Methoxyadiantifoline 10 mg/kg i.v. significantly increased the arrhythmia- inducing dose of aconitine in anaesthetized rats, and that of ouabain in anaesthetized guinea pigs. It markedly prevented ventr icular fibrillation induced by chloroform. Methoxyadiantifoline is also effective in preventing reperfusion-induced arrhythmias in anaesthetized rats. It was demonstrated that methoxyadiantifoline slowed heart rate significantly, and prolonged P-R and Q-Tc interval of ECG in rats.

Methoxyadiantifoline ( MAF) is a new alkloid isolated from Thalictrum Omeience W.T.Wang.During 3 min reperfusion after 10 min of coronary ligation, MAF 5 ?mol/L significantly decreased the incidence of isolated rat hearts with ventricular arrhythmias ( VF and VT ) . It delayed the onset of ventricular fibrillation and shortened its duration and markedly prolonged the time of normal sinus rhythm. It also significantly decreased the release of LDH from the myocardium in isolated rat hearts. In addition , MAF 5 ?mol/L could decrease the heart rate and coronary resistance. The results suggest that MAF possessed protective effects on the reperfusion injury in isolated rat hearts.

OBJECTIVETo investigate the therapeutic effect of soft tissue expansion combined with follicular unit extraction( FUE) for burn cicatricial bald.

METHODS48 patients with burn cicatricial bald (> 25 cm2) were treated in three stages. The expanders were implanted on the first stage. After expansion for 8 weeks, the expanders were taken out and local flaps were transferred. One year later, follicular unit extraction( FUE) was applied on the bald area.

RESULTS48 cases were followed up for 5 years with satisfactory cosmetic results. The VAS assessment of satisfaction on hair appearance after three-staged surgery was 8.2 ± 2.1.

CONCLUSIONSSoft tissue expansion combined with FUE has a reliable effect for burn cicatricial bald.

Alopecia ; etiology ; surgery ; Burns ; complications ; surgery ; Female ; Hair ; transplantation ; Hair Follicle ; transplantation ; Humans ; Male ; Surgical Flaps ; transplantation ; Tissue Expansion ; methods ; Tissue Expansion Devices

Objective:To explore the interventional effect of β-sitosterol on ovalbumin(OVA)-induced allergic asthma rats and its potential mechanism.Methods:SD male rats were randomly divided into normal group(CON),model group(M),positive drug dexamethasone group(DEX,0.075 mg/kg)and β-sitosterol group(Sit,50 mg/kg).A rat model of allergic asthma was estab-lished by intraperitoneal injection of OVA with aluminum hydrogen solution,and nebulized inhalation of OVA to stimulate.Rats were given intragastric administration 30 min before aerosol challenge,and after continuous administration for 7 days,the indicators of cough and asthma and tracheal phenol red excretion were detected.HE staining was used to observe pathological changes of lung tis-sue.Flow cytometry was used to detect reactive oxygen species(ROS)generation,apoptosis level and ratios of Th17 and Treg cells in peripheral blood.Biochemical method was used to detect contents of MDA,and activities of T-SOD and GSH-Px in rat lung tissues.ELISA was used to detect levels of Th17 and Treg-related cytokines(TNF-α,IL-4,IL-6,IL-17A,and IL-35).Results:Compared with model group,β-sitosterol significantly prolonged the incubation period of cough and gasp in rats with allergic asthma,reduced the frequency of cough and gasping,and promoted the excretion of phenol red in trachea;significantly reduced inflammatory infiltration in lung tissue of asthmatic rats;observably reduced MDA content in lung tissue,ROS of primary lung cell and apoptosis levels of asthmatic rats,increased the activities of T-SOD and GSH-Px;markedly reduced proportion of Th17 cells and levels of pro-inflammatory cyto-kines TNF-α,IL-4,IL-6 and IL-17A,increased proportion of Treg cells and levels of anti-inflammatory cytokine IL-35.Conclusion:β-sitosterol can ameliorate airway inflammation and oxidative damage in OVA-induced allergic asthmatic rats,and its mecha-nism may be related to the regulation of β-sitosterol on Th17/Treg immune imbalance and oxidative stress response.