Hereditary erythrocyte glucosephosphate isomerase (GPI) deficiency is thefourth most common cause of non-spherocytic hemolytic anemia. A case of GPI deficiencywas confirmed after screening a panel of 18 red cell enzymes and GSH. The GPI variantwas characterized by biochemical parameters including GPI activity in erythrocytes andplasma, low substrate activity, electrophoretic mobility, pH optimum, Michaelis constant(Km), thermostability, and substrate analogue (GAL-6-P) utilization rate. A new GPIvariant was found and was designated as GPI-Guangzhou.

Inspection of the complexion is one of the characteristics of traditional Chinese medical diagnosis. Traditional Chinese medicine puts high emphasis on inspection of the complexion and there exists detailed discussion on inspection of facial expression in Neijing. The so-called inspection of facial expression is a method to diagnose diseases according to the theory of five Zang-organs matching five elements and five colors by distinguishing various changes of facial color, such as green, red, yellow, white and black based on yin and yang doctrine and five elements theory. Nowadays, more and more experts have introduced color optical theory and modern devices into the modern research field of traditional Chinese medical diagnosis with the development of color optical theory and the renewal of determining devices, such as digital camera, color differentiation meter and spectrophotometer, to make the research more scientific and objective and avoid the deviations caused by human factors. The modern study of traditional Chinese medicine diagnosis has made fare progress, consequently enriching the contents of its facial color observation and giving a more scientific explanation of it. However, the devices being used now are still disunited; the data may be unilateral and cannot contain the whole information. So the most important task is to invent and use scientific devices conforming better with the theory of five colors observation in traditional Chinese medicine.

OBJECTIVE: To observe the correlation between serum level of TXB2, 6-Keto-PGF1alpha and liver metastasis. METHODS: The metastatic model was made by injection of W256 carcinosarcoma. Rats were randomly divided into two groups: rats with blood stasis group and control group. Rats in control group were given normal saline via abdominal cavity once a day. Rats in blood stasis group were injected adrenalin in the fourteenth day. Tumor size and liver metastasis were observed. Serum TXB2 and 6-Keto-PGF1alpha were tested by radioimmunoassay. RESULTS: Tumor size in rats with blood stasis was significantly smaller than that of the control group (P<0.01). Occurrence of liver metastasis in rats with blood stasis was significantly lower than that of the control group (P<0.01). The values of 6-Keto-PGF1alpha, TXB2, and TXB2/6-Keto-PGF1alpha were higher in the group with blood stasis. CONCLUSION: In the status of blood stasis, W256 carcinosarcoma grows slowly, and liver metastasis increases insignificantly, with the elevations of 6-Keto-PGF1alpha, TXB2 and TXB2/6-Keto-PGF1alpha.

Objective To develop a rapid method based on ARMS, named four primers allele-specific PCR(4p-AS PCR), to detect the most common non-deletional ?-thalassemia mutation Hb Constant Spring(Hb CS) by PCR technique. Methods The 4p-ASPCR was used to detect the Hb CS mutation of ?-thalassemia in 38 DNA samples of Hb H disease patients and using PCR-RE and DNA sequencing to confirm the results. Results Among the 38 Hb H disease patients 15 cases was revealed to carry Hb CS, 16 cases were deletional Hb H, and 7 cases need to be defined.Conclusion A simple, rapid and reliable method, named 4P-ASPCR, to detect Hb CS mutation have been developed. It is also may be useful in screen other point mutations such as Hb Quong Sze.

The ubiquitin-proteasome pathway is responsible for the degradation of most cellular proteins in eukaryotes.It regulates almost all cellular activities, including cell proliferation, differentiation, apoptosis, gene transcription, and DNA repair.The dysfunction of the ubiquitin-proteasome pathway is associated with the pathogenesis of numerous human diseases, including cancer and neurodegenerative diseases.The marketed proteasome inhibitors have been successfully used to treat multiple myeloma and mantle cell lymphoma.Furthermore, novel inhibitors against the components of the ubiquitin-proteasome pathway are under developed and exhibit promising therapeutic effects in vivo.This paper will briefly introduce the progress on the drug discovery related to the ubiquitin-proteasome pathway.

To select appropriate descriptors for response of the patient-reported outcome (PRO) scale for the main symptoms of patients with chronic obstructive pulmonary disease (COPD) complicated with pulmonary heart disease.

To observe the effects of Shengmai Injection on enhancing efficacy and reducing toxicity of 5-fluorouracil (5-FU).

Smoothened (SMO) is a member of sonic hedgehog homology (SHH) signaling pathway. It plays a key role as a bridge between patched-1 (PTCH-1) and Gli. Aberrant SHH expression can be detected in various malignant tissues, and the expression in pancreatic cancer stem cells is higher apparently. SHH signals are closely associated with self-duplication of cancer stem cells, formation of tumor vessels as well as matrixes. SMO antagonists such as cyclopamine, GDC-0449 and so on show potential to inhibit activity of SHH signaling, and arrest the growth as well as metastases of tumors. Recently, a few of SMO antagonists have been studied in phase I clinical trials and some are in phase II, meanwhile, phase I or II trials of SMO antagonists to treat pancreatic cancer are performed currently. As the classical SMO antagonist, cyclopamine is extracted from a medicinal plant. Perhaps researchers may be able to determine more effective SMO-targeting drugs from herbal medicines in the future.

Objective: To investigate the effects of Qingyi Huaji (QYHJ) decoction, a compound traditional Chinese herbal medicine, on tumor inhibition rate and serum levels of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha) in nude mice with transplanted tumors of human pancreatic cancer. Methods: The tumor-bearing mice model was established by subcutaneously inoculating with xenografts of pancreatic cancer into the right armpit of 40 BALB/c nude mice. After successful modeling, the mice were randomly divided into untreated group (Arabic gum), capecitabine group, low-dose QYHJ decoction group (36 g/kg) and high-dose QYHJ decoction group (72 g/kg), with 10 mice in each group. Citrate buffer solution (containing 5% Arabic gum), capecitabine suspension and QYHJ decoction were administered to four groups by gavage respectively. After 5-week treatment, the concentrations of serum IL-6, IL-8 and TNF-alpha were examined by enzyme-linked immunosorbent assay (ELISA) using blood sample from eye socket. Then the mice were euthanized by cervical dislocation. Tumor weight and the tumor inhibition rate were calculated. Results: Tumor weight in the low-dose QYHJ decoction group decreased significantly as compared with the untreated group (P<0.05). Serum levels of IL-6 and TNF-alpha in low- and high-dose QYHJ groups were extremely significantly lower than those in the untreated group (P<0.01). Serum level of IL-8 in the low-dose QYHJ group was significantly lower than that in the untreated group (P<0.05). Correlation analysis showed that transplanted tumor weight of the mice was linearly positively correlated with serum levels of IL-6, IL-8 or TNF-alpha (P<0.01). Conclusion: Conventional dose of QYHJ decoction is effective in suppressing pancreatic carcinoma in nude mice. The mechanism may be related to down-regulation of serum cytokines such as IL-6, IL-8 and TNF-alpha.

AIM: To clone human ?-globin gene carrying a thalassemic mutation IVS II654(C→T) and establish a eukaryotic expression system for high-level expression of human ? IVS II654 gene in mouse erythroleukaemia(MEL) cells. METHODS: The fragments of human ? 654 gene isolated from the ? thalassemia patients homozygous for the ? 654 mutation were amplified by PCR, and cloned to plasmid pBGT51. Then, the human ? LCR and ? 654 gene were subcloned from plasmid pBGT51 to the stable mammalian expression vector pcDNA3.1+ together, and the MEL cells were transfected with this vector using commercially available cationic lipid FuGENE6. The MEL cells were induced for further maturation by DMSO and the expression of human ? 654 gene in the MEL cells was identified by RT-PCR. RESULTS: A mammalian expression system of human ? thalassemic mutation ?IVS II654(C→T) was established. CONCLUSION: The level and the reliability of expression of human ? 654 gene in the MEL cells in vitro are similar to that in vivo in human body. This may be a valuable gene therapy model for human ? thalassemic mutation ?IVS II654(C→T).