AIM: To observe the changes in subfoveal choroidal thickness ( SFCT ) after intravitreal injections of ranibizumab ( IVR ) for macular edema secondary to retinal vein occlusion ( RVO) .
METHODS:Thirty-six eyes of 36 patients with macular edema secondary to RVO) were treated with 0. 5mg IVR monthly for 3mo and received additional IVR as needed over the following 1a period. SFCT of the all eyes ( the affected eyes with RVO and unaffected fellow eyes ) was measured by enhanced depth imaging optical coherence tomography images before and after the IVR.
RESULTS: The mean SFCT of the affected eyes with RVO decreased from 246. 7±115. 0μm at baseline to 220. 5±102.0μm at 1mo (P<0.05), 198.3± 114.0μm at 6mo (P<0.01), 212. 6± 96. 0μm at 12mo (P<0. 01). Whereas the fellow eyes changed from 229. 4±108. 0μm at baseline to 226. 3±107. 0μm at 1mo (P>0. 05), 228. 6±127. 0μm at 6mo (P>0.05), 223.6±101.0μm at 12mo(P>0.05). There were statistically significant difference between affected eyes with RVO and unaffected fellow eyes.
CONCLUSION: The SFCT is decreased after IVR for macular edema secondary to RVO. IVR seems to affect the hemorheology of the choroid.

OBJECTIVE:To observe clinical efficacy and safety of Mailuoning injection in adjunctive treatment of acute cere-bral infarction. METHODS:A total of 65 patients with acute cerebral infarction selected from neurology department of our hospital were divided into control group(32 cases)and observation group(33 cases)according to random number table. Control group was given conventional treatment. Observation group was additionally given Mailuoning injection 10 mL added into 0.9% sodium chlo-ride injection 250 mL intrnrenously,ivgtt,qd,on the basis of control group. Both group were treated for 15 d. Clinical efficacy as well as serum levels of ox-LDL,BNP and MMP-9,NIHSS score before and after treatment,the occurrence of ADR were com-pared between 2 groups. RESULTS:The response rate of observation group was 90.91%,which was significantly higher than 65.63%,with statistical significance(P<0.05). Before treatment,there was no statistical significance in serum levels of ox-LDL, BNP or MMP-9,NIHSS score between 2 groups (P>0.05). After treatment,serum levels of ox-LDL,BNP and MMP-9,NIHSS score in 2 groups were all decreased significantly,and the observation group was significantly lower than the control group,with statis-tical significance (P<0.05). There was no statistical significance in incidence of ADR between 2 groups (P>0.05). CONCLU-SIONS:Mailuoning injection has significant therapeutic efficacy for acute cerebral infarction,can significantly reduce serum levels of ox-LDL,BNP and MMP-9,promotes neurological function and the recovery of patients with cerebral infarction with good safety.

NMDA-induced excitotoxicity cause severe neuronal damage including apoptosis and necrosis. The present study was aimed to evaluate the proportion of NMDA-induced apoptosis of rat cortical neurons and discover signal transduction mechanism. Caspase inhibitor and lactate dehydrogenase (LDH) assay were used to study the NMDA-induced apoptosis. To explore the involved signal pathways, the primary culture of rat cortical neurons were pretreated by the inhibitors of three MAPK pathways, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. With 2 h of NMDA treatment, cellular apoptosis was measured by caspase-3 activity, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) and Annexin V staining. The results showed that: (1) Caspase-dependent apoptosis accounted for 22.49% in NMDA-induced neuronal death; (2) Pretreatment with p38 MAPK inhibitor SB203580 (10 μmol/L) significantly decreased NMDA-mediated caspase-3 activity by 30.43% (P < 0.05). However, ERK inhibitor PD98059 (20 μmol/L) or JNK inhibitor SP600125 (20 μmol/L) did not influence caspase-3 activity; (3) Pretreatment with SB203580 significantly reduced the number of NMDA-induced TUNEL-positive cells by 33.10% (P < 0.05). PD98059 (20 μmol/L) or SP600125 (20 μmol/L) did not show obvious effect; (4) Pretreatment with SB203580 (10 μmol/L) significantly reduced the number of NMDA-induced early apoptotic neurons by 55.56% (P < 0.05). Also, SP600125 (20 μmol/L) significantly decreased the amount of late apoptotic/dead cells by 67.59% (P < 0.05). There was no effect of PD98059 (20 μmol/L). These results indicate that: (1) NMDA induces neuronal apoptosis besides necrosis; (2) p38 MAPK, but not JNK and ERK, is involved in NMDA-induced neuronal apoptosis, and inhibition of the apoptotic signaling pathway contributes to neuroprotection; (3) JNK activation might contribute to NMDA-induced neuronal necrosis rather than apoptosis.
Animals ; Anthracenes ; pharmacology ; Apoptosis ; Caspase 3 ; metabolism ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; Imidazoles ; pharmacology ; JNK Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; MAP Kinase Signaling System ; N-Methylaspartate ; pharmacology ; Neurons ; cytology ; Primary Cell Culture ; Pyridines ; pharmacology ; Rats ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors

To investigate the effects of 2-(4-methoxycarbonyl-2-tetradecyloxyphenyl)carbamoylbenzoic acid (CX09040) on protecting pancreatic β cells, the β cell dysfunction model mice were induced by injection of alloxan into the caudal vein of ICR mice, and were treated with compound CX09040. Liraglutide was used as the positive control drug. The amount and the size of islets observed in pathological sections were calculated to evaluate the β cell mass; the glucose stimulated insulin secretion (GSIS) test was applied to estimate the β cell secretary function; the oral glucose tolerance test (OGTT) was taken to observe the glucose metabolism in mice; the expressions of protein in pancreas were detected by Western blotting. The effects on the target protein tyrosine phosphatase 1B (PTP1B) were assessed by the PTP1B activities of both recombinant protein and the intracellular enzyme, and by the PTP1B expression in the pancreas of mice, separately. As the results, with the treatment of CX09040 in alloxan-induced β cell dysfunction mice, the islet amount (P<0.05) and size (P<0.05) increased significantly, the changes of serum insulin in GSIS (P<0.01) and the values of acute insulin response (AIR, P<0.01) were enhanced, compared to those in model group; the impaired glucose tolerance was also ameliorated by CX09040 with the decrease of the values of area under curve (AUC, P<0.01). The activation of the signaling pathways related to β cell proliferation was enhanced by increasing the levels of p-Akt/Akt (P<0.01), p-FoxO1/FoxOl (P<0.001) and PDX-1 (P<0.01). The effects of CX09040 on PTP1B were observed by inhibiting the recombinant hPTP1B activity with IC50 value of 2.78x 10(-7) mol.L-1, reducing the intracellular PTP1B activity of 72.8% (P<0.001), suppressing the PTP1B expression (P<0.001) and up-regulating p-IRβ/IRβ (P<0.01) in pancreas of the β cell dysfunction mice, separately. In conclusion, compound CX09040 showed significant protection effects against the dysfunction of β cell of mice by enlarging the pancreatic β cell mass and increasing the glucose-induced insulin secretion; its major mechanism may be the inhibition on target PTP1B and the succedent up-regulation of β cell proliferation.
Alloxan ; Animals ; Benzoates ; pharmacology ; Biological Assay ; Disease Models, Animal ; Glucose ; metabolism ; Glucose Tolerance Test ; Insulin ; secretion ; Insulin Resistance ; Insulin-Secreting Cells ; drug effects ; Liraglutide ; pharmacology ; Mice ; Mice, Inbred ICR ; Molecular Weight ; Pancreas ; drug effects ; enzymology ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 ; antagonists & inhibitors ; Signal Transduction

OBJECTIVETo explore the relationship between methylenetetrahydrofolate reductase (MTHFR) gene polymorphism and microsatellite instability (MSI) in patients with gastric cancer.

METHODSMTHFR gene C677T and A1298C polymorphism were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and MSI was examined with PCR.

RESULTSMTHFR gene C677T and A1298C polymorphisms were analyzed on 122 gastric cancers and 110 normal controls The genotype frequencies of MTHFR 677CC, 677CT and 677TT were 47.5%, 39.3% and 13.1% on patients with gastric cancer, and 48.5%, 42.6%, 8.9% in the controls respectively. There was no significant difference of genotype frequency between the two groups (P > 0.05). The individuals with 677CT genotype, 677TT genotype and 677CT + TT genotype exhibited significantly reduced risk (OR = 0.38,95% CI: 0.15-0.98; OR = 0.26,95% CI: 0.03-2.18 and OR = 0.36,95% CI: 0.07-0.98) of developing gastric cardia cancer compared with those harboring the wild-type(677CC). The individuals with 677TT genotype having a 3.03-fold (95% CI: 1.07-8.65) increased risk of developing gastric corpus cancer. The genotype frequency of MTHFR 1298AA, 1298AC and 1298CC were 59.8%, 36.1% and 4.1% in gastric cancer patients, and 57.4%, 7.6%, 5.0% in the controls, respectively. The distribution of MTHFR A1298C genotype was not significantly different between gastric cancer and controls (P > 0.05). The individuals with 1298CC genotype had a reduced risk of developing gastric antrum cancer (OR = 0.41- fold, 95% CI: 0.03-2.18, 0.05-3.72) when comparing with those having 1298AA genotype. Patients with MSI+ gastric cancer had an increased frequency of the MTHFR 677TT genotype when comparing with those suffering from MSI- gastric cancer (P = 0.009) and with controlled subjects (P = 0.008). There was no significant association found between MTHFR A1298C polymorphism and MSI (P>0.05).

CONCLUSIONPolymorphism of MTHFR C677T was associated with increased risk on gastric corpus cancer and reduced risk on gastric cardia cancer. The polymorphism of MTHFR A1298C was associated with reduced risk for gastric antrum cancer while MSI pathway was possibly involved in the development of gastric cancer with MTHFR 677TT genotype.

Adult ; Aged ; Aged, 80 and over ; Case-Control Studies ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Microsatellite Instability ; Middle Aged ; Polymorphism, Genetic ; Stomach Neoplasms ; genetics

OBJECTIVETo observe the anti-tumor effect of combination TNF-related apoptosis-inducing ligand (TRAIL) with aspirin on liver cancer cell line, SMMC-7721.

METHODSThe survival fraction of SMMC-7721 cells was measured by MTT assay, apoptosis rate and cell cycle was determined by flow cytometry, and the expression of apoptosis-related gene was identified by western blot.

RESULTSThe survival fraction of SMMC-7721 cells treated with 300 ng/ml TRAIL, 3 mmol/L or 10 mmol/L aspirin alone was 82.76%, 81.34% and 71.29% respectively, and the survival fractions of SMMC-7721 cells treated with TRAIL and 3 mmol/L or 10 mmol/L aspirin were 43.54% and 37.8% respectively. The apoptosis rates of SMMC-7721 cells induced by TRAIL and 3 mmol/L or 10 mmol/L aspirin were higher than that induced by TRAIL or aspirin alone (34.76% and 38.56% vs 21.25%, 1.89% and 6.08%), and G0/G1 arrest was observed under TRAIL and aspirin. The expression of Bcl-2 in SMMC-7721 cells treated by 3 mmol/L or 10 mmol/L aspirin decreased markedly, but no effect on Bax.

CONCLUSIONThe cooperative anti-tumor effect of aspirin and TRAIL may be related to the inhibition of the expression of Bcl-2 by aspirin

Antineoplastic Combined Chemotherapy Protocols ; pharmacology ; Apoptosis ; Apoptosis Regulatory Proteins ; Aspirin ; pharmacology ; Cell Survival ; drug effects ; Humans ; Membrane Glycoproteins ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; antagonists & inhibitors ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Cells, Cultured ; Tumor Necrosis Factor-alpha ; pharmacology

Aim To explore the effect of gypenosides on proliferation and apoptosis of human gastric cancer cells SGC-7901 and AGS and its mechanism. Methods Different concentrations of gypenosides were cultured with human gastric cancer cells SGC-7901 and AGS. Cell viability assay was used to detect cell proliferation activity, and the IC

Objective To observe the improving effect in joint function of moderate skeletal fluorosis treated by traditional Chinese medication(main ingredient was Strychnine).MethodsFrom December 2007 to July 2009,120 moderate skeletal fluorosis patients met the inclusion criteria were divided into the treatment group(60 cases)and the control group(60 cases)in the skeletal fluorosis hospital of Xinzhou,the treatment group was given basic treatment and traditional Chinese medication,the control group wa8 given basic treatment and placebo.The treatment lasted 12 weeks,follow up 24 weeks.Before treatment,after treatment 4 weeks,8 weeks,12 weeks,36 weeks,a third party evaluate comprehensive function of both upper and lower limb and joint dysfunction.Results The main effect of both drugs was statistically significance in the scores of the upper forearm in the finger by touching the posterior contralateral ear, upper arm touched by the finger back in the opposite corner subscapularis function, lower limb function and single-joint dysfunction(F values were 4.08,14.32,35.81,13.02, all P<0.05), the main effect of time also was significant (F values were 82.63,72.82,277.33,328.16, all P<0.05),①the upper forearm in the finger by touching the posterior contralateral ear functions:At the time of 8,12 weeks,scores of the treatment group were lower than those of before treatment and control group (all P<0.05);At the time of 36 weeks,scores of the treatment group were lower than that 12 weeks(all P<0.05);At the time of 8,12,36 weeks, scores of the control group were lower than those of before treatment(all P < 0.05);②upper arm function, namely fingers touching the opposite corner subscapularis:At the time of 4,8,12 weeks, scores of the treatment group were lower than those of before treatment(all P<0.05); At the time of 36 weeks, scores of the treatment group were lower than that 12 weeks(all P<0.05); At the time of 8,12,36 weeks, scores of the treatment group were lower than those of the control group (all P<0.05);③Lower extremity functions: At the time of 8,12 weeks,scores of the treatment group were lower than those of before treatment and control group (all P<0.05);At the time of 36 weeks, scores of the treatment group were lower than that 12 weeks(all P<0.05) ; At the time of 8,12,36 weeks, scores of the control group were lower than those of before treatment (all P<0.05);④single joint functions:At the time of 4,8,12 weeks,scores of the treatment group were lower than those of before treatment(all P<0.05); At the time of 36 weeks,scores of the treatment group were lower than that 12 weeks(all P<0.05) ; At the time of 8,12,36 weeks, scores of the control group were lower than those of before treatment(all P<0.05);At the time of 4,8,12,36 weeks, scores of the treatment group were lower than those of control group(all P<0.05);⑤At the end of treatment and follow-up,the improvement rate in joint functions in the treatment group were 88.33% (53/60),93.33% (56/60); the control group were 28.07%(16/57),40.35%(23/57), (Fisher test, P<0.01,X2=56.21, P<0.01). ConclusionTraditional Chinese medication(its main ingredient is Strychnine), an effective drug for improving joint dysfunction in patients suffering from moderate skeletal fluorosis, is simple and effective.

OBJECTIVE To discuss the correlation between effectual time and the curative effect in patients with all frequency descending sudden deafness. METHODS According to effectual time,the subjects were divided into first week effectual group and second week effectual group and the curative effect of each group was compared. RESULTS In patients with flat descent sudden deafness, the curative rate of the first week effectual group was higher than that of the second week effectual group, but there was no significant difference between the two groups(χ2=1.599, P =0.206). Meanwhile, the total significant effective rate of the first week effectual group was higher than that of the second week effectual group, without obvious difference between the two groups(χ2=0.124, P =0.725). Furthermore, in patients with total deafness type of sudden deafness, the curative rate of the first week effectual group was higher than that of the second week effectual group, showing no remarkable difference between the two groups(χ2=2.493, P =0.114). Besides, there was no remarkable difference in the comparison of the total significant effective rate (χ2=2.308, P =0.129), which was higher in the first week effectual group than that in the second week effectual group. CONCLUSION The course of treatment should be at least 2 weeks in patients with all frequency descending sudden deafness after onset.

OBJECTIVETo investigate the proportion of Th22 cells in peripheral blood of patients with acute lymphoblastic leukemia (ALL) and evaluate its significance.

METHODSThe proportions of Th22 cells in peripheral blood of B-ALL and T-ALL patients before therapy (group 1), B-ALL and T-ALL patients in complete remission (ALL-CR, group 2) and healthy donors (group 3) were evaluated by flow cytometry. The cytokines IL-22, TGF-β, TNF-α and IL-6 in peripheral blood of each group were measured by enzyme-linked immunosorbent assay (ELISA). The levels of IL-22 mRNA in peripheral blood mononuclear cells of each group were examined by reverse transcription-PCR (RT-PCR).

RESULTSThe percentages of Th22 cells and the levels of IL-22, TNF-α, IL-6 and IL-22 mRNA in B-ALL and T-ALL patients before therapy were (0.44 ± 0.10)%, (10.9 ± 3.4) ng/L, (110.7 ± 26.5) ng/L, (60.2 ± 13.8) ng/L, 0.17 ± 0.04 and (0.46 ± 0.11)%, (11.2 ± 3.5) ng/L, (114.6 ± 27.0) ng/L, (58.7 ± 12.4) ng/L, 0.19 ± 0.04, respectively; Which in B-ALL and T-ALL patients in complete remission were(0.59 ± 0.15)%, (14.3 ± 4.1) ng/L, (142.5 ± 32.7) ng/L, (83.7 ± 18.9) ng/L, 0.25 ± 0.06 and(0.60 ± 0.15)%, (14.6 ± 4.3) ng/L, (140.4 ± 31.4) ng/L, (81.4 ± 18.2) ng/L, 0.26 ± 0.06, significantly lower than those in healthy donors \[(1.24 ± 0.31)%, (19.7 ± 6.6) ng/L, (238.3 ± 50.4) ng/L, (138.0 ± 27.1) ng/L, 0.49 ± 0.09\] (P < 0.01). The percentages of Th22 cells and the levels of IL-22, TNF-α, IL-6 and IL-22 mRNA in group l were lower than those in group 2 (P < 0.05), there was not significant difference between B-ALL and T-ALL (P > 0.05). But the levels of TGF-β in B-ALL and T-ALL patients before therapy \[(30.6 ± 8.2) ng/L, (31.4 ± 8.8) ng/L\] and in complete remission \[(24.2 ± 5.8) ng/L, (25.1 ± 6.1) ng/L\] were significantly higher than those in group 3\[(9.6 ± 2.8) ng/L\] (P < 0.01). However, the level of TGF-β in group 1 was higher than that of group 2 (P < 0.05), there was not significant difference between B-ALL and T-ALL (P > 0.05).

CONCLUSIONBoth the number and function of Th22 cells reduced in ALL patients. Th22 cells might be negatively correlated with ALL progression. The lower levels of TNF-α and IL-6, and overexpression of TGF-β in ALL patients might suppress the differentiation of Th22 cells.

Adolescent ; Adult ; Case-Control Studies ; Humans ; Interferon-gamma ; metabolism ; Interleukin-6 ; metabolism ; Interleukins ; metabolism ; Leukocytes, Mononuclear ; metabolism ; Middle Aged ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; blood ; RNA, Messenger ; genetics ; T-Lymphocytes, Helper-Inducer ; metabolism ; Transforming Growth Factor beta ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism ; Young Adult