Child, Preschool ; Coronary Vessel Anomalies ; physiopathology ; Coronary Vessels ; physiopathology ; Female ; Humans ; Pulmonary Artery ; abnormalities

Objective To observe the effect of Qi-strengthening and blood-activating Chinese patent medicine Qigui Ershen Granules on the carotid intima-media thickness(IMT ) , atheromatous plaque scores, serum fibroblast growth factor 23 (FGF23) and Klotho protein levels, and oxidation- and inflammation-associated indicators in carotid atherosclerosis patients. Methods Fifty-two carotid atherosclerosis patients were randomized into Chinese medicine group and western medicine group, 26 cases in each group. Chinese medicine group was treated with Qigui Ershen Granules orally, and western medicine group was treated with Atorvastatin Calcium Tablets orally. The mediation for the two groups lasted for 24 continuous weeks. Carotid ultrasonography was performed before and after treatment for the examination of carotid IMT and plaque Crouse scores. Double antibody sandwich enzyme-linked immunosorbent assay(ELISA) was applied for the detection of serum Klotho, FGF23, interleukin 1(IL-1) and tumor necrosis factorα(TNF-α) levels, and radio-immuno-precitation method was used for the assay of serum reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) levels. The clinical efficacy of the two groups was evaluated by the scores of Qi deficiency syndrome and blood stasis syndrome before and after treatment. Results (1) In western medicine group, 5 cases dropped out and were excluded, and a total of 21 cases completed the trial; in Chinese medicine group, 3 cases dropped out and were excluded, and a total of 23 cases completed the trial.(2) After treatment for 24 continuous weeks, IMT and Crouse scores of the plaque in the two groups were obviously reduced(P < 0.01 compared with those before treatment) , but the differences of IMT and the scores between the two groups were insignificant after treatment(P > 0.05). (3) Serum Klotho protein level was increased while FGF23 was decreased in Chinese medicine group after treatment (P < 0.01 compared with those before treatment); no obvious changes of serum Klotho protein and FGF23 levels were found in western medicine group before and after treatment(P > 0.05). The effects of Chinese medicine on increasing Klotho protein level and decreasing FGF23 level were superior to those of western medicine (P<0.01). (4) After treatment, serum IL-1, TNF-α, ROS and MDA levels were decreased and serum SOD level was increased in the two groups (P < 0.01 compared with those before treatment). The differences of the above indexes were insignificant between the two groups after treatment(P > 0.05).(5) The scores of Qi deficiency syndrome and blood stasis syndrome in Chinese medicine were decreased after treatment (P < 0.01), but showed no significant changes in western medicine group (P > 0.05). Chinese medicine group had better effect on improving the scores of Qi deficiency syndrome and blood stasis syndrome than western medicine group(P < 0.01).(6) After treatment, the total effective rate for improving Qi deficiency syndrome and blood stasis syndrome in Chinese medicine group was 82.61%, 78.26%, and that in western medicine group was 28.57%, 14.28%respectively, the difference being significant (P<0.01). Conclusion Qi-strengthening and blood-activating Qigui Ershen Granules have certain effects on counteracting atherosclerosis, inflammatory aging and oxidation.

Animals ; Humans ; Hydrogen Sulfide ; metabolism ; Inflammation ; metabolism

OBJECTIVETo investigate the expression of CXCR4 in cultured human dental pulp cells (HDPC) in vitro and the corresponding ligand SDF-1alpha level of HDPC supernatants stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha), and to explore the role of SDF-1alpha on the proliferation and the migration of HDPC.

METHODSThe expression of CXCR4 in HDPC was detected by immunocytochemistry technique and indirect immunofluorescence technique. The culture supernatants of HDPC were collected after HDPC had been simulated by LPS and TNF-alpha of different concentrations for 48h and then the SDF-1alpha level was assayed by quantitative sandwich ELISA. Meanwhile, the effects of recombinant human SDF-1alpha (rhSDF-1alpha) on the proliferation and the migration of HDPC at different concentrations were observed by MTT and Boyden Chamber Assay.

RESULTSCXCR4 was expressed in cytomembrane of HDPC and SDF-1alpha was secreted into their normal cell supernatants with a concentration of (4513.55 +/- 962.92) ng/L. The secretion of SDF-1alpha was both significantly decreased by stimulation with LPS and TNF-alpha (P < 0.05). In addition, rhSDF-1alpha stimulated the HDPC proliferation at the concentrations of 50, 100, 200 microg/L (P < 0.01) and increased the chemotactic migration of HDPC significantly after 9h's incubation with the concentrations of 50, 100 microg/L (P < 0.05).

CONCLUSIONSSDF-1alpha accelerated the proliferation and the migration of HDPC which expressed CXCR4. SDF-1-CXCR4 axis may play a role in repair of pulp injury.

Cell Movement ; Cell Proliferation ; Cells, Cultured ; Chemokine CXCL12 ; metabolism ; Dental Pulp ; cytology ; metabolism ; Humans ; Receptors, CXCR4 ; metabolism

AIMTo detect the expression of HSP25 in rat dental follicles both in vivo and vitro, and explore the underlying mechanism of HSP25 on the proliferation and differentiation of rat dental follicle cells (DFCs).

METHODOLOGYImmunohistochemistry was performed to detect the expression of HSP25 in mandibles of postnatal rats on days 1, 3, 5, 7, 9 and 11 in vivo. In vitro, the expression of HSP25 in DFCs was detected by an indirect immunofluorescence assay. Thiazolyl blue tetrazolium bromide (MTT) assay, flow cytometry and alkaline phosphatase (ALP) assay were used to identify the time-course effect mediated by different concentrations of recombinant murine HSP25 of 0, 1, 10, 50 and 100 ng/mL on rat DFCs.

RESULTSExpression of HSP25 was not detected in dental follicles of the rats until day 5 after birth, but became up-regulated in a time-dependent manner till day 11. HSP25 was detected in the cytoplasm of cultured rat DFCs. No significant difference could be observed in the proliferation of DFCs after stimulation with different concentrations of HSP25 on days 1, 2 and 3 (P > 0.05). HSP25 at concentrations of 50 ng/mL and 100 ng/mL up-regulated the ALP activity of DFCs on day 9 (P < 0.05).

CONCLUSIONHSP25-immunoreactivity increased chronologically during the development of dental follicles. The protein had no significant effect on cell proliferation but may play a role in cementoblast/osteoblast differentiation of DFCs.

Alkaline Phosphatase ; analysis ; Ameloblasts ; cytology ; Animals ; Cell Culture Techniques ; Cell Differentiation ; physiology ; Cell Proliferation ; Coloring Agents ; Cytoplasm ; ultrastructure ; Dental Sac ; cytology ; growth & development ; Flow Cytometry ; Fluorescent Antibody Technique, Indirect ; HSP27 Heat-Shock Proteins ; analysis ; physiology ; Odontoblasts ; cytology ; Rats ; Rats, Sprague-Dawley ; Tetrazolium Salts ; Thiazoles ; Tooth Germ ; cytology ; Up-Regulation ; physiology

OBJECTIVETo investigate the expression of macrophage migration-inhibitory factors (MIF) in clinically healthy and inflamed human pulp tissues and the effects of rhMIF on the proliferation of human dental pulp cells (HDPC).

METHODSImmunohistochemistry was used to detect the localization of MIF expression in clinically healthy pulp and inflamed pulp tissues. Quantitative real-time polymerase chain reaction (PCR) was performed to evaluate the mRNA levels of MIF in pulp specimens. In addition, the culture supernatants of HDPC were collected after HDPC was stimulated by lipopolysaccharide (LPS) for 24 h, and then the MIF levels were assayed by quantitative sandwich enzyme-linked immunosorbent assay. Meanwhile, the effects of rhMIF on the proliferation of HDPC at different concentrations for 24 and 48 h were observed by cell counting kit-8 (CCK-8).

RESULTSMIF was mainly distributed in odontoblasts of healthy pulp tissue, however, in inflamed pulp tissue, it was widely detected in fibroblasts, inflammatory infiltrates and endothelial cells as well as odontoblasts. Quantitative real-time PCR showed that there was no significant difference in MIF mRNA levels between inflamed pulps and healthy pulps (P > 0.05). Additionally, the secretion of MIF was significantly increased by stimulation with LPS at the concentration of 0.1 and 1.0 mg/L [(1772.58 ± 495.05), (1692.58 ± 337.45) ng/L] (P < 0.05), and the concentration was (1048.53 ± 161.81) ng/L in control group. rhMIF stimulated the HDPC's proliferation at the concentration of 10, 30, 60 µg/L for 24 and 48 h.

CONCLUSIONSMIF was expressed in pulp tissue and its expression was increased after stimulation by LPS. rhMIF increased the proliferation of HDPC. These results suggest that MIF may be involved in the process of pulpal inflammation.

Cell Proliferation ; Cells, Cultured ; Dental Pulp ; cytology ; pathology ; Dose-Response Relationship, Drug ; Humans ; Lipopolysaccharides ; administration & dosage ; pharmacology ; Macrophage Migration-Inhibitory Factors ; genetics ; metabolism ; Pulpitis ; metabolism ; pathology ; RNA, Messenger ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

The aim of this study was to evaluate the homing capabilities of hematopoietic stem/progenitor cells (HSPCs) derived from human placenta tissues (PT). Single cell suspension of human PT was prepared by mechanical method. The expression levels of homing-related adhesion molecules (HRAM) including CD11a, CD49d, CD44, CD49e, CD62L and CD54 on CD34(+) cells and the percentages of CD34(+) cells and their subpopulations in nucleated cells (NC) from fresh human PT, umbilical cord arterial blood (UCAB) and umbilical cord venous blood (UCVB) were detected by using flow cytometry. The results showed that the percentage of CD34(+) cells and CD34(+)CD38(-) cells in placenta were higher than those in UCAB and UCVB. There were no significant difference in percentage of HSPC between UCAB and UCVB. Placenta-derived CD34(+) cells strongly expressed CD11a, CD49d, CD44, CD49e and CD54, among which expression levels of CD49e and CD54 on placenta-derived CD34(+) cells were significantly higher than those on UCAB and UCVB-derived CD34(+) cells. While the percentage of CD34(+)CD62L(+) cells in placenta was only lower than that in UCVB. It is concluded that human placenta is rich in HSPC. Moreover, the expression levels of most HRAM in CD34(+) cells from PT are higher than those from UCAB and UCVB or are close to them. It suggested that HSPCs derived from PT might have stronger homing capabilities than those from UCB.
Antigens, CD34 ; biosynthesis ; Cell Adhesion Molecules ; biosynthesis ; Fetal Blood ; cytology ; Hematopoietic Stem Cells ; metabolism ; Humans ; Hyaluronan Receptors ; biosynthesis ; Integrin alpha5 ; biosynthesis ; Intercellular Adhesion Molecule-1 ; biosynthesis ; Placenta ; cytology

OBJECTIVETo evaluate the effect of intravenous immunoglobulin (IVIG) and vitamin C on the progression of experimental autoimmune myocarditis(EAM).

METHODSFifty-two Balb/c mice were randomized into six groups: The blank group received no treatment, the remaining 5 groups were immunized with 100mug emulsified porcine myosin at d 1 and d 7. Different agents were injected from d 1, SVitC group:150 mg/kg*d(-1)vitamin C; LVitC group: 300 mg/kg*d(-1)vitamin C; IVIG group: 1 g/kg*d(-1)IVIG; IVIG+VitC group: 1 g/kg*d(-1)IVIG and 150 mg/kg*d(-1)vitamin C; The control group same volume of normal saline. All mice were sacrificed at d 21, and serum TNF-alpha levels were detected with enzyme linked immunosorbent assay (ELISA). The ratio of heart to body weight(C/W), spleen to body weight(S/W) and kidney to body weigh(R/W) were calculated. The spleens and heart were examined pathologically and/or immunohistochemically.

RESULTCompared with those of control group, inflammatory cells infiltration in the myocardium and calcification in the pericardiume in SVitC and LVitC groups were extenuated. There were inflammatory cells infiltrating in the myocardium sparely and no calcification in the pericardium in IVIG and IVIG+VitC groups. The size of spleens enlarged especially in IVIG and IVIG+VitC groups. White and red pulps of spleens were hyperplastic microscopically. The C/W of treatment groups decreased significantly compared with that of control group. The S/W of therapy groups and control group was significantly higher than that of blank group; and the S/W of IVIG and IVIG + VitC groups was significantly higher than that of SVitC and LVitC groups. The R/W in each groups had no significant difference. The TNF-alpha level in SVitC and LVitC groups was a little lower than that in control group; TNF-alpha level in IVIG and IVIG+VitC groups was significantly lower than that of control group. Wide fluorescence stripe was found along extracellular matrix surrounding the damaged cardiomyocytes of control group. Both density and intensity of fluorescence in SVitC and LVitC groups were lower than those of control group. There were much wider fluorescence stripe and strengthened intensity in IVIG and IVIG + VitC groups. The myofilaments were in wild disorder and sarcomere had severe breakage in control group. Moreover, chondriosome hypertrophy and vacuolar degeneration were found. The damage lessened in SVitC and LVitC groups. Both myofilaments and sarcomeres in IVIG and IVIG + VitC groups were almost normal, and the chondriosome was normal.

CONCLUSIONIVIG and vitamin C have some protective and therapeutic effect on the progression of EAM by decreasing pathological damage of myocardium and depressing TNF-alpha production, and IVIG combined with vitamin C is more effective.

Animals ; Ascorbic Acid ; administration & dosage ; Autoimmune Diseases ; drug therapy ; Drug Therapy, Combination ; Female ; Immunoglobulins, Intravenous ; administration & dosage ; Injections, Intravenous ; Male ; Mice ; Mice, Inbred BALB C ; Myocarditis ; drug therapy ; Random Allocation ; Tumor Necrosis Factor-alpha ; blood ; gamma-Globulins ; administration & dosage

OBJECTIVETo explore the predisposing factors for postoperative epilepsy in patients with gliomas.

METHODSA total of 258 glioma patients with complete clinical data receiving cranial surgeries were analyzed retrospectively. With gender, age, predominant symptoms, positive signs, history of preoperative epilepsy, time of epilepsy onset, tumor location, surgical approaches, cortical injury, arterial and venous injury, scope of tumor resection, postoperative edema, tumor pathology, tumor recurrence, number of operation, radiation therapy as the independent variables, the occurrence of postoperative epilepsy was analyzed as the dependent variable using logistic regression to identify the risk factors for postoperative epilepsy.

RESULTSHistory of preoperative epilepsy, surgical approaches, postoperative edema, tumor pathology and tumor recurrence were identified as the risk factors for postoperative epilepsy in glioma patients.

CONCLUSIONSPostoperative epilepsy severely affected the quality of life of glioma patients, and rigorous treatment targeting the risk factors may decrease the occurrence of postoperative epilepsy.

Adult ; Brain Neoplasms ; surgery ; Causality ; Epilepsy ; epidemiology ; Female ; Glioma ; surgery ; Humans ; Male ; Middle Aged ; Postoperative Complications ; epidemiology ; Retrospective Studies ; Risk Factors ; Young Adult

We report on a patient with a partial deletion on the short arm of chromosome 18 (del 18p), who presented with dysmorphic features and delayed developmental milestones as well as with a patent ductus arteriosus (PDA) and pulmonary valve stenosis (PS). Several forms of congenital heart disease (CHD) are found in about 10% of patients with del (18p), but coexisting PDA and PS have not been reported. Del (18p) must be considered in patients with characteristic phenotypic abnormalities and congenital heart disease, including a combination of PDA and PS.
Child, Preschool ; Chromosome Banding ; *Chromosome Deletion ; Chromosomes, Human, Pair 18/*genetics ; Ductus Arteriosus, Patent/genetics/*pathology ; Humans ; Karyotyping ; Male ; Pulmonary Valve Stenosis/genetics/*pathology