Mongolian folk medicine, the important part of Mongolian medicine, is the main means, method and weapon of disease prevention, treatment and health care. Mongolian materia medicas are the important literatures of guiding the healthy development of the modern Mongolian medicine with a long and dazzling history. Since the founding of new China, a new history chapter of Mongolian folk medicine was opened under the attention and support from all levels of party and government. This paper intends to provide comprehensive insight into the rapid development of Mongolian folk medicine. The resources, phytochemistry, quality standard, pharmacology, dosage forms reform and production were reviewed to expound the process that Mongolian folk medicine was developed from traditional practices to scientific development
Medicine, Mongolian Traditional ; standards ; Science

Objective To explore the expression of hypoxia-inducible factor-1?(HIF-1?) protein and its mRNA in cultured cortical neurons after hypoxia,ischemia or hypoxia-ischemia(HI) and explore the possibilities of HIF-1? gene therapy in HI neurons.Methods The in vitro models of HI,pure hypoxia and pure ischemia were established using embryonic day 16-18 rats cortical neurons.Immunohistochemical and in-situ hybridization were performed to examine the expression of HIF-1? protein and its mRNA at different reperfusion time points in neurons.Results The expression of HIF-1? protein was very week in normoxic cultured neurons,but was up-regulated while treated with hypoxia and(or) ischemia.HIF-1? expression reached peak at 4 to 8 h after reperfusion with HI,which were statistically significant higher than that at other time points(Pa=0),and decreased gradually at 12 h.Furthermore,HIF-1? protein expression was significantly higher in HI group compared with that in the pure hypoxia or ischemia group(Pa=0).HIF-1? mRNA reached peak immediately after HI,decreased gradually at 2 h,and returned to the baseline at 8 h after reperfusion.Conclusions HIF-1? expression on cortical neurons is regulated differently with hypoxia,ischemia or HI treatment,HIF-1? gene therapy for HI neurons maybe a useful method in the future studies.

OBJECTIVETo examine the effects of rat marrow stromal cells (rMSCs) on gene expression of local brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) after injection of rMSCs into Cistern Magnum of adult rats subjected to traumatic brain injury (TBI).

METHODSA modified Feeney's TBI model was created in 48 adult rats. rMSCs were harvested from 3-month-old rats, and injected into Cistern Magnum in 24 rats subjected to TBI (Group cell transplantation). Saline was given through Cistern Magnum to another 24 rats subjected to TBI (Group saline control). Animals were sacrificed 1, 2 and 3 weeks after intervention, and special brain tissue blocks were dissected for total RNA extraction from each block. BDNF and NGF mRNA were reverse-transcribed into cDNA and further expanded by polymerase chain reaction (PCR). The expression of target genes was evaluated using semi-quantitative methods.

RESULTSGroup cell transplantation had higher BDNF and NGF gene expressions than Group saline control during a period of less than 3 weeks (P<0.05).

CONCLUSIONSrMSCs transplantation via Cistern Magnum in rats subjected to traumatic brain injury can enhance expressions of local brain NGF and BDNF to a certain extent.

Animals ; Bone Marrow Transplantation ; Brain Injuries ; metabolism ; therapy ; Brain-Derived Neurotrophic Factor ; genetics ; Disease Models, Animal ; Electrophoresis, Agar Gel ; Gene Expression ; Immunoenzyme Techniques ; Nerve Growth Factor ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Stromal Cells ; Up-Regulation

Aged ; Animals ; China ; epidemiology ; Disease Outbreaks ; Female ; Humans ; Male ; Middle Aged ; Orientia tsutsugamushi ; Scrub Typhus ; epidemiology

OBJECTIVETo assess the reaction of cytokines induced killer (CIK) cells treatment in hematopoietic injury at different levels on patients with benzene poisoning and seek a novel, safe and effective immunotherapy for benzene poisoning.

METHODSCIK cells were in vitro activated by interleukin-2 (IL-2) and granulocyte-macrophage-colony-stimulating factor (GM-CSF) from the peripheral blood mononuclear cells (PBMC). Thirty-two patients with benzene poisoning were treated with CIK cells. Nineteen patients with mild or moderate benzene poisoning in the control group were treated with VitB4, batilol, leucogen, inosine and stanozolol. The results for treatment of 12 patients with aplastic anemia induced by severe benzene poisoning (the efficacy rate and the case fatality rate) were analyzed. The change of T-lymphocyte subset analyzed by flow cytometry was also observed before and after treatment.

RESULTSFor mild or moderate benzene poisoning, the increase of WBC and RLT in CIK group was higher than that in the control group (P < 0.05). The CD(4)/CD(8) levels were significantly increased after CIK treatment. And for severe benzene poisoning, the effective rate of the CIK group was 91.7% and the mortality rate was 0%.

CONCLUSIONCIK treatment is safe and effective for hematopoietic injury caused by benzene poisoning. The mechanism may be related with the immune modulation of CIK treatment on immunodeficiency of patients with benzene poisoning.

Adult ; Benzene ; poisoning ; Cytokine-Induced Killer Cells ; immunology ; Female ; Follow-Up Studies ; Humans ; Immunotherapy ; Male ; Middle Aged ; Treatment Outcome ; Young Adult

OBJECTIVETo detect alterations of microsatellite loci [transforming growth factor beta receptor II (TGF-betaRII)(A)(10), TGF-betaRII(GT)(3), hMSH3(A)(8), hMSH6(C)(8), Bax(G)(8), IGFIIR(G)(8), IGFIIR(CT)(3)] and point mutations of TGF-betaRII (TGF-betaRII 452/454, TGF-betaRII 533).

METHODSPCR-SSLP, microdissection-PCR-SSLP, PCR-SSCP, clone sequencing and immunohistochemistry were used.

RESULTSThe mutation rate of TGF-betaRII(A)(10) in RER+ (replication error positive) colorectal carcinomas was 33% (3/9). Similar mutations were also observed in adenomas with severe dysplasia. No mutations at other microsatellite loci were found. RER+ colorectal cancers mainly occurred in male patients at a young age and were more common in the colon than in the rectum (P < 0.05).

CONCLUSIONSRER+ colorectal cancers were found in young males and commonly located in the colon. A one third mutation rate in TGF-betaRII(A)(10) in these patients is lower than that observed in western populations, which may imply diverse pathways of carcinogenesis of RER+ colorectal carcinoma. TGF-betaRII(A)(10) mutation may play a role in the transforming process from an adenoma with severe dysplasia to a full blown carcinoma.

Adult ; Aged ; Colorectal Neoplasms ; genetics ; Female ; Humans ; Male ; Microsatellite Repeats ; Middle Aged ; Point Mutation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases ; Receptors, Transforming Growth Factor beta ; genetics

In order to provide plenty of information about the relationship between its structure and function,the structure of a novel housefly pupae D-galactose binding lectin with the molecular weight 55kDa and immune acitivity was analyzed preliminarily.In the first place,oligosaccharide chain was confirmed to be existed in this kind of novel housefly pupae lectin by the method of gel staining,and then its structure was analyzed with the help of protein sequencing instrument,spectrophotometer color contrast,?-elimination reaction,infrared spectroscopy and atomic force microscopy.This kind lectin was a global-shaped monomer with the diameter 75 nm or so and the protein and oligosaccharide content 97.36% and 2.1% respectively.Peptide chain and oligosaccharide chain was linked by O-glycoside bond with the N-terminal blocked and the sugar ring alpinum type.All above was the reliable theory for further analysis of structure.

OBJECTIVETo study the gene mutation in a patient with multiple exostoses, identify the disease-causing gene mutation.

METHODSPolymerase chain reaction and DNA sequencing were used to screen the EXT1 or EXT2 gene mutation, while mismatch primer amplification and restriction endonuclease digestion were performed to confirm the mutation.

RESULTSBy DNA sequencing, a mutation in the seventh intron was detected and located at 26 bp of 3' splice site upstream in EXT1 gene, which was unreported before. Mismatch primer amplification and restriction fragment length polymorphism analysis suggested that this mutation was not detected in the normal control.

CONCLUSIONThe mutation 1633-26(C-->A) may be the disease-causing mutation in this patient with multiple exostoses.

DNA Mutational Analysis ; Exostoses, Multiple Hereditary ; genetics ; Female ; Humans ; Mutation ; N-Acetylglucosaminyltransferases ; genetics ; Young Adult

OBJECTIVETo explore the role of NF-E2-related factor 2(Nrf2) and its related factors in the progression of nonalcoholi steatohepatitis (NASH) by investigating the alterations of lipid metabolism and liver histopathology as well as the changes of mRNA and protein expression levels of Nrf2 and its related factors in rats during NASH progression.

METHODSMale SD rats were randomly divided into normal group and model group, which were administrated with high fat diet to establish nonalcoholic steatohepatitis model. The rats from both groups were randomly killed at the end of 4, 12 weeks respectively. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) were detected in the serum and liver tissue; Changes in fat deposition in liver tissue were determined by oil red O staining. HE staining were used to observe the pathological changes of liver tissue and to calculate nonalcoholic fatty liver disease (NAFLD) activity score (hepatic steatosis, inflammation and ballooning degeneration of liver cells). The expression of Nrf2 in liver was detected by immunohistochemical staining. The mRNA and protein levels of Nrf2 and related factors in liver were determined by Realtime PCR and Western blot, respectively.

RESULTSAfter 4 weeks of high fat diet, the levels of ALT, AST, TC in rat serum and TC, TG, LDL-C in liver were significantly increased compared with that of the normal group (P < 0.01, P < 0.05). After 4 weeks of high fat diet, the levels of ALT, AST, TC, TG in serum and TC, TG, LDL- C in liver increased further (P < 0.01, P < 0.05). Until the 12th week, the content of HDL-C in liver was significantly lower than that of the normal group (P < 0.05). At the end of the 4th or the 12th week, lipid droplets in the model rat liver cells were heavily dyed red and hepatic steatosis increased severely, with ballooning degeneration of liver cells. With the extension of high fat diet feeding time, fat deposition in the liver tissue, hepatic steatosis, NAFLD score, Nrl2 expression were significantly increased (P < 0.01). Expression levels of mRNA and protein of Nrf2, heme oxyenase 1(HO1), NADPH quinone oxidoreductase 1(NQO1), γ-glutamylcysteine synthethase (γ-GCS), glutathione S-transferase (GST) in the model rats increased or decreased at the end of the 4th or the 12th week differentially, (P < 0.01, P < 0.05) with the more significant changes at the end of the 4th week than the 12th week.

CONCLUSIONNrf2 and its related factors may be involved in the occurrence and development of nonalcoholic fatty liver disease, which may play an important role in the process of NASH formation.

Alanine Transaminase ; metabolism ; Animals ; Aspartate Aminotransferases ; metabolism ; Cholesterol ; metabolism ; Diet, High-Fat ; Dipeptides ; metabolism ; Disease Progression ; Glutathione Transferase ; metabolism ; Heme Oxygenase (Decyclizing) ; metabolism ; Lipid Metabolism ; Liver ; pathology ; Male ; NAD(P)H Dehydrogenase (Quinone) ; metabolism ; NF-E2-Related Factor 2 ; metabolism ; Non-alcoholic Fatty Liver Disease ; metabolism ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; metabolism

OBJECTIVESTo observe the role of PPARgamma during the activation process of hepatic stellate cells (HSC).

METHODSBy morphology and RT-PCR, we study the changes of expression of PPARgamma in culture-activated HSC or in vivo activated HSC induced by dimethylnitrosamine (DMN).

RESULTSIn vitro, the expression level of PPARgamma in freshly isolated HSC (0.72+/-0.01) significantly reduced to 0.48+/-0.03 on the third day of culture (t = 19.8372, P<0.01), and reduced 70% on the seventh culture-day and could not be detected after the second passage. In vivo, HSC freshly isolated from normal control rats expressed PPARgamma (0.76+/-0.01). During the development of rat liver fibrosis induced by DMN, the expression level significantly reduced to 0.46+/-0.02 after the third injection of DMN (t = 29.5318, P<0.01), and reduced 66% on the end of first week and could not be detected on the end of second and third week.

CONCLUSIONThe expression of PPARgamma might play an important role on the maintenance of resting-form of HSC, and the reduction of expression of PPARgamma might be an early event during the activation process of HSC.

Animals ; Liver ; cytology ; Liver Cirrhosis ; etiology ; pathology ; Male ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; physiology ; Transcription Factors ; physiology