Search

The effectiveness of acupuncture in acute stroke remains largely untested and unproved. A randomized, controlled trial was carried out to study the feasibility of acupuncture in combination with conventional supportive treatment for acute stroke patients. A total of 30 patients, aged 46-74, with the onset of symptoms within 36 h were enrolled into the study after appropriate screening. All patients gave informed consent. Basing on the same supportive treatment, patients were randomly assigned to a treatment with or without acupuncture. The procedure and acupoint selection were discussed and decided through several meetings of a group of senior acupuncture doctors in Taiwan. Acupuncture was applied 3 times/week for 4 weeks. During the study period, there were no problems in conducting this trial in terms of patient availability and acceptance, and physician cooperation. A significantly better neurologic outcome was observed in the acupuncture group on day 28 and day 90. The improvement in neurologic status was greatest in patients with a poor neurologic score at baseline. There were no important side effects except for one episode of dizziness related to acupuncture treatment. The data and results of this study will be used as a guideline for planning a full-scale clinical trial, e.g. sample size calculation, method of randomization with stratification of prognostic factors, choosing acupuncture points and technique of acupuncture.

Complex regional pain syndrome (CRPS) is a disease with unclear pathophysiology. The condition is characterized by pain, soft tissue change, vasomotor change, and even psychosocial disturbance. It may affect the upper more than the lower extremities, and the distal more than the proximal. The trigger factors include carpal tunnel release, Dupuytren's repair, tendon release procedures, knee surgery, crush injury, ankle arthrodesis, amputation, and hip arthroplasty. Rarely, it has been associated with stroke, mastectomy, pregnancy, and osteogenesis imperfecta. Herein, we present a rare case of a patient who was diagnosed with CRPS after transradial cardiac catheterization. CRPS was first diagnosed due to hand swelling, allodynia, paresthesia, and the limited range of motion of interphalangeal, metacarpophalangeal, and wrist joints, with the preceding factor of transradial cardiac catheterization, and was then confirmed by a three-phase bone scan. After intensive physical therapy with hydrotherapy, manual soft tissue release, and occupational therapy for the hand function, there was much improvement in range of motion and hand function. There was no allodynia or painful sensation in the follow-up. After training, the functional status of this patient was adequate for daily activity.

beta-Lapachone, a novel anticancer drug, induces various human carcinoma cells to undergo apoptotic cell death. However, we report here that, in human osteocarcinoma (U2-OS) cells, beta-lapachone induces necrosis rather than apoptosis. beta-Lapachone-induced necrotic cell death in U2-OS cells was characterized by propidium iodide uptake, cytochrome c release, a decreased mitochondrial membrane potential, and ATP depletion. The mitochondrial potential transition (MPT), including the reduction of the mitochondrial transmembrane potential and the release of mitochondrial cytochrome c, occurred in beta-lapachone-treated cells; cotreatment of these cells with cyclosporin A, an inhibitor of MPT pore, failed to prevent necrotic cell death. This indicates that the MPT transition does not play a crucial role in this process. Furthermore, beta-lapachone-induced necrosis was independent of oxidative stress and caspase activation. However, excessive poly(ADP-ribose) polymerase (PARP) activation and subsequent depletion of intracellular NAD(+) and ATP were seen in beta-lapachone-treated U2-OS cells. Cotreatment with a PARP inhibitor, 3-aminobenzamide, decreased beta-lapachone-induced PARP activation and provided significant protection from necrosis by preventing depletion of intracellular NAD(+) and ATP. Taken together, our results suggest that PARP plays an important role in the signaling pathway for beta-lapachone-induced necrosis in U2-OS cells.