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Biomedical subjects

D Huang

Publications and source records attributed to D Huang.

At least 55 records · Page 3Linked to original sources

[Confirmation of patulous eustachian tube syndrome by Tubo-tymanoaerodynamic graphy].

OBJECTIVE: To compare the advantage of tympanogram, Morimitsu's method and Tubotymanoaerodynamic graphy (TTAG) in the confirmation of patulous eustachian tube syndrome. METHOD: Twenty ears with patulous eustachian tube syndrome diagnosed clinically were selected. The tympanogram, Morimitsu's method and TTAG were examined in these ears and the positive rate was estimated. RESULT: The confirmation of patulous eustachian tube syndrome by tympanogram, Morimitsu's method and TTAG was 5, 12 and 20 ears in 20 ears with patulous eustachian tube syndrome. The positive rate was 25%, 60% and 100% respectively. TTAG also was useful in following-up. CONCLUSION: TTAG is an important method for diagnosis and following-up in patulous eustachian tube syndrome.

Acoustic Impedance Tests↗

[Role of epithelial cell proliferation and apoptosis in human middle ear cholesteatoma].

OBJECTIVE: To determine the role of middle ear epithelial cell proliferation and apoptosis in the pathogenesis of human cholesteatoma. METHOD: 33 cholesteatoma, 25 auditory meatal skin of cholesteatoma and 10 normal human auditory meatal skin were detected by using immunohistochemistry analysis for cell proliferation with Ki 67, PCNA and PCNA antibody and TUNTEL methods for cell apoptosis. RESULT: PCNA expression and apoptosis cells exists different quantity in cholesteatoma, auditory metal skin of cholesteatoma and normal human auditory meatal skin and distributes in various cell layer. There were positive correlation between p53 and PCNA as well as negative correlation between p53 and apoptosis. CONCLUSION: The dyregulation of proliferation and apoptosis in keratinocyte is important in pathogenesis of cholesteatoma.

Adolescent↗

[Some biological characteristics of genetically engineered insecticidal Pseudomonas fluorescens].

Plasmid stability, Antifungal activity, plant-colonizing ability, UV resistance and inseticidal activity in field were analysed for the engineered Pseudomonas fluorescens (Pf) strain IPP202. The results indicated that the recombinant plasmid in IPP202 was very stable after successive diluting culturing and after continuous culturing, There was no significant change in the properties beneficial to plants, such as antifungal activity and plant-colonizing ability as compared with the original strain P303. IPP202 was much more resistant to UV than Bt strain HD73. The control effect in field against cotton boll worm in field was close to that of a locally used Bt-chemical mixture in normal applied concentration. All the data indicated that the engineered Pf strain was a one with prosperous future after further study.

Animals↗

[The orientation and its significance of water channel protein in the mouse inner ear].

OBJECTIVE: To examine the distribution of various subtypes of water channel protein (aquaporin, Aqp) in various structures of the mouse inner ear. METHODS: Thirty mice with white color were used in this study and were cardiacally perfused. The temporal bones were taken out and were processed and sectioned by paraffin-embedded technique. The sections were labeled with fluorescent antibody by immunohistochemical method. The distribution of Aqp1, 3, 4, 5, 7, 9 were confirmed in the inner ear of mouse. RESULTS: The constant and clear fluorescent reaction could be observed in the inner ear tissue with the first antibody concentration of 1:200 for Aqp-1 and 1:100 for Aqp-3, 7, 9. But the reaction of Aqp-4 and 5 could not be found with the concentration of 1:50, even 1:30. Aqp-1 was labeled in the round window membrane, spiral ligament, endolymphatic sac and duct, utricle and saccule and the wall of inner ear blood vessel; Aqp-3 in the spiral limb, vestibular lip, internal and external sulci, basilar membrane and basilar membrane crest, endolymphatic sac and duct, membranous semicircular canal and utricle and saccular macula; Aqp-7 in the stria vascularis, basilar membrane, Reissner's membrane, utricle and saccule and their maculae; Aqp-9 in the spiral limb, vestibular lip internal and external sulci, Reissner's membrane, membranous semicircular canal, saccule and its macula. CONCLUSION: Aqp-1, 3, 7, 9 were extensively distributed in various tissues of mouse inner ear. Their distribution sites and reaction degree were different, and mainly located in the structures related to the endolymph.

Animals↗

[Multiple factors analysis of intraoperative bleeding and recurrence of juvenile nasopharyngeal angiofibromas].

OBJECTIVE: To study the effect of surgical treatment of juvenile nasopharyngeal angiofibromas and the factors influencing intra-operative bleeding and recurrence. METHODS: Thirty-four patients with juvenile nasopharyngeal angiofibromas treated surgically in Chinese PLA General Hospital between 1986 and 1999 were studied retrospectively. The relationship between surgical treatment, intraoperative bleeding, recurrence and age, duration, staging, preoperative treatment, times of previous operation, operative approaches was statistically analyzed. RESULTS: The tumors were totally resected in 30 patients, and five patients(16.7%) recurred during a mean follow-up of 77 months. The mean recurrence time after operation was 3.2 months (1-6 months). The amount of intraoperative bleeding correlated well with the age, duration, staging, preoperative treatment, and surgical approaches (P < 0.05), but not with times of previous operation (P > 0.05). Recurrence was not correlated with the age, duration, preoperative treatment and surgical approaches (P > 0.05), but correlated with staging (P < 0.05). CONCLUSION: The factors significantly influencing the intraoperative bleeding were the age, duration and staging. Recurrence was correlated with the tumor stages, incomplete resection or the exceedingly malignant activity of the tumor. Radiotherapy, with a dose of 30Gy, is an adjuvant therapy for incompletely resected, or residual tumors.

Adolescent↗

[The role of fibrinolysis in pathogenesis of middle ears adhesions].

OBJECTIVE: To investigate the role of fibrinolysis in pathogenesis of middle ears adhesions. METHODS: The amount of Tissue-type Plasminogen Activator (tPA) of 28 sections from 6 ears with adhesive otitis media (AOM) and of 22 sections from 6 normal ears was examined by Super Sensitive Biotin-Streptavidin (SSBSA) method. Amount of Fibrin of 11 sections from 3 ears with significant adhesions was compared with that of 12 sections from 3 normal ears. Qualitative analysis of light microscopy with computer-assisted image system was employed. RESULTS: In adhesive ears, tPA stains were negative in 11 of 28 sections and faint positive were 10 of 28 sections, while Fibrin stains were positive in 6 of 11 sections and strong positive were in 3 of 11 sections. In normal ears, tPA stains positive were in 8 of 22 sections and strong positive were 10 of 22 sections, meanwhile, fibrin stains were negative in 8 of 12 sections and faint positive were in 3 of 12 sections. Quantitative analysis showed that the amount of tPA was 16.70 +/- 5.11 and 39.84 +/- 6.26 in ears with AOM and normal ones respectively (P < 0.05). CONCLUSION: In adhesive ears the amount of tPA was less than that in the normal ears, whereas, the amount of Fibrin was greater in ears with AOM than that in normal ears. It indicates that fibrinolysis involved in the process of adhesion formation of AOM, which may acts as a key factor.

Fibrin↗

[Surgical treatment of craniofacial recurrent carcinoma].

OBJECTIVE: The patients with craniofacial recurrent cancers after the radiation, chemical and operative therapies were often not able to get effective treatment because their lesions involved in the nervous and vascular structure and the re-radiation therapy was not suitable or chemical therapy was not sensitive to the tumor as well. To improve their survival quality, prevent the fatal complication and prolong their life, the surgical treatment for them was advised. METHOD: Six patients were treated surgically. According to the lesion of extension and position, the different incisions were respectively made. The neoplasms of these patients were resected piece by piece because they usually involved in the important structures, such as the internal carotid artery and cavernous sinus. Then, local defect was repaired with different methods on basis of the individual condition. So, this type of operation could be called as non-defined operation. RESULTS: The lesions in all 6 patients invaded the eye, meninges and encephala, skull base, cavernous sinus and other important structures. After surgical intervene, the patients were all more than one year survival except for one of the patients who died of serous bleeding with corrupted rupture of internal carotid artery. Three patients survived for 4, 5 and 12 years, respectively. CONCLUSION: The craniofacial recurrent carcinomas in late stage could be resected by the non-defined operation, which could prolong the patients life and achieve the desired effect.

Adult↗

[Rat hearing loss and hearing organs mitochondrial DNA4834 deletions associated with hypercholesteremia].

OBJECTIVE: To determine whether or not the rat hypercholesteremia contributes to hearing organs mtDNA4834 deletion and involves in the development of hearing loss. METHODS: The rat hypercholesteremia model (n = 38) was established by feeding with high cholesterol diet and the control group (n = 22) with common diet for 6 months. The rats were tested for auditory sensitivity using auditory brainstem response (ABR). Twenty-one left cochleae and 27 left cochlear nuclei from experimental group and 10 left cochleae and 13 left cochlear nuclei from control group were harvested. The total DNA of them was extracted. mtDNA was amplified by nest PCR to examine the presence of mtDNA4834 deletion. RESULTS: Our result showed: (1) There is a significant increase in serum cholesterol level and ABR threshold in the experimental group. (2) The mitochondrially-encoded tRNA and ND1 segments were amplified from all samples, as well as mtDNA4834 deletions. (3) The incidence of mtDNA4834 deletions in hearing organs of hypercholesteremia rats was significantly higher than that of the control group (P < 0.05). CONCLUSION: Extended hypercholesteremia can induce hearing loss, and mtDNA4834 deletion in hearing organs may be one of the pathogenic mechanisms.

Animals↗

MYCN expression is not prognostic of adverse outcome in advanced-stage neuroblastoma with nonamplified MYCN.

PURPOSE: The clinical significance of MYCN expression in children with neuroblastoma (NB) remains controversial. To determine the prognostic significance of MYCN expression in the absence of MYCN amplification, we analyzed MYCN mRNA and protein expression in tumors from 69 patients. PATIENTS AND METHODS: Sixty-nine NB tumor samples with nonamplified MYCN from patients with stage C or D disease were obtained from the Pediatric Oncology Group Neuroblastoma Tumor Bank. MYCN mRNA was analyzed using a real-time reverse transcriptase polymerase chain reaction assay, and MYCN protein was examined by Western blot analyses. RESULTS: The estimated 5-year event-free survival (EFS) and survival (S) rates plus SE for the cohort were 57% +/- 17% and 60% +/- 16%, respectively. Infants younger than 1 year had significantly higher rates of EFS and S than children >/= 1 year of age (P =.003 and P <.001, respectively); patients with stage C disease had better outcome than those with stage D NB (P <.001); and patients with hyperdiploid tumors had better outcome than those with diploid NB (P <.001). Surprisingly, outcome was slightly better for patients with high versus low levels of MYCN mRNA expression (4-year S, 70% +/- 13% v 50% +/- 16%; P =.290), and for patients with tumors that expressed MYCN protein (4-year S, 73% +/- 19% v 53% +/- 15%, respectively; P =.171). CONCLUSION: High levels of MYCN expression are not prognostic of adverse outcome in patients with advanced-stage NB with nonamplified MYCN. A trend associating high levels of MYCN expression with improved outcome was observed.

Blotting, Western↗

Correlation of mutations of the SH2D1A gene and epstein-barr virus infection with clinical phenotype and outcome in X-linked lymphoproliferative disease.

The purposes of this study were to determine the frequency of mutations in SH2D1A in X-linked lymphoproliferative disease (XLP) and the role of SH2D1A mutations and Epstein-Barr virus (EBV) infection in determining the phenotype and outcome of patients with XLP. Analysis of 35 families from the XLP Registry revealed 28 different mutations in 34 families-large genomic deletions (n = 3), small intragenic deletions (n = 10), splice-site (n = 3), nonsense (n = 3), and missense (n = 9) mutations. No mutations were found in 25 males, so-called sporadic XLP (males with an XLP phenotype after EBV infection but no family history of XLP) or in 9 patients with chronic active EBV syndrome. Of 304 symptomatic males in the XLP Registry, 38 had no evidence of EBV infection at first clinical manifestation. When fulminant infectious mononucleosis (FIM) was excluded, there was no statistical difference in the frequency of EBV infectivity in the other XLP phenotypes. Furthermore, there was no difference at age of first clinical manifestation between EBV(+) and EBV(-) males or in survival when patients with FIM were excluded. In conclusion, it was found that mutations in the SH2D1A gene are responsible for XLP but that there is no correlation between genotype and phenotype or outcome. It was also found that though EBV infection often results in FIM, it is unnecessary for the expression of other manifestations of XLP, and it correlates poorly with outcome. These results suggest that unidentified factors, either environmental or genetic (eg, modifier genes), contribute to the pathogenesis of XLP.

Alternative Splicing↗

Schwann cell-conditioned medium inhibits angiogenesis.

Neuroblastomas are biologically heterogeneous tumors that consist of two main cell populations: neuroblastic/ganglionic cells and Schwann cells. The amount of Schwannian stroma strongly impacts prognosis, and favorable outcome is associated with tumors that are Schwannian stroma rich/stroma dominant. At the present time, there is controversy regarding the origin of Schwann cells in neuroblastoma tumors. However, recent studies have suggested that the Schwann cells in mature neuroblastoma tumors may be normal cells that produce soluble substances that enhance the survival and differentiation of neuroblastoma cell lines. Previously, we reported that in neuroblastoma, high vascular index correlated with clinically aggressive disease. In contrast, tumors with favorable histology and abundant Schwannian stroma had low tumor vascularity. As a first step toward investigating whether Schwann cells also play a role in inhibiting angiogenesis in neuroblastoma tumors, we examined the ability of conditioned medium collected from normal human Schwann cells to affect basic fibroblast growth factor- and vascular endothelial growth factor-induced endothelial cell proliferation and migration and in vivo angiogenesis. In vitro angiogenesis assays were also performed with conditioned medium collected from Schwann cells derived from a Schwannian stroma-dominant neuroblastoma tumor. Our results indicate that Schwann cells derived from either adult nerve or tumor tissue produce a potent inhibitor(s) of angiogenesis. Expression studies revealed tissue inhibitor of metalloproteinase (TIMP)-2 in conditioned medium collected from both normal and tumor-derived Schwann cells. In addition, TIMP-2 was detected in the cytoplasm of Schwann cells and ganglion cells in stroma-rich/stroma-dominant neuroblastoma tumors by immunohistochemistry studies. We postulate that the low level of vascularity and more benign clinical behavior of Schwannian stroma-rich/stroma-dominant neuroblastoma tumors result from the Schwann cell production of TIMP-2 and/or other inhibitors of angiogenesis.

Adult↗

Differential ligand-dependent protein-protein interactions between nuclear receptors and a neuronal-specific cofactor.

Nuclear receptors are transcription factors that require multiple protein-protein interactions to regulate target gene expression. We have cloned a 27-kDa protein, termed NIX1 (neuronal interacting factor X 1), that directly binds nuclear receptors in vitro and in vivo. Protein-protein interaction between NIX1 and ligand-activated or constitutive active nuclear receptors, including retinoid-related orphan receptor beta (RORbeta) (NR1F2), strictly depends on the conserved receptor C-terminal activation function 2 (AF2-D). NIX1 selectively binds retinoic acid receptor (RAR) (NR1A) and thyroid hormone receptor (TR) (NR1B) in a ligand-dependent manner, but does not interact with retinoid X receptor (RXR) (NR2B) or steroid hormone receptors. Interestingly, NIX1 down-regulates transcriptional activation by binding to ligand-bound nuclear receptors. A 39-aa domain within NIX1 was found to be necessary and sufficient for protein-protein interactions with nuclear receptors. Northern blot analysis demonstrates low-abundance RNA messages only in brain and neuronal cells. In situ hybridization and immunohistochemistry revealed that NIX1 expression is restricted to the central nervous system and could be confined to neurons in the dentate gyrus of the hippocampus, the amygdala, thalamic, and hypothalamic regions. In summary, protein-protein interactions between the neuronal protein NIX1 and ligand-activated nuclear receptors are both specific and selective. By suppressing receptor-mediated transcription, NIX1 implements coregulation of nuclear receptor functions in brain.

3T3 Cells↗

Dinucleotide repeat expansion in the CTLA-4 gene leads to T cell hyper-reactivity via the CD28 pathway in myasthenia gravis.

CD28 is required to promote T cell proliferation and cytokine production, while the cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) functions as a negative modulator for T cell activation. We previously reported that alleles with longer PCR products (designated as allele xx) in an (AT)n polymorphism in Ctla-4 are associated with myasthenia gravis with thymoma, while the shortest allele, 86, is negatively associated with the disease. Here, we demonstrate that serum IL-2 sRalpha increases parallel to the length of (AT)n in Ctla-4. Periphereal blood mononuclear cells (PBMC) from patients with Ctla-4 xx/xx contained higher activity of telomerase than patients bearing Ctla-4 86/86. Blockade of CTLA-4 increased the telomerase activity in PBMC stimulated by acetylcholine receptor in vitro. There was a positive correlation between the expression of CD28 and CTLA-4 on anti-CD3 activated PBMC, suggesting a balance between CD28 and CTLA-4. Cells from patients with Ctla-4 xx/xx had the highest level of T cell proliferative responses upon the addition of anti-CD28 antibodies to the anti-CD3 containing culture system while cells from patients with Ctla-4 86/xx had an intermediate and cells from patients with Ctla-4 86/86 the lowest increase. The current results point to the (AT)n in Ctla-4 as a myasthenia gravis facilitating mutation under certain permissive environments by influencing the T cell reactivity via the CD28 pathway.

Abatacept↗

Structural distortions in mer-M(H)3(NO)L2 (M = Ru, Os) and their influence on intramolecular fluxionality and quantum exchange coupling.

Molecules of the type mer-M(H)3(NO)L2 [M = Ru (1), Os (2); L = PR3] are characterized on the basis of 1H NMR T1min values and IR spectra as pseudo-octahedral trihydrides significantly distorted by compression of the cis H-M-H angles to approximately 75 degrees. The distortion, uncharacteristic of six-coordinate d6 complexes, is rationalized with DFT (B3LYP) calculations as being driven by increased H-to-M sigma donation and by the exceptional pi-accepting ability of linear NO+. In both 1 and 2, hydrides undergo intramolecular site exchange with delta HHH++(1) = 10-11 kcal/mol and delta HHH++(2) = 16-20 kcal/mol, depending on L, whereas for mer-Ru(H)3(NO)(PtBu2Me)2 (1b), moderate exchange couplings (up to 77 Hz) are featured in the low-temperature 1H NMR spectra, in addition to chemical exchange. On the basis of experimental and theoretical results, a dihydrogen intermediate is suggested to mediate hydride site exchange in 1. The cis H-M-H distortion shortens the tunneling path for the exchanging hydrides in 1, thereby increasing the tunneling rate; diminishes the "conflict" between trans hydrides in the mer geometry; and decreases the nucleophilicity of the hydrides. The generality of the observed structural distortion and its dependence on the ligand environment in late transition metal tri- and dihydrides are discussed. A less reducing metal center is generally characterized by greater distortion.

Journal Article↗

Leptin induces insulin-like signaling that antagonizes cAMP elevation by glucagon in hepatocytes.

Although many effects of leptin are mediated through the central nervous system, leptin can regulate metabolism through a direct action on peripheral tissues, such as fat and liver. We show here that leptin, at physiological concentrations, acts through an intracellular signaling pathway similar to that activated by insulin in isolated primary rat hepatocytes. This pathway involves stimulation of phosphatidylinositol 3-kinase (PI3K) binding to insulin receptor substrate-1 and insulin receptor substrate-2, activation of PI3K and protein kinase B (AKT), and PI3K-dependent activation of cyclic nucleotide phosphodiesterase 3B, a cAMP-degrading enzyme. One important function of this signaling pathway is to reduce levels of cAMP, because leptin-mediated activation of both protein kinase B and phosphodiesterase 3B is most marked following elevation of cAMP by glucagon, and because leptin suppresses glucagon-induced cAMP elevation in a PI3K-dependent manner. There is little or no expression of the long form leptin receptor in primary rat hepatocytes, and these signaling events are probably mediated through the short forms of the leptin receptor. Thus, leptin, like insulin, induces an intracellular signaling pathway in hepatocytes that culminates in cAMP degradation and an antagonism of the actions of glucagon.

3',5'-Cyclic-AMP Phosphodiesterases↗

Schwann cell-conditioned medium inhibits angiogenesis in vitro and in vivo.

BACKGROUND: Neuroblastomas are biologically heterogeneous tumors that consist of two main cell populations: neuroblastic/ganglionic cells and Schwann cells. The amount of Schwannian stroma strongly impacts prognosis. Low tumor vascularity, localized stage, and favorable outcome are associated with tumors that are Schwannian stroma-rich/stroma-dominant. PROCEDURE: To investigate if Schwann cells play a role in inhibiting angiogenesis in neuroblastoma tumors, we examined the ability of human Schwann cell-conditioned medium to affect bFGF- and VEGF-induced endothelial cell proliferation and migration, and in vivo angiogenesis. RESULTS: Schwann cell-conditioned medium significantly inhibited bFGF- and VEGF-induced endothelial cell proliferation and migration. This effect appears to be specific for endothelial cells as smooth muscle cell and fibroblast proliferation were not inhibited by this medium. Schwann cell-conditioned medium also inhibited in vivo angiogenesis in rat corneal assays. CONCLUSIONS: Schwann cells produce a potent inhibitor(s) of angiogenesis that may be responsible for the low level of vascularity and more benign clinical behavior of Schwannian stroma-rich/stroma-dominant neuroblastoma tumors. Studies to identify the inhibitor(s) are ongoing.

Cell Division↗