In Order to screen antidiarrhea drugs, the standard operation of mice diarrhea model replicated with leave of Cassia angustifolia vahl was introduced. In experiments, diarrhea index expressed with loose stool ineidence rate multiplied by loose stool grade was used as main index. It thoroughly mirrors indi. vidual diarrhea degree and possesses comparability. The result indicates that diarrhea index in mice presented normal distribution. The index between animal model groups kad no difference as well as no differcnce was found in model mice of same group for six consecutive days, with good reproduclbility. It is recommended that the model can be used for the screening of antidiarrhea drugs.

The estrogen related receptor family member Esrrb (Estrogen related receptor β) is a gene that expresses in the early stage of embryo and plays an important role in the core pluripotent network. Its function has been analyzed in human and mouse, although no report so far related to pig. Therefore, to explore its mechanism of transcriptional regulation and expression pattern, we cloned a 3.3 kb pig ESRRB promoter by PCR and constructed the green fluorescence protein (GFP) reporter vector pE3.3. We used these vectors to study the ESRRB expression pattern in 293T, Hela and C2C12. Sequence was analyzed for regulatory elements that share homology to known transcription factor binding sites by TFSEARCH and JASPER program. Some pluripotency related genes such as SMAD, STAT3, MYC, KLF4 and ESRRB have been found within the 3.3 kb sequence by co-transfected pig ESRRB promoter and these potential regulators. We found that ESRRB only expressed in 293T and SMAD could activate ESRRB expression obviously. To determine the core promoter region, a series of ESRRB promoter fragments with gradually truncated 5'-end were produced by PCR and inserted into pGL3-Basic vector. After transient transfection into 293T, dual luciferase assay was used to measure these promoter activities. The result suggested that the core promoter of pig ESRRB located within -25 bp to -269 bp region. These results suggest that these transcription factor binding sites and the core promoter region may be essential for transcriptional regulation of pig ESRRB gene.
Animals ; Binding Sites ; Cloning, Molecular ; Estrogen Receptor beta ; genetics ; Genetic Vectors ; HeLa Cells ; Humans ; Mice ; Promoter Regions, Genetic ; Swine ; genetics ; Transcription Factors ; Transfection

Objective:To study on GFW-inducing tumor apoptosis and to find the experimenting basis for utilizing GFW in cancei theiapy.Methods:S180 mouse sarooma model was used to detect inhibiting effects of GFW on tumor grouth in viro,Morphological changes were observed by electron microscopy and flow cytometer was used for determination apoptosis.The protein expression of p21 and the mRNA expression of Survivin were evaluated by immunohistochemistry and in situ hybridization.Results:For S180 sarcoma ,the inhibiting rate of GFW was 38.93%.Apoptosis was 17.79% detected by flow cytomety.Typical apoptotic cells and apoptotic bodies were observed through electron microscope. Chromatin was found gathering as aggregates in nucleus or under nucleus membrane and the nuclear body formed at the same time. Survivin mRNA decreased markedly in the GFW group when compared with the model group(P

Objective To study the effect of Guizhi Fuling Wan(GFW) on tumor apoptosis and apply the experimenting basis of GFW's development and utilization.Methods The S180 mice sarcoma model was used to detect the inhibitory effects of GFW,observe the ultrastructural change by electron microscopy,and the flow cytometer was used for apoptosis determination.The protein expression of P21waf/cip and the mRNA expression of Survivin were evaluated by immunohistochemistry and in situ hybridization.Results For S180 sarcoma,the inhibition ratio of GFW was 38.93%.The apoptosis was 17.79% by the flow cytometer.Some typical apoptotic cells and apoptotic bodies were observed through electron microscope.Chromatin gathered at the side of cell,the nucleus turned into the nucleus band and nucleus projected.Survivin mRNA markedly declined in the GFW group when compared with that in the model group(P

OBJECTIVE:To improve the monitoring and reporting system of adverse drug use(ADR)in medical organiza?tions.METHODS:The current situation of monitoring and reporting system of ADR in medical organizations were analyzed.RESULTS&CONCLUSION:In our country the running of the ADR monitoring and reporting system is left to be improved and optimized.

Objective To explore the value of MRI in diagnosis of fetal meconium peritonitis.Methods Seven meconium peritonitis fetuses proved by surgery and pathology were enrolled.The prenatal MRI findings and clinical data were analyzed retrospectively.Results Six fetuses showed a large amount of ascites,intestinal tube floating in the abdomen,small intestine gathered together.One fetus showed a giant abdominal cystic mass,with bowel compressed,displaced and uneven dilated.Four fetuses showed small colon and rectum,or without meconium signal.Two fetuses were accompanied by bilateral hydrocele.Amniotic fluid increased in 3 cases.After the neonates were born,1 case of them died from sudden heart rate decline during operation,1 case died from severe pulmonary edema after operation,and 5 cases survived after operation.Conclusion MRI has some features in the prenatal diagnosis of meconium peritonitis,which can provide an important basis for postpartum treatment and evaluation of prognosis.

N-Benzyl matrinol was obtained by hydrolysis, benzylation and reduction reaction from matrine. A series of hybrids (8a-8n) from (phenylsulfonyl)furoxan and N-benzyl matrinol were synthesized and biologically evaluated as anti-hepatocellular carcinoma agents. All target compounds were evaluated for anti-proliferative activity against human hepatocellular Bel-7402, SMMC-7721, Bel-7404, and HepG2 cells in vitro by MTT method. The results indicated that all of these compounds had potent anti-proliferative activity which were more potent than their parent compound and 5-FU, especially 8a-8h and 8j showed the strongest anti-HCC HepG2 cell activity with IC50 values of 0.12-0.93 μmol x L(-1).

Objective To study the effects of medicated serum with total saponins from Rhizoma Dioscreae Nipponicae (RDN) on VEGF mRNA expression and AP-1 activity in rat synovial cell strain RSC-364 induced by IL-17 and TNF-α. To investigate the mechanism about total saponin from RDN inhibition of angiogenesis. Methods Medicated serum of total saponins from RDN and tripterygium (positive control) were prepared. Rat synovial cells RSC-364 were divided into four groups: the blank control,IL-17+TNF-α model,tripterygium medicated serum,and total saponins medicated serum groups. After one hour of incubation,all groups except for the blank control were incubated with both IL-17(10 μg·L-1 ) and TNF-α(10 μg·L-1 ) for 24 hours. VEGF mRNA expression in RSC-364 was detected by PrimeScriptTM real-time quantitative PCR (RT-PCR) detection kit,and the AP-1 DNA-binding activity was detected by electrophoretic mobility shift assay (EMSA). Results Compared with the control blank group,both of the VEGF mRNA expression and AP-1 activity in rat synovial cell strain RSC-364 induced by IL-17 and TNF-α increased remarkably (P<0. 05,P<0.01). The VEGF mRNA expression and AP-1 activity in tripterygium medicated serum group and total saponins medicated serum group were remarkably lower than those of the model control group (P<0.05). There was no significant difference between the two medicated serum groups. Conclusion Serum medicated with total saponins from RDN can remarkably decrease VEGF mRNA expression and AP-1 activity,indicating that the total saponins from RDN could influence VEGF secretion by inhibiting the AP-1 signal transduction pathway,VEGF is the key factor of angiogenesis,thereby to restrain angiogenesis.

OBJECTIVETo study the anti-tumor activity of SPS in vivo and in vitro and the cytotoxicity of CTL cells, NK cells of T739 lung cancer in mice.

METHODThe transplanted tumor model of S180 Sarcoma was established with KM mouse. The SPS was adminished i.p. for 10 d, the tumor weight was detected. The transplanted tumor model of LA795 lung cancer was established with T739 mouse and SPS was adminished i.p. for 10 d and the tumor weight and the cytotoxicity of CTL cells, NK cells were detected. The Anti-tumor activity of SPS on three types of tumor cells in vitro was observed with trypan blue exclusion staining.

RESULTSPS 40 mg x kg(-1) can significantly inhibit the growth of S180 Sarcoma in mice and inhibitory rate was 51.33% (P<0.01). It can also inhibit the growth of LA795 lung cancer in mice and the tumor volume was reduced obviously for 3.29 mm3 (P<0.05). It can remarkably enhance the cytotoxicity of splenic CTL cells, NK cells in tumor-bearing (P<0.05).

CONCLUSIONSPS have anti-tumor effects, the mechanism of the anti-tumor activity may be related to enhance the cytotoxicity of CTL cell and NK cell.

Animals ; Antineoplastic Agents ; administration & dosage ; Carthamus tinctorius ; chemistry ; metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Killer Cells, Natural ; immunology ; Lung Neoplasms ; drug therapy ; immunology ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Plant Extracts ; administration & dosage ; Polysaccharides ; administration & dosage ; T-Lymphocytes, Cytotoxic ; immunology ; Tumor Burden ; drug effects

Spastic paraplegia type 4 (SPG4) is the most common type of autosomally inherited spastic paraplegia. Its main clinical features include typical simple hereditary spastic paraplegia, with neurological impairments limited to lower limb spasticity, hypertonic bladder dysfunction, and mild weakening of lower limb vibration sensation, without accompanying features such as nerve atrophy, ataxia, cognitive impairment, seizures, and muscle tone disorders. SPAST is the main pathogenic gene underlying SPG4, and various pathogenic SPAST variants have been discovered. This disease has featured a high degree of clinical heterogeneity, and the same pathogenic variant can have different age of onset and severity among different patients and even within the same family. There is a lack of systematic research on the correlation between the genotype and phenotype of SPG4, and the pathogenic mechanism has remained controversial. This article has provided a review for the clinical characteristics, pathogenic gene characteristics, correlation between the genotype and phenotype, and pathogenic mechanism of this disease, with an aim to provide reference for its clinical diagnosis and treatment.
Humans ; Spastic Paraplegia, Hereditary/genetics* ; Mutation ; Spastin/genetics* ; Paraplegia/genetics* ; Phenotype