AIM: To study the determination of dl-tetrahydropalmatine (THP) in Chi nese traditional patent medicines by TLC-Scanning from the viewpoint of the pro cess control of manufacture. METHODS: To select the 5 kinds of representative drugs and its prep arations contained, THP was extracted with solvent method. The mobile phase contains diethylamine. THP w as separated with high-efficiency silica gel plate or handcrafted silica gel p late. Iodine was used for chronogenic agent and fluorescence defectiion for dete rmination. TLC-Scanning results were compared with HPLC. RESULTS: The method is practicable, the result is correlative with the HPLC. CONCLUSION: TLC-Scanning is fit for the quality control of the Chi nese traditional patent medicine in the process of manufacture.

OBJECTIVETo establish a predicting model of survival rates and to evaluate the weighted contributions of each key prognostic factor of the patients with salivary adenoid cystic carcinoma (SACC).

METHODSOne hundred and eighteen follow-up cases with SACC were analyzed for the survival study with retrospective cohort method. Ten possible clinical and pathologic factors were selected. A multivariate analysis was performed by Cox proportional hazard model and prognostic index (PI) was calculated. According to the PI, all cases were divided into three risk subgroups respectively: lower, intermediate and higher risk subgroups. Ten-year survival rate and median survival time were calculated and the predicting models of survival rates were established.

RESULTSThe significant prognostic factors influencing the survival rate were age at diagnosis, clinical presentation, TNM clinical stage, treatment, surgical margins (P < 0.05). The predicting formula was PI = 0.031X(2) + 0.665X(5) + 0.420X(6)-0.576X(7) + 0.999X(10). According to the value of PI, the prognosis of the patients was significantly different among the three subgroups (P < 0.05). In the three risk subgroups, 10-year survival rates were 83.56%, 31.45% and 11.20% respectively, the median survival time was 18 years, 7 years and 4 years respectively.

CONCLUSIONSThe established predicting model of survival rates can predict the prognosis of the patients with SACC.

Adolescent ; Adult ; Aged ; Carcinoma, Adenoid Cystic ; mortality ; surgery ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Prognosis ; Salivary Gland Neoplasms ; mortality ; surgery ; Survival Rate ; Young Adult

Humans ; Thyroid Neoplasms/pathology* ; Carcinoma, Papillary/pathology* ; World Health Organization ; Adenocarcinoma, Follicular/pathology*

This study was aimed to establish an experimental mouse model of combined transgenic inhibition of both multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and inward rectifier potassium current (Ik1), and to observe whether the specific inhibition of both CaMKII and Ik1 can bring about any effects on cardiac remodeling. Mice were divided into 4 groups: wild type (WT), CaMKII inhibited (AC3-I), Ik1 inhibited (Kir2.1-AAA) and combined inhibition of both CaMKII and Ik1 (AC3-I+Kir2.1-AAA). Mice in each group received electrocardiogram (ECG) and echocardiography examination. ECG in the condition of isoproterenol (ISO) injection was also checked. The whole cell patch clamp technique was used to measure Ik1 and the transient outward potassium current (Ito) from enzymatically isolated myocytes of left ventricle. In the condition of basal status, no significant changes of heart rate, PR interval and QRS interval were observed. No mouse showed ventricular arrhythmias in all of the 4 groups. After ISO injection, each group presented no significant ventricular arrhythmias either. The indexes measured by M-mode (motion-mode) and two-dimensional echocardiography had no significant differences among the four groups. Ik1 in AC3-I group was significantly higher than those in other three groups (P < 0.01) because of the results brought about by CaMKII inhibition. Among the latter three groups, both Kir2.1-AAA group and AC3-I+Kir2.1-AAA group had a significant reduced Ik1 compared with that of WT group, which was due to the Ik1 inhibition (P < 0.01). Ito in AC3-I group was higher than that of the other three groups (P < 0.01), but there were no significant differences in Ito among WT, Kir2.1-AAA and AC3-I+Kir2.1-AAA groups. Thus, combined transgenic myocardial CaMKII and Ik1 inhibition eliminated the up-regulation of Ik1 in CaMKII inhibited mice, and had no effects on cardiac remodeling including heart structure and function as well as arrhythmias at the basic and ISO conditions. The results of this study may provide a basis for the further investigation of combined inhibition of CaMKII and Ik1 in pathogenic cardiac remodeling.
Animals ; Arrhythmias, Cardiac ; Brugada Syndrome ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; physiology ; Cardiac Conduction System Disease ; Disease Models, Animal ; Electrocardiography ; Heart ; physiology ; Heart Conduction System ; abnormalities ; Heart Ventricles ; Isoproterenol ; Mice ; Mice, Transgenic ; Patch-Clamp Techniques ; Potassium Channels, Inwardly Rectifying ; physiology ; Up-Regulation ; Ventricular Remodeling