Objective To observe clinical effect of treating diabetic peripheral neuropathy with Shuxuetong injection combined herbal oral administration. Methods A total of 51 patients with diabetic peripheral neuropathy were randomly recruited into a control group and a treatment group. The control group was treated with western medicine, and the treatment group was treated with Shuxuetong injection combined with Buyang Huanwu decoction. The clinical effect was observed in both groups after the treatment. Results The total effective rate was 88.5% and 68.0% in the treatment group and the control group respectively. The clinical effect in the treatment group was significantly higher than that of the control group (P＜0.05). Conclusion The effects of Shuxuetong injection combined herbal oral administration on diabetic peripheral neuropathy was better than western medicine.

Taking Naegleria australiensis, a species of pathogenic free-living amoeba (isolated in Shanghai in 1986), as antigen, two cell lines which provided potentially permanent source of monoclonal antibodies were established by lymphocytic hybridoma technique. The results of identification showed that: (1) the two cell lines could secret two different kinds of McAbs; (2) both of the McAbs were IgG (by gel diffusion); (3) McAbs produced in BALB/c mice were at high concentrations. One of them had a titer of ≥1 : 8 192 and the other≥l : 1 024 (by enzyme linked immunosorbent assay). A decline of the titers after purification by salting-out method was shown. One of the purified McAbs had a titer of≥1: 2 024 and the other≥l : 128.We have adopted two ways of recovering cryopreserved cells : ordinary recovering and "direct" recovering. The latter way was more practical because it could reduce the cycle of antibody production, and avoid contamination and chromosome variation. Experiments with different doses of cells revealed that, if the latter way was used, the optimal dose was 3 to 5 ? 106 cells per mouse.

OBJECTIVE:To study the influence of reduced glutathione(GSH) on serum liver fibrosis index and cytokines in patients with chronic hepatitis B(CHB) . METHODS:96 patients with CHB were randomly divided into the treatment group(treated with GSH) and control group. The serum levels of TGF-?1,TNF-?,hyaline acid(HA) ,type Ⅳcollagen(C-Ⅳ) ,laminin(LN) ,Alanine aminotransferase(ALT) and Aspartate Aminotransferase(AST) were measured by specific-ELISA and RIA assay before and after treatment. Healthy group made up of 30 healthy volunteers. RESULTS:Before treatment the serum levels of ALT,AST,TGF-?1,TNF-?,HA,C-Ⅳ and LN in CHB group were significantly increased,as compared with heatthy group(P

Objective To investigate the role of astroglial glutamate-glutamine shuttle in the development of neuropathic pain (NP) in rats. Methods Forty-eight adult male SD rats weighing 200-230 g were randomly divided into 8 groups (n =6 each): Ⅰ control group (group C);Ⅱ sham operation group (group S);group ⅢNP;Ⅳ-Ⅶ 0.01, 0.03, 0.05 and 0.10 mmol/L methionine sulfoximine (MSO, an inhibitor of glutamine synthetase (GS)) group (group M1-4 );Ⅷ MSO + glutaminate group (group MG). In group C no operation was performed. In group S the sciatic nerve was only exposed but not ligated. NP was induced by ligation of the tibial nerve and commom peroneal nerve according to the technique described by Dixon. After the establishment of the model, intrathecal PBS 50 μl was injected in group NP, IT 0.01, 0.03, 0.05 and 0.10 mmol/L MSO 50 μl was injected intrathecally in group M1-4, and 0.05 mmol/L MSO 50 μl was injected intrathecally and then 0.25 mmol/L glutamine 50 μl was injected intrathecally 15 min later in group MG. Mechanical pain threshold was measured 1 week before ligation (T0 , baseline), 1 week after ligation (T1) and 15, 30, 45 and 60 min after injection of MSO (T2-5). Then rats were killed and the lumbar segment of the spinal cord was removed for determination of the expression of glial fibrillary acidic protein (GFAP) and GS and the co-expression (GFAP/GS) in the dorsal horn.Results Mechanical pain threshold was significantly lower at T1-5 in group MG and NP and at T2-4 in group M3.4 ,and the expression of GFAP, GS and GFAP/GS was significantly higher in group MG,NP and M3 than in group S and C ( P ＜ 0.05) .Conclusion Astroglial glutamate-glutamine shuttle in the spinal cord is involved in the development of neuropathic pain in rats.

Objective To investigate the proliferation inhibition and the apoptosis induction effect of brucine on human chronic myeloid leukemia cell line HL-60 cells.Methods HL-60 cells were exposed to various dosages of brucine 24,48,72 h respectively,MTT method was used to assay the growth inhibition effect of brucine on HL-60 cells and the IC50 of brucine was evaluated at the same time.The morphology was observed by AO/EB stains.The cell apoptosis and cell cycle was tested by flow cytometry with Annexin V-FITC/PI double staining and PI labeling respectively.Results The results indicated that the brucine displayed significant anti-proliferative effect on HL-60 cells in a dose-and time-dependent manner,with IC50 value of 211.8 μg/ml(24 h),107 μg/ml(48 h),83 μg/ml(72 h)respectively.The most significant inhibition was observed at 320 μg/ml for 48 h.In this condition,apoptosis morphology was induced by brucine with nuclear chromatin condensation,most of the nuclears were orange stained and condensation-like or bead-like,which was consistent with the Annexin V-FITC/PI results.The cell apoptosis rates were(2.1±1.1)％,(21.3±1.2)％,(38.6±1.3)％,(58.5±4.1)％,(75.3±0.87)％and(66.2±0.75)％in different dose of brucine,respectively.At the same time,the cell cycle analysis results showed that the cell ratio in G0/G1 phase was decreased while in G2/M and sub-G0 phases was increased,comparing with blank control group.Conclusion Brucine can inhibit cell growth dramatically,which may be related to the cell apoptosis and the cell cycle arrest.

This article reports one hepatic echinococcosis patient complicated with systemic sclerosis. His clinical manifesta?tions were the progressive fibrosis of the skin,sour regurgitation,and belching. The blood examination showed that eosinophils was reduced,and antinuclear antibody(ANA)was positive at 1∶100 in cytoplasm particle type. He was given prednisone ace?tate 25 mg,q. d.,aspirin 100 mg,q. d.,centella triterpenes cream 12 mg t. i. d.,esomeprazole 40 mg q. d.,and domperidone 10 mg t. i. d. After one week,the Rodnan skin score reduced from 27 to 17. The liver hydatid cyst resection was performed,and the follow?up showed that his clinical manifestations improved and the Rodnan skin score reduced further.

The central nervous system (CNS) plays a key regulatory role in glucose homeostasis. In particular, the brain is important in initiating and coordinating protective counterregulatory responses when blood glucose levels fall. This may due to the metabolic dependency of the CNS on glucose, and protection of food supply to the brain. In healthy subjects, blood glucose is normally maintained within a relatively narrow range. Hypoglycemia in diabetic patients can increase the risk of complications, such as heart disease and diabetic peripheral neuropathy. The clinical research finds that the use of traditional Chinese medicine (TCM) has a positive effect on the treatment of hypoglycemia. Here the authors reviewed the current understanding of sensing and counterregulatory responses to hypoglycemia, and discuss combining traditional Chinese and Western medicine and the theory of iatrogenic hypoglycemia in diabetes treatment. Furthermore, the authors clarify the feasibility of treating hypoglycemia on the basis of TCM theory and CNS and have an insight on its clinical practice.

Objective To study the function of interleukin (IL)-25 for rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) differentiation as well as on the expression of extracellular regulating protein kinase (ERK) and matrix metalloproteinases-3 (MMP-3).Methods The differences on ERK1/2 and MMP-3 protein levels were tested in RA-FLS of RA patients and healthy controls,then IL-17A (10 ng/ml) was tested when the RA-FLS were co-stimulated with different concentrations of IL-25 (0.01,0.1,1 and 10 ng/ml) and IL-17A(10 ng/ml) for 24 hours respectively.The expression of ERK1/2 and MMP-3 protein was detected by the Western blot.T test was used for the comparison between different groups.Results The expression of ERK1/2 (1.71±0.17) and MMP-3 (0.50±0.13) proteins in RA-FLS was higher than the healthy controls (0.50±0.15,0.17±0.05) (t=-9.13,P＜0.01 and t=-4.10,P＜0.05),after stimulated with IL-17A,the expression of ERK1/2 (0.77±0.22) and MMP-3 (0.59±0.13) proteins in RA-FLS were increased compared with the untreated groups (0.18±0.35,0.04±0.03) (t=-4.69,P＜0.01 and t=-7.47,P＜0.01).With increase of the concentration on IL-25,the level of ERK1/2 (0.54±0.26,0.48±0.18,0.48±0.23,0.23±0.06) and MMP-3 (0.58±0.09,0.59±0.14,0.21±0.04,0.04±0.02) in RA-FLS which were stimulated by IL-17A was decreased slowly (t=4.22,P＜0.05 and t=4.95,P＜0.01 and t=7.47,P＜0.01).Conclusion IL-25 can inhibit the stimulation of IL-17A on ERK1/2 and MMP-3 fractionally,which implies that it may take part in the development of RA through this pathway and may be a target for the RA treatment.

Objective To observe the efficacy and safety of tocilizumab combined with methotrexate (MTX) in the treatment of refractory adult-onset Still's disease (AOSD), and to explore whether it is possible to reduce the dose of tocilizumab when disease is under control. Methods Twenty-eight patients with refractory AOSD received the treatment of tocilizumab (8 mg/kg, Intravenous infusion every 4 weeks, and reduced to 8 mg/kg every 8 weeks after 6 months of remission) combined with MTX (12.5 mg oral intake per week). The clinical efficacy, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), ferritin level and dose change of glucocorticoid (GC) were observed prior to treatment initiation and 2, 4, 8, 12, 24, 36, 48 weeks after treatment. All adverse reactions were recorded. The Chi-square test and repetitive measure analysis of variance were used for statistical analysis. Results Compared with the baseline levels, our results showed that after 8-weeks of treatment with tocilizumab all patients had normal body temperature, while skin rash, joint swelling and pain disappeared. CRP [(125.4 ±48.3) mg/L, (6.1 ±2.5) mg/L vs (4.9 ±1.8) mg/L , F=77.034, P<0.01], ESR [(103±31) mm/1 h, (17±7) mm/1 h vs (16±4) mm/1 h, F=55.73, P<0.01], white blood cells count [(18.1± 5.3)×109/L, (8.2±2.9)×109/L vs (7.2±2.1)×109/L, F=24.71, P<0.01], neutrophils count [(16.7±4.9)×109/L, (6.1± 2.2)×109/L vs(4.9±2.3)×109/L, F=35.295, P<0.01], blood platelets [(312±83)×109/L, (199±40)×109/L vs (204± 47)×109/L, F=7.139, P<0.01], hemoglobin [(100±9) g/L, (116±9) g/L vs (277±102) g/L, F=9.852, P<0.01], ferritin level [(3542±1313) ng/ml, (2342±923) ng/ml vs (277±102) ng/ml), F=34.232, P<0.01] were improved significantly, clinical symptoms and laboratory tests continued to improve at week 12, 24, 36 and 48, the doseof prednisone was reduced from (71.4±20.7) mg/d to (55.0±11.1) mg/d (P<0.05) After 2 weeks, and the dosage was gradually reduced to 3.3±2.1 mg/d (P<0.05) at the end of 48 weeks. Five (17.9％) patients discontinued prednisone after 36 weeks, and 7 (25％) patients at week 48, no serious adverse events were found during the treatment. Conclusion Tocilizumab can rapidly and significantly improve clinical symptoms and laboratory tests of patients with refractory AOSD and it also can help with the reduction of GC dosage. In addition, the disease remains stable after the dose reduction of tombuzumab. The safety profile is good.

OBJECTIVE: To explore the genetic basis for a patient with episodic ataxia and pyramidal tract signs. METHODS: The patient was subjected to high-throughput sequencing, Sanger sequencing and analysis of dynamic variant site associated with spinocerebellar ataxias (SCA). RESULTS: The patient was an adolescent male presenting with episodic ataxia, bilateral knee hyper-reflexia and ankle clonus. By genetic testing, he was found to harbor a c.1159-1162dupAAGT variant of PDHA1 gene. The same variant was not found in his parents and elder sister. No abnormalities were found by SCA dynamic variant screening. The patient was diagnosed as pyruvate dehydrogenase E1alpha deficiency due to variant of the PDHA1 gene. CONCLUSION The de novo c.1159-1162dupAAGT variant of the PDHA1 gene probably underlies the disease in the proband. Patients with pyruvate dehydrogenase E1alpha deficiency have complex phenotypes and very few have pyramidal tract involvement, which may be attributed to abnormal early neuronal development.