A multicenter, randomized, controlled trial testing the effects of acupuncture on allergic rhinitis.

BACKGROUND: The aim of this study was to evaluate the efficacy and safety of acupuncture in the treatment for allergic rhinitis. METHODS: This study was a multicenter, randomized, parallel-controlled study. Participants were randomized to either the active acupuncture, sham acupuncture, or waitlist groups. The active and sham acupuncture groups received acupuncture treatment three times per week for 4 weeks. In the sham group, minimal acupuncture at nonacupuncture points was used. The waitlist group did not receive any acupuncture treatment. RESULTS: Of the 238 participants, 97, 94, and 47 individuals were assigned to the active acupuncture, sham acupuncture, and waitlist group, respectively. After the treatment, the difference in the total nasal symptom score (TNSS) was significantly reduced in the active acupuncture group compared with the sham acupuncture (difference: -1.03, 95% confidence interval [CI]: -1.96, -0.09, P = 0.03) and waitlist (difference: -2.49, 95% CI: -3.68, -1.29, P < 0.0001). The active acupuncture group exhibited a significant change in the total non-nasal symptom score (TNNSS) compared with the waitlist (difference: -0.78, 95% CI: -1.22, -0.34, P = 0.0002), but not the sham acupuncture group (difference; 0.15, 95% CI: -0.21, 0.5, P = 0.56). Both active and sham acupuncture treatments resulted in significant improvements in TNSS and TNNSS compared to baseline. CONCLUSION: Active acupuncture showed a significantly greater effect on symptoms of allergic rhinitis than either sham acupuncture or no active treatment. The symptoms of allergic rhinitis decreased significantly after treatment in the both acupuncture and sham acupuncture groups. Acupuncture appears to be an effective and safe treatment for allergic rhinitis.

Mutations in the cardiac troponin I gene associated with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM), the most common cause of sudden death in the young, is an autosomal dominant disease characterized by ventricular hypertrophy accompanied by myofibrillar disarrays. Linkage studies and candidate-gene approaches have demonstrated that about half of the patients have mutations in one of six disease genes: cardiac beta-myosin heavy chain (c beta MHC), cardiac troponin T (cTnT), alpha-tropomyosin (alpha TM), cardiac myosin binding protein C (cMBPC), ventricular myosin essential light chain (vMLC1) and ventricular myosin regulatory light chain (vMLC2) genes. Other disease genes remain unknown. Because all the known disease genes encode major contractile elements in cardiac muscle, we have systematically characterized the cardiac sarcomere genes, including cardiac troponin I (cTnI), cardiac actin (cACT) and cardiac troponin C (cTnC) in 184 unrelated patients with HCM and found mutations in the cTnI gene in several patients. Family studies showed that an Arg145Gly mutation was linked to HCM and a Lys206Gln mutation had occurred de novo, thus strongly suggesting that cTnI is the seventh HCM gene.