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C Dai

Publications and source records attributed to C Dai.

At least 19 recordsLinked to original sources
PubMed2001

Gene polymorphisms of homocysteine metabolism-related enzymes in Chinese patients with occlusive coronary artery or cerebral vascular diseases.

The mutations in homocysteine (Hcy) metabolism-related enzyme genes including methylenetetrahydrofolate reductase (MTHFR) C677T, cystathionine beta-synthase (CBS) 844ins68, and methionine synthase (MS) A2756G have been identified as genetic risk factors for thromboembolic events. It has been noticed that these gene mutations have heterogeneous distributions among different ethnic groups or geographic areas. The data on the prevalence of the gene mutations in Chinese population is not yet available. In the present study, we have investigated the frequency of the MTHFR C677T, CBS 844ins68, and MS A2756G mutations in 102 patients with ischemic stroke (IS), 73 patients with myocardial infarction (MI) and 100 healthy controls. The distributive frequencies of the gene variations are as follows: In the IS, MI and control groups, the mutant homozygote for MTHFR C677T is 15 (14.7%), 8 (11.7%) and 16 (16.0%), respectively, and the T allele frequency is 37.7%, 33.6% and 39.5%, respectively; the heterozygote for CBS 844ins68 is 1 (1.0%), 1 (1.4%) and 5 (5.0%), respectively; the heterozygote for MS A2756G is 18 (17.6%), 14 (19.2%) and 17 (17.0%), and the G allele frequency is 8.8%, 11.0% and 9.5%, respectively. The carrier of both MS A2756G and MTHFR C677T (combined mutations) is 14 (12.7%), 8(11.0%) and 12(12.0%), respectively. There is no statistically significant difference between the patient groups and the control group in the frequencies of these single mutation or combined mutations. The heterozygosity of CBS 844ins68 yields an odds ratio (OR) of 0.19 (95% confidence interval (CI) 0.02-1.43) for IS and 0.26 (95% CI 0.03-2.31) for MI. The T allele of MTHFR C677T yields an OR of 0.93 for IS (95% CI 0.62-1.39) and 0.77 for MI (95% CI 0.50-1.21). The G allele of MS A2756G yields an OR of 0.92(95% CI 0.47-1.81) for IS and 1.17 (95% CI 0.58-2.37) for MI. Our results suggest that neither single mutation nor combined mutations in MTHFR C677T, CBS 844ins68 and MS A2756G represent an independent risk factor for increasing IS and coronary artery disease risks in Chinese population. However, CBS 844ins68 may be a protective factor against vascular thromboembolic disease. The prevalence of CBS 844ins68 and MS A2756G in Chinese population is obviously lower than in Western Caucasian population.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2001

Glioma models.

Gliomas are primary central nervous system tumors that arise from astrocytes, oligodendrocytes or their precursors. Gliomas can be classified into several groups according to their histologic characteristics, the most malignant of the gliomas is glioblastoma multiforme. In contrast to the long-standing and well-defined histopathology, the underlying molecular and genetic bases for gliomas are only just emerging. Many genetic alterations have been identified in human gliomas, however, establishing unequivocal correlation between these genetic alterations and gliomagenesis requires accurate animal models for this disease. Here we are reviewing the existing animal models for gliomas with different strategies and our current knowledge on the important issues about this disease, such as activation of signal transduction pathways, disruption of cell cycle arrest pathways, cell-of-origin of gliomas, and therapeutic strategies.

Animals↗
PubMed2001

PDGF autocrine stimulation dedifferentiates cultured astrocytes and induces oligodendrogliomas and oligoastrocytomas from neural progenitors and astrocytes in vivo.

We present evidence that some low-grade oligodendrogliomas may be comprised of proliferating glial progenitor cells that are blocked in their ability to differentiate, whereas malignant gliomas have additionally acquired other mutations such as disruption of cell cycle arrest pathways by loss of Ink4a-Arf. We have modeled these effects in cell culture and in mice by generating autocrine stimulation of glia through the platelet-derived growth factor receptor (PDGFR). In cell culture, PDGF signaling induces proliferation of glial precursors and blocks their differentiation into oligodendrocytes and astrocytes. In addition, coexpression of PDGF and PDGF receptors has been demonstrated in human gliomas, implying that autocrine stimulation may be involved in glioma formation. In this study, using somatic cell type-specific gene transfer we investigated the functions of PDGF autocrine signaling in gliomagenesis by transferring the overexpression of PDGF-B into either nestin-expressing neural progenitors or glial fibrillary acidic protein (GFAP)-expressing astrocytes both in cell culture and in vivo. In cultured astrocytes, overexpression of PDGF-B caused significant increase in proliferation rate of both astrocytes and neural progenitors. Furthermore, PDGF gene transfer converted cultured astrocytes into cells with morphologic and gene expression characteristics of glial precursors. In vivo, gene transfer of PDGF to neural progenitors induced the formation of oligodendrogliomas in about 60% of mice by 12 wk of age; PDGF transfer to astrocytes induced the formation of either oligodendrogliomas or mixed oligoastrocytomas in about 40% of mice in the same time period. Loss of Ink4a-Arf, a mutation frequently found in high-grade human gliomas, resulted in shortened latency and enhanced malignancy of gliomas. The highest percentage of PDGF-induced malignant gliomas arose from of Ink4a-Arf null progenitor cells. These data suggest that chronic autocrine PDGF signaling can promote a proliferating population of glial precursors and is potentially sufficient to induce gliomagenesis. Loss of Ink4a-Arf is not required for PDGF-induced glioma formation but promotes tumor progression toward a more malignant phenotype.

Animals↗
PubMed2001

Increased expression of the INK4a/ARF locus in polycythemia vera.

The retinoblastoma (Rb), cyclin-dependent kinase (CDK), and CDK inhibitor genes regulate cell generation, and deregulation can produce increased cell growth and tumorigenesis. Polycythemia vera (PV) is a clonal myeloproliferative disease where the mechanism producing increased hematopoiesis is still unknown. To investigate possible defects in cell-cycle regulation in PV, the expression of Rb and CDK inhibitor gene messenger RNAs (mRNAs) in highly purified human erythroid colony-forming cells (ECFCs) was screened using an RNase protection assay (RPA) and 11 gene probes. It was found that RNA representing exon 2 of p16(INK4a) and p14(ARF) was enhanced by 2.8- to 15.9-fold in 11 patients with PV. No increase of exon 2 mRNA was evident in the T cells of patients with PV, or in the ECFCs and T cells from patients with secondary polycythemia. p27 also had elevated mRNA expression in PV ECFCs, but to a lesser degree. Because the INK4a/ARF locus encodes 2 tumor suppressors, p16(INK4a) and p14(ARF) with the same exon 2 sequence, the increased mRNA fragment could represent either one. To clarify this, mRNA representing the unique first exons of INK4a and ARF were analyzed by semiquantitative reverse transcription-polymerase chain reaction. This demonstrated that mRNAs from the first exons of both genes were increased in erythroid and granulocyte-macrophage cells and Western blot analysis showed that the INK4a protein (p16(INK4a)) was increased in PV ECFCs. Sequencing revealed no mutations of INK4a or ARF in 10 patients with PV. p16(INK4a) is an important negative cell-cycle regulator, but in contrast with a wide range of malignancies where inactivation of the INK4a gene is one of the most common carcinogenetic events, in PV p16( INK4a) expression was dramatically increased without a significant change in ECFC cell cycle compared with normal ECFCs. It is quite likely that p16(INK4a) and p14(ARF) are not the pathogenetic cause of PV, but instead represent a cellular response to an abnormality of a downstream regulator of proliferation such as cyclin D, CDK4/CDK6, Rb, or E2F. Further work to delineate the function of these genes in PV is in progress. (Blood. 2001;97:3424-3432)

Aged↗
PubMed2001

The first general method for palladium-catalyzed Negishi cross-coupling of aryl and vinyl chlorides: use of commercially available Pd(P(t-Bu)(3))(2) as a catalyst.

With a single protocol, commercially available Pd(P(t-Bu)(3))(2) can effect the Negishi cross-coupling of a wide range of aryl and vinyl chlorides with aryl- and alkylzinc reagents. The process tolerates nitro groups, and it efficiently generates sterically hindered biaryls. In addition, a high turnover number (>3000) can be achieved.

Journal Article↗
PubMed2001

Experimental study on facial nerve regeneration with or without geniculate ganglionectomy.

OBJECTIVE: To investigate regeneration of the distal facial nerve following nerve grafting within the tympanic segment with geniculate ganglion preservation or dissection. DESIGN: Randomized controlled trial. SUBJECTS: Twenty-three adult New Zealand albino rabbits were used in this study. INTERVENTIONS: A 2-mm tympanic segment of the facial nerve was removed, and the greater auricular nerve was harvested for grafting in all animals. In group 1 (10 rabbits), the geniculate ganglion was preserved. In group 2 (13 rabbits), the geniculate ganglion was dissected. Mastoidal and extratemporal segments of the facial nerve were harvested 3 months postoperatively for histological examination by electron microscopy. RESULTS: The number of myelinated axons in normal facial nerves was 1819.6 +/- 535.6. In group 1, the number of myelinated axons was 123.6 +/- 31.1, and, compared with normal facial nerves, the diameter of the regenerative axons was decreased and the sheath thickness in the regenerative fiber was diminished. In group 2, the number of myelinated axons was 515.1 +/- 103.1, while the myelin sheath thickness was proportionate to axon diameter. (Data are given as mean +/- SD.) CONCLUSION: Geniculate ganglionectomy may improve motor axon regeneration.

Animals↗
PubMed2001

Systemic administration of naked plasmid encoding hepatocyte growth factor ameliorates chronic renal fibrosis in mice.

The progression of chronic renal diseases is considered as an irreversible process that eventually leads to end-stage renal failure characterized by extensive tissue fibrosis. At present, chronic renal fibrosis is incurable and the incidence of affected patients is on the rise worldwide. In this study, we demonstrate that delivery of hepatocyte growth factor (HGF) gene via systemic administration of naked plasmid vector markedly ameliorated renal fibrosis in an animal model of chronic renal disease induced by unilateral ureteral obstruction. A high level of exogenous HGF protein was detected in the obstructed kidneys following intravenous injection of naked plasmid encoding human HGF. Delivery of human HGF gene induced a sustained activation of extracellular signal-regulated kinases-1 and -2 in the obstructed kidneys. Exogenous HGF expression dramatically inhibited alpha-smooth muscle actin expression, attenuated renal interstitial accumulation and deposition of collagen I and fibronectin. In addition, exogenous HGF suppressed renal expression of pro-fibrogenic cytokine TGF-beta1 and its type I receptor in vivo. These results suggest that systemic administration of naked plasmid vector introduces a high level of exogenous HGF to the diseased kidneys, and that HGF gene transfer may provide a novel therapeutic strategy for amelioration of chronic renal fibrosis in vivo.

Actins↗
PubMed2001

[Study on homocysteine metabolism related enzymes gene mutations in Chinese patients with ischemic cardiovascular and cerebrovascular diseases].

OBJECTIVE: To explore the significance of gene mutations of cystathionine beta-synthase (CBS844ins68), methionine synthase (MS A2756G) and methylenetetrahydrofolate reductase (MTHFR C677T) in ischemic cardiovascular and cerebrovascular diseases. METHODS: The genotypes of CBS 844ins68, MS A2756G and MTHFR C677T were determined by PCR-based assay in 102 patients with brain infarction, 73 with myocardial infarction and 100 healthy controls. RESULTS: The prevalences of CBS 844ins68 and MS A2756G in the cohort studied were somewhat lower than that in western Caucasian populations. There were no significant differences in the frequencies of CBS 844ins 68, MS A2756G and MTHFR C677T mutations between the patient the and control groups. However, the heterozygous form of CBS 844ins 68 tended to be more prevalent in the controls than in the patients. CONCLUSION: Gene mutations as CBS 844ins 68, MS A2756G and MTHFR C677T may not be independent risk factors for ischemic cardiovascular and cerebrovascular disease in Southern Chinese Han population. The prevalences of CBS 844ins 68 and MS A2756G may vary with different ethnic groups or geographic regions.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2001

Monocyte chemoattractant protein-1 expression in renal tissue is associated with monocyte recruitment and tubulo-interstitial lesions in patients with lupus nephritis.

OBJECTIVE: To investigate the pattern of monocyte chemoattractant prolein-1 (MCP-1) distribution in the renal interstitium and evaluate its pathogenic role in tubulo-interstitial lesions in patients with lupus nephritis, the distribution of MCP-1 in renal tissue was observed. METHODS: Eighteen female patients with biopsy-proven lupus nephritis were enrolled in this study. No intensive immunosuppresive therapy was used in these patients during the 3 months prior to renal biopsy. The distribution of MCP-1, infiltration of CD68+ (macrophage/monocyte), CD4+ and CD8+ cells in the tubulo-interstitium of patients with lupus nephritis was detected using immunohistochemical staining with specific antibodies. Renal specimens from patients with minimal change glomerulonephritis were used as controls. RESULTS: MCP-1 protein was widely distributed in the renal tissue of patients with lupus nephritis, mainly located at the baso-lateral surface of tubular epithelial cells (16/18 biopsies), and on the wall of interstitial blood vessels (9/18 biopsies). In contrast, tubular MCP-1 staining was weak and rare in renal tissue from controls (7.4 +/- 6.2% vs 26.7 +/- 22.8%, P < 0.01). Tubulo-interstitial infiltration of CD68+, CD4+ and CD8+ cells was markedly increased in patients with lupus nephritis as compared to controls. The tubular expression of MCP-1 was strongly associated with the amount of CD68+ cell infiltration in the interstitium (r = 0.5420, P < 0.05) and the extent of interstitial fibrosis. There was no correlation between MCP-1 production in tubules and the degree of urinary protein excretion in patients with lupus nephritis (r = 0.0547, P > 0.05). CONCLUSIONS: The expression of MCP-1 in the renal tubules and vascular wall was markedly increased in patients with lupus nephritis. The overproduction of MCP-1 in renal tissue may contribute to monocyte recruitment in the interstitium and thus result in tubulo-interstitial damage in lupus nephritis.

Adult↗
PubMed2001

[An experimental study of repairing nerve gap with acellular basal lamina tubes].

OBJECTIVE: To develop an effective new material for repair of nerve defects. METHODS: The 4-week pre-degenerative and normal sciatic nerve segments of SD rats were extracted with the detergent lysophosphatidylcholine, which resulted in acellular nerve basal lamina tubes, called EDNG (extracted degenerative nerve grafts) and ENG (extracted normal nerve grafts) respectively. The morphology of the acellular nerve basal lamina tubes was revealed by conventional histological examinations, transmission electron microscopy and immunohistochemistry method. The basal lamina tubes, as allografts, were used to repair a 15 mm-gap of sciatic nerve in Wistar rats. In the control group nerve autografts (NAG) was applied. Evaluation included general observation, electromyographic examination, muscle measurement and histological observation of serial sections at 12 weeks after surgery. RESULTS: The EDNG had more ideal frame, better resilience than ENG. There was no any cell debris in EDNG, whereas in the inner wall of the tubes immunohistochemical analysis revealed clear positive staining and strong immunoreactivity of laminin under immunoelectron microscopy. After peripheral nerves were repaired, all the animals of the three groups had restoration of function to a certain extent. The result of the NAG group was the best, the EDNG group was the next and the ENG group was the inferior. CONCLUSION: This new material offers a possible solution to repair of a short defect of a peripheral nerve.

Animals↗
PubMed2001

[Effects of blood transfusion on cellular immuno-function in patients with laryngeal carcinoma].

OBJECTIVE: To explore the influence of blood transfusion on cellular immunofunction in patient with laryngeal carcinoma. METHOD: EPICS-XL flow cytometry was used to measure T cell subgroup, NK cell and CD28 in 36 patients with laryngeal carcinoma pre-operation and 2 weeks post-operation. Patients were divided into allotransfusion group and non-transfusion group. Comparison was conducted between the 2 groups. RESULT: 1. Comparison with normal population, decreasing of CD3, CD4, NK cell and CD28 in the 36 patients pre-operation was statistically significant (P < 0.01). 2. Decreasing of CD3, CD4, NK cell and CD28 was statistically significant post-operation (P < 0.05). 3. In the non-transfusion group change of CD3, CD4, CD8, NK cell and CD28 post-operation was statistically insignificant (P > 0.05). CONCLUSION: While cellular immunofunction is generally low in patients with laryngeal carcinoma, allotransfusion will reduce further. It makes contribution to spreading and metastasis of carcinoma easier.

Aged↗
PubMed2001

[The effect of culture conditions on the fatty acid composition in the mycelium of the Cephalosporium sp].

The optimal condition of Cephalosporium sp. to culture mycelia and accumulate polyunsaturated fatty acid (PUFA) was researched. The optimal culture condition to get mycelium productivity was: maltose 60 g/L, KNO3 3 g/L, initial pH 6.0, 100 mL medium in 500 mL flask, seeding 25% (v/v), 25 degrees C culture it for 10 days. The optimal condition to accumulation PUFA proportion to total fatty acid was: glucose 10-20 g/L, NH4Cl or (NH4)2SO4 3 g/L, initial pH 4.0, 100 mL medium in 500 mL falsk, seeding 10-20% (v/v) and lighted it when it was cultured. It was suggested that two step could be used in the producing progress. A proposal was put forward that the oileic acid transformed to linoleic acid was the key step to produce PUFA. This proposal gave a base to research the optimal culture condition and enzyme regulation.

Acremonium↗
PubMed2001

[Expression of bcl-2 in facial motoneurons and its ultrastructural localization following facial nerve injury].

OBJECTIVE: To explore the expression of bcl-2 in facial motoneurons and its subcellular distribution. METHODS: Wistar rats were used in this study. Facial nerve transection was performed at stylomastoid foramen or internal acoustic meatus. Facial nerve crush was made at stylomastiod foramen. The animal survived for 1, 3, 7, 15, 30 and 60 days respectively. Facial nucleus was treated with bcl-2 monoclonal antibody or bcl-2 DIG-labelling probe and studied with immunohistochemistry and in situ hybridization. The bcl-2 positive motoneuron was investigated with immuno-electron microscope. RESULTS: It was demonstrated that bcl-2 protein level was corresponded with bcl-2 mRNA expression. The level of bcl-2 expression in facial motoneurons was high in normal facial nerve. It increased on the first day and declined on the third day post-transection in facial motoneuron. It reached the lowest level on the 15th days following facial nerve injury (P < 0.05). The expression recovered to normal level in two months (P > 0.05). After facial nerve transected, the reduction of bcl-2 expression was more significant when facial nerve transected close to facial nucleus than that far from facial nucleus (P < 0.05). Comparing to facial nerve transection in stylomastoid foramen, there was more intensive bcl-2 expression following facial nerve crush (P < 0.05). Further study showed that bcl-2 primarily resided in the nuclear envelop, endoplasmic reticulum and mitochondrial membrane. CONCLUSIONS: These data indicated that high level bcl-2 protein may prevent facial motoneuron death following facial nerve injury. It is suggested that overexpression bcl-2 by transgene may prevent facial motoneurons death.

Animals↗
PubMed2001

[Facial paralysis in temporal bone trauma].

OBJECTIVE: To study the cause and treatment of facial paralysis in temporal bone trauma. METHODS: A retrospective review of 28 patients with facial paralysis resulting from temporal bone trauma was conducted, House-Brackmann(H-B) system was used to evaluate the recovery of facial nerve function, U test was employed for statistic analysis. RESULTS: Twenty-six cases underwent following up facial nerve function of all patients was recovery partly after surgery, 46% cases reached H-B II, 84% cases reached H-B III, comparing facial nerve decompression within 4 months of injury to beyond 4 months of injury, recovery to H-B II or more of facial nerve function was 60% and 0%, respectively. The difference was significant(P < 0.05). CONCLUSION: Surgery decompression is effective on facial nerve palsy caused by temporal bone trauma. It is recommended that surgery decompression be carried out as soon as possible since a better prognosis is obtained if it is performed within four months after injury.

Adolescent↗
PubMed2001

Expression and glycosylation of rotavirus strain SA11 VP4 protein in a recombinant adenovirus.

OBJECTIVE: Using a recombinant human adenovirus to express modified VP4 gene of rotavirus SA11 strain. METHODS: A whole VP4 gene was obtained with PCR and induced the signal peptide at the gene N terminal. The chimera gene was cloned into pCMV plasmid that consists of human cytomegalovirus promoter, and then the gene was cloned to the transfer vector of human adenovirus type 5. Homologous recombination was performed by co-transfection to 293 cell lines with recombinant plasmid and viral genome using CaPO4 precipitation. RESULTS: No mutation was found in the whole VP4 gene sequence of 2362 base pair. The expressed product in recombinant adenovirus was confirmed to be specific and more antigenicity by indirect immunofluorescence assay. Both the Western blot and immunoprecipitation assay showed that the molecular mass of the expressed protein was higher than the wild type VP4 protein, and that the modified product was corresponding to a glycosylation of VP4 protein. CONCLUSION: To modify the target gene might be an effective method to enhance the stability, antigenicity and immunogenicity of expressed protein.

Adenoviruses, Human↗
PubMed2000

Astrocytes give rise to oligodendrogliomas and astrocytomas after gene transfer of polyoma virus middle T antigen in vivo.

The cells of origin for oligodendrogliomas and astrocytomas are not known but are presumed to be oligodendrocyte and astrocyte precursors, respectively. In this paper we report the generation of mixed gliomas from in vivo transformation of glial fibrillary acidic protein (GFAP)-positive cells (differentiated astrocytes) with polyoma virus middle T antigen (MTA). MTA is a powerful oncogene that activates a number of signal transduction pathways, including those proposed to be involved in gliomagenesis, and has been shown to induce tumors in many cell types. We have achieved transfer of MTA expression specifically to GFAP(+) cells in vivo using somatic cell gene transfer, and find resultant formation of anaplastic gliomas with mixed astrocytoma and oligodendroglioma morphological features. We conclude that GFAP- expressing astrocytes, with appropriate signaling abnormalities, can serve as the cell of origin for oligodendrogliomas, astrocytomas, or mixed gliomas.

Animals↗
PubMed2000

Combined activation of Ras and Akt in neural progenitors induces glioblastoma formation in mice.

Gliomas are the most common primary malignant brain tumours and are classified into four clinical grades, with the most aggressive tumours being grade 4 astrocytomas (also known as glioblastoma multiforme; GBM). Frequent genetic alterations in GBMs (refs 2-5) result in stimulation of common signal transduction pathways involving Ras, Akt and other proteins. It is not known which of these pathways, if any, are sufficient to induce GBM formation. Here we transfer, in a tissue-specific manner, genes encoding activated forms of Ras and Akt to astrocytes and neural progenitors in mice. We found that although neither activated Ras nor Akt alone is sufficient to induce GBM formation, the combination of activated Ras and Akt induces high-grade gliomas with the histological features of human GBMs. These tumours appear to arise after gene transfer to neural progenitors, but not after transfer to differentiated astrocytes. Increased activity of RAS is found in many human GBMs (ref. 11), and we show here that Akt activity is increased in most of these tumours, implying that combined activation of these two pathways accurately models the biology of this disease.

Animals↗