The theory of formulas corresponding to syndromes is one of the characteristics of Treatise on Cold Damage and Miscellaneous Diseases (Shanghan Zabing Lun) and one of the main principles in applying classic prescriptions. It is important to take effect by following the principle of formulas corresponding to syndromes. However, some medical practitioners always feel that the actual clinical effect is far less than expected. Six errors in the use of classic prescriptions as well as the theory of formulas corresponding to syndromes are the most important causes to be considered, i.e. paying attention only to the local syndromes while neglecting the whole, paying attention only to formulas corresponding to syndromes while neglecting the pathogenesis, paying attention only to syndromes while neglecting the pulse diagnosis, paying attention only to unilateral prescription but neglecting the combined prescriptions, paying attention only to classic prescriptions while neglecting the modern formulas, and paying attention only to the formulas but neglecting the drug dosage. Therefore, not only the patients' clinical syndromes, but also the combination of main syndrome and pathogenesis simultaneously is necessary in the clinical applications of classic prescriptions and the theory of prescription corresponding to syndrome. In addition, comprehensive syndrome differentiation, modern formulas, current prescriptions, combined prescriptions, and drug dosage all contribute to avoid clinical errors and improve clinical effects.

The theory of ascending and descending activities of qi is one basic theory that guides diagnosis and treatment of disease clinically. It has been esteemed by ancient physicians throughout their academic thinking and clinical diagnosis. As a kind of unbalanced disease in the whole body, the basic internal mechanism of tumor formation may be caused by unbalanced ascending and descending activities of qi. Better clinical efficacy is liable to get by applying the theory of ascending and descending activities of qi in cancer treatment. Therefore, we hope to provide a reference for clinicians from the following aspects: historical status and academic value of the theory of ascending and descending activities of qi, case examples and classical prescriptions.
Humans ; Neoplasms ; diagnosis ; therapy ; Qi

Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Estrogen Antagonists ; pharmacology ; Glioma ; pathology ; Humans ; Protein Kinase C ; antagonists & inhibitors ; Tamoxifen ; pharmacology

Dysprosium ; Endophthalmitis ; etiology ; Humans ; Quartz

Humans ; Medicine, Chinese Traditional ; Qi ; Thymoma ; surgery ; therapy

Objective To investigate the in vitro effect of low dosage of paclitaxel on normal murine bone marrow-derived dendritic cells(mDCs)and its role in reactivating tumor-pulsed DCs. Methods The concentration of paclitaxel which could induce 30% apoptosis of 3LL cell lines was figured out.mDCs were generated from murine bone marrow precursors.Cell culture insert system was used and four groups were divided as following: mDC,mDC+3LL,mDC+ low dose of paclitaxel,and mDC+3LL with 30% apoptosis induced by low dose of paclitaxel.The phenotypes,chemoattractive function to MIP1? and MIP-3?,and viability in activating allogeneic T cell proliferation of DCs in the four groups were analysed. Results Paclitaxel of 50 nmol/L could induce 30% apoptosis of 3LL,and had protective effects on DCs.It could stimulate the maturation of mDCs by up-regulating the phenotypes of CD11cCD80,CD11cCD86,CD11cCD40 and CD11cCDIab,and could enhance the chemoattractive function to chemokine MIP-3?.Compared with those cocultured with 3LL,DCs pulsed with apoptosis antigen of 3LL cell which was induced by 50 nmol/L paclitaxl up-regulated the phenotype of CD11cCD40,enhanced the the chemoattractive function to MIP1? and MIP-3?,and activated the proliferation of T cells. Conclusion Paclitaxel of 50 nmol/L can stimulate the maturation of DC,and can partially recover the phenotype and function of tumor-pulsed DC.

Objective: To observe the tropism of bone marrow stromal cells (BMSCs) to intracranial glioma and their differentiation in the brain of rats bearing glioma, and to investigate the corresponding mechanism. Methods: The in vitro tropism of cultured BMSCs to glioma cells, vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor(FGF), platelet derived growth factor (PDGF) were observed under microscope and detected by performing Transwell experiment. The in vivo tropism of BMSCs to intracranial glioma was observed by immunofluorescence method. The differentiation of BMSCs was induced in vitro and observed. After BMSCs were transplanted in the brain of glioma-bearing rats for 15 days, their in vivo differentiation was observed by immunofluorescence staining. Results: BMSCs displayed obvious in vitro tropism to glioma, PDGF, and EGF and in vivo tropism to intracranial glioma. They could migrate to satellite lesions of glioma in vivo. BMSCs were induced to differentiate into neural progenitor cells (8.4% ± 3.5%), neurons (53.7% ± 7.4%), and astrocytes (22.3% ± 5.2%) in vitro. After being transplanted into the brain of glioma-bearing rats, they also differentiated into neural progenitor cells (8.3% ± 3.6%), neurons (15.7% ± 4.3%) and astrocytes (32.5% ± 7.2%). There was significant difference in the differentiation ratio to neurons between in vitro and in vivo experiments (P< 0.05), but the differentiation ratios to neural progenitor cells and astrocytes had no significant difference (P>0.05). Conclusion: BMSCs display extensive tropism to glioma. The direction of the differentiation of BMSCs may be related with local microenvironment.

Background Researches have suggested that the defocus can induce the change of static visual acuity,but whether it produce influence on dynamic visual acuity is not clear.Objective This study was to investigate the impact of myopic defocus on static visual acuity and dynamic visual acuity and explore the essential difierence between static visual acuity and dynamic visual acuity. Methods Forty volunteers were enrolled in this trial.including 20 adults with the age of 27.4±1.64 years and 20 children with the age of 11.70+1.49 years.All the eyes of subjects received regular examined to excluded the eye disease with the best corrected vision of ≥1.0 D,astigmatism of ≤0.75 D and anisometropia ＜1.50 D.+1.00 D,+1.50 D,+2.00 D,+2.50 D slasses were ware respectively for the defocus on the foundation of full correction.Dynamic visual acuity was inspected by using selfmade DVA-I training software.and static visual acuity wag tested by static visual acuity chart (Precision Vision,CAT.NO.2125).This clinical trial complied with the Helsinki Declaration and obtained the approval of Ethic Committee of Wenzhou Medical College.Written informed consent was received from each individual prior to the protocol. Results The dynamic and static visual acuities were gradually decreased with the elevation of defocus (F=506.907,P=0.000).No significant differences were found between static visual acuity and dynamic visual acuity in adult or children at various defocus(P＞0.05).The regression linear analysis showed that a positive correlation between static visual acuity with defoeus(R2=0.819,t=26.72,P=0.000) or dynamic visual acuity with defoeus(R2=0.826,t=27.42,P=0.000).The slope and intercept between defocus with static visual acuity were steeper than that between defocus and dynamic visual acuity (slope:F=34.18,P=0.000;intercept:F=1005.56,P=0.001). Conclusion The effect of defocus on static visual acuity is different from that of dynamic visual acuity.It could be speculated that dynamic visual acuity is related not only to refractive systems but also other factor.

Background The circulating endothelial progenitor cells (EPCs)play an important role in postnatal vasculogenesis and restoration of endothelial injury.Previous investigation illustrated that a reduced ocular blood flow and vascular dysfunction caused by endothelial dysfunction plays a role in the pathogenesis of glaucoma.However,endothelial system accommodation is accomplished with the circulating EPCs.Objective The present trail was to investigate EPCs change in patients with primary acute angle-closure glaucoma (PACG)and explore the role of EPCs in the pathogenesis of PACG. MethodsA prospective cohort study was designed.Thirty patients with PACG were enrolled in Tianjin Medical University General Hospital as PACG group,and 20 normal subjects served as control group.Periphery bloodsamples were obtained fromall the patients and thenstained with saturating concentrations of monoclonal antibodies,FITC-conjugated anti-CD34 and CD133 mAb.EPCs identified by CD34,CD133 were enumerated by flow cytometry,and the correlation between EPCs change and its relative factors was analyzed.Informed consent was obtained from each subject before any medical procedure. Results No significant differences were found in age,gender,vascular-related risk factor,blood biochemical indicators between PACG group and normal contol group(P＞0.05 ),but a higher intraocular pressure( IOP)was displayed in PACG group compared with normal control group ( P =0.00 ).The numbers of EPCs were ( 48 ± 22 ) cells/ml in PACG group and ( 65 ± 20 )cells/ml in normal control group with a significant difference between them (P=0.004).In PACG group,the numbers of EPCs were(60± 19 )cells/ml and (34 ±7 )cells/ml respeetively in phase 1 and phase 3 of optical nerve damage (Z=-3.015,P=0.002 ).There was a negative correlation between EPCs numbers and baseline IOP within a certain range( r=-0.835,P＜0.05 ).However,no obvious correlations were seen between EPCs numbers and blood lipid Level,blood glucose level or glaucoma course ( r =0.343,P =0.227 ; r =-0.203,P =0.419 ; r =0.198,P =0.610 ).The EPCs numbers in PACG patients with cardiovascular disease were(56±22)cells/ml and that of without PACG were (35± 15 ) cells/ml( P =0.005 ). ConclusionsThe numbers of EPCs decrease in PACG patient.These results imply that EPCs might play role during the restore of the optical nerve damage in PACG eye.

Carcinoembryonic Antigen ; metabolism ; Carcinoma in Situ ; immunology ; pathology ; virology ; Carcinoma, Ductal, Breast ; immunology ; pathology ; virology ; Cervical Intraepithelial Neoplasia ; immunology ; pathology ; virology ; DNA, Viral ; analysis ; Diagnosis, Differential ; Female ; Human papillomavirus 16 ; genetics ; isolation & purification ; Humans ; Ki-67 Antigen ; metabolism ; Uterine Cervical Dysplasia ; immunology ; pathology ; virology ; Uterine Cervical Neoplasms ; immunology ; pathology ; virology