• The Korean Journal of Pain
• /
• v.6 no.2
• /
• pp.275-279
• /
• 1993

Reflex sympathetic dystrophy is a syndrome characterized by persistent, burning pain, hyperpathia, allodynia & hyperaesthesia in an extremity, with concurrent evidence of autonomic nervous system dysfunction. It generally develops after nerve injury, trauma, surgery, et al. The most successful therapies are directed towards blocking the sympathetic intervention to the affected extremity by regional sympathetic ganglion block or Bier block with sympathetic blocker; other traditional treatments include transcutaneous electrical stimulation, immobilization with cast & splint, physical therapy, psychotherapy, administration of sympathetic blocker, calcitonin, corticosteroid and analgesic agents. The purpose of this report is to evaluate and describe the effects of magnetic resonance following unsatisfactory results with traditional treatments of RSD. A 17 year old female patient, 1 year earlier, had received excision and drainage of pus at the right femoral triangle due to an injury caused by a stone. Afterwards, she experienced burning pain, knee joint stiffness, and muscle dystrophy of the right thigh, especially when standing and walking. Despite a year of number of traditional treatments such as: lumbar sympathetic block, continuous epidural analgesia, transcutaneous electrical stimulation, & administration of predisolone, her pain did not improve. Surprisingly, the patients was able to walk free from pain and difficulty after just one application of magnetic resonance. The patient has been successfully treated with further treatment of two to three times a week for approximately ten weeks. More recently, magnetic resonance has been demonstrated to produce effective results for the relief of pain in a variety of diseases. From our experiences we recognize magnetic resonance as a therapeutic modality which can provide excellent results for the treatment of RSD. It has been suggested that polysynaptic reflex which are disturbed in RSD may be modulated normally on the spinal cord level through the application of magnetic resonance.

• Journal of Applied Biological Chemistry
• /
• v.66
• /
• pp.213-220
• /
• 2023

The most common skin disease, acne, often occurs in adolescence, but it is also detected/observed in adults due to air pollution and drug abuse. One of the causative agents of acne, Cutibacterium acnes (C. acnes) plays a role in the development of skin acne by inducing inflammatory mediators. Torreya nucifera (TN) is an evergreen tree of the family Taxaceae, having well reported antioxidant, anti-proliferative, liver protection, and nerve protection properties. Improvement of these bioactive properties of natural products is one of the purposes of natural product chemistry and pharmaceuticals. We believe biorenovation could be one improvement strategy that utilizes microbial metabolism to produce unique derivatives having enhanced bioactivity. Therefore, in this study, the C. acnes-induced RAW264.7 inflammation model was used to evaluate the anti-inflammatory activity of the biorenovated Torreya nucifera product (TNB). The results showed improved viability of TNB-treated cells compared to TN-treated cells in the concentration range of 50, 100, and 200 ㎍/mL. At non-toxic concentrations, TNB inhibited the production of nitric oxide and prostaglandin E2 by suppression of inducible nitric oxide synthase and cyclooxygenase-2 protein expression. TNB also attenuated the expression of interleukin-1β, interleukin-6, interleukin-8, and tumor necrosis factor-α induced by C. acnes. Furthermore, TNB inhibited the nuclear factor-κB signaling pathway, a transcription factor known to regulate inflammatory mediators. Based on these results, this study suggests the potential of using TNB as natural material for the treatment of acnes and thus, supporting our postulation of biorenovation as an bioactivity improvement strategy.

• Journal of Yeungnam Medical Science
• /
• v.10 no.2
• /
• pp.451-474
• /
• 1993

Lidocaline if frequently administered as a component of an anesthetic : for local or regional nerve blocks, to mitigate the autonomic response to laryngoscopy and tracheal intubation, to suppress the cough reflex, and for antiarrythmic therapy. Diazepam dectease the potential central nervous system (CNS) toxicity of local anesthetic agents but may modify the sitmulant action of lidocaine in addition to their own cardiovascular depressant. The potential cardiovascular toxicity of local anesthetics may be enhanced by the concomitant administration of diazepam. This study was designed to investigate the effects of lidocaine dose and pretreated diazepam to cardiovascular system and plasma concentration of lidocaine. Lidocaine in 100 mcg/kg/min, 200 mcg/kg/min, and 300 mcg/kg/min was given by sequential infusion to dogs anesthetized with halothane-nitrous oxide (Group I). And in group II, after diazepam pretreatment, lidocaine was infused by same way when lidocaine was administered in 100 mcg/kg/min, the low plasma levels ($3.97{\pm}0.22-4.48{\pm}0.36$ mcg/ml) caused a little reduction in cardiovascular hemodynamics. As administered in 200 mcg/kg/min, 300 mcg/kg/min, the higher plasma levels ($7.50{\pm}0.66-11.83{\pm}0.59$ mcg/ml) reduced mean arterial pressure (MAP), cardiac index (CI), stroke index (SI), left ventricular stroke work index (LVSWI), and right ventricular stroke work index (PVSWI) and increased pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), systemic vascular resistance index (SVRI), but was associated with little changes of heart rate (HR), mean pulmonary artery pressure (MPAP), and pulmonary vascular resistance index (PVRI). When lidocaine with pretreated diazepam was administered in 100 mcg/kg/min, the low plasma level, the lower level than when only lidocaine administered, reduced MAP, but was not changed other cardiovascular hemodynamics. While lidocaine was infused in 200 mcg/kg/min, 300 mcg/kg/min in dogs pretreated diazepam, the higher plasma level ($7.64{\pm}0.79-13.79{\pm}0.82$ mcg/ml) was maintained and was associated with reduced CI, SI, LVSWI and incresed PAWP, CVP, SVRI but was a little changes of HR, MPAP, PVRI. After $CaCl_2$ administeration, CI, SI, SVRI, LVSWI was recovered but PAWP, CVP was rather increased than recovered. The foregoing results demonstrate that pretreated diazepam imposes no additional burden on cardiovascular system when a infusion of large dose of lidocaine is given to dogs anesthetized with halothanenitrous oxide. But caution may be advised if the addition of lidocaine is indicated in subjects who have impared autonomic nervous system and who are in hypercarbic, hypoxic, or acidotic states.