OBJECTIVE:To prepare Xiaozhong zhitong cataplasma,establish a method for its quality control and to observe its clinical efficacy on orthopedic patients(30 cases).METHODS:Based on the precompounded prescription order of Xiaozhong zhitong powder with water soluble polymer substance as base material which were evenly mixed with the drug extractives before being applied on non-woven fabric to prepare Xiaozhong zhitong cataplasma.The clinical efficacy was compared between the trial group(Xiaozhong zhitong cataplasma) and the control group(Xiaozhong zhitong powder).RESULTS:The prepared Xiaozhong zhitong cataplasma had smooth surface and uniform thickness,with a satisfactory stability achieved within 3 months at a dosage of 0.715 6 g?100 cm-2.The total effective rate in the trial group(93.3%) was significantly higher than in the control group(76.7%)(P

OBJECTIVE:To investigate the use of antibiotics in the inpatients of our hospital.METHODS:The medical records of inpatients from Jan.2004 to Dec.2006 randomly selected in our hospital were analyzed statistically in respect to the irrational use of antibiotics.RESULTS:Of the total 1,120 inpatient medical records examined,843(75.3%) used antibiotics,56 involved irrational use of antibiotics,which manifested as improper in dosage,dosage regimen,drug combination or solvents selection etc.CONCLUSION:The irrational use of antibiotics is quite common,thus the role of clinical pharmacists should be strengthened to promote rational use of antibiotics in clinical practice.

Objective To evaluate the clinical efficacy and analyze relevant prognostic factors of simultaneous integrated boost intensity-modulated radiation therapy ( SIB-IMRT ) for esophageal squamous cell carcinoma. Methods A total of 101 patients diagnosed with esophageal squamous cell carcinoma received SIB-IMRT from 2009 to 2015. The prescribed dose of PTV was 5040 cGy/28 times ( 180 cGy/time) and the dose for planning gross tumor volume (PGTV) was 6020 cGy/28 times (215 cGy/time) or 6160 cGy/28 times ( 220 cGy/time) simultaneously. The total treatment time was 5. 5 weeks ( once a day, 5 times a week).The adverse events, mode of treatment failure,l-,3-and 5-year local control (LC) and overall survival ( OS) rates were observed. Results The quantity of patients who completed the 1-,3-and 5-year follow-up was 101, 84 and 45, respectively. The 1-,3-and 5-year LC rates were 81. 6％,70. 4％ and 68. 4％, respectively. The 1-, 3-and 5-year OS rates were 72. 3％, 49. 4％ and 45. 2％, respectively. The median survival time was 36 months. Univariate and multivariate analyses showed that clinical staging ( stageⅠ/Ⅱ/Ⅲ) and tumor response ( complete remission/ partial remission/no remission ) were the prognostic factors of OS (P=0. 016,0. 000,0. 005,0. 000).There were no significant differences in the LC and OS between the two groups of 215 cGy and 220 cGy (P=0. 283,0. 951).The incidence rates of grade 1,2,3 acute pneumonitis were 10. 9％(11/101),2. 0％(2/101) and 2. 0％(2/101), respectively. The incidence rates of grade 1, 2, 3 acute esophagitis were 63. 4％( 64/101 ) , 10. 9％( 11/101 ) and 4. 0％( 4/101 ) , respectively. No acute esophageal perforation or hemorrhage occurred. Five patients experienced late pneumonitis ( two died) . One case developed late lemostenosis, two cases developed esophageal perforation and hemorrhage, and two patients experienced esophageal hemorrhage. The patients treated with a fractionated dose of 220 cGy had a higher incidence rate of acute pneumonitis and upper gastrointestinal adverse reactions than those receiving 215 cGy ( P= 0. 062, 0. 024 ) . The local failure and recurrence accounted for 62. 5％ of all treatment-related failures. Conclusions SIB-IMRT yields high long-term clinical efficacy and tolerable adverse events in the treatment of esophageal squamous cell carcinoma. Compared with the dose of 215 cGy, the fractionated dose of 220 cGy fails to improve LC and OS rates, whereas enhances the risk of adverse events. The clinical staging and short-term clinical efficacy are the prognostic factors of survival rate.

OBJECTIVE To explore the regulatory effects of baicalin on the proliferation and migration of human periodontal ligament stem cells （hPDLSCs） induced by lipopolysaccharide （LPS） and Janus protein tyrosine kinase 2 （JAK2）/signal transduction and transcription activator 3 （STAT3） signaling pathways. METHODS hPDLSCs were divided into control group， LPS group， different concentration baicalin groups （0.1， 1 and 10 mg/L）. ELISA method and CCK-8 assay were used to determine the contents of cell inflammatory factors [interleukin 6 （IL-6）， IL-1β and tumor necrosis factor-α （TNF-α）] and cell viability， so as to screen the optimal concentration of baicalin for follow-up pathway validation experiments. The cells were then divided into control group， LPS group， optimal baicalin concentration group and inhibitor group （10 μg/mL LPS+1 mg/L baicalin +3 μmol/L JAK2/STAT3 pathway inhibitor AG490）. After treated for 24 h， the proliferation rate of hPDLSCs， apoptosis rate， migration rate， invasion cell number， mRNA and protein expressions of Cyclin D1 and caspase-3， the expression of JAK2/STAT3 pathway-related proteins were all detected. RESULTS According to cell inflammatory factors and cell viability， 1 mg/L was selected as the optimal concentration of baicalin. Compared with control group， cell proliferation rate， migration rate， invasion cell number， Cyclin D1 mRNA and protein expression were significantly decreased in LPS group， while cell apoptosis rate， caspase-3 mRNA and protein expression， p-JAK2 and p-STAT3 protein expression were significantly increased （P＜0.05）. After treated with 1 mg/L baicalin， the above indexes were reversed significantly （P＜0.05）. The improvement of above indexes in the inhibitor group was more obvious （P＜0.05）. CONCLUSIONS Baicalin can promote the proliferation， migration and invasion of LPS-induced hPDLSCs and inhibit their apoptosis and inflammation by blocking the JAK2/STAT3 pathway.

Oral potentially malignant disorders (OPMDs) are precursors of oral squamous cell carcinoma (OSCC). Deregulated cellular energy metabolism is a critical hallmark of cancer cells. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) plays vital role in mitochondrial energy metabolism. However, the molecular mechanism of PGC1α on OPMDs progression is less unclear. Therefore, we investigated the effects of knockdown PGC1α on human dysplastic oral keratinocytes (DOKs) comprehensively, including cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ETC), reactive oxygen species (ROS), oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake. We found that knockdown PGC1α significantly inhibited the proliferation of DOKs in vitro and tumor growth in vivo, induced S-phase arrest, and suppressed PI3K/Akt signaling pathway without affecting cell apoptosis. Mechanistically, downregulated of PGC1α decreased mtDNA, ETC, and OCR, while enhancing ROS, glucose uptake, ECAR, and glycolysis by regulating lactate dehydrogenase A (LDHA). Moreover, SR18292 (an inhibitor of PGC1α) induced oxidative phosphorylation dysfunction of DOKs and declined DOK xenograft tumor progression. Thus, our work suggests that PGC1α plays a crucial role in cell proliferation by reprograming energy metabolism and interfering with energy metabolism, acting as a potential therapeutic target for OPMDs.
Humans ; Carcinoma, Squamous Cell/metabolism* ; Cell Proliferation ; DNA, Mitochondrial ; Energy Metabolism ; Glucose ; Mouth Neoplasms/metabolism* ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism* ; Phosphatidylinositol 3-Kinases ; Reactive Oxygen Species