Advance on chemical constituents and pharmacological activities of Stellera plants have been conducted. The chemical constituents include terpenes, coumarins, flavonoids, lignans, volatile oils, and other compounds. Pharmacological studies showed that diterpenoids and biflavones showed strong activities, such as antitumor, anti-HIV, and immune regulations. This review hopes to provide a scientific basis for further research and explorations of the medicinal values of the genus.
Animals ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Humans ; Molecular Sequence Data ; Molecular Structure ; Thymelaeaceae ; chemistry ; classification

Animals ; Animals, Newborn ; Cells, Cultured ; Cyclic AMP ; metabolism ; Glucagon-Like Peptide 1 ; pharmacology ; Insulin ; secretion ; Islets of Langerhans ; drug effects ; secretion ; Peptide Fragments ; pharmacology ; RNA, Messenger ; genetics ; Rats

OBJECTIVEThe relationship between selenium deficiency and the changes of synaptic structure in the CA3 area of hippocampus were studied in the third generation rats.

METHODSA selenium deficiency model was established by feeding rats with selenium-deficient food. The rats were divided into 4 groups: control (Se+I+), selenium deficiency (Se-I+), iodine deficiency (Se+I-), and both deficient group (Se-I-). The hippocampuses were dissected from the third generation rats on the 21st gestational day and the ultrastructural features of hippocampal synapses were observed with electron microscope. The length of active zone, synaptic curvatures, post-synaptic density (PSD) and synaptic cleft were quantitatively described.

RESULTSCompared with the control, the length of active zone and the thickness of PSD were significantly decreased in Se-I+, Se+I- and Se-I- groups [(261.7 +/- 50.1) nm, (286.7 +/- 41.6) nm and (220.8 +/- 61.6) nm contrast to (312.4 +/- 47.7) nm, P < 0.01], so were the synaptic curvatures in Se-I+, Se+I- and Se-I- groups [(22.9 +/- 6.3) nm, (27.5 +/- 8.6) nm and (25.2 +/- 6.5) nm contrast to (48.1 +/- 12.3) nm, P < 0.01]; the width of synaptic cleft were also decreased significantly in Se-I- [(11.1 +/- 3.3) nm contrast to (16.1 +/- 4.0) nm, P < 0.01].

CONCLUSIONSelenium deficiency might cause changes of neuronal functions at the synaptic level, and furthermore, affect learning and memory.

Animals ; Female ; Hippocampus ; pathology ; Iodine ; deficiency ; Male ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency ; Synapses ; pathology ; ultrastructure

Adult ; Antidotes ; administration & dosage ; therapeutic use ; Female ; Humans ; Insecticides ; poisoning ; Parathion ; poisoning ; Poisoning ; drug therapy ; Pralidoxime Compounds ; administration & dosage ; therapeutic use ; Treatment Outcome

Adult ; Aortic Valve ; microbiology ; pathology ; Autopsy ; Brain ; microbiology ; pathology ; Endocarditis, Bacterial ; complications ; microbiology ; pathology ; Female ; Heart Ventricles ; microbiology ; pathology ; Humans ; Mitral Valve ; pathology ; Sepsis ; complications ; microbiology ; pathology ; Substance Abuse, Intravenous ; complications ; microbiology ; pathology ; Young Adult

China ; epidemiology ; Hexanes ; toxicity ; Humans ; Occupational Diseases ; epidemiology ; Trichloroethylene ; toxicity

Objective　To investigate the effects of glucagon-like peptide 2 (GLP-2) on recovery of small intestinal epithelia from radiation injury in mice. Methods　Mice received a single 8 Gy dose of total body irradiation from 60Co gamma ray followed by treatment with GLP-2 or vehicle. DNA and protein content in small intestinal mucosa were measured, and small intestine was processed for histological examination with light microscope and scanning electron microscope. Results　Small intestinal mucosal DNA and protein content, villus height, and villus number significantly decreased in irradiated mice, partial villus tips were ulcerated. GLP-2 administration caused increase in DNA and protein content, villus height, and villus number as compared with irradiated control group. Meanwhile, the villus tips were lack of ulceration. Conclusion　GLP-2 can promote recovery of small intestinal epithelia from radiation injury in mice.

Objective　To study the effect of glucagon-like peptide 2 (GLP-2) on mitogen-activated protein kinase (MAPK) activity in small intestinal epithelia in mice after radiation injury and its relation with the change of small intestinal epithelial proliferation. Methods　Mice were given a single dose of 8 Gy of total body 60Co gamma irradiation and then divided into GLP-2 and control groups. The activity of MAPK and proliferation rate in small intestinal epithelia were measured. Results　The activity of MAPK in small intestinal epithelia was higher in GLP-2-treated mice than in irradiated mice, and the proliferation rate in small intestinal epithelia significantly increased in GLP-2-treated mice. These two indices were of significantly positive correlated. Conclusion　GLP-2 can promote small intestinal epithelial proliferation in irradiated mice, and this may be related to activation of MAPK in small intestinal epithelia.

OBJECTIVETo assess how trace element selenium and B27 supplements affect the neural stem cell (NSc) differentiation in vitro.

METHODSThe development and differentiation of NSc from the newborn rat were observed with primary culture and subculture during treating by sodium-selenite, and selenium-methyl-cysteine (SMC). The immunocytochemistry techniques were used to identify the NSc and mature protein expression with neuron marker beta-tubulin, astrocyte marker GFAP, and oligodendrocyte marker CNPase. The neurosphere morphology and neurite outgrowth were observed.

RESULTSAdding the complete B-27 serum-free supplement, Selenium could promote the neurosphere viability, development and differentiation. Without selenium and B-27, neurosphere could not survive and differentiate. Without B-27 in the medium but there containing selenium, the neurosphere could promote the viability and development into neuron, astrocyte and oligodendrocyte, as compared with the no-containing B-27 and selenium groups, these differentiated cells might have more quantity, more branches and better morphological nerve net. The count of the neuron, astrocyte and oligodendrocyte was 11.2/Hp, 16.1/Hp and 9.3/Hp.

CONCLUSIONSThe selenium should be very important for neural stem cells' survival. Selenium could promote the neurosphere cells differentiation and development.

Animals ; Animals, Newborn ; Cell Differentiation ; drug effects ; Cell Survival ; drug effects ; Cells, Cultured ; Culture Media, Serum-Free ; pharmacology ; Cysteine ; analogs & derivatives ; pharmacology ; Female ; Glial Fibrillary Acidic Protein ; metabolism ; Immunohistochemistry ; Male ; Neurons ; cytology ; drug effects ; metabolism ; Organoselenium Compounds ; pharmacology ; Rats ; Rats, Wistar ; Selenium ; pharmacology ; Selenocysteine ; analogs & derivatives ; Sodium Selenite ; pharmacology ; Stem Cells ; cytology ; drug effects ; metabolism ; Tubulin ; metabolism

Background Human paired box gene 6 (PAX6)encodes a transcriptional regulator.It is essential for eye and brain morphogenesis.Mutation of PAX6 gene isresponsible for many congenital ocular malformations,such as aniridia.Aniridia is a autosomal dominant inheritance mode.Objective In this study,PAX6 gene mutation was analyzed in three Chinese families with aniridia through polymerase chain reaction (PCR) and sequencing.Methods The blood specimens were collected from 5 suffers and normal individuals of 3 aniridia families to extract DNA.The sequences of extron 4-13 were designed based on PAX6 gene.The primer was amplified by PCR and sequenced and compared with the known PAX6 gene sequence.This study complied with Declaration of Helsinki and approved by ethic committee of Sichuan University.Written informed consent was obtained from each individual before any medial examination.ResultsThere were 5 suffers in the 3 families.A heterozygous mutation (c.718 C＞T) in PAX6 gene was identified in 2 patients of family A.This mutation caused an amino acid substitution of arginine to termination codon at position 240 ( p.Arg240X) of PAX6 protein.No similar change in the normal families.No any the alteration of PAX6 gene was detected in family B whatever suffers and normal individuals.In family C,a deletion mutation of c.331 delG ( p.Val111 SerfsX13 ) in PAX6 gene was found.The deletion of one base caused frame shift mutation of PAX6 protein,and no such mutation was seen in other families.Conclusions Mutation of PAX6 gene appeares to be causative mutations of the disease in family A and C.