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D Huang

Publications and source records attributed to D Huang.

At least 73 records · Page 4Linked to original sources

Functions of Pho85 cyclin-dependent kinases in budding yeast.

Pho85 is a multifunctional cyclin-dependent kinase (Cdk) in Saccharomyces cerevisiae that has emerged as an important model for the role of Cdks in both cell cycle control and other processes. Pho85 was originally discovered as a regulator of phosphate metabolism but roles for Pho85 in glycogen biosynthesis, actin regulation and cell cycle progression have since been discovered. Ten genes encoding known or putative Pho85 cyclins (Pcls) have been identified and the Pcls appear to target Pho85 to specific cellular functions and substrates. In this chapter, we review the functions of the various Pcl-Pho85 complexes in budding yeast. We focus on the known biological roles of Pho85 with an emphasis on Pho85 substrates and cyclin-Cdk specificity.

Amino Acid Sequence↗

Chemokines and chemokine receptors in inflammation of the nervous system: manifold roles and exquisite regulation.

This article focuses on the production of chemokines by resident glial cells of the nervous system. We describe studies in two distinct categories of inflammation within the nervous system: immune-mediated inflammation as seen in experimental autoimmune encephalomyelitis (EAE) or multiple sclerosis (MS) and post-traumatic inflammation. We provide evidence that chemokines play a role in amplifying the inflammatory reaction in EAE (and, probably, MS). In the context of neural trauma, chemokines appear to be primary stimuli for leukocyte recruitment. Strikingly, expression of monocyte chemoattractant protein (MCP)-1 and interferon-gamma-inducible protein-10 (IP-10) are largely restricted to astrocytes or other glial cells in these diverse pathological states. The remainder of the review focuses on studies that address the molecular mechanisms which underlie transcriptional regulation of three astrocyte-derived chemokines: MCP-1, IP-10 and beta-R1/interferon-gamma-inducible T-cell chemoattractant (I-TAC). Based on these studies, we propose that the complex promoters of these genes are marvelously organized for flexible and efficient response to challenge. In the case of MCP-1, several different stimuli can elicit gene transcription, acting through a conserved mechanism that includes binding of inducible transcription factors and recruitment of the constitutive factor Sp1. For IP-10 and beta-R1/I-TAC, it appears that efficient gene transcription occurs only in highly inflammatory circumstances that produce aggregates of simultaneous stimuli. These characteristics, in turn, mirror the expression patterns of the endogenous genes: MCP-1 is expressed under a variety of circumstances, while IP-10 appears primarily during immune-mediated processes that feature exposure of resident neuroglia to high levels of inflammatory cytokines.

Autoimmune Diseases of the Nervous System↗

Complete primary structure, chromosomal localisation, and definition of polymorphisms of the gene encoding the human interleukin-12 p40 subunit.

Owing to the importance of interleukin (IL)-12 in regulating immune responses, we have determined the complete genomic sequence and organization of the gene encoding its p40 subunit. The genomic sequence was determined and was compared to cDNA sequences to derive exon/intron boundaries. Unusually, both the first and last of the eight exons of this gene are not translated. An extensive search identified several polymorphisms in IL-12p40, including repeat elements in introns 2 and 4 and a polymorphic Taql site in the 3'UTR. However, no polymorphisms were found which could result in amino acid substitutions. This finding places constraints on any preferential involvement of alleles of IL-12p40 in contributing to autoimmune, inflammatory or infectious diseases.

Chromosome Mapping↗

beta2-adrenergic receptor gene polymorphisms in myasthenia gravis (MG).

The beta2-adrenergic receptor (beta2-AR) belongs to the group of G-protein coupled receptors and is present mainly on skeletal and cardiac muscle cells and lymphocytes. The gene encoding beta2-AR (ADRB2) displays a moderate degree of heterogeneity in the human population. The distribution of polymorphisms at amino acid positions 16, 27 and 164 is changed in asthma, hypertension and obesity. We have earlier reported a decreased density of the beta2-AR on peripheral blood mononuclear cells and the presence of beta2-AR antibodies in patients with MG. Since certain polymorphisms affect the function of the beta2-AR, it was of interest to analyse these in MG. Using allele-specific polymerase chain reaction amplification, we revealed an over-representation of homozygosity for Arg16 and a lower prevalence of homozygosity for Gly16 in MG patients compared with healthy individuals. The increased frequency of homozygosity for Arg16 was due to a contribution from patients with generalized MG but not from patients with only ocular disease. Homozygosity for Glu27 was negatively associated with both the presence of beta2-AR antibodies and severity of disease. Moreover, acetylcholine receptor (AChR) antibodies were more often present in patients being homozygous for Gln27. Our results imply that homozygosity for Arg16 confers susceptibility to generalized MG, and that certain polymorphisms at amino acid position 27 are associated with subgroups of patients.

Adolescent↗

In situ detection of AP sites and DNA strand breaks bearing 3'-phosphate termini in ischemic mouse brain.

Our aims were to examine whether oxidative DNA damage was elevated in brain cells of male C57BL/6 mice after oxidative stress, and to determine whether neuronal nitric oxide synthase (nNOS) was involved in such damage. Oxidative stress was induced by occluding both common carotid arteries for 90 min, followed by reperfusion. Escherichia coli exonuclease III (Exo III) removes apyrimidinic or apurinic (AP) sites and 3'-phosphate termini in single-strand breaks, and converts these lesions to 3'OH termini. These ExoIII-sensitive sites (EXOSS) can then be postlabeled using digoxigenin-11-dUTP and Klenow DNA polymerase-I, and detected using fluorescein isothiocyanate-IgG against digoxigenin. Compared with the non-ischemia controls, the density of EXOSS-positive cells was elevated at least 20-fold (P < 0.01) at 15 min of reperfusion, and remained elevated for another 30 min. EXOSS mainly occurred in the cell nuclei of the astrocytes and neurons. Signs of cell death were detected at 24 h of reperfusion and occurred mostly in the neurons. Both DNA damage and cell death in the cerebral cortical neurons were abolished by treatment with 3-bromo-7-nitroindazole (30 mg/kg, intraperitoneal), which specifically inhibited nNOS. Our results suggest that nNOS, its activator (calcium), and peroxynitrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W., Liu, P. In situ detection of AP sites and DNA strand breaks bearing 3'-phosphate termini in ischemic mouse brain.

Animals↗

Novel intertypic recombinants of epstein-barr virus in the chinese population.

Among 34 Epstein-Barr virus isolates from nonimmunocompromised Chinese donors, we identified three intertypic recombinants with type 1 sequences at the EBNA2 locus and type 2 sequences at some or all of the EBNA3A, -3B, and -3C loci. These appear to have arisen from independent, evolutionarily recent recombination events; such events may be commoner in nonimmunocompromised populations than hitherto imagined.

Base Sequence↗

Polymorphisms in CTLA-4 but not tumor necrosis factor-alpha or interleukin 1beta genes are associated with Wegener's granulomatosis.

OBJECTIVE: The genetic factors predisposing to Wegener's granulomatosis (WG) are largely unknown. T cells are clearly involved in the disease, as are the proinflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin 1beta (IL-1beta). The cytotoxic T lymphocyte associated antigen-4 (CTLA-4) suppresses antigen-specific immune responses by opposing the CD28 pathway, and is crucial for a balanced T cell activation. Genetic variations in the TNF-alpha, IL-1beta, and CTLA-4 genes could thus be important in WG. METHODS: Polymorphisms in the genes coding for TNF-alpha, IL-1beta, and CTLA-4 were analyzed in 32 Swedish Caucasian patients and 109 ethnically matched controls. Results. A strong association of Ctla-4 (AT)n microsatellite to WG contrasts to the negative finding of associations between TNF-alpha NcoI, IL-1beta TaqI restriction fragment length polymorphism, and WG. The prevalence of the shortest Ctla-4 allele was decreased in patients with WG compared with healthy individuals (p < 0.0001, pc < 0.0016). CONCLUSIONS: This is the first report of a T cell related gene in association with WG. The Ctla-4 itself, or a gene close to Ctla-4, may thus contribute to the pathogenesis of WG by allowing an increased T cell activation by antigen.

Abatacept↗

Relationship between expression of type III collagen and phenotype of vascular smooth muscle cells in neointimal of stented coronary artery.

OBJECTIVE: To investigate the secretive features of type III collagen in restenosis of the stented coronary artery and the relationship between the expression of type III. collagen and vascular smooth muscle cells (VSMCs). METHODS: An animal model of restenosis was established by implanting oversized tantalum stents into the coronary arteries in 26 dogs. At the 7th, 14th and 28th days after implantation, the stented coronaries were harvested. Transmission electronic microscopy and immunohistochemistry were employed to investigate the features of type III collagen secretion and VSMCs' phenotype. The expression of type III collagen was quantified and compared for the three stages. RESULTS: Migration and proliferation of VSMCs were the main features at the 7th day after injury. At the 14th day, proliferation of VSMCs reached the peak while much more secretion of collagen was noticeable. VSMCs began to transform from the synthetic phenotype to the contractile phenotype at the 28th day, when a great quantity of collagen was also secreted. The quantity of secreted type III collagen was greater at the 14th and 28th day than that at the 7th day (P < 0.05). The stain density of type III collagen was positively correlated to neointimal thickness at both of 14th and 28th day. CONCLUSION: The pathological bases of restenosis are variant in different period of restenosis formation. Type III collagen may play an important role in the late stage of restenosis after coronary stenting.

Animals↗

Two cases of combined liver-kidney transplantation.

OBJECTIVES: To report the clinical experiences of simultaneous hepatorenal transplantation. METHODS: We performed simultaneous hepatorenal transplantation in one patient with liver cirrhosis of hepatitis B and uremia of chronic nephritis on February 1, 1999 and one patient with liver cirrhosis of hepatitis B complicated by hepatorenal syndrome on March 12, 1999. The donors were heart arrest cases. Rapid multiple organ harvesting techniques and UW solution infusion in situ were used. Liver and kidney transplantation were orthotopic and ordinary methods, respectively. Immunosuppressive drugs consisted of cyclosporine, Cellcept, ALG and cortstco steroids. Lamividine was used on day 50 and day 40 postoperation, respectively. RESULTS: Both transplanted organs rapidly achieved normal function postoperation and the patients recovered well but suffered mild kidney rejection day 110 postoperation in No 1 patient. In No 2 patient, acute renal function failure, mental symptoms, muscle spasm, cerebral artery thrombosis, inhalation pneumonia and chronic liver graft rejection ensured sequentially but were controlled. The patients have survived for more than nine and eight months, respectively, with normal life quality. CONCLUSIONS: Combined hepatorenal transplant is a radical treatment method for liver and kidney function failure and requires more comprehensive techniques than isolated single organ transplantation. Preventing the recurrence of hepatitis B by oral lamividine may be a key to long-term survival.

Adult↗

[Minimal residual disease in bone marrow in patients with Ewing's sarcoma detected by RT-PCR amplification of EWS-FLI-1 fusion gene transcript].

OBJECTIVE: To set up a system for sensitively detecting minimal Ewing's sarcoma cells in bone marrow. METHODS: Ewing's sarcoma cell line T1 cells were serially diluted with normal bone marrow cells so that the concentration of tumor cells was 10(-3), 10(-4), 10(-5), 10(-6), 10(-7), and 0, respectively. Total RNA was isolated from these samples and cDNA was synthesized. EWS-FLI-1, a fusion gene formed due to chromosome translocation, was amplified with PCR. Bone marrow samples from five patients with Ewing's sarcoma patients with tumor metastasis were examined for EWS-FLI-1 transcript. RESULTS: T1 cells could be detected when one was present in 10(6) normal bone marrow cells. Thus the sensitivity of detection was 10(-6). A 434 bp EWS-FLI-1 transcript was detected in five Ewing's sarcoma patients examined at the time of diagnosis. After complete remission, EWS-FLI-1 was still positive on RT-PCR in 3 patients, although BM pathological examination was negative in all cases. CONCLUSION: RT-PCR for EWS-FLI-1 is sensitive enough to detect minimal residual Ewing's sarcoma cells in the bone marrow. It can identify residual tumor cells in pathologically negative bone marrow specimens.

Bone Marrow Cells↗

[Major dissection after PTCA is a strong independent predictor of early luminal deterioration].

OBJECTIVE: To investigate the early natural course of dissection after PTCA and its relation to early luminal deterioration. METHODS: One hundred and five patients who underwent relook coronary arteriography within 24 hours of PTCA were retrospectively analyzed. The patients were subdivided into no dissection and type A, B, C, D, and E dissection. Minimal luminal diameter (MLD) was measured immediately after PTCA and at relook coronary arteriography. The changes were correlated with the severity of the dissections. RESULTS: Immediately after PTCA, the MLD in all 6 groups was > 2.0 mm. Except for type A dissection, the MLD, however, was deteriorated significantly at the relook coronary arteriography next day. The factors contributing to the deterioration were analyzed by covariance analysis, which showed a significant linear relation with the MLD immediately after PTCA and the type of dissection. Multivariate stepwise regression analysis was used to investigate if the patients' demographic factors and coronary lesion characteristics were also related to the MLD deterioration. The results showed that multivessel disease and the type of dissection were two independent risk factors of the MLD deterioration. CONCLUSION: Even if the results immediately after PTCA were acceptable, MLD will deteriorate over time. The degree of the deterioration was not only related to elastic recoil, but also to the type of dissection. Type C, D and E dissections were unstable, causing much more damage to the MLD than type A and B dissections, which mandated immediate stent implantation to prevent early luminal deterioration and late restenosis. Stent implantation was usually unnecessary in type A and B dissections. Multivessel disease was also involved in the process of the MLD deterioration. The mechanism is unclear, but might be related to coronary lesion characteristics.

Angioplasty, Balloon, Coronary↗

[Detection of minimal residual disease in childhood hematological malignancies and its clinical significance].

OBJECTIVE: Exploring the detection of minimal residual malignant cells in bone marrow from children with hematological malignancies to predict the prognosis. METHODS: Seventy-five patients with acute lymphoblastic leukemia (ALL), stage IV non-Hodgkin's lymphoma or stage IV neuroblastoma were studied. Complete remission was maintained for over 3 months before the detection. Minimal residual disease was detected by polymerase chain reaction (PCR) for IgH and TcRgamma rearrangements in lymphoid tumors by reverse transcriptase-polymerase chain reaction (RT-PCR) for neuroblastoma patients. RESULTS: Thirty five patients were positive for minimal residual disease, and 21 of them (60%) relapsed 3 - 40 months later, while only 7 (17%) negative patients relapsed (chi(2) = 12.59, P < 0.01). CONCLUSION: Minimal residual disease detection in bone marrow by PCR might predict prognosis in some childhood hematological malignancies.

Adolescent↗

[The effects of lipoproteins on human vascular endothelial gap junctional intercellular communication].

The effects of HDL, LDL and ascorbic acid on cultured human vascular endothelial gap junctional intercellular communication (GJIC) were observed using fluorescence recovery after photobleaching assay under confocal laser scanning microscopy in this study. The results showed that in culture, human vascular endothelial cells could produce functional gap junctions. The fluorescence recovery rates of the LDL group were 6.691 +/- 2.634, 4.153 +/- 2.125 and 2.441 +/- 0.720 respectively; when these rates were compared with the control and with each other, significant differences were found(P < 0.05). When the fluorescence recovery rates of the HDL group and Vitamin C group were compared with the control, no significant differences were found(P > 0.05). The fluorescence recovery rates of the LDL + HDL group were 3.500 +/- 0.890, 4.339 +/- 1.126 and 5.243 +/- 1.278(n = 15) respectively, when these rates were compared with the control and with each other, significant differences were found (P < 0.05). These suggested that LDL should be able to inhibit GJIC in human vascular endothelial cells, and the inhibition could be diminished by HDL or ascorbic acid. Inhibition of vascular endothelial GJIC may be one of the atherosclerogenic mechanisms of LDL, whereas HDL and ascorbic acid may be conducive to the improvement of endothelial GJIC. But it may also be only a compensatory behavior of endothelial cells to injuries.

Arteriosclerosis↗

[Response to milrinone treatment in patients with chronic congestive heart failure].

The objective of this study was to examine the efficacy of milrinone in chronic congestive heart failure. In this randomized, double-blind, placebo-controlled trial, 30 patients with class III or IV chronic congestive heart failure were randomly assigned to receive milrinone (n = 15) or placebo (n = 15). The results showed that in the milrinone group, stroke volume increased from 38.50 +/- 5.34 to 64.93 +/- 6.46 ml (P < 0.001), cardiac output increased from 3.39 +/- 0.42 to 5.28 +/- 0.55 L/min (P < 0.001), cardiac index increased from 2.01 +/- 0.42 to 3.21 +/- 0.57/min/m2 (P < 0.001) and ejection fraction increased from 0.23 +/- 0.05 to 0.35 +/- 0.06(P < 0.001). In the placebo group, no hemodynamic effects were found. Milrinone favourably influenced the symptoms and heart function in 11/15(73.3%) patients. In the placebo group, only 4/15(26.7%) patients had such response (P < 0.05). These data indicate that milrinone is effective for improving the hemodynamics status and heart function in patients with chronic heart failure.

Adolescent↗

[Effect of calcium on adherence of Streptococcus mutans MT6R(serotype c) surface protein P1].

OBJECTIVE: To study effects of calcium on the adherence of Streptococcus mutans MT6R(serotype c) surface protein P1 to saliva-coated hydroxyapatite(S-HA). METHODS: The surface protein P1 of Streptococcus mutans MT6R was purified by PAGE and labeled with 131I(131I-P1). The adherence amount of 131I-P1 to S-HA in different calcium concentration liquid was measured. RESULTS: The amount of 131I-P1 adherence to S-HA in 0, 0.1, 0.25, 0.5, 1.0, 1.5, 2.0 mmol/L, and calcium was 7175 + 183, 7516 + 192, 8850 + 215, 9335 + 204, 10087 + 228, 10179 + 224 and 10200 + 317 cpm, respectively(P < 0.01). The calcium concentration from 0 to 1.0 mmol/L, the amount of 131I-P1 adherence was increased statistically(P < 0.05), calcium concentration from 1.0 mmol/L to 2.0 mmol/L, the amount of 131I-P1 adherence was increased unstatistically(P > 0.05). CONCLUSION: Calcium promoted the adherence of surface protein P1 to the S-HA. This result suggested that calcium was involved in the adherence of Streptococcus mutans MT6R (serotype c) surface protein P1.

Bacterial Adhesion↗

[Transthoracic three-dimensional echocardiography for determination of left ventricular mass in patients with dilated cardiomyopathy].

This study was performed to compare left ventricular mass (LVM) measurement by one- (1D), two- (2D) and 3D echocardiography with magnetic resonance imaging (MRI) in patients with dilated cardiomyopathy (DCM). 36 patients with DCM underwent imaging by conventional 1D and 2D echocardiography as well as transthoracic 3D echocardiographic data acquisition. Also patients were imaged with cardiac MRI. LVM was determined. There was no significant correlation (r = 0.42, P > 0.05) for measuring LVM between 1D echocardiography and MRI in patients with DCM. A significant correlation was obtained between 2D echocardiography and MRI (r = 0.64, P < 0.01) and between 3D and MRI (r = 0.78, P < 0.01) in determination of LVM. Compared with 1D and 2D echocardiography, the 3D analysis achieved a significantly higher agreement with the MRI results (1D; 399.2 g, 2D: 285.9 g, 3D: 172.6 g versus MRI: 199.1 g). Interobserver variability was 5.1% for measuring LVM by 3D echocardiography. These results suggest that LVM of patients with DCM can be accurately determined by transthoracic 3D echocardiography and this method could be used in clinical practice.

Adolescent↗