Acupuncture Points ; Acupuncture Therapy ; instrumentation ; Catgut ; Female ; Humans ; Infertility, Female ; blood ; therapy ; Moxibustion ; Treatment Outcome

OBJECTIVE:To explore the relevant factors that led to the adverse drug reaction(ADR)of netilmicin.METHODS:ADR cases resulted from netilmicin reported in12kinds of Chinese periodicals from1998to2003were analyzed statistically.RESULTS:The ADR of netilmicin involved multiple organs and systems,the clinical manifestation were compli-cated and diversified,which manifested mainly on the renal toxicity,toxicity of nervous system and allergic reaction.CON-CLUSION:Clinician and pharmacists should be alert to the ADR of netilmicin and keep using drugs rationally.

Antigens, CD34 ; metabolism ; Craniotomy ; Diagnosis, Differential ; Follow-Up Studies ; Hemangiosarcoma ; metabolism ; pathology ; surgery ; Humans ; Male ; Middle Aged ; Skull ; pathology ; surgery ; Skull Neoplasms ; metabolism ; pathology ; surgery ; Vimentin ; metabolism

Objective To study the molecular biology of rifampin-depending M. Tuberculosis. Methods The seguence (a 319-bp DNA fragment) of rpoB gene were analyzed by automated DNA sequencing machine. (2) The fingerprints of genomic DNA were obtained by random amplified polymorphic DNA (RAPD) fingerprinting. (3)The protein electrophoresis of bacterium by SDS-polyacrylamide gel (SDS-PAG).(4) The cases of pulmonary tuberculosis by rifampin-depending strains were retrospectively analyzed. Results (1) rpoB gene sequenced: The point mutationrate of rifampin-depending strainswas 96.7%(29/30) and that of rifampin-residtant strains 81.1%(30/37), P

T were also detected in the controls.Conclusion Nephrotic syndrome may be associated with NPHS2 identified in children.

Objective To observe the effect of gheocorticoid by oral medication or intrathoracic iniection on the expression of IL-6,IL-8 and sIL-2R in gerum and pleural fluid in patients of tuberculous pleurisy.Methods Twenty tuberculous pleurisy patients were treated with ghcocortieoid by oral medication (oral group)and 20 cases by intrathoracic injection(injection group).ELISA wag employed to detect the levels of IL-6,IL-8 and sIL-2R in serum and pleural fluid before treatment and 3,6 and 9 days after treatment.Results The levels of serum IL-6 and IL-8 decreased and sIL-2R increased obviously in injection group at 3,6 and 9 days after treatment(P＜0.01).Meanwhile the levels of IL-6 and IL-8 in pleural fluid decreased and sIL-2R increased obviously(P＜0.01).The levels of IL-6 and IL-8 were significantly lower and the levels of aIL-2R were significantly higher in injection group than those in oral group(P＜0.01).One month after treatment,the rate of complete absorpion of pleural fluid was higher in injection group(80%)than thatin oral group(45%),the rate of pachynsis pleurae was lower in injection group(10%)than that in oral group(40%),P＜0.05.Conclusions Intrathoracic injection of ghcocorticoid shows stronger suppression of cellular immune function in cavum pleurae and weaker suppression of the general immune sysmm than oral medication.Intrathoracic injection of glucocorticoid can increase the therapeutic effect and decrease side effect in tuberculous pleurisy.

Objective To study the effect of docosahexaenoic acid ( DHA ) and eicosapentaenoic acid (EPA) on cognition impairment and huntingtin associated protein 1 ( HAP1 ) expression in hippocampus of rat model with Alzheimer' s disease(AD). Methods Forty healthy Sprague-Dawley rats were randomly divided into control group, AD group, DHA group and EPA group on average. Alcl3 was injected intraperitoneally and D-galac tose was injected into subcutaneous to establish the model of rat with AD. ABC method of immunohistochemistry was used to observe the expression level of HAP1 in the hippocampus. Morris water maze was used to study the spatial learning and memory in rats. Results Compared with control group,the HAP1-positive neurons of hippo campus decreased and poorer performance in Morris water maze test was observed in AD group. Compared with AD group, DHA and EPA treatments significantly caused the decreases in escape latency and searching distance in the Morris water maze test. The number of HAP1- positive cells in DG region of DHA group(43.57 ±6.14) increased obviously compared with AD group( 28.56 ± 4.23 ) (P ＜ 0.05 ＝. Conclusion The immunoreactivities of HAP1 decrease in hippocampus of AD rat. The applications of DHA and EPA in AD rats significantly improve the ability of learning and memory;and the mechanisms may be related to the decrease of HAP1 expressions in hippocampus.

Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Paraffin Embedding ; RNA, Neoplasm ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; methods

ObjectiveTo investigate the clinical efficacy of Jin’s eye three-needle acupuncture as main therapy for acquired paralytic strabismus.MethodSeventy patients with acquired paralytic strabismus were randomly allocated to acupuncture and Western medication groups. Both groups of enrolled patients took prednisone,methycobal, vitamin B1and vitamin B12. In addition, theacupuncture group received Jin’s eye three-needle acupuncture as main therapy. The clinical therapeutic effects and adverse reactions were observed after four and eight weeks of treatment.ResultThe total efficacy rate was 75.0% in the acupuncture group and 51.6% in the Western medication group after four weeks of treatment and 90.6% in the acupuncture group and 77.4% in the Western medication group after eight weeks of treatment. There were statistically significant differences between the two groups (P<0.05). Patients in the acupuncture group occasionally had acupuncture syncope and local blood stasis. Both groups had no special discomforts.ConclusionJin’s eye three-needle acupuncture has a quick and definite therapeutic effect on acquired paralytic strabismus.

Objective To explore the therapeutic efficacy of the water soluable photosensitizer D-galactopyranosyl zinc phthalocyanines (T1)-mediated photodynamic therapy (PDT) applied to HepG2 human hepatocellular carcinoma cells in vitro and in vivo,as well as its mechanism.Methods HepG2 cells in their logarithmic growth phase were cultured and divided into different concentrations ofT1 (0 μM,0.06 μM,0.125 μM,0.25 μM,0.5 μM and 1 μM).Methyl thiazolyl tetrazolium (MTT) assays were employed to determine the effect of the T1-PDT on the proliferation of the HepG2 cells.Cell apoptosis and necrosis were measured using a cell analyzer with Annexin VFITC/PI/Hochest33342 triple-staining.The reactive oxygen species (ROS) and the mitochondrial membrane potentials of the HepG2 cells were detected using fluorescence microscopy.Confocal microscopic assays were used to observe T1's subcellular localization on the HepG2 cells.Real-time quantitative polymerase chain reactions (RT-PCRs)were used to detect any apoptosis of Bcl-2-and Bax-related genes.H-22-bearing mice were used to calculate the antitumor rate of T1-PDT,and the expression levels of Bcl-2 and Bax mRNA were detected using RT-PCRs.Twenty-four healthy mice were randomly divided into a control group,a low-dose group,a middle-dose group and a high-dose group,each of 6.Each group was given different doses of T1-PDT and the tumor inhibition rate was calculated.Results The MTT assays showed that T1-PDT could significantly inhibit HepG2 cell growth,but T1 or PDT alone had little effect.The confocal microscope assay showed that T1 was mainly localized in the mitochondria in HepG2 cells with little in the lysosome.Cell analyzer results showed that T1-PDT could induce HepG2 apoptosis.The ROS levels of HepG2 cells increased after T1-PDT.The RT-PCR results showed that T1-PDT could increase the expression of Bax and decrease the expression of Bcl-2.The in vivo experiments demonstrated that T1-PDT significantly inhibited the growth of H-22-xenografied tumors.Conclusions T1-mediated PDT has a significant lethal effect on HepG2 cells in vitro and in vitro.The lethal effect of PDT on cancer cells is shown in the apoptosis and can be attributed to T1's subcellular localization in the mitochondria,increasing ROS levels,and regulating apoptosis-related genes.