Vascular or endoluminal stent is a stent implanted in the lesion site to support stenosis vessels based on luminal balloon expansion,to reduce vascular elasticity recoil and remoulding,and maintain blood flow patent.Some stents can also prevent vascular restenosis.Stent size,surface coverage,radial supporting,extensibility,longitudinal recoil,fatigue test,material composition,corrosion-resistance,coagulation,surface roughness and biocompatibility(blood compatibility) are performance parameters to evaluate the stents.Vascular or endoluminal stent has been widely used in arterial and venous systems and non-vessel luminal systems.The incidence of complications following stenting is 11.6%,including acute or subacute thrombogenesis,restenosis,or stent dislocation.It is commonly demonstrated that intrastent restenosis is caused by hyperblastosis.

Animals ; Cell Culture Techniques ; methods ; Cell Separation ; methods ; Culture Media ; Epithelial Cells ; cytology ; Respiratory System ; cytology ; Swine

To investigate the immune regulatory effects of human bone marrow mesenchymal stem cells on alloantigen T lymphocyte in vitro, human MSCs were isolated and expanded from bone marrow cells, and identified with cell morphology, and the phenotypes were assessed by immunohistochemistry and flow cytometry. As the stimulation factor of T lymphocytes proliferation, either PHA or dendritic cells isolated from cord blood were cocultured with CD2(+) T lymphocytes from peripheral blood mononuclear cells by magnetic beads with or without MSC in 96-well plats for seven days. T cell proliferation was assessed by [(3)H]-thymidine incorporation using a liquid scintillation counter. T cell subsets, Th1, Th2, Tc1 and Tc2 were analyzed by flow cytometry after co-culture of CD2(+) T cells with MSCs for 10 days. The results showed that a significant decrease of CD2(+) T cell proliferation was evident when MSC were added back to T cells stimulated by DC or PHA, and an increase of Th2 and Tc2 subsets were observed after co-culture of MSC with T lymphocytes. It is suggested that allogeneic MSC can suppress T cell proliferation in vitro and the cause of that was partly depend on interaction of cells and the alteration of T cell subsets.
Bone Marrow Cells ; cytology ; immunology ; CD2 Antigens ; immunology ; Cell Communication ; immunology ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Flow Cytometry ; Humans ; Immunohistochemistry ; Mesenchymal Stromal Cells ; cytology ; immunology ; T-Lymphocyte Subsets ; cytology ; immunology ; T-Lymphocytes ; cytology ; immunology

OBJECTIVETo explore the relationship between angiotensin converting enzyme (ACE) gene single nucleotide polymorphisms (SNP) and premature coronary heart disease (PCHD) patients with blood stasis syndrome (BSS).

METHODSrs4343, rs4293, and rs4267385 were selected at SNP from ACE gene. Allele and genotype were detected. Frequencies of allele and genotype were compared by using time-of-flight mass spectrometry technique (TOF-MS).

RESULTSCompared with the healthy control group, genotype of rs4293 and rs4267385 in ACE gene were similar, but there was statistical difference in polymorphisms and allele frequencies of rs4343 in the I and II group (P < 0.05, P < 0.01). The frequency of G allele was higher in the 3 groups than in the healthy control group (P < 0.05, P < 0.01). The relative risk analysis showed that the risk for PCHD occurrence in G allele carriers at rs4343 (GG +AG) was 3. 6 times the risk in non-G allele carriers (95% CI: 1.224-10.585, P = 0.02). There was also statistical difference in sex, age, TC, and TG after adjusted Logistic regression analysis (OR = 3.994, 95% CI: 1.230-12.974, P = 0.021).

CONCLUSIONThe polymorphism at rs4343 (G2350A) might be one of risk factors for PCHD occurrence, but not a predisposing factor for PCHD patients of BSS.

Alleles ; Case-Control Studies ; Coronary Artery Disease ; genetics ; Gene Frequency ; Genotype ; Humans ; Medicine, Chinese Traditional ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Single Nucleotide ; Risk Factors

OBJECTIVETo evaluate the time course of granulocyte-colony-stimulating-factor (G-CSF), estrogen and various doses of atorvastatin on endothelial progenitor cells (EPCs) mobilization.

METHODA total of 48 male New Zealand White rabbits were treated with placebo, estrogen (0.25 mg.k(-1).d(-1)), Atorvastatin (2.5, 5, or 10 mg) and G-CSF (50 microg/rabbit/d), respectively. Peripheral EPCs number was surveyed weekly for 4 weeks by FACS analysis (double-positive for PE-CD34/FITC-CD133) and under fluorescent microscope (double-positive for FITC-UEA-1/Dil-acLDL). Serum nitric oxide (NO) and lipids were also measured at the third week.

RESULTSPeripheral EPCs was significantly increased in G-CSF treated animals and remained constant for 4 weeks compared to placebo treated animals. Atorvastatin increased peripheral EPCs dose-dependently from 2.5 to 5 mg and peaked at the third week while peripheral EPCs number was not affected by 10 mg.k(-1).d(-1) atorvastatin during the first 3 weeks and was significantly higher only in the fourth week compared to placebo group. Estrogen also significantly increased peripheral EPCs at the third and fourth week compared to placebo group. At the third week, serum NO was similar in G-CSF group, significantly higher in atorvastatin 5 mg.k(-1).d(-1) and estrogen groups while significantly lower in atorvastatin 10 mg.k(-1).d(-1) group compared to placebo group. Serum lipids were similar among various groups.

CONCLUSIONAtorvastatin, estrogen and G-CSF could mobilize EPCs. The mobilization efficacy is as follows: G-CSF > atorvastatin 5 mg.k(-1).d(-1) > estrogen > atorvastatin 2.5 mg.k(-1).d(-1) > atorvastatin 10 mg.k(-1).d(-1). NO might partly contribute to the mobilizing effect of estrogen and atorvastatin.

Animals ; Atorvastatin Calcium ; Endothelial Cells ; cytology ; drug effects ; Estrogens ; pharmacology ; Granulocyte Colony-Stimulating Factor ; pharmacology ; Heptanoic Acids ; pharmacology ; Hypolipidemic Agents ; pharmacology ; Lipids ; blood ; Male ; Nitric Oxide ; blood ; Pyrroles ; pharmacology ; Rabbits ; Recombinant Proteins ; Stem Cells ; drug effects

The calbindin D-28k (CB)-containing neurons in the interstitial nucleus of the spinal trigeminal tract (INV) that receive visceral and orofacial somatic nociceptive information and emanate projections to the parabrachial nuclei (PB) were investigated by the triple-labeled methods of fluorogold (FG) retrograde tracing combined with Fos and CB proteins immunofluorescence histochemistry in the rat. The results showed (1) in the perioral stimulation group, a large number of FG-retrograde labeled and Fos-immunoreactive neurons were found in the paratrigeminal nucleus (PaV) and the dorsal paramarginal nucleus (PaMd) of the INV ipsilateral to FG and formalin injection made to the PB and lips, respectively, while a lot of CB-immunoreactive neurons were distributed in the INV bilaterally; (2) a majority of the FG-retrograde labeled neurons (77.3%) were double-labeled with CB, and 40.7% of them were double-labeled with Fos; about 38.5% of FG/CB double-labeled neurons were FG/CB/Fos triple-labeled in the INV; and (3) in the upper alimentary tract stimulation group, the distribution and the numbers of FG-retrograde labeled, CB-immunoreactive neurons and FG/CB double-labeled neurons in the INV were similar to those of the perioral stimulation group as described above, except that the Fos immunoreactive neurons were distributed in the INV bilaterally, approximately 41.9% of the FG-retrograde labeled neurons were FG/Fos double-labeled, and over half (52.0%) of those double-labeled neurons were FG/CB/Fos triple-labeled. The results indicate that a part of CB-containing neurons in the INV receive orofacial somatic and visceral nociceptive information and that these neurons sent projections directly to the PB. The CB-containing neurons might play an important role in the transmission of the peripheral nociceptive information from INV to PB.
Animals ; Calbindins ; Face ; innervation ; Male ; Medulla Oblongata ; physiology ; Nerve Tissue Proteins ; metabolism ; Neural Pathways ; physiology ; Neurons ; metabolism ; physiology ; Nociceptors ; physiology ; Pain ; metabolism ; physiopathology ; Pons ; physiology ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein G ; metabolism ; Trigeminal Nucleus, Spinal ; physiology ; Viscera ; innervation

This paper retrospectively summarized and analyzed observation of the disease and nursing care of 17 patients with pregnancy-associated fulminant type 1 diabetes and intrauterine fetal demise.Through timely supplying blood capacity and improving renal perfusion,maintaining blood glucose homeostasis and acid-alkali,potassium balance,safety of the patients was guaranteed;by providing effective psychological nursing,puerperal dietary guidance and discharge guidance,patients' rehabilitation was improved.As a result,16 patients were in stable condition,and dead babies were delivered.Major bleeding event occurred in one patient after delivering the dead baby,and the patient developed shock as well as liver and kidney failure.The patient was transferred to ICU for further treatment and became stable and was discharged after two months.

OBJECTIVETo investigate the distribution of GAD67 and the co-localization with bNOS in the main olfactory bulb of GAD67-GFP knock-in mouse.

METHODSPolymerase chain reaction was applied to identify the genotype of GAD67-GFP knock-in mouse, the animals were sacrificed and frozen sections of olfactory bulb were prepared. The Nissl-staining was performed to show an framework of the neuron in the olfactory bulb. The distribution of GAD67 and co-localization with bNOS were detected by immunofluorescence technique.

RESULTSThe proportion of GAD67-positive cells among DAPI-positive cells were (42.98 ± 0.92)% in glomerular layer, (23.64 ± 0.84)% in mitral cell layer and (77.75 ± 0.84)% in granule cell layer; the bNOS-positive cells mainly existed in glomerular layer and mitral cell layer, very few in granule cell layer. No co-localization of GAD67 and bNOS in granule cell layer and mitral cell layer was found, but there was dispersed distribution in glomerular layer.

CONCLUSIONGAD67-positive neurons mainly appear in glomerular layer and granule cell layer, and the bNOS is mostly expressed in glomerular layer and mitral cell layer; while the co-localization of GAD67 and bNOS only occurs in glomerular layer of olfactory bulb.

Animals ; Gene Knock-In Techniques ; Glutamate Decarboxylase ; genetics ; metabolism ; Green Fluorescent Proteins ; genetics ; metabolism ; Mice ; Mice, Transgenic ; Neurons ; metabolism ; Nitric Oxide Synthase Type I ; metabolism ; Olfactory Bulb ; metabolism ; Tissue Distribution

OBJECTIVETo investigate the effect of urokinase on hepatic fibrogenesis in rats.

METHODSHepatic fibrosis was induced in rats by complex pathogenic factors including subcutaneous injections of carbon tetrachloride, alcohol and cholesterol feeding. Animals were randomly divided into 3 groups: normal control group, hepatic fibrosis group (complex pathogenic factors for 6 weeks), UK prevention group (complex pathogenic factors+UK for 6 weeks). The animals were sacrificed at the end of week 6. The expression of alpha-SMA, uPA, PAI-1, TGFb1, TIMP-1, collagen type I and type III proteins in hepatic fibrosis tissue was detected by immunohistochemistry, the expression of PAI-1 and TGFb1 mRNA in the hepatic fibrosis tissue was quantified by real time RT-PCR. The serum levels of hyaluronicacid (HA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin (TBil) and the content of liver hydroxyproline (Hyp) were detected using ELISA kits.

RESULTSThe serum ALT, AST, TBil, HA and the content of liver Hyp were (46.66+/-6.30) U/L, (126.26+/-31.65) U/L, (31.11+/-4.20) micromol/L, (109.70+/-18.81) microg/L and (0.98+/-0.09) mg/(g liver), respectively, in UK prevention group, which were significantly lower than those [(101.57+/-11.97) U/L, (205.89+/-56.26) U/L, (67.75+/-2.75) micromol/L, (184.43+/-32.36) microg/L and (1.65+/-0.16) mg/(g liver), respectively] in hepatic fibrosis group (q = 3.3801-20.0061, P < 0.01). The levels of a-SMA, collagen type I, type III, TIMP-1, PAI-1, TGFb1 proteins were (299.27+/-37.36), (210.05+/-27.17), (192.94+/-24.48), (213.70+/-32.21), (204.25+/-17.92), (205.97+/-23.81), respectively, in UK prevention group, which were significantly lower than those [(418.83+/-30.21), (323.77+/-21.53), (302.37+/-31.43), (376.63+/-25.19), (313.53+/-26.67) and (327.42+/-36.75), respectively] in hepatic fibrosis group. The level of uPA protein was increased, and the expression of PAI-1, TGFb1 mRNA in hepatic fibrosis tissue was decreased in UK prevention group.

CONCLUSIONIn the early stage of hepatic fibrogenesis, urokinase can attenuate the progression of rat hepatic fibrosis via upregulation of uPA, downregulation of TGFb1, and inhibition of HSC activation.

Actins ; metabolism ; Animals ; Disease Models, Animal ; Hydroxyproline ; metabolism ; Liver ; drug effects ; metabolism ; pathology ; Liver Cirrhosis, Experimental ; chemically induced ; metabolism ; pathology ; prevention & control ; Liver Function Tests ; Male ; Plasminogen Activator Inhibitor 1 ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Tissue Inhibitor of Metalloproteinase-1 ; genetics ; metabolism ; Transforming Growth Factor beta1 ; genetics ; metabolism ; Urokinase-Type Plasminogen Activator ; pharmacology

OBJECTIVETo survey the incidence of acute febrile reaction in elderly patients receiving intravenous zoledronic acid for osteoporosis and identify the related factors.

METHODSThirty-eight elderly patients with osteoporosis were hospitalized and treated with intravenous infusion of 5 mg zoledronic acid in 2010. The incidence of acute fever reaction was observed in these patients , and the time of fever onset, duration, average maximum temperature, and antipyretic drug used were recorded. The patients with and without acute febrile reaction were compared for age, duration of osteoporosis, sex ratio, use of parathyroid hormone before zoledronic acid treatment, β-fragment of collagen breakdown, calcitonin, osteocalcin, serum calcium, and use of anti-osteoporosis drugs before the treatment.

RESULTSAcute fever reaction occurred in 12 (31.6%) of the patients. Two of the patients had fever on the day of zoledronic acid treatment, and the other patients developed fever after the first day of treatment, with a mean duration of 1 day and a maximum temperature of (38.5∓0.84) degrees celsius;. The fever was treated with a mean of 3.55∓1.21 pseudoephedrine tablets. The patients with fever showed significantly higher parathyroid hormone levels before treatment than those without fever (P<0.05); osteocalcin, calcitonin, β-fragment of collagen breakdown, or serum calcium showed no significant difference between the two groups.

CONCLUSIONAcute febrile reaction, often moderate and transient, is common in elderly patients receiving intravenous zoledronic acid for osteoporosis, and its occurrence is possibly associated with parathyroid hormone levels before the treatment.

Aged ; Aged, 80 and over ; Bone Density Conservation Agents ; administration & dosage ; adverse effects ; China ; epidemiology ; Diphosphonates ; administration & dosage ; adverse effects ; Female ; Fever ; chemically induced ; Humans ; Imidazoles ; administration & dosage ; adverse effects ; Incidence ; Infusions, Intravenous ; Male ; Osteoporosis ; drug therapy ; Parathyroid Hormone ; blood