Objective To explore the difference of treating carpal tunnel syndrome (CTS) with needling Yangchi point and moxibustion on Yangchi point.Methods 38 cases of CTS were randomly recruited into a treatment group (19 cases) and a control group (19 cases).The treatment group was treated with electric acupuncture on Yangchi point and the control group was treated with moxibustion on Yangchi point.VAS (visual analogue scale) and GSS (overall symptom score table) scores were measured before and after the treatment.Results After the treatment VAS,GSS scores were (3.95± 1.87),(13.42±7.81) in the treatment group and (4.26±2.38),(14.63±9.97) in the control group,both decreased than those in the same group before the treatment [treatment group were (6.89± 1.56),(25.58±8.09) ; the control group were (5.79± 1.69),(20.37±8.67)],and the difference between the two groups was significant (t=-3.06,-3.39,P＜0.05).3 months follow-up after the treatment,the value of VAS and GSS scores in treatment group were (3.29±2.31)％ and (8.06±7.77); in the control group were (3.28±2.95) and (10.44±9.82),both decreased than those in the same group before the treatment [treatment group were (6.76± 1.56),(24.76±8.17); the control group were (5.78± 1.73),(20.33± 8.92) (P＜0.05)].The difference of VAS score was not significant between the two group (t=-1.49,P＞0.05); while the difference of GSS score showed statistical difference between the two groups (t=-2.64,P＜0.05).Conclusion Acupunctureon Yangchi point can effectively improve pain,numbness and motor activity in patients with the carpal tunnel syndrome.

AIM　To study the glucose and lipids metabolis m and insulin sensitivity of MSG rats during their growing period, and to evalua te the effects of insulin sensitizer pioglitazone on the model rats. MET HODS　Body weights were measured regularly, and glucose and insulin tole rance tests were taken. In their 3 and 10 months old, rats were given insulin se nsitizer pioglitazone orally, then the effects on serum glucose, triglyceride, c holesteral, free fatty acid and insulin concentrations were determined. RESULTS　Compared with normal rats, a slight but significant increase of glucose in MSG rats was revealed. The serum triglyceride, cholesteral, free fat ty acid and insulin concentrations were significantly higher in model rats. More over, gluconeogenesis increased significantly, and insulin tolerance showed abno rmal. However, glucose tolerance was nearlly normal. Pioglitazone could ameliora te all these metabolic disorders. CONCLUSION　Obesity and insuli n resistance were induced by injecting monosodium glutamate (MSG) to neonatal Wi star rats. Pioglitazone can significantly improve the insulin sensitivity of MSG rats. These results suggested that MSG obese rats can be used as an easily acce ssible and inexpensive insulin resistance animal model for evaluating the effica cy and mechanisms of antidiabetic agents.

PurposeTo study the effect of phospholipid on the ability of HDL3 mediated cholesterol efflux from rat skin fibroblasts. Methods At the present of phosphatidylcholine (PC) or sphingomyelin (SPM), to measure the changes of HDL3-mediated cellular cholesterol efflux, cellulax phospholipid content and balance between free cholesterol and cholesteryl ester.Results① BSA (control) ,HDL3,PC,SPM, PC + HDL3 and SPM + HDL3 group mediated 4.70 %, 31.55 %, 7.35 %, 8.06 %,42.95 % and 46.98 % of cellular cholesterol efflux from the cells respectively. ② After the incubation of the cells with BSA, HDL3, HDL3 +SPM and HDL3 + PC, the cellular phosphorous content in PC(PC-p) and SPM (SPM-p) were 20.02,5.56; 17.56,5.28; 18.62,7.00 and 22.50,5.52 μg/plate respectively. ③ After the incubation of the cell with PC and SPM, ratio of free cholesterol to total cholesterol were 49.65 and 59.57 respectively. The ratio was 48.64 before incubation.ConclusionsO PC and SPM couldn' t mediated directly cellular cholesterol effiux, but they could enhance significantly HDL3 mediated cellular cholesterol efflux, and this ability of SPM was stronger than PC. ① With cellular cholesterol efflux,a part of cellular PC went out of the cells, but the content of cellular SPM didn' t change significantly. ③ SPM could induce cholesterol ester to convert into free cholesterol in the cells.

Aged ; Antibodies, Monoclonal, Murine-Derived ; therapeutic use ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Bleomycin ; therapeutic use ; Dacarbazine ; therapeutic use ; Doxorubicin ; therapeutic use ; Hodgkin Disease ; drug therapy ; pathology ; Humans ; Leukemia, Hairy Cell ; drug therapy ; pathology ; surgery ; Male ; Mitoxantrone ; administration & dosage ; Neoplasms, Multiple Primary ; drug therapy ; pathology ; surgery ; Rituximab ; Splenectomy ; Vidarabine ; administration & dosage ; analogs & derivatives ; Vinblastine ; therapeutic use

Diagnosis, Differential ; Gene Rearrangement ; Hodgkin Disease ; genetics ; metabolism ; pathology ; Humans ; Lymphoma, B-Cell ; genetics ; metabolism ; pathology ; Lymphoma, Large B-Cell, Diffuse ; genetics ; metabolism ; pathology ; Mediastinal Neoplasms ; genetics ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism

Accidents, Occupational ; prevention & control ; statistics & numerical data ; Adult ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Poisoning ; epidemiology ; prevention & control

Diagnosis, Differential ; Humans ; Lymphoproliferative Disorders ; diagnosis ; Stomach ; Stomach Neoplasms ; diagnosis

Peroxisome proliferator activated receptor(PPAR), a member of the hormone receptor superfamily, is a key regulating factor in adipocyte differentiation and lipids metabolism. Recently, with the increased understanding of the precise mechanisms of TZD, thiazolidinedione class of insulin sensitizer, PPAR? has also been identified as the major functional receptor for the drugs. In the study of the relationship between PPAR and insulin resistance, considerable gaps appeared. TZD induced activation of PPAR? is known to promote insulin sensitivity. More interestingly, however, PPAR? +/- heterozygous mice were shown to be less susceptible to insulin resistance. These findings suggest that the relationship between PPAR activation and insulin sensitivity improvement is not simplely positively related. A better understanding of the role of PPAR in insulin action system will be critical in developing more efficacious and safe agents that act on PPAR and benefit patients with type 2 diabetes.

[Objective] To investigate doctor Xu Qing Lingtai’s vitality academic thought. [Methods] Using traditional philological research methods, through a careful reading medical books of Xu Lingtai, combined with various Chinese medicine theory, summarize his vitality academic thought. [Re-sult] The study refines that Xu Lingtaivitalityacademic thought can be summarized as: Xu thought vitality is the first righteous cause for doctors to treat diseases; doctors shal get to the bottom and care vitality. In theory, he viewed that the innate vitality comes before the blood and Qi. The true viscera essence is the sub-strength of vitality. In clinical thinking, he actual y applied the theory in 3 aspects:diagnosing diseases with vitality, evil and vitality com-bined and using warm-dry drugs with caution. [Conclusion] Xu Lingtai inherited the former based on the theory and put forwardstrength theory.Hisvitality theory is unique not only in the theory of traditional Chinese medicine essence, but also has great features in the clinical syndrome differentiation. Its doctrine has important reference value on clinical medicine.

The de novo transcription of hTERT gene represents a rate-limiting step in the activation of human telomerase.The expression of hTERT is strictly regulated with several oncogene products and tumor suppressor gene products in normal cells.The construction of a reverse-transcriptional virus vector that contains the promoter of hTERT without losing its specificity can dramatically augment the expressions of anticancer genes in telomerase-positive cancer cells,which prompts the use of an hTERT promoter for anticancer gene therapies.Firstly,we briefly introduce the structure and regulation of hTERT gene,and then we also review the present knowledge of its biological function in cancer progression.