Objective:Comparing the effect of different doses of simvastatin in lowering the serum lipid.Methods:79 patients were randomized into group A and group B,and were given simvastatin 10 mg*d-1 (group A) and 20 mg*d-1 (group B),respectively for a total of 8 weeks.Results:Comparing with baseline,in group A,TC,TG,LDL-C were decreased by 23.4%,20.0% and 30.7%,respectively (P＜0.01); HDL-C was increased by 17.5%.The content of serum TC,TG and LDL-C was decreased to the normal range in 12.8%,28.2% and 15.4% of the patients in group A.For the group B,TC,TG,LDL-C were decreased by 32.7%,22.8% and 42.8%,respectively (P＜0.01); HDL-C was increased by 13.7%.The content of serum TC,TG and LDL-C was decreased to the normal range in 65.0%,57.5% and 65.0% of the group B patients.Conclusion:Oral intake of 20 mg of simvastatin once a day can effectively reduce the serum lipid.The patients can well tolerate and no obvious side effect was observed in our study.

According to the requirement of simulated actual combat,based on the traditional contents of sanitary reconnaissance of water source,this paper introduced some practical knowledge and skills in drinking water under emergency,including water source search,utilization,drinking principles and some measures to reduce the loss of body water.These practices enriched and consum- mated the subject of sanitary reconnaissance of water source.

OBJECTIVEThe present study was undertaken to design antisense oligodeoxynucleotides (AS-ODNs) of glial glutamate transporter-la (GLT-1a) and to evaluate the effectiveness of the designed AS-ODNs on the expression of GLT-1a.

METHODSFive sequences of GLT-1a AS-ODNs were designed according to the C terminus specific sequences of GLT-1a mRNA using antisense design software of IDT Com- pany. Western blot analysis was used to evaluate the inhibition effects of the five GLT-1a AS-ODNs on the expression of GLT-la.

RESULTSThe sequence of GLT-1a AS-ODNs with sequence of 5'-GGTTCTTCCTCAACACTGCA-3' could specifically inhibit the expression of GLT-1a in the hippocampal CA1 subfield of rats, while it had no effect on the expression of GLT-1b. This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. It could also significantly inhibit the cerebral ischemic preconditioning (CIP)-induced up-regulation in the expression of GLT-1a. The magnitude of the inhibition in sham, Cef- or CIP-treated rats was similar by more than 60%.

CONCLUSIONFrom the designed five sequences of GLT-1a AS-ODNs, we obtained an effective sequence which can specifically inhibit the expression of GLT-1a.

Animals ; CA1 Region, Hippocampal ; metabolism ; Excitatory Amino Acid Transporter 2 ; antagonists & inhibitors ; metabolism ; Ischemic Preconditioning ; Oligonucleotides, Antisense ; genetics ; RNA, Messenger ; Rats ; Up-Regulation

·AIM: To detect the effect of CTGF on the apoptosis in the diabetic retina with small interfering RNAs (siRNA) targeting with CTGF. ·METHODS: A total of 60 rats were divided into six groups including control group, diabetic 4,8,12,16 weeks group, and interference group. Diabetic rats were induced by STZ intra-peritoneal. At 4, 8, 12, 16 weeks after diabetic setting up, retinas were obtained from control, diabetic rats and diabetic animals treated by intravitreal injection of CTGFsiRNA to suppress the expression of CTGF mRNA. Retinal cells apoptosis was detected by Tunnel staining and mRNA expression of CTGF was analyzed by RT-PCR.·RESULTS: The levels of CTGF and the apoptosis in the retinas of diabetic rats were significantly higher than those in the controls. Apoptosis occurred at 4 weeks after a diabetic model setting up, became serious with the diabetes developing, while CTGF elevated at 8 weeks. The cell apoptosis counts increased to 25.8cells/mm2 at 24 weeks of diabetes. SiRNA-mediated inhibition of CTGF mRNA resulted in a significant decrease in apoptosis. Significant correlations were found between CTGF and apoptosis in the retina.·CONCLUSION: These results suggest that CTGF might be involved in retinal cells apoptosis which is a characteristic of early diabetic retina. siRNA targeting CTGF seems to have the advantage of ameliorating retinal cells lost.

Objective To improve the diagnosis and treatment of ureteral cancer. Methods A retrospective analysis of 24 cases of primary ureteral cancer treated from January 1990 to March 2005 was performed.The diagnostic value of ultrasound,IVU,CT,MRU and the patients' outcomes were reviewed. There were 19 males and 5 females aged 38-72 years(mean,59 years).The tumors were on the left side in 16 cases and on the right in 8.Of the 24 cases,17(71%)had gross hematuria and 7(29%)had micro- scopic hematuria.Urine cytology was performed in 16 cases with a positive rate of 6.3%.B-ultrasonic exami- nation showed hydronephrosis in 19 cases(79%)and low-echo space-occupying disease of middle-inferior ureter in 3(12%).IVU demonstrated hydronephrosis in 20 cases(83%)and filling defect of the diseased ureter in 3(12%).Retrograde pyelography showed filling defect of the diseased ureter in 16(76%)of 21 cases(5 cases had failure of intubation).CT scan was performed in 20 cases,indicating thickening of the ureteral wall and infiltration of the cancer in 14(70%).In 3 cases who had undergone spiral CT thin layer scan and 1 of 3 cases who had undergone MRU,the definite diagnosis was made.Results All the 24 pa- tients underwent surgical treatment.Among them,nephroureterectomy and bladder cuff or partial resection were performed in 18 cases,and nephrectomy and partial ureterectomy in 6 cases.Postoperative pathology showed transitional cell carcinoma in 23 cases,and adenoma in 1.Of the 14 cases during 1990-1999 peri- od,1,5,3,2,2 and 1 cases had survival time of 1,2,3,4,5 and 6 years,respectively.Of the 10 cases during 2000-2005 period,3 were lost to follow-up;2 survived for 3 years and 2,for 1 year;the other 3 who have survived near 5 years have been followed till now.Conclusions IVU and retrograde urography are the most common diagnostic measures for primary ureteral cancer.They can be used in combination with other imaging study to reduce missed diagnosis rate.The 5-year survival rate was lower because of late pathologic stage of the tumors in the patients of this series.

To determine whether the pathological changes caused by injury to the spinal cord can be correlated with values obtained by the Magnetic Motor Evoked Potential (MEPs) technique, we studied spinal cords from 41 adult cats who were divided into 4 groups. The groups ranged from normal cats whose spinal cords were not compressed, to slightly, moderately and severely injured. MEPs were recorded before compression and in 30 minutes, 6 hours, 1 week, 2 week and 4 week after the compression unit was installed. Pathological changes with increased pressure were seen in blood vessels, nerve cells and fibers, Nissl substance and the central canal. A reversal of pathological changes was observed in slight or moderate injury during the 4 weeks of the experiment. Extensive injury, however, caused irreversible changes in the nerve cells with loss of motor function. The latency of MEPs at 30 minutes and 6 hours in the slightly injured group was 0.37 and 0.38 times greater than the baseline and returned to normal levels in 4 weeks. In the moderately injured group, the latency was increased 0.77 and 0.81 times and in the severely injured 1.32 and 1.36 times over the baseline. Recovery in the second group was partial and not at all in the severely injured. Thus, there appears to be good correlation between observed pathological changes, motor functions and MEPs.

Objective To investigate the expression and clinical significance of P-selectin (CD62P) in bone marrow hematopoietic stem cells of patients with acute leukemia (AL). Methods The CD62P expression in bone marrow mononuclear cells of 15 healthy donors and 56 untreated patients with AL, were examined by flow cytometry. Results The average rate of CD62P expression was (6.72±7.64) % in hematopoietic stem cells (CD+45 CD+34 CD-38) of the 38 patients with acute myeloid leukemia (AML), was (3.46±2.51) % in hematopoietic stem cells (CD+45 CD+34 CD+19) of the 12 patients with B-acute lymphoblastic leukemia (B-ALL), and was (6.23±4.95) % in hematopoietic stem cells (CD+45 CD+34 CD+7) of 6 patients with T-acute lymphoblastic leukemia (T-ALL). The expression rates in those AL patients were higher than that in the healthy controls (1.04 ±1.23) % (t = 2.847, 3.284, 3.091, respectively, P ＜0.01), while there was no difference between the control group and the group who reach CR after routine treatment (t =1.932, P ＞0.05). Furthermore, the leukocyte,hemoglobin and platelet count in CD+62P patients with AML and T-ALL were significantly higher than CD-62P ones (t =4.153, 8.095, 8.289, 7.235, 8.692, 9.832, respectively, P ＜0.05), but there was no significant difference between CD+62P and CD-62P patients with B-ALL (t =0.340, 1.142, 0.019, respectively, P ＞0.05).Conclusion The CD62P is one of the markers of platelet activation, and its expression varies in different types of AL. The CD62P in hematopoietic stem cells of AL could be regarded as a new sign for the leukemic stem cells, as well as a helpful prognostic indicator in treatment response assessment.

Objective To evaluate the effect of curcumin on cognitive dysfunction in a rat model of trigeminal neuralgia.Methods Thirty healthy adult male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n=10 each) using a random number table:sham operation group (Sham group),trigeminal neuralgia group (TN group),and trigeminal neuralgia + curcumin group (TN + Cur group).Trigeminal neuralgia was produced by injecting cobra venom solution 4 μl into the sheath of the infraorbital nerve in TN and TN + Cur groups.Starting from 15 days after establishment of the model,1.5 ml peanut oil was injected through a gastric tube into stomach twice a day (in the morning and at night) for 28 consecutive days in TN group,and curcumin 45 mg/kg (dissolved in 1.5 ml peanut oil) was injected through a gastric tube into stomach twice a day (in the morning and at night) for 28 consecutive days in TN + Cur group.The cognitive function was assessed using Morris water maze test after the end of treatment.The escape latency,swimming speed,ratio of time of staying at the target quadrant,and the number of times the animals crossing the platform were recorded.The pathological changes in the hippocampal CA1 region were observed with an electron microscope.The ultrastructure of neurons,organelles and synapses in the hippocampal CA1 region was examined with a transmission electron microscope.Results There was no significant difference in the swimming speed between the three groups (P＞0.05).Compared with Sham group,the escape latency on 1st-4th days was significantly prolonged,the ratio of time of staying at the target quadrant was decreased,and the number of times the animals crossing the platform was decreased in TN group,and the escape latency was significantly prolonged on 3rd and 4th days in TN + Cur group (P＜0.01).Compared with TN group,the escape latency on 2nd-4th days was significantly shortened,the ratio of time of staying at the target quadrant was increased,the number of times the animals crossing the platform was increased (P＜0.01),and the pathological changes of hippocampal tissues were attenuated in TN + Cur group.Conclusion Curcumin can improve cognitive dysfunction in a rat model of trigeminal neuralgia.

Objective To evaluate the effect of combined treatment with gonadotropin-releasing hormone analog(GnRHa)and recombinant human growth hormone(rhGH)on predicted adult height(PAH)in girls with central precocious puberty(CPP).Methods Fifteen girls with CPP,whose growth velocity during GnRHa treatment had been less than 4 cm/year,were given additional rhGH treatment at a dose of 1 U?kg~(-1)?w~(-1),sc, for 4-13 months.Comparisons of growth velocity,height SDS for bone age(HtSDS_(BA))and PAH were performed before and after the combined treatment.Results During rhGH combined with GnRHa therapy,growth velocity increased significantly[(7.4?1.7)cm/year vs (3.2?0.7)cm/year baseline,P＜0.01].In 7 girls treated with rhGH and GnRHa for more than 9 months,growth velocity in the second 6 months[(6.5?1.0)cm/year]was slightly lower than that in the first 6 months[(8.8?1.1)cm/year],being both faster than that of baseline [(3.2?0.8)cm/year].There was a significant increase in rhGH-duration corrected change of HtSDS_(BA) [(0.35?0.15)/6 month vs (0.12?0.18 )/6 month baseline,P＜0.01]and PAH[(3.2_+1.4)cm/ 6 month vs (1.4?1.1)cm/6 month baseline,P＜0.01].Conclusion In girls with CPP showing a marked decrease in growth velocity during GnRHa treatment,the combined rhGH and GnRHa treatment remarkably improves growth velocity and PAH.

Objective To study the effects of urinary kallidinogenase (kallikrein) on focal cerebral blood flow (CBF) following cerebral infarction in rats by laser speckle imaging.Methods Permanent middle cerebral artery occlusion (MCAO) was induced in male Sprague-Dawley rats by the intraluminal filament technique.Laser speckle imaging was used to measure CBF in the ischemic cortical area and middle cerebral artery territory.The brain was stained with 2,3,5-triphenyltetrazolium chloride (TTC) to determine the infarct size.Neurological deficit score was measured.Results CBF increased in both hemispheric cortical area and MCA territory on the first and second days following urinary kallikrein administration at high dose but not at low dose.Larger blood vessel diameter and increased blood flow velocity were noticed in the high dose group in some arteries when compared to the low dose group and normal saline control group.At 36 h after cerebral ischemia,the brain infarct size was 10.14% ±3.02% ,25.99% ±3.90% and 27.10% ±3.32% in high, low dose and normal saline control groups,respectively.The infarct size was significantly smaller in the high ( F = 61.14, P<0.01 ) but not low dose group when compared to the normal saline control group.The neurological deficit was milder in the high dose group but not the other two groups at 4 h after cerebral ischemia; however, there were no differences among the groups at 36 h after MCAO.Conclusions Urinary kallidinogenase can reduce cerebral infarction volume and neurological deficit in rats following focal cerebral ischemia.These effects may be attributed to enhanced collateral circulation and improved CBF in the hemispheric cortical area and MCA territory.