Biomedical subjects

L Song

Publications and source records attributed to L Song.

At least 55 records · Page 3Linked to original sources

PubMed2001

Molecular phylogeny and species identification of pufferfish of the genus Takifugu (Tetraodontiformes, Tetraodontidae).

The phylogenetic relationships and species identification of pufferfishes of the genus Takifugu were examined by use of randomly amplified polymorphic DNA (RAPD) and sequencing of the amplified partial mitochondrial 16S ribosomal RNA genes. Amplifications with 200 ten-base primers under predetermined optimal reaction conditions yielded 1962 reproducible amplified fragments ranging from 200 to 3000 bp. Genetic distances between 5 species of Takifugu and Lagocephalus spadiceus as the outgroup were calculated from the presence or absence of the amplified fragments. Approximately 572 bp of the 16S ribosomal RNA gene was amplified, using universal primers, and used to determine the genetic distance values. Topological phylogenic trees for the 5 species of Takifugu and outgroup were generated from neighbor-joining analysis based on the data set of RAPD analysis and sequences of mitochondrial 16S rDNA. The genetic distance between Takifugu rubripes and Takifugu pseudommus was almost the same as that between individuals within each species, but much smaller than that between T. rubripes, T. pseudommus, and the other species. The molecular data gathered from both analysis of mitochondria and nuclear DNA strongly indicated that T. rubripes and T. pseudommus should be regarded as the same species. A fragment of approximately 900 bp was amplified from the genome of all 26 T. pseudommus individuals examined and 4 individuals of intermediate varieties between T. rubripes and T. pseudommus. Of the 32 T. rubripes individuals, only 3 had the amplified fragment. These results suggest that this fragment may be useful in distinguishing between T. rubripes and T. pseudommus.

Journal Article↗

PubMed2001

Oxidized LDL differentially regulates MMP-1 and TIMP-1 expression in vascular endothelial cells.

We have reported recently that oxidized low-density lipoprotein (oxLDL) stimulates matrix metalloproteinase-1 (MMP-1) expression in human vascular endothelial cells. The present study was conducted to examine the effect of oxLDL on expression of Tissue inhibitor of metalloproteinase-1 (TIMP-1), an endogenous inhibitor of MMPs, in human vascular endothelial cells. Our enzyme-linked immunosorbent assay and Northern blot analysis showed that oxLDL inhibited TIMP-1 secretion and expression by human umbilical vein endothelial cells. In contrast, PMA stimulated TIMP-1 expression and secretion. Both oxLDL and PMA increased MMP-1 expression and secretion significantly as previously reported. Inhibition by oxLDL of TIMP-1 expression was also observed in human aortic endothelial cells. Collagenase activity as detected by an enzymatic activity assay demonstrated, as expected, an increase in collagenase activity in the culture medium from oxLDL-treated cells as compared with that from untreated cells. The presented data indicates that oxLDL differentially regulates TIMP-1 and MMP-1 expression, whereas PMA coordinately regulates TIMP-1 and MMP-1 in vascular endothelial cells. The lack of coordination in the secretion of MMP-1 and TIMP-1 induced by oxLDL leads to an increased collagen-degrading activity that may contribute to destabilization of atherosclerotic plaques.

Cells, Cultured↗

PubMed2001

Mutation analysis of the potassium chloride cotransporter KCC3 (SLC12A6) in rolandic and idiopathic generalized epilepsy.

Genetic predisposition plays a major role in the etiology of idiopathic epilepsies. The common epilepsy syndromes display a complex pattern of inheritance, with an unknown number of genes contributing to seizure susceptibility. During the last decade linkage studies have narrowed down several candidate regions for susceptibility loci of idiopathic epilepsies. Several lines of evidence point to the existence of an epilepsy susceptibility gene on chromosome 15q14. Evidence for linkage to this region has thus been reported for juvenile myoclonic epilepsy, common subtypes of idiopathic generalized epilepsy (IGE), in addition to the EEG trait 'centrotemporal spikes' in families with rolandic epilepsy. The chromosomal region 15q14 harbours several candidate genes that are involved in the regulation of neuronal excitability. One of the most promising candidate genes is the brain-expressed potassium chloride cotransporter KCC3, given that this class of ion transporter has been implicated in the regulation of neuronal chloride activity. We therefore performed a mutation analysis of KCC3 in the index patients of 23 IGE-families as well as of 16 families with rolandic epilepsy which where selected by positive evidence for linkage to D15S165. Four novel single nucleotide exchanges (SNPs) were identified, none of which change the coding sequence. These results do not support a major role for KCC3 in the etiology of rolandic epilepsy or common subtypes of IGE.

Carrier Proteins↗

PubMed2001

Nicastrin binds to membrane-tethered Notch.

The presenilins and nicastrin, a type 1 transmembrane glycoprotein, form high molecular weight complexes that are involved in cleaving the beta-amyloid precursor protein (betaAPP) and Notch in their transmembrane domains. The former process (termed gamma-secretase cleavage) generates amyloid beta-peptide (Abeta), which is involved in the pathogenesis of Alzheimer's disease. The latter process (termed S3-site cleavage) generates Notch intracellular domain (NICD), which is involved in intercellular signalling. Nicastrin binds both full-length betaAPP and the substrates of gamma-secretase (C99- and C83-betaAPP fragments), and modulates the activity of gamma-secretase. Although absence of the Caenorhabditis elegans nicastrin homologue (aph-2) is known to cause an embryonic-lethal glp-1 phenotype, the role of nicastrin in this process has not been explored. Here we report that nicastrin binds to membrane-tethered forms of Notch (substrates for S3-site cleavage of Notch), and that, although mutations in the conserved 312-369 domain of nicastrin strongly modulate gamma-secretase, they only weakly modulate the S3-site cleavage of Notch. Thus, nicastrin has a similar role in processing Notch and betaAPP, but the 312-369 domain may have differential effects on these activities. In addition, we report that the Notch and betaAPP pathways do not significantly compete with each other.

Alzheimer Disease↗

PubMed2001

Association of a mutation in the beta3-adrenergic receptor gene with obesity and response to dietary intervention in Chinese children.

UNLABELLED: This study aimed to determine whether the Trp64Arg mutation in the beta3-adrenergic receptor beta3-adr) gene is related to childhood obesity and the response to dietary intervention for obesity. The study included 311 healthy children aged 8-11 y selected at random from 4 primary schools in Beijing. Fasting insulin and lipids were measured and anthropometry was carried out for all samples. The mutation of the beta3-adr gene was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. Forty-seven obese children were selected and divided into two groups. One group received dietary intervention (36 subjects); the other served as the control group (11 subjects). After 3 mo of dietary intervention, anthropometry was carried out again in 47 obese children. The frequency of the mutated allele was similar in 73 overweight and 238 normal-weight children (0.18 and 0.17, respectively). Adjusted for age and sex. there was no significant difference in body mass index (BMI) and the levels of fasting lipids and insulin between those with and without the mutation of the 311 children. However, after 3 mo of dietary intervention. increases in weight and BMI were significantly lower in obese children without the mutation than in the control group (2.41 +/- 0.56 vs 4.43 +/- 0.70. p < 0.05: 0.48 +/- 0.24 vs 1.55 +/- 0.35, p < 0.05. respectively), but the changes in weight and BMI in obese children with the mutation were similar to the results in the controls (4.32 +/- 0.69 vs 4.43 +/- 0.70; 1.47 +/- 0.32 vs 1.55 +/- 0.35). CONCLUSION: The Trp64Arg mutation of the beta3-adr gene may predict the result of dietary intervention in obese children to some extent, but it was not a major factor affecting weight in Chinese children.

Analysis of Variance↗

PubMed2001

Cellular localization of gelatinases and tissue inhibitors of metalloproteinases during follicular growth, ovulation, and early luteal formation in the rat.

The matrix metalloproteinase (MMP) system consists of a proteolytic component, the metalloproteinases, and an associated class of tissue inhibitors of metalloproteinases (TIMPs). We investigated the cellular localization of the TIMPs and the gelatinase family of MMPs throughout the latter stages of follicular growth and during the periovulatory period. Immature female rats were injected with eCG, and ovaries were collected at the time of eCG administration (0 h) and at 6, 12, 24, or 36 h after eCG injection (i.e., follicular development group). A second group of animals (periovulatory) was injected with eCG followed by hCG 48 h later, and ovaries were collected at 0, 12, and 24 h after hCG. Ovaries were processed for the cellular localization of gelatinase or TIMP mRNA or gelatinolytic activity. Gelatinase mRNA (MMP-2 and MMP-9) was localized to the theca of developing follicles and to the stroma. Following a hCG stimulus, MMP-2 mRNA increased as the granulosa cells of preovulatory follicles underwent luteinization during formation of the corpus luteum (CL). MMP-9 mRNA remained predominantly in the theca during this period. In situ zymography for gelatinolytic activity demonstrated a pattern of activity that corresponded with the localization of MMP-2 and MMP-9 mRNA around developing follicles. Gelatinolytic activity was observed at the apex of preovulatory follicles and throughout the forming CL. The mRNA for TIMP-1, -2, and -3 was localized to the stroma and theca of developing follicles. TIMP-3 mRNA was present in the granulosa cells of certain follicles but was absent in granulosa cells of adjacent follicles. At 12 h after hCG, luteinizing granulosa cells expressed TIMP-1 and TIMP-3 mRNA, but TIMP-2 mRNA was at levels equivalent to the background. In the newly forming CL at 24 h after hCG administration, the luteal cells expressed TIMP-1, -2, and -3 mRNA, although the pattern of cellular expression was unique for each of the TIMPs. These findings demonstrate that the MMPs and TIMPs are in the cellular compartments appropriate for impacting the remodeling of the extracellular matrix as the follicle grows, ovulates, and forms the CL.

Animals↗

PubMed2001

Quantitative assessment of cranial defect healing and correlation with the expression of TGF-beta.

Circular parietal defects from 3 to 12 mm in diameter were made in 45 6-month old skeletally mature guinea pigs, and animals were sacrificed after survival periods of 3 days to 12 weeks. The original defect was harvested in continuity with a rim of surrounding bone and the adjacent dura and pericranium. After 12 weeks, all 3 and 5 mm defects were completely covered by a bridge of bone, while residual defects were noted within the 8 and 12 mm wounds. Percentage of new bone formation was significantly higher within 3 mm defects, than in all larger defects at each time interval from 1 week on (P < .05), reaching a mean of 93% in 3 mm defects and remaining below a mean of 31% in the remaining defect sizes. Immunolocalization demonstrated an osteogenic front in which the osteoblasts stained strongly for all isoforms of TGF-beta, with the intensity decreasing after the majority of the defects had reossified; this front was located at the advancing bone edge of the defect as well as the endocranial side adjacent to the dura. In conclusion, isoforms of TGF-beta are upregulated during a limited "window" of time corresponding to the period of calvarial reossification, and are localized to osteoblasts within an osteogenic front at the periphery and dural surfaces of the defects.

Animals↗

PubMed2001

Lymphocytes are important in early atherosclerosis.

Lymphocytes represent a potentially important proinflammatory cell that localizes to atherosclerotic lesions. To determine whether they contribute to lesion development, atherosclerosis-prone (LDLR(-/-)) mice were crossed with lymphocyte-deficient (RAG1(-/-)) mice to generate double knockout progeny. After 8 weeks on a Western-type diet (WTD), lesion development was reduced by 54% in double knockout mice, as compared with matched LDLR(-/-) controls. However, these significant differences in lesion area gradually subsided as the WTD was continued for 12 and 16 weeks. Consistent with this observation, histological studies determined that lesion initiation and early progression were delayed in RAG1/LDL-R double knockout mice. Differences in lesion area did not correlate with any significant alterations in plasma lipid levels. These studies suggest that lymphocytes play an important role early in atherogenesis.

Animals↗

PubMed2001

[A study of phenylketonuria heterozygotes screening in married population of Tianjin area].

OBJECTIVE: To find out a method that is simple and reliable for screening phenylketonuria(PKU) heterozygotes. METHODS: Detecting and analyzing plasma phenylalanine(Phe) and tyrosine(Tyr) from 101 known-PKU heterozygotes and 2023 married people by means of a high performance liquid chromatograph. RESULTS: Significant differences were observed between known- PKU heterozygotes and screening population in plasma Phe, Phe/Tyr and Phe(2)/Tyr. The values of plasma Phe, Phe/Tyr and Phe(2)/ Tyr from 94.1% known-PKU heterozygotes were higher than mean+2s of those values from screening population. According to the limits of mean+2s, 81 cases were screened out from the 2023 married people. It was the first time to get the actual heterozygote frequency of 4% from population. CONCLUSION: The biochemical method mentioned above is available for use in screening PKU heterozygotes.

Adult↗

PubMed2001

[Changes in erythrocyte rheologic properties after mild burn injury].

The changes in erythrocyte deformability and osmotic fragility were studied with an animal model of mild burn injury. The results showed that after the burn injury there was a gradual decrease with time at first and then a recovery in erythrocyte deformability. Maximum deformation index [(DI)max], integration deformation index (IDI) and osmotic fragility of RBCs drawn just after burn were almost identical to those before burn injury. (DI)max and IDI significantly decreased at 1, 2 h but not at 4, 7 h when compared with those before burn injury, however, the RBCs were less deformable at 4, 7 h. Erythrocyte osmotic fragility significantly increased only at 4 h after burn injury when compared at the time points of 0, 1, 2, 4, 7 h after burn with that before burn injury. The results indicated that the lesion in (DI)max and IDI, and the increase in osmotic fragility might be only related to the body fluid factors in this animal model. The decrease in erythrocyte deformability and the increase in erythrocyte osmotic fragility did not synchronize, suggesting that the changes might come about not by the same mechanism.

Animals↗

PubMed2001

[Effect of tissue factor pathway inhibitor on the adhesion of platelet onto polyethylene and polyvinylchloride membranes].

Tissue factor pathway inhibitor(TFPI) is the major inhibitor of the extrinsic pathway of the blood coagulation cascade. Our previous study showed that TFPI could obviously prolong the blood coagulation time on the surface of polyethelene(PE) and polyvinylchloride(PVC) membranes in vitro and decrease the generation of thrombus on Dacron membrane in vivo. In the present study, the effect of TFPI on the adhesion of platelet onto PE and PVC membranes was investigated. PE or PVC membrane was cut into small pieces and incubated in 96-well culture plate with GST or GST-TFPI fusion protein at 4 degrees C over night. Freshly collected rabbit blood was mixed with 3.8% sodium citrate. Platelet-rich plasma was separated by centrifugation and then incubated with the treated membranes at 37 degrees C for 30 minutes. The membranes were then washed, fixed, and freeze-dehydrated Adhesion of platelet was observed through scanning electronic microscope. The result showed that GST-TFPI treatment significantly decreased the number of platelet adhered on the membrane when compared with the GST and control group, and it suggested that TFPI might have a great potential to be used as an anticoagulant for improving the hemocompatibility of biomaterials.

Animals↗

PubMed2001

Intravascular local gene transfer mediated by protein-coated metallic stent.

OBJECTIVE: To assess the feasibility, efficiency and selectivity of adenovirus-mediated gene transfer to local arterial wall by protein-coated metallic stent. METHODS: A replication-defective recombinant adenovirus carrying the Lac Z reporter gene for nuclear-specific beta-galactosidase (Ad-beta gal) was used in this study. The coating for metallic stent was made by immersing it in a gelatin solution containing crosslinker. The coated stents were mounted on a 4.0 or 3.0 mm percutaneous transluminal coronary angioplasty (PTCA) balloon and submersed into a high-titer Ad-beta gal viral stock (2 x 10(10) pfu/ml) for 3 min, and then implanted into the carotid arteries in 4 mini-swines and into the left anterior descending branch of the coronary artery in 2 mini-swines via 8F large lumen guiding catheters. The animals were sacrificed 7 (n = 4), 14 (n = 1) and 21 (n = 1) days after implantation, respectively. The beta-galactosidase expression was assessed by X-gal staining. RESULTS: The results showed that the expression of transgene was detected in all animal. In 1 of carotid artery with an intact intima, the beta-gal expression was limited to endothelial cells. In vessels with denuded endothelium, gene expression was found in the sub-intima, media and adventitia. The transfection efficiency of medial smooth muscle cells was 38.6%. In 2 animals sacrificed 7 days after transfection, a microscopic examination of X-gal-stained samples did not show evidence of transfection in remote organs and arterial segments adjacent to the treated arterial site. CONCLUSIONS: Adenovirus-mediated arterial gene transfer to endothelial, smooth muscle cells and adventitia by protein-coated metallic stent is feasible. The transfection efficiency is higher. The coated stent may act as a good carrier of adenovirus-mediated gene transfer and have a potential to prevent restenosis following PTCA.

Adenoviridae↗

PubMed2001

Association and contribution of ERK to IL-6-induced activation of signal transducer and activator of transcription in a human myeloma cell line.

OBJECTIVE: To investigate the regulation effect of protein kinase ERK on the activation of transcription factor STAT3 in response to IL-6 in the Sko-007 human myeloma cell line. METHODS: Electrophoretic mobility shift assay (EMSA) and immunoprecipitation (IP) were used to show the activation of STAT3 and ERK in Sko-007 cells in the presence and absence of IL-6. Antisense oligonucloetides of ERK (ERK-AS) were transfected into Sko-007 cells to specifically inhibit the expression and activity of ERK. The changes in the activation of STAT3 in the transfected cells were also exhibited by EMSA. Direct binding between STAT3 and ERK was analyzed by co-IP. RESULTS: Both STAT3 and ERK were activated in Sko-007 cells stimulated with IL-6. ERK-AS inhibited STAT3 activation by IL-6. Moreover, activated ERK could form a complex with STAT3 in Sko-007 cells. CONCLUSION: ERK can bind STAT3 directly and be required for its maximal activation in Sko-007 cells stimulated by IL-6.

DNA, Antisense↗

PubMed2001

[Immunorelated pancytopenia].

OBJECTIVE: A report of a group of patients with pancytopenia which might be related to abnormal immunity. METHODS: The clinical and laboratory features of 29 patients with positive bone marrow mononuclear cell (BMMNC) Coombs tests were analyzed. RESULTS: Most of these cases were pancytopenia with normal or decreased bone marrow cellularities and increased normoblasts. They were all found to have negative results of conventional hemolysis tests and hematopoietic nutrient determination and had no evidence of malignant clonal hematopoiesis. However, all of them showed positive BMMNC-Coombs test and good response to corticosteroids. CONCLUSION: Immunorelated pancytopenia might be caused by abnormal immunity (especially autoantibody) mediated destruction or abnormal function of blood cells. It is beneficial to differentiate immunorelated pancytopenia from aplastic anemia or myelodysplastic syndromes.

Adolescent↗

PubMed2001

[Sequential intensified immunosuppressive therapy combining with hematopoietic growth factors in the treatment of severe aplastic anemia].

OBJECTIVE: To explore more effective regimen for reducing early mortality of severe aplastic anemia (SAA) and improving therapeutic effectiveness. METHODS: Antilymphocyte globulin/antithymocyte globulin (ALG/ATG) and cyclosporine A (CsA) (sequential intensified immunosuppressive therapy, SIIST), with or without hematopoietic growth factors (HGFs) were administered to 73 SAA patients in a prospective randomized clinical trial to test the effectiveness of the addition of HGFs for the patients. RESULTS: The response rate of SIIST with HGFs group was significantly higher than that of SIIST alone group (89.2% vs 63.9%), with lower rates of early infection (24.3% vs 55.3%) and mortality (4.0% vs 16.7%), shorter duration of cytopenia and blood transfusion dependence and faster recovery of bone marrow hematopoiesis. The addition of HGFs to SIIST was tolerated well in all patients. There was no difference in the treatment outcome of the two groups with GM-CSF plus Epo or G-CSF plus Epo. CONCLUSION: The use of HGFs in combination with SIIST could reduce early infection and mortality rates and, therefore, improve the response rates in SAA patients.

Adolescent↗

PubMed2001

[Study on the transformation from myelodysplastic syndromes into acute leukemias].

OBJECTIVE: To study the patterns of transformation from myelodysplastic syndromes (MDS) into acute leukemias (AL). METHODS: Leukemic transformation of MDS patients was dynamically followed up and the clinical manifestations, peripheral blood and bone marrow pictures, karyotypes, immunophenotypes, response to treatment and prognosis of post MDS acute leukemia (postMDS-AL) were observed. RESULTS: During the past eight year and seven months, 21 (13.91%) of 151 MDS patients progressed to overt leukemia with a median interval of 5 (1 - 21) months. There were no significant differences among the rates of leukemia from RA, RAEB and RAEB-t groups. The transformation was developed either gradually or rapidly. There were five parameters related to the leukemic transformation: under 40 years of age, pancytopenia, more than 0.15 blasts in bone marrow, at least two types of abnormal karyotype and combined chemotherapy. All of the 21 post MDS-AL were acute myeloid leukemia (AML); and most of them were M(2), M(4) and M(5). Two (9.52%) post MDS-AML developed extramedullary infiltration. Leukopenia was found in 47.62% of patients. Two third of the patients, whose bone marrows were generally hypercellular, showed neutropenias. After evolving into AML, 8 (47.06%) patients developed abnormal karyotypes. High expression of immature myeloid antigens, including CD(33) (49.83 +/- 24.50)%, CD(13) (36.38 +/- 33.84)%, monocytic antigen CD(14) (38.50 +/- 24.60)%, and stem cell marker CD(34) (34.67 +/- 30.59)% were found on bone marrow mononuclear cells of post MDS-AML cases. In some cases, lymphoid antigens, such as CD(5), CD(7), CD(9) and CD(19) were coexisted with myeloid antigens. A low complete remission rate (31.25%) and short survival duration with median survival of 6 (1 - 28) months were found in patients with post MDS-AML treated by induction therapy. CONCLUSION: MDS was at high risk of evolving into AML, either gradually or rapidly. Patients with post MDS-AML had specific biologic features and worse prognoses.

Acute Disease↗

PubMed2001

[The expression of glucocorticoid receptor beta messenger RNA in peripheral white blood cells of hormone-resistant nephrotic syndrome patients].

OBJECTIVE: To study the molecular mechanism contributing to hormone resistance of nephrotic syndrome. METHODS: The specific hormone binding sites of receptor was determined by radioligand binding assay. Messenger RNA of receptor was determined by quantitative reverse transcription-polymerase chain reaction. RESULTS: No significant differences of specific hormone binding sites of peripheral white blood cells were observed among hormone-sensitive patients, hormone-resistant patients and healthy volunteers. However, in hormone-resistant patients, GR alpha/GR beta mRNA ratio decreased significantly as compared with that of hormone-sensitive patients and healthy volunteers. CONCLUSION: Results of the experiments indicated that the increased expression of GR beta, which leads to the decrease of the GR alpha/GR beta ratio, may be one of the mechanism responsible for hormone resistance in some nephrotic syndrome patients.

Binding Sites↗

PubMed2001

[Guided tissue regeneration with Biomesh membrane for Class II furcation defects].

OBJECTIVE: The objective of this study was to investigate clinical significance of the guided tissue regeneration (GTR) by using Biomesh membrane to the treatment of Class II furcation defects. METHODS: Totally 8 molars with Class II furcation defects of 6 periodontitis patients were treated. The clinical effects of GTR were evaluated by measuring changes of pocket probing depths (PPD), clinical attachment levels (CAL), and alveolar bone on X-ray films prior to and 6 months after the surgery. RESULTS: All patients had no swollen or pain reaction on these surgery areas after the surgery, and the PPD was reduced and the CAL was gain significantly 6 months after the surgery. The new alveolar bone formation was demonstrated. CONCLUSION: The GTR with Biomesh membrane is a good therapy method for Class II furcation defects.

Adult↗