We compared the clinical efficacy of a short-term intervention of 308-nm excimer laser with that of narrow-band UVB (NBUVB) phototherapy for vitiligo patients to see the early response. Twenty-three symmetrically patterned patches of vitiligo on 8 patients were selected. Vitiligo patches on one side of the body were treated 2 times per week for a maximum of 20 treatments with the excimer laser, and NBUVB phototherapy was used on patches on the other side. Improvement (repigmentation) was assessed on a visual scale via serial photographs taken every five treatments and scored as follows: 0, or=75% improvement. At five treatments, the excimer laser-treated patches had an average score of 0.26, compared with 0.04 for patches treated with NBUVB phototherapy. A slightly higher repigmentation (p>0.05) in the excimer treated area was thus observed. At 10, 15, or 20 treatments, the differences between the average scores were significant: 0.83, 1.17, and 1.39 for the excimer-treated patches, and 0.17, 0.30, and 0.74 for the NBUVB pho-totherapy-treated areas (p<0.05). In conclusion, the 308-nm excimer laser appears to be more effective than NBUVB phototherapy, as it produces more rapid and profound repigmentation.
Adult ; Chlorides/*therapeutic use ; Comparative Study ; Female ; Humans ; Lasers/*therapeutic use ; Male ; Middle Aged ; Treatment Outcome ; *Ultraviolet Therapy ; Vitiligo/pathology/*radiotherapy ; Xenon/*therapeutic use

OBJECTIVETo study the effectiveness of radiation synovectomy with (188)Re-sulfide.

METHODSTwenty rabbit models of joint synovitis were injected intra-articularly with different doses of (188)Re-sulfide from 7.4 to 37.0 MBq. By pathological examination, the effects of (188)Re-sulfide on synovium and cartilage were evaluated. Clinically, 10 joints of 7 cases of hemophilic arthritis with (188)Re-sulfide radiation synovectomy were performed. MRI was taken before and after the synovectomy to evaluate the treatment effects.

RESULTSIn rabbit models, when (188)Re-sulfide dose larger than 14.8 MBq, the radiation effect on synovitis was remarkable, including thinning the thickened synovium and reducing the inflammatory cells. When radio-activity dose increased to 37.0 MBq, pathological damage was noted in cartilage. Clinical trial demonstrated that radiation synovectomy by (188)Re-sulfide could reduce the frequencies of intra-articular hemorrhage. MRI showed that edema and villi reduced.

CONCLUSIONSRadiation synovectomy using (188)Re-sulfide is effective on synovitis in hemophilic arthritis.

Animals ; Chlorides ; therapeutic use ; Disease Models, Animal ; Follow-Up Studies ; Hemophilia A ; complications ; Humans ; Injections, Intra-Articular ; Rabbits ; Rhenium ; therapeutic use ; Ruthenium Radioisotopes ; therapeutic use ; Sulfides ; Synovial Membrane ; radiation effects ; Synovitis ; etiology ; pathology ; radiotherapy

AIMTo investigate the effect of melatonin on learning and memory impairment in mice induced by aluminum chloride and its possible mechanism.

METHODSMice were treated with intracerebroventricular (icv) injection of 2 microL 5% aluminum chloride solution, once a day for 5 d. At the same time, the mice were given intraperitoneally melatonin 0.6, 3 and 15 mg.kg-1, once a day for 14 d. The passive avoidance of the mice was assessed by step-through test on day 15 after the last icv injection, and then the place navigation and spatial probe ability by Morris water maze were tested. After the spatial probe test, the activities of total superoxide dismutase (T-SOD), CuZn superoxide dismutase (CuZn-SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in the cerebral cortex and hippocampus of mice brain were determined.

RESULTSMelatonin ameliorated significantly the impairment of passive avoidance memory, the place navigation and spatial probe ability of mice induced by aluminum chloride. Melatonin was found to prevent significantly the decline of T-SOD, CuZn-SOD and GSH-Px activities, the increase of MDA content in the cortex and hippocampus of mouse brain induced by aluminum chloride.

CONCLUSIONThe results suggest that melatonin improves significantly the learning and memory impairment in mice induced by aluminum chloride, and this effect may be attributed to its antioxidation.

Aluminum Compounds ; Alzheimer Disease ; chemically induced ; metabolism ; Animals ; Antioxidants ; therapeutic use ; Cerebral Cortex ; drug effects ; metabolism ; Chlorides ; Glutathione Peroxidase ; metabolism ; Hippocampus ; drug effects ; metabolism ; Male ; Malondialdehyde ; metabolism ; Melatonin ; therapeutic use ; Memory Disorders ; drug therapy ; Mice ; Random Allocation ; Superoxide Dismutase ; metabolism

BACKGROUNDIncreasing evidence suggests that many neurons may die through apoptosis in Alzheimer's disease (AD). Mitochondrial dysfunction has been implicated in this process of neuronal cell death. One promising approach for preventing AD is based upon anti-apoptosis to decrease death of nerve cells. In this study, we observed the memory improving properties of curcumin in mice and investigated the neuroprotective effect of curcumin in vitro and in vivo.

METHODSThe mice were given AlCl(3) orally and injections of D-galactose intraperitoneally for 90 days to establish the AD animal model. From day 45, the curcumin group was treated with curcumin for 45 days. Subsequently, the step-through test, neuropathological changes in the hippocampus and the expression of Bax and Bcl-2 were carried out to evaluate the effect of curcumin on the AD model mice. In cultured PC12 cells, AlCl(3) exposure induced apoptosis. The MTT assay was used to measure cell viabilities; flow cytometric analysis to survey the rate of cell apoptosis; DNA-binding fluorochrome Hoechst 33258 to observe nuclei changes in apoptotic cells and Western blot analysis of Bax, Bcl-2 to investigate the mechanisms by which curcumin protects cells from toxicity.

RESULTSCurcumin significantly improved the memory ability of AD mice in the step-through test, as indicated by the reduced number of step-through errors (P < 0.05) and prolonged step-through latency (P < 0.05). Curcumin also attenuated the neuropathological changes in the hippocampus and inhibited apoptosis accompanied by an increase in Bcl-2 level (P < 0.05), but the activity of Bax did not change (P > 0.05). AlCl(3) significantly reduced the viability of PC12 cells (P < 0.01). Curcumin increased cell viability in the presence of AlCl(3) (P < 0.01). The rate of apoptosis decreased significantly in the curcumin group (P < 0.05) when measured by flow cytometric analysis. Curcumin protected cells by increasing Bcl-2 level (P < 0.05), but the level of Bax did not change (P > 0.05).

CONCLUSIONSThis study demonstrates that curcumin improves the memory ability of AD mice and inhibits apoptosis in cultured PC12 cells induced by AlCl(3). Its mechanism may involve enhancing the level of Bcl-2.

Aluminum Compounds ; toxicity ; Alzheimer Disease ; drug therapy ; psychology ; Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Chlorides ; toxicity ; Curcumin ; pharmacology ; therapeutic use ; Disease Models, Animal ; Female ; Learning ; drug effects ; Memory ; drug effects ; Mice ; Neuroprotective Agents ; pharmacology ; PC12 Cells ; Rats

AIMTo study the effect of modified starfish sterol [C03, succinic acid (5-epiandroene-17-one-3beta-ol) diester] on experimental arrhythmias.

METHODSArrhythmias were induced by drugs (Aco, Oua, BaCl2 and adrenalin) i.v., ligating the left anterior descending coronary artery and electricity.

RESULTSC03 71.4 mg x kg(-1) (ig) was shown to increase the dose of Oua inducing VP, VT, VF and CA in guinea pigs (P < 0.01); C03 (26.8, 80.4 mg x kg(-1)) was found to increase the dose of Aco inducing VF and CA in rats (P < 0.01); C03 (8.9, 26.8, 80.4 mg x kg(-1)) increase the dose of barium chloride and delay the onset time of ventricular arrhythmias (P < 0.01); C03 (14.1, 42.3 mg x kg(-10) shorten time of recovering induced by adrenalin in rabbits (P < 0.01); C03 (80.4 mg x kg(-1)) was shown to reduce the number of ventricular arrhythmias induced by coronary artery ligation in rats (P < 0.05), C03 increase VFT induced by electricity in rabbits, VFT of C03 14.1 mg x kg(-1) increased from (5.1 +/- 2.5) V to (11.0 +/- 2.7) V (P < 0.01), 42.3 mg x kg(-1) increased from (6.1 +/- 1.7) V to (15 +/- 5) V (P < 0.01).

CONCLUSIONStarfish sterol has anti-arrhythmic effect.

Aconitine ; Animals ; Anti-Arrhythmia Agents ; therapeutic use ; Arrhythmias, Cardiac ; chemically induced ; physiopathology ; prevention & control ; Barium Compounds ; Cats ; Chlorides ; Epinephrine ; Guinea Pigs ; Materia Medica ; isolation & purification ; therapeutic use ; Mice ; Ouabain ; Rabbits ; Rats ; Starfish ; chemistry ; Sterols ; isolation & purification ; therapeutic use ; Ventricular Fibrillation ; physiopathology

OBJECTIVETo examine the protective effect of Ginkgo biloba leaf extract (GbE) on learning and memory deficit induced by aluminum chloride (AlCl(3)), and explore its mechanisms.

METHODSThe rat models with learning and memory deficit were induced by administering via gastrogavage and drinking of AlCl(3) solution. And the model rats were treated with GbE at the dose of 50, 100, 200 mg/kg every day for 2 months accompanied with drinking of AlCl(3) solution, respectively. Their abilities of spatial learning and memory were tested by Morris water maze, and the acetylcholinesterase (AChE) activity in serum was assayed with chemical method, the AChE expression in hippocampus was observed by immunohistochemistry assay, and then quantitative analysis was done by BI 2000 image analysis system.

RESULTSLearning and memory deficit of rats could be induced by AlCl(3) solution (P < 0.01), and AChE expressions in rats hippocampus were increased (P < 0.01); GbE ameliorated learning and memory deficit and reduced AChE expression in rats hippocampus in a dose-dependent manner, while GbE significantly increased serum AChE activity at the dose of 200 mg/kg each day (P < 0.05).

CONCLUSIONGbE can ameliorate learning and memory deficit induced by AlCl(3), which may be due to its inhibition of the AChE expression in hippocampus.

Acetylcholinesterase ; metabolism ; Aluminum Compounds ; toxicity ; Animals ; Chlorides ; toxicity ; Dose-Response Relationship, Drug ; Ginkgo biloba ; Hippocampus ; enzymology ; Immunohistochemistry ; Male ; Maze Learning ; drug effects ; Memory Disorders ; chemically induced ; prevention & control ; Neuroprotective Agents ; therapeutic use ; Phytotherapy ; Plant Extracts ; therapeutic use ; Plant Leaves ; Plant Structures ; Rats ; Rats, Wistar ; Reaction Time

AIMTo study the protective effect and mechanism of osthol on learning and memory impairment of mice with acute senile model induced by AlCl3.

METHODSAfter s.c. AlCl3 60 mg.kg-1 for 7 d and i.p. osthol 15 and 7.5 mg.kg-1 for 12 d, using step-through test and step-down test, the effect of osthol on learning and memory was observed and the glutathione peroxidase (GSH-PX) activities in blood and superoxide dismutase (SOD) activities in plasma and cerebrum were measured.

RESULTSOsthol 15 and 7.5 mg.kg-1 significantly improved the capability of memory and enhanced the activities of GSH-PX and SOD in AlCl3 treated mice.

CONCLUSIONOsthol shows protective effect on brain memory impairment of mice in acute senile model induced by AlCl3. Perhaps the mechanism is involved in enhancing the activities of GSH-PX and SOD, clearing away the free radical, protecting the brain neuron from the harm of lipoperoxide.

Acute-Phase Reaction ; Aging ; drug effects ; metabolism ; Aluminum Compounds ; pharmacology ; Animals ; Avoidance Learning ; drug effects ; Brain ; enzymology ; Chlorides ; pharmacology ; Cnidium ; chemistry ; Coumarins ; isolation & purification ; pharmacology ; therapeutic use ; Female ; Glutathione Peroxidase ; blood ; Male ; Memory Disorders ; chemically induced ; enzymology ; prevention & control ; Mice ; Plants, Medicinal ; chemistry ; Random Allocation ; Superoxide Dismutase ; metabolism