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.

Cultural considerations in developing church-based programs to reduce cancer health disparities among Samoans.

OBJECTIVES: We examined receptivity to developing church-based cancer programs with Samoans. Cancer is a leading cause of death for Samoans, and investigators who have found spiritually linked beliefs about health and illness in this population have suggested the Samoan church as a good venue for health-related interventions. DESIGN: We interviewed 12 pastors and their wives, held focus groups with 66 Samoan church members, and engaged a panel of pastors to interpret data. All data collection was conducted in culturally appropriate ways. For example, interviews and meetings started and ended with prayer, recitation of ancestry, and an apology for using words usually not spoken in group setting (such as words for body parts), and focus groups were scheduled to last five hours, conferring value to the topic and allowing time to ensure that cancer concepts were understood (increasing the validity of the data collected). RESULTS: We found unfamiliarity with the benefits of timely cancer screening, but an eagerness to learn more. Church-based programs were welcome, if they incorporated fa'aSamoa (the Samoan way of life) -- including a strong belief in the spiritual, a hierarchical group orientation, the importance of relationships and obligations, and traditional Samoan lifestyle. This included training pastors to present cancer as a palagi (White man) illness versus a Samoan (spiritual) illness, about which nothing can be done, supporting respected laity to serve as role models for screening and witnesses to cancer survivorship, incorporating health messages into sermons, and sponsoring group education and screening events. CONCLUSION: Our findings inform programming, and our consumer-oriented process serves as a model for others working with minority churches to reduce cancer health disparities.

Rat bite fever without fever.

Rat bite fever is a rarely reported acute febrile bacterial illness caused by Streptobacillus moniliformis or Spirillum minus following a rat bite. It is classically characterised by abrupt onset of fever with rigors, myalgias, headache, and the appearance of a generalised maculopapular petechial skin rash. Polyarthritis complicates the course of the disease in up to 50% of infected patients, and numerous hurdles can make the diagnosis particularly difficult in the absence of fever or rash, as in the present case. A high degree of awareness is necessary to make the correct diagnosis in such cases. Diagnosis has important prognostic implications as the disease is potentially lethal, but easily treatable.

Plasma apolipoprotein(a) co-deposits with fibrin in inflammatory arthritic joints.

Extravascular coagulation and diminished fibrinolysis are processes that contribute to the pathology of both inflammatory arthritis and atherosclerosis. We hypothesized that, given its homology with plasminogen, apolipoprotein (apo) (a), the distinctive glycoprotein of the atherogenic lipoprotein (Lp) (a), may be equally implicated in inflammatory arthritis. We detected the presence of apo(a) as part of Lp(a) in human arthritic synovial fluid. The abundance of apo(a) in synovial fluid rose in proportion to plasma apo(a) levels and was higher in inflammatory arthritides than in osteoarthritis. In addition, apo(a) immunoreactive material, but not apo(a) transcripts, was detected in inflammatory arthritic synovial tissues. These data indicated that synovial fluid apo(a) originates from circulating Lp(a) and that diffusion of Lp(a) through synovial tissue is facilitated in inflammatory types of arthritis. In synovial tissues, apo(a) co-localized with fibrin. These observations could be reproduced in a model of antigen-induced arthritis, using transgenic mice expressing human Lp(a). Although in this mouse model the presence of apo(a) did not change the severity of arthritis, the co-localization of apo(a) with fibrin in synovial tissue suggests that, in humans, apo(a) may modulate locally the fibrinolytic activity and may thus contribute to the persistence of intra-articular fibrin in inflammatory arthritis.

Amelioration of collagen-induced arthritis by thrombin inhibition.

The deleterious role of fibrin deposition in arthritic joints prompted us to explore the effect of the thrombin inhibition on the course of collagen-induced arthritis (CIA) in the mouse. CIA was induced in male DBA/1J mice using native chicken type II collagen. The thrombin inhibitor polyethyleneglycol-hirudin (PEG-hirudin) was given for 16 days, starting 20 days after the first immunization (preventive treatment) or at the onset of clinical signs of arthritis (curative treatment). All the mice treated with PEG-hirudin had a significantly prolonged clotting time compared with control mice. PEG-hirudin, administered in a preventive way, led to significantly reduced incidence and severity of CIA during most of the treatment period, as assessed by clinical scoring. Accordingly, histological features showed a significant diminution of synovial hyperplasia in PEG-hirudin-treated mice compared with untreated mice. There was also a significant downmodulation of the synovial proinflammatory IL-1beta and IL-12p35 cytokine mRNAs in treated mice. Intra-articular fibrin, evaluated by immunohistochemistry, was significantly reduced in treated mice compared with control mice and correlated with both clinical and histological scorings. Most importantly, once arthritis was established, PEG-hirudin also showed a curative effect. In conclusion, PEG-hirudin can both prevent the onset of CIA in a dose-dependent manner and ameliorate established arthritis, suggesting that thrombin inhibition may offer a new therapeutic approach in arthritis.

Differential removal of thymidine nucleotide analogues from blocked DNA chains by human immunodeficiency virus reverse transcriptase in the presence of physiological concentrations of 2'-deoxynucleoside triphosphates.

Removal of 2',3'-didehydro-3'-deoxythymidine-5'-monophosphate (d4TMP) from a blocked DNA chain can occur through transfer of the chain-terminating residue to a nucleotide acceptor by human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT). ATP-dependent removal of either d4TMP or 3'-azido-3'-deoxythymidine-5'-monophosphate (AZTMP) is increased in AZT resistant HIV-1 RT (containing D67N/K70R/T215F/K219Q mutations). Removal of d4TMP is strongly inhibited by the next complementary deoxynucleoside triphosphate (50% inhibitory concentration [IC(50)] of approximately 0.5 microM), whereas removal of AZTMP is much less sensitive to this inhibition (IC(50) of >100 microM). This could explain the lack of cross-resistance by AZT-resistant HIV-1 to d4T in phenotypic drug susceptibility assays.

Effect of thrombin inhibition on synovial inflammation in antigen induced arthritis.

OBJECTIVE: To determine the effect of the thrombin inhibitor, hirudin, on the pathogenesis of murine antigen induced arthritis (AIA). METHODS: AIA was induced by intra-articular injection of methylated bovine serum albumin in the knee joints of previously immunised mice. Hirudin (injected subcutaneously 3 x 200 microg/mouse/day) was given over 13 days, starting three days before arthritis onset, and its anticoagulant effect monitored by clotting times. Arthritis severity was evaluated by technetium-99m ((99m)Tc) uptake in the knee joints and by histological scoring. In addition, intra-articular fibrin deposition was examined by immunohistochemistry, and synovial cytokine mRNA expression measured by RNase protection. RESULTS: Joint inflammation, measured by (99m)Tc uptake, was significantly reduced in hirudin treated mice at days 7 and 10 after arthritis onset. Histologically, synovial thickness was markedly decreased in hirudin treated mice compared with untreated ones. By contrast, no difference in articular cartilage proteoglycan content was found between both groups. Intra-articular fibrin deposition and synovial interleukin 1beta mRNA levels, were slightly reduced ( approximately 20%) in arthritic joints from hirudin treated mice compared with untreated ones at day 10 of AIA. CONCLUSION: Hirudin reduces joint inflammation associated with AIA by fibrin-dependent and independent mechanisms.

Effect of interleukin 17 on proteoglycan degradation in murine knee joints.

OBJECTIVE: To evaluate the effect of murine interleukin 17 (IL17) on cartilage catabolism and joint inflammation by direct intra-articular injection of the cytokine into murine knee joints. METHODS: Knees of normal C57 Bl mice were injected once or repeatedly with recombinant IL17 or IL1beta. Inflammation was estimated by technetium-99m pertechnetate ((99)Tc) uptake and histological scoring of tissue sections. Proteoglycan depletion was evaluated by histological scoring of safranin O stained sections. Effects on proteoglycan synthesis were studied by (35)SO(4) incorporation. RESULTS: A single intra-articular injection of IL17 (10 ng/knee) produced effects very similar to those of IL1beta (10 ng/knee). No inflammation was detected at six or 24 hours by (99)Tc uptake. However, safranin O staining showed depletion of proteoglycan at 48 hours. Repeated injections of IL17 induced joint inflammation and cartilage proteoglycan depletion as shown by histological scoring. Unlike IL1beta, proteoglycan depletion induced by IL17 seemed to be the result of increased degradation only, as no suppression of (35)SO(4) incorporation was seen. CONCLUSION: These findings confirm, in vivo, the catabolic effects of IL17 on cartilage. IL17 is thus the first T cell cytokine showing a direct catabolic effect on cartilage in addition to stimulatory effects on macrophages and synoviocytes, making it a potentially important cytokine in the pathogenesis of arthritis.

A mechanism of AZT resistance: an increase in nucleotide-dependent primer unblocking by mutant HIV-1 reverse transcriptase.

Mutations in HIV-1 reverse transcriptase (RT) give rise to 3'-azido-3'-deoxythymidine (AZT) resistance by a mechanism that has not been previously reproduced in vitro. We show that mutant RT has increased ability to remove AZTMP from blocked primers through a nucleotide-dependent reaction, producing dinucleoside polyphosphate and extendible primer. In the presence of physiological concentrations of ATP, mutant RT extended 12% to 15% of primers past multiple AZTMP termination sites versus less than 0.5% for wild type. Although mutant RT also unblocked ddAMP-terminated primers more efficiently than wild-type RT, the removal of ddAMP was effectively inhibited by the next complementary dNTP (IC50 approximately equal to 12 microM). In contrast, the removal of AZTMP was not inhibited by dNTPs except at nonphysiological concentrations (IC50 > 200 microM).

Propionibacterium avidum sacroiliitis and osteomyelitis.

The anaerobic Gram-positive bacterium Propionibacterium avidum is a common inhabitant of the skin with low pathogenicity. We report a case of P. avidum sacroilitis, psoas abscess and osteomyelitis in a 67-year-old male who had recently undergone surgical repair of an inguinal hernia. The organism was recovered from blood cultures, a bone biopsy specimen and specimens from the abscess. The spectrum of bone and joint infections caused by Propionibacterium is discussed. Infection by Propionibacterium spp. should be considered in patients with bone and joint infections.

Mechanisms of error discrimination by Escherichia coli DNA polymerase I.

The mechanism of base selection by DNA polymerase I of Escherichia coli has been investigated by kinetic analysis. The apparent KM for the insertion of the complementary nucleotide dATP into the hook polymer poly(dT)-oligo(dA) was found to be 6-fold lower than that for the noncomplementary nucleotide dGTP, whereas the Vmax for insertion of dATP was 1600-fold higher than that for dGTP. The ratio of Kcat/KM values for complementary and mismatched nucleotides of 10(4) demonstrates the extremely high specificity of base selection by DNA polymerase I and is in agreement with results obtained with a different template-primer, poly(dC)-oligo(dG) [El-Deiry, W. S., Downey, K. M., & So, A. G. (1984) Proc. Natl. Acad. Sci. U.S.A. 81, 7378]. Studies on the effects of phosphate ion on the polymerase and 3'- to 5'-exonuclease activities of DNA polymerase I showed that, whereas the polymerase activity was somewhat stimulated by phosphate, the exonuclease activity was markedly inhibited, being 50% inhibited at 25 mM phosphate and greater than 90% inhibited at 80 mM phosphate. Selective inhibition of the exonuclease activity by phosphate also resulted in inhibition of template-dependent conversion of a noncomplementary dNTP to dNMP and, consequently, markedly affected the kinetic constants for insertion of noncomplementary nucleotides. The mutagenic metal ion Mn2+ was found to affect error discrimination by both the polymerase and 3'- and 5'-exonuclease activities of DNA polymerase I.(ABSTRACT TRUNCATED AT 250 WORDS)

Molecular mechanisms of manganese mutagenesis.

The mechanism by which DNA polymerase discriminates between complementary and noncomplementary nucleotides for insertion into a primer terminus has been investigated. Apparent kinetic constants for the insertion of dGTP and dATP into the hook polymer d(C)194-d(G)12 with Escherichia coli DNA polymerase I (large fragment) were determined. The results suggest that the high specificity of base selection by DNA polymerase I is achieved by utilization of both Km and Vmax differences between complementary and noncomplementary nucleotides. The molecular basis for the increased error frequency observed with DNA polymerase I in the presence of Mn2+ has also been investigated. Our studies demonstrate that when Mn2+ is substituted for Mg2+, there is a higher ratio of insertion of incorrect to correct dNTP by the polymerase activity, accompanied by a decreased hydrolysis of a mismatched dNMP relative to a matched dNMP at the primer terminus by the 3',5' exonuclease activity. Kinetic analysis revealed that in the presence of Mn2+, the kcat for insertion of a complementary dNTP is reduced, whereas the catalytic rate for the insertion of a mismatched nucleotide is increased. The apparent Km values for either complementary or noncomplementary nucleotide substrates are not significantly altered when Mg2+ is replaced by Mn2+. The rate of hydrolysis of a mismatched dNMP at the primer terminus is greater in the presence of Mg2+ vs. Mn2+, whereas the rate of hydrolysis of a properly base-paired terminal nucleotide is greater in Mn2+ vs. Mg2+. These studies demonstrate that both the accuracy of base selection by the polymerase activity and the specificity of hydrolysis by the 3',5' exonuclease activity are altered by the substitution of Mn2+ for Mg2+.

Intestinal permeability and inflammation in rheumatoid arthritis: effects of non-steroidal anti-inflammatory drugs.

The suggestion that the intestinal mucosa may be abnormally permeable and a site of absorption of antigens in rheumatoid arthritis was tested by the use of a 51Cr-EDTA (edetic acid) absorption test. 24 patients with rheumatoid arthritis excreted significantly more 51Cr-EDTA than did 34 controls. Intestinal permeability was normal in untreated patients but almost invariably abnormal in patients treated with non-steroidal anti-inflammatory drugs. Studies in patients with osteoarthritis showed that the permeability abnormalities were due to an effect of NSAIDs on both the proximal and the distal intestine and that the effect was systemically mediated. Indium-111-labelled leucocyte scans showed ileocaecal inflammation in 6 of 9 patients on or recently on NSAIDs. Although increased intestinal permeability does not seem to be important in the pathogenesis of rheumatoid arthritis, the administration of NSAIDs may lead to loss of intestinal integrity, thus facilitating antigenic absorption and perhaps contributing to persistence of the disease.