OBJECTIVE:To prepare cholecalciferol(VitD3)microcapsules and establish a method for their quantitative determination.METHODS:Microcapsules were prepared by complex coacervation method and VitD3 content was determined by HPLC.RESULTS:The prepared microcapsules had well-distributed particle size with average particle size of(103.9?26.2)?m and encapsulation efficiency of(90.8?2.68)%.The linear range of VitD3 was 0.1～1.0 ?g?mL-1(r=0.999 3)with mean recovery rate of 98.65% and a dissolution rate of above 75% at 45 min.CONCLUSION:VitD3 microcapsules was successfully prepared by the established method,and the established content determination method was proved to be simple and feasible.

The pharmacognostical study on root of An-gelica tsinlingensis K. T. Fu was reported in thispaper. The resouce, content of essential oil, mor-philogical and histological characteristics of thisroot all were investigated. Active components con-taining in the root were examined by TLC. The re-sults of the study mentioned above has also beencompared with that of Angelica sinensis (Oliv.)Diels. 8 common metal elements (Pb, Cr, Cu,Zn, Mn, Fe, Mg, Ca) were alos determined byusing atomic absorption spectrophotomtry. Scien-tific evidences for usage, development and drawingup quality standard of Angelica tsinlingensis K. T.Fu were provided.

The fibroblasts have long been considered as structural elements and playing a main role in wound healing. Recent studies indicated that fibroblasts are heterogenic cells and function as resident sentinel cells in inflammatory reaction. When activated by substances released during tissue injury or derived from infectious microorganisms or by proinflammatory cytokines, tissuespecific fibroblasts can transiently produce certain chemokines and initiate a cascade of inflammatory reaction. In addition fibroblasts can produce prostanoids that participate in inflammatory and immune responses. In this review, the new role of fibroblasts in regulation of inflammation and immune reactions and possible molecular mechanism will be discuss.

Background and purpose: L-asparaginase (L-Asp) is an important drug in the treatment of childhood lymphoid neoplasms at present, but a lot of adverse reactions of L-Asp were observed. Pegasparaginase (PEG-Asp) is available in China in recent years. This study aimed to explore efifcacy and side-effect of PEG-Asp as ifrst-line treatment in childhood acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LBL). Methods:A total number of 211 ALL or LBL patients were treated with CCLG 2008 or BFM-90 protocol with PEG-Asp or L-Asp between Apr. 2008 and Mar. 2013;42 patients, among whom, were 35 ALL patients and 7 LBL patients, were treated with PEG-Asp as ifrst-line treatment;169 patients were treated with L-Asp as ifrst-line treatment (including 53 patients treated with L-Asp during induction protocol; with PEG-Asp during consolidate protocol). The clinical outcome and adverse reaction of PEG-Asp with L-Asp were observe and compared. Results: There were 35 ALL patients in PEG-Asp ifrst-line treatment group and the complete remission rate after 1 course of PEG-Asp was 97.1%,however, which was 83.3%of high risk ALL patients. The complete remission rate of 7 LBL patients of PEG-Asp ifrst-line treatment group was 57.1%. There was no signiifcant difference between 2 groups (P>0.05). Thirty-four patients relapsed including 5 patients of PEG-Asp ifrst-line treatment group, 16 patients of L-Asp ifrst-line treatment group and 13 patients treated with L-Asp during induction protocol and with PEG-Asp during consolidate protocol. Thirty-one patients died including 3, 18, 10 patients in 3 groups respectively. Twenty-two patients died of relapse, 4 died without remission, 5 died of complications. There was also no signiifcant difference between 2 groups (P>0.05). The incidence rates of adverse reactions were 47.6% and 63.3% respectively. Anaphylaxis, liver functions abnormalities, blood coagulation abnormalities, gastrointestinal reaction, hyperglycemia and pancreatitis were common in our patients. The incidence rate of anaphylaxis in PEG-Asp as ifrst-line treatment group was lower than other groups (P=0.03). But there was no signiifcant difference been observed in the incidence of other adverse reaction. Conclusion: The short-term efifcacy of PEG-Asp as the ifrst-line treatment in childhood leukemia and lymphoma was satisfactory and the incidence rate of anaphylaxis was lower. However, we will still pay much attention to adverse reaction monitoring of PEG-Asp.

This study is to evaluate the curative effect of repairing the flexor tendons defect in the fibroosseous sheath by transferring the near flexor digitorum superficial tendons. Thirty-two cases (39 fingers) with acute flexor tendon defect in Zone I were repaired by transferring the flexor digitorum superficial tendons. Early protected passive motion was advocated postoperatively. All cases were followed up for 11 to 23 months. The outcome of fingers were excellent in 24,good in 12 and fair in 3 by TAM score. The percentage of excellent and good outcome was 92. 3%. Microrepair of fresh flexor tendons defect in Zone II by transferring flexor digitorum superficial tendons combined with early protected passive motion can prevent the adhension of tendons effectively and restore finger function earlier.

Objective To improve the recognition of aggressive natural killer-cell leukemia(ANKL)complicating muhiple organ failure(MOF).Methods A Fare case of ANKL was reported,and the related literatures were reviewed. Results One case of ANKL was diagnosed by bone marrow morphology and immunophenotypes of CD2,CD16,CD56,who developed multiple organ failure involving in liver,kidney,heart,lung,severe metabolic acidosis,tumour lysis syndrome and disseminated intravascular coagulation(DIC)in course of the disease and chemotherapy.VP regimen and symptomatic treatment were performed,and the disease could be stable shortly but died of the failure of lung and heart soon. Conclusion ANKL has a fulminant clinical course and diffuse infihration of tumor cells resulted in multiple organ failure with poor response to treatment and unfavorable prognosis.

BACKGROUND:It is shown in past researches that total saponin of ginseng has the effect of promoting multiplication of bone marrow hematopoietic stem cells and progenitor cells in vitro, and promoting secretion of bone marrow hemotopoietic factors, however there has been little researches on the effect of multiplication of bone marrow stromal cells.OBJECTIVE: To investigate the effect of ginsenoside Rg1 on pig's bone marrow stromal cells multiplication in vitro.DESIGN: A controlled observation.SETTING:Department of Cardiology and Department of Dermotology,First Affiliated Hospital, Nanjing Medical University; Department of Pharmacology, Nanjing Medical University.MATERIALS: The experiment was conducted at the Cardiovascular Pharmaceutical Laboratory of Nanjing Medical University from January 2002 to February 2003. The experimental pigs ahd the powder of ginsenoside Rg1were chosen METHODS :The bone marrow stromal cells cultured in vitro were divided as control and experimental groups. For experimental group insenoside Rg1 in different concentrations (10-7,5×10-7,10-6,5×104 mol/L)were added for induction culture, and for control group the media of the same volume was added. The multiplication conditions of bone marrow stromal cells were respectively detected by fibroblast colony forming in vitro, tritiated thymidine {[3H]TdR} incorporation and MTT.MAIN OUTCOME MEASURES: ① The effect of ginsenoside Rgl on the fibroblast colony forming units of bone marrow stromal cells in vitro. ②The effect of ginsenoside Rg1 on [3H]TdR incorporation of bone marrow stromal cells. ③ The effect of ginsenoside Rg1 on bone marrow stromal cells multiplication detected by MTT.RESULTS:① The effect of ginsenoside Rg1 on the fibroblast colony forming units of bone marrow stromal cells in vitro: The numbers of units in experimental group were all higher than that in control group (P ＜ 0.05-P ＜ 0.01),especially obvious in (5-50)×10-7 mol/L experimental group, reaching peak in the concentration being 10-6 mol/L. ② The effect of ginseno side Rg1 on [3H]TdR incorporation of bone marrow stromalcells: As the concentration of ginsenoside Rg1 was 10-6 mol/L, the [3H]TdR incorporation efficiency of bone marrow stromal cells was obviously higher that that in control group (P ＜ 0.05-P ＜ 0.01), and the effect was enhanced as the dosage increased. ③ The effect of ginsenoside Rgl on bone marrow stromal cells multiplication detected by MTT: The value of absorbance in experimental group was obviously higher than that in control group (P ＜ 0.05-P ＜ 0.01), and it was dose-dependent. CONCLUSION: Ginsenoside Rg1 had an effect of multiplication on pig's bone marrow stromal cells in vitro, and it was dose-dependent.

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells.OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2.DESIGN: A completely randomized controlled trial.SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University.MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children' s Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine treated group randomly, with 10 rats in each group.METHODS: In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue.pholipase A2) and type Ⅱ phospholipase A2 (cytoplasmic phospholipase A2)in brain tissue were measured in rats in all the groups.pholipsse A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group [(57.8 ±7.2),(42.5±6.1), (17.1±5.3)%, P＜ 0.05-0.01], and it was a litter lower in nimodipine brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group [(775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L,P ＜ 0.05-0.01], and it was lower in nimodipine group than in ischemia group (P ＜ 0.01).that in sham operation group [(82.9±0.5), (80.0±1.1), (72.1±0.01)%, P ＜ 0.05-0.01], and it was lower in nimodipine treated group than that in ischemia group (Ppase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased.CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.

AIM: To investigate the effect of PMA(phorbol 12-myristate 13-acetate) on the expression of CD18 and the mechanism. METHODS: The technique of quantitative RT-PCR analysis was used to measure the expression of CD18 mRNA in U937 cells treated by PMA. RESULTS: PMA could significantly induce CD18 mRNA expression in a dose and time-dependent manner. The induction effects of PMA on CD18 mRNA could be inhibited obviously by Myr (2 ?mol/L), a specific inhibitor of PKC, and APDC, an inhibitor of NF-?B, but not be inhibited by curcumin, a inhibitor of transcriptional factor AP-1. CONCLUSION: PMA enhanced the expression of CD18 via the pathway of PKC. Transcriptional factor NF-?B, but not AP-1, was essential for the gene transcription of CD18 in U937 cells treated by PMA.