.71; 95% confidence interval, 1.4-53.9; P = 0.020; multivariate model adjusting for clinical presentation). CONCLUSION: ApoE genotype may influence the risk of ICH in the natural course of brain AVM. The identification of genetic predictors of ICH risk may facilitate estimation of AVM natural history risk and individualize clinical decision-making and therapeutic recommendations.

Tumor necrosis factor-alpha-238G>A promoter polymorphism is associated with increased risk of new hemorrhage in the natural course of patients with brain arteriovenous malformations.

BACKGROUND AND PURPOSE: Identification of single-nucleotide polymorphisms (SNPs) associated with increased risk of new intracranial hemorrhage (ICH) after brain arteriovenous malformation (BAVM) diagnosis would facilitate risk stratification and identify potential targets for therapeutic intervention. METHODS: Patients with BAVM were longitudinally followed. Primary outcome was new ICH after diagnosis; censoring events were last follow-up or any BAVM treatment. We genotyped 4 promoter SNPs in 2 inflammatory cytokine genes: interleukin-6 (IL-6-174G>C; IL-6-572G>C) and tumor necrosis factor-alpha (TNF-alpha-238G>A; TNF-alpha-308G>A). Association of genotype with risk of new ICH was screened using chi2; SNPs associated with new ICH were further characterized using Cox proportional hazards. RESULTS: We genotyped 280 patients (50% female; 59% white, mean+/-SD age at diagnosis 37+/-17 years; 40% presenting with ICH). TNF-alpha-238G>A was associated with increased risk of new ICH after diagnosis (chi2; P=0.003). After adjusting for age, race/ethnicity, and clinical presentation, the risk of new ICH was increased for patients with TNF-alpha-238 AG genotype (hazard ratio, 4.01; P=0.015). No other SNP was found to be associated with new ICH. CONCLUSIONS: A TNF-alpha SNP was associated with increased risk of new ICH in the natural course of BAVMs. The role of inflammatory cytokines in the pathogenesis of BAVM hemorrhage merits further study.

Use of limbal ring-rod for radiological localisation of ocular foreign body.

The limbal ring-rod and the proportional geometric drawing method provide a simple, inexpensive, and fairly accurate measure for the radiological localisation of ocular foreign bodies, and the results simulate those of orbital tomography.