No abstract available.
Carcinogenesis* ; Oenothera biennis*

No abstract available.
Animals ; Euonymus* ; Mice*

No abstract available.
Animals ; Capsaicin* ; Macrophages, Peritoneal* ; Mice*

No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*

No abstract available.
Animals ; Cyclophosphamide* ; Food Deprivation* ; Mice*

Case histories of isolated and complete volar dislocation of the carpal scaphoid have rarely been reported .We report here another such case. On examination, the wrist was moderately swollen and tender over its volar aspect. Radiographs showed isolated, complete volar dislocation of the scaphoid. We used open reduction with K-wire fixation as treatment. After four weeks of operative reduction the patient had undertaken neurolysis due to median nerve compression symptom (carpal tunnel syndrome). At six weeks, the K-wires were removed and the patient was allowed to do a range of motion exercise. Twenty months after injury, the wrist was asymptomatic and had a mid-range of active motion without instability. There was no roentgenographic evidences of scapholunate dissociation or avascular necrosis
Dislocations* ; Humans ; Median Nerve ; Necrosis ; Range of Motion, Articular ; Wrist

Capsaicin, the pungent principle of hot peppers, is a neurotoxin that depletes unmyelinated primary sensory neurons (polymodal nociceptors) of neuropeptides like tachykinins. However, the role of capsaicin-sensitive sensory nerve in the production of cytokines, penicillin V (PEV)-induced active fatal anaphylaxis and other immune responses is not yet fully established. Neonatal mice were pretreated s.c. with a single injection of 10 ug of capsaicin per mouse in volume of 20 ul within 5 days of age. Using 5-8 week old mice pretreated as neonates with capsaicin, the capsaicin- pretreated and vehicle-treated control mice were examined for various parameters of immune responses described above. For the induction of active fatal anaphylaxis with PEV, 8 week old mice pretreated as neonates and age-matched capsaicin- untreated control mice were sensitized i.p. with 500 ug of PEV-ovalbumin conjugate plus 2*10(9) B. pertussis and 1.0 mg alum and challenged i.v. with PEV-bovine serum albumin conjugate 14 days later. It was found that neonatal capsaicin-pretreatment significantly enhanced contact hypersensitivity to TNCB and hemagglutination response to SRBC, but significantly inhibited the proliferation response of rnurine splenocyte to Con A and LPS. Interestingly, neonatal capsaicin pretreatment significantly inhibited the intensity of PEV-induced active fatal anaphylaxis and decreased the mortality due to anaphylactic shock. It also significantly inhibited LPS- induced production of cytokines such as TNF-a, IL-1B, IL-6, IL-10, and IL-12. The capsaicin-pretreatment also resulted in an inhibition of the activation of NF-kB. Taken together, these data showed for the first time that neonatal capsaicin-pretreatment significantly inhibited an antibiotic (PEV)-induced anaphylaxis and production of various cytokines, and suggest that capsaicin-sensitive primary sensory nerve may play an important regulatory role in active fatal anaphylaxis and cytokine production, thus potentially presenting tools for immune intervention. In particular, the data presented also indicated the possibility to selectively down-modulate cytokine production and NF-kB activation may offer a broad application for therapeutic intervention in neuroimmunological diseases and other pathological situations.
Anaphylaxis ; Animals ; Capsaicin* ; Cytokines ; Denervation* ; Dermatitis, Contact ; Hemagglutination ; Humans ; Infant, Newborn ; Interleukin-10 ; Interleukin-12 ; Interleukin-6 ; Mice ; Mortality ; Neuropeptides ; NF-kappa B ; Penicillin V ; Sensory Receptor Cells ; Serum Albumin ; Tachykinins ; Whooping Cough

PURPOSE: It is not clear that the development of glomerular injury and aggravation by tumor necrosis factor alpha (TNF-alpha) is related to intrarenal or serum concentration of TNF-alpha. So, we studied the relationship between the concentration of TNF-alpha and aggravation of glomerular damage in the Henoch-Schonlein nephritis(HSN) and idiopathic nephrotic syndrome(INS). METHODS: We collected the sera and urines of 21 patients with Henoch-Schonlein purpura(HSP) and 22 patients with INS visited Chungbuk National University hospital from March 1998 to March 2001. The concentration of TNF-alpha in the sera and urines were measured by sandwich ELISA. RESULTS: Serum TNF-alpha levels in the HSP patients with renal involvement were significantly higher than those without renal involvement(P=0.009). But urine TNF-alpha levels have no correlation with renal involvement(P=0.088). In the HSN patients, proteinuria have a significant correlation with serum TNF-alpha levels(P=0.004) but less correlation with urine TNF-alpha levels(P=0.053). Otherwise, proteinuria have no correlation with serum TNF-alpha levels(P=0.763) but have a significant correlation with urine TNF-alpha levels(P=0.007) in INS. CONCLUSION: These result suggest that the serum concentration of TNF-alpha would be important to glomerular involvement in HSP. And, it is interesting that proteinuria shows a significant relation with serum TNF-alpha levels in the HSN, but with urine TNF-alpha levels in the INS. This means the major production of TNF-alpha may be originated by extrarenal inflammation in the HSN and by intrarenal tubulo-interstitial damage due to proteinuria in the INS.
Chungcheongbuk-do ; Enzyme-Linked Immunosorbent Assay ; Humans ; Inflammation ; Nephritis* ; Nephrotic Syndrome* ; Proteinuria* ; Tumor Necrosis Factor-alpha*

No abstract available.
Osteomyelitis* ; Radionuclide Imaging*

Glycopyrrolate, a synthetic quarternary ammonium compound, has a similar pharmacologic property to that of scopolamine, a belladonna alkaloid. Since glycopyrrolate, a quarternary ammonium compound, dose not readily cross the blood brain barrier, it has less central effect than that of scopoiamine a tertiary-amine compound. The authors administered a small dose of scopolamine and glycopyrrolate to human volunteers, and examined the effect on the heart rate ofr both drugs. The results were as follows: 1) A small dose of scopolamine(0.1mg) showed significnat decrease in the heart rate. 2) A small dose of gylcopyrrolate(0.1mg) indeced little change in the heart rate. 3) A small dose of gylcopyrrolate(0.1mg), 10minutes after glycopyrrolate(0.1mg), showed marked increase in the heart rate. 4) A small dose of scopolamine(0.1mg), given 10 minutes after glycopyrrolate (0.1mg), showed tendency for decrease in heart kate. 5) A small dose of gylcopyrrolate(0.1mg), 10 minutes afterscopolamine(0.1mg), showed significant increases in the heart rate. 6) Scopolamine induced bradycardia was suppressed by an additional dose of glycopyrrolate and a preceding dose of glycopyrrolate.
Humans