Objective To investigate the features of chronic prostatitis during puberty(CPP)and the effects of pelvic floor biofeedback therapy.Methods Totally,25 CPP children (mean age,16 years) and 15 children (mean age,16 years) with normal lower urinary tract as controls were included.In CPP group,NIH-CPSI scores were evaluated,expressed prostatic secretions (EPS) were examined,and bacterial culture was done;and CPP patients were categorized based on the definitions of NIH types.In both groups, urodynamic examination was performed,including evaluation of uroflow curve,maximum flow rate (Q_(max)), post-voiding residual urine (PVR),detrusor-sphincter dyssynergia (DSD),maximum detrusor pressure (P_(det,max))and maximum urethral closure pressure (MUCP).CPP patients underwent biofeedback therapy, and 10 weeks later the effects were assessed.Results In CPP group,NIH typing showedⅡ,ⅢA andⅢB in 1,3 and 21 cases,respectively.Before treatment in CPP and control groups,the incidence of staccato voiding (20 cases vs 1 case),DSD (22 cases vs 1 case),Q_(max)(10.7?3.7 vs 15.0?4.3ml/s),PVR (7.7?4.1vs 3.2?2.6ml),P_(det,max)(115.1?33.6vs 76.8?16.6cm H_2O)and MUCP(176.5?45.7 vs 86.2?28.5cm H_2O)all showed significant differences between the 2 groups(P＜0.05).In CPP group,the differences in pain(4.6?2.2 vs 2.1?1.6),urination (7.9?2.0vs 2.2?1.7),life impact (9.4?2.2vs 2.6?2.1)and total scores(22.0?5.2vs 7.0?4.2) of NIH-CPSI and Q_(max)(10.7?3.7 vs 14.9?5.6) between pre-and post-biofeedback were significant (P＜0.05).Conclusions The main type of CPP is categoryⅢB.The primary symptom is voiding disorder,which leads to greater psychological stress in patients.Children with CPP have pelvic floor dysfunctions and multiple abnormal urodynamic param- eters.The short-term effect of biofeedback strategies for CPP is satisfactory.

6.24 mmol/L) and sixty healthy persons in the health center of our hospital were investigated as hyperhpidemia group (Hyperlipidemias) and control group (Controls) respectively.Hyperlipidemias were given simvastatin 20 mg?d~(-1) for twelve weeks (Statins).Blood samples of ulnar vein were extracted from Statins at the end of twelve weeks as well as Controls and Hyperhpidemias at the beginning of the experiment. Blood serum,plasma and mononuclearcell were extracted and stored at a refrigerator of-80℃.The level of plasma angiotensinⅡwas detected by the method of radioimmunity.While the expression of RANTES mRNA and protein on mononuclearcell were assessed by real time reverse transcription polymerse chain reaction and Western blot respectively.Results①The plasma angiotensinⅡof Hyperlipidemias was higher than that of Controls [(92.13?22.03) vs (50.85?12.12),P

AIMTo study the effect of ginkgolide B from Ginkgo leave on action potential (AP), L-type calcium current (I(Ca) - L) and delayed rectifier potassium current (I(K)) in normal and ischemic guinea pig ventricular myocytes.

METHODSWith the standard microelectrode technique to record action potential and whole-cell variant patch-clamp technique to record calcium and potassium current.

RESULTS(1) Under normal condition, ginkgolide B shortened APD and had no effect on RP, AP and V(max). Ginkgolide B also increased I(K) in a concentration dependent manner and had no significant effect on I(Ca) - L (2) Under ischemia condition, it was observed that shortening of APD, APA, decrease V(max) and depolarization of RP was induced by ischemia, but ginkgolide B could attenuate above--mentioned changes. (3) Under ischemia condition, I(Ca) - L and I(K) were inhibited, perfusion with ischemia solution containing ginkgolide B could reverse the decrease of I(Ca) - L and I(K).

CONCLUSIONGinkgolide B had protective effect on ischemic myocardium to prevent ischemic arrhythmia.

Action Potentials ; drug effects ; Animals ; Calcium Channels, L-Type ; drug effects ; Delayed Rectifier Potassium Channels ; drug effects ; Ginkgolides ; pharmacology ; Guinea Pigs ; Heart Ventricles ; drug effects ; Lactones ; pharmacology ; Myocardial Ischemia ; metabolism ; Myocytes, Cardiac ; drug effects ; metabolism ; Patch-Clamp Techniques

Fragile X syndrome (FXS) is one of the most prevalent mental retardations. It is mainly caused by the loss of fragile X mental retardation protein (FMRP). FMRP is an RNA binding protein and can regulate the translation of its binding RNA, thus regulate several signaling pathways. Many FXS patients show high susceptibility to epilepsy. Epilepsy is a chronic neurological disorder which is characterized by the recurrent appearance of spontaneous seizures due to neuronal hyperactivity in the brain. Both the abnormal activation of several signaling pathway and morphological abnormality that are caused by the loss of FMRP can lead to a high susceptibility to epilepsy. Combining with the research progresses on both FXS and epilepsy, we outlined the possible mechanisms of high susceptibility to epilepsy in FXS and tried to give a prospect on the future research on the mechanism of epilepsy that happened in other mental retardations.
Brain ; physiopathology ; Epilepsy ; etiology ; genetics ; pathology ; Fragile X Mental Retardation Protein ; genetics ; metabolism ; Fragile X Syndrome ; complications ; genetics ; Humans ; RNA-Binding Proteins ; metabolism

With whole-cell variant patch-clamp and laser scanning confocal microscope technique, we examined the effect of ginkgolide B (GB) from ginkgo leaves on L-type calcium current and cytosolic [Ca(2+)](i) in guinea pig ischemic ventricular myocytes. The results showed that under normal conditions, at a test voltage of 0 mV, GB had no significant effect on I(Ca,L); and during ischemia, the peak Ca(2+) current reduced by 37.71%, and the I-V curve of I(Ca,L) was shifted upward. 1 micromol/L GB reversed the change induced by ischemia, a result being significantly different from those of the ishemia group (P<0.05).Under control condition, 0.1,1,10 micromol/L GB decreased intracellular calcium concentration by 10.58%, 17.27% and 16.35% (n=12, 12, 10, P<0.01-0.001), respectively. With perfusion of ischemic solution for 12 min, intracellular calcium concentration increased by 20.15%. After a 12 min-perfusion of ischemic solution containing 1 micromol/L nifedipine or 5 mmol/L NiCl2, intracellular calcium concentration increased by 18.18% (P>0.05 vs ischemia) and 11% (P<0.05 vs ischemia), respectively. After 12 min of perfusion with ischemic solution containing 1 micromol/L GB, intracellular calcium concentration increased by 9.6% (P<0.05 vs ischemia). It is shown that GB could reverse the decrease of I(Ca,L) and partially inhibit calcium overload during ischemia.
Animals ; Calcium ; metabolism ; Calcium Channels, L-Type ; drug effects ; Cell Hypoxia ; Cytosol ; metabolism ; Ginkgolides ; pharmacology ; Guinea Pigs ; Heart Ventricles ; cytology ; Lactones ; pharmacology ; Male ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocytes, Cardiac ; drug effects ; metabolism ; Patch-Clamp Techniques ; Plant Extracts ; pharmacology

The complete coding sequences of Eya gene family was amplified by standard PCR fromhuman tissues or cells cDNA library.The product of PCR was cloned into the eukaryotic expression vector pcDNA3-FLAG,generating pcDNA3-FLAG-Eya1～4.Thenhuman embryo kidney 293T cells were transfected with the recombinant plasmids and the expression of Eya genes were identified by Western blot.Transcriptional assay using a reporter containing myogenin enhance factor indicated that expression of Eya cooperation with Six in 293T cells affected the Myogenin gene expression.The expression vectors of Eya genes were constructed and confirmed by restriction enzyme digestion and DNA sequence analysis.Transcriptional assay using a reporter containing myogenin enhance factor indicated that expression of Eya in coordination with Six in 293T cells stimulated the Myogenin gene expression.Eya proteins are transcriptional activator of Six and can improve the activity of myogenin promoter.

Objective To evaluate the clinical effect in the treatment of the young patients(≤45 years old) with acute myocardial infarction(AMI)underwent emergent percutaneous transluminal coronary angioplasty(PTCA) combined with Lipo-PGE_1.Methods 39 patients with AMI(paroxysm within 12 hours),were underwent emergent PTCA(coronary stem performed in some patients),including 18 cases which were treated combined with Lipo-PGE_1 in the mean time.And the clinical efficacy and the results of short-period follow-up were recorded.Results The in- farctive vasculars were re-open in 37 patients(23 cares were routinely placed translunrinal srents),and the successful rate was 94.9 %.Those who also used Lipo-PGE_1 were re-open in 17 patients.The successful rate was 94.4 %,their ST segments on EKG 30 minutes after operations reduced significantly than that of patients who did not use Lipo- PGE_1,their cardial functions were also improved significantly 24 hours after operations and no side effects on blood pressure and heart rate were observed.Conclusion The emergent PTCA combined with Lipo-PGE_1 for acute my- ocardial infarction can protect the cardial function and show a better early therapy effect.

OBJECTIVETo understand the epidemiological characters of Kashin-Beck disease (KBD) in nuclear families, and to probe the pathogenetic mechanism and its etiology.

METHODSClinical diagnosis was used to identify nuclear families in KBD areas. Based on the clinical manifestation of parents in the nuclear families, 4938 nuclear families were divided into four types. According to the seriousness in KBD areas, prevalence of offspring and family aggregation in low, middle and high prevalence areas were formed and data was analyzed.

RESULTS(1) Type of nuclear family was associated to the degree of disease seriousness in the areas. (2) There was an aggregation of disease among the offsprings in the nuclear families of medium and high prevalence diseased areas. (3) There was an aggregation of offspring in the nuclear family of both parents or father alone who were suffered from KBD. (4) The prevalence of offspring in nuclear family of both parents with KBD was obviously higher than that in the nuclear family with single parent or neither having KBD.

CONCLUSIONThe degree of diseased areas seemed to influence the seriousness of KBD in individuals. The prevalence of parents in nuclear families might play a role in the pathogenesis of KBD.

Adolescent ; Adult ; Child ; Child, Preschool ; China ; epidemiology ; Endemic Diseases ; Family Health ; Female ; Humans ; Male ; Middle Aged ; Nuclear Family ; Osteoarthritis ; epidemiology ; Prevalence ; Selenium ; deficiency

Objective To investigate the effects of dominant-negative truncation mutant?NTCF4, lacking the N-terminal form of TCF4 gene,on biological characteristics of renal cancer cell line GRC-I and explore the molecular mechanisms.Methods GRC-I cell was transfected with pCDNA3-?NTCF4 eukary- otie expression plasmid,pCDNA3 empty vector to construct the stable cell line GRC-I/?NTCF4 and GRC-I/ Mock respectively.The morphological changes of stable cells were observed and the cells growth curve was detected through light microscope.The cellular proliferation activities were determined using the MTT assay. The protein expression of Wnt pathway downstream target gene C-Myc and Cox-2 was evaluated by immuno- cytoehemieal method and Western Blot analysis.Results After the dominant-negative?NTCF4 gene was permanently expressed,the GRC-I/?NTCF4 stable cells morphologically showed that appearance changed from circular to long-spindle shape,growth rate decreased with less karyosehisis found,malignant pheno- types reversed to normal renal tubular cells.MTT assay revealed that the proliferation activities of GRC-1/?NTCF4 cells were inhibited by 11.2%-35.5% compared with GRC-I cells (P＜0.05),while the GRC- I/Mock cells have no difference with the control cells.Immunocytochemical analysis and Western Blot showed that the C-Myc and Cox-2 protein expression level of GRC-I/?ANTCF4 cells were significantly sup- pressed in comparison with that of GRC-I/Mock and GRC-I cells.Conclusions The dominant-negative truncation mutant?NTCF4 could partially inhibit the growth of renal cancer cells and down-regulate the pro- tein expression of Wnt pathway target gene C-Myc and Cox-2.These findings provide a experimental founda- tion for applying cell signal therapy to renal cell cancer by blocking the Wnt signaling pathway.

OBJECTIVETo assess the changes of neurobehavioral function in a neonatal mouse model of excitotoxic brain damage.

METHODSFifty-five 5-day-old ICR neonatal mice were randomly assigned to three groups: blank (no intravenous) control (n=20), saline control (n=20) and excitotoxic brain damage model (ibotenic acid treatment, n=15). Behavioral function was evaluated by the surface righting reflex test (postnatal days 6-10), the swimming test (postnatal days 8-12) and the Y-maze discrimination learning test (postnatal days 33-34).

RESULTSRighting time in the surface righting reflex test in the ibotenic acid treatment group on postnatal days 6-10 was more prolonged than that in the two control groups (p<0.05). Swimming test scores in the ibotenic acid treatment group were significantly lower than those in the two control groups (p<0.05). In the Y-maze discrimination learning test, the mice from the ibotenic acid treatment group performed significantly worse than two control groups, presenting with increased learning times (19.79+/-2.42 vs 16.29+/-2.48 or 16.30+/-2.37; p<0.05) and achieving a lower correct percentage (86.7% vs 96.5% or 95.0%) (p<0.05).

CONCLUSIONSThe developmental reflexes and learning and memory functions were impaired in neonatal mice following excitotoxic brain damage. Behavioral testing is useful in the evaluation of early developmental reflexes and long-term neurobehavioral outcome in neonatal mice with excitotoxic brain damage.

Animals ; Animals, Newborn ; Behavior, Animal ; drug effects ; Brain ; drug effects ; Excitatory Amino Acid Agonists ; toxicity ; Female ; Ibotenic Acid ; toxicity ; Male ; Maze Learning ; drug effects ; Mice ; Mice, Inbred ICR ; Swimming