Biomedical subjects

Hongyan Jiang

Publications and source records attributed to Hongyan Jiang.

7 recordsLinked to original sources

PubMed2006

Oxidative imbalance in the aging inner ear.

The mammalian inner ear loses its sensory cells with advancing age, accompanied by a functional decrease in balance and hearing. This study investigates oxidant stress in the cochlea of aging male CBA/J mice. Glutathione-conjugated proteins, markers of H2O2-mediated oxidation, began to increase at 12 months of age; 4-hydroxynonenal and 3-nitrotyrosine, products of hydroxyl radical and peroxynitrite action, respectively, were elevated by 18 months. Immunoreactivity to these markers was stronger in the supporting cells (Deiters and pillar cells) than the sensory cells and appeared later (23 months) in spiral ganglion cells and in the stria vascularis and spiral ligament. Conversely, antioxidant proteins (AIF) and enzymes (SOD2) decreased by 18 months in the organ of Corti (including the sensory cells) and spiral ganglion cells but not in the stria vascularis. These results suggest the presence of different reactive oxygen species and differential time courses of oxidative changes in individual tissues of the aging cochlea. An imbalance of redox status may be a component of age-related hearing loss.

Aging↗

PubMed2006

Kanamycin alters cytoplasmic and nuclear phosphoinositide signaling in the organ of Corti in vivo.

Aminoglycoside antibiotics strongly bind to phosphoinositides and affect their membrane distribution and metabolism. Kanamycin treatment also disrupts Rac/Rho signaling pathways to the actin cytoskeleton in the mouse inner ear in vivo. Here, we investigate the influence of kanamycin on phosphoinositide signaling in sensory cells (hair cells) of the mouse cochlea. Immunoreactivity to phosphatidylinositol-3,4,5-trisphosphate (PIP3) decreased in the organ of Corti, especially in outer hair cells, after 3-7 days of drug treatment, whereas imunoreactivity to phosphatidylinositol-4,5-bisphosphate (PIP2) increased. Immunoreactivity to PIP2 was present at the apical poles of outer hair cells, but appeared in their nuclei only after drug treatment. Furthermore, nuclear PIP2 formed a complex with histone H3 and attenuated its acetylation in outer hair cells. In agreement with reduced PIP3 signaling, phosphorylated Akt decreased in both the cytoplasm and nuclei of outer hair cells after kanamycin treatment. This study suggests that kanamycin disturbs the balance between PIP2 and PIP3, modifies gene transcription via histone acetylation and diminishes the PI3K/Akt survival pathway. These actions may contribute to the death of outer hair cells, which is a consequence of chronic kanamycin treatment.

Animals↗

PubMed2006

Rac/Rho pathway regulates actin depolymerization induced by aminoglycoside antibiotics.

Stress stimuli can lead to remodeling of the actin cytoskeleton and subsequent alteration of cell adhesion and permeation as well as cell functions and cell fate. We investigated redox-dependent Rho GTPase-linked pathways controlling the actin cytoskeleton in the inner ear of the CBA mouse, by using aminoglycoside antibiotics as a noxious stimulus that causes loss of sensory cells via the formation of reactive oxygen species. Kanamycin treatment in vivo interfered with the formation of F-actin, disturbed the arrangement of beta-actin in the stereocilia of outer hair cells, and altered the intermittent adherens junction/tight junction complexes between outer hair cells and supporting cells. The drug treatment also activated Rac1 and promoted the formation of the complex of Rac1 and p67phox while decreasing the activity of RhoA and reducing the formation of the RhoA/p140mDia complex. In inner-ear-derived cell lines, expression of mutated Rac1 changed the structural arrangement of F-actin and diminished the immunoreactivity of p140mDia. These findings suggest that actin depolymerization induced by kanamycin is mediated by Rac1 activation, followed by the formation of superoxide by NADPH oxidase. These changes will ultimately contribute to aminoglycoside-induced loss of hair cells.

Actins↗

PubMed2005

Light-induced shape-memory polymers.

Materials are said to show a shape-memory effect if they can be deformed and fixed into a temporary shape, and recover their original, permanent shape only on exposure to an external stimulus. Shape-memory polymers have received increasing attention because of their scientific and technological significance. In principle, a thermally induced shape-memory effect can be activated by an increase in temperature (also obtained by heating on exposure to an electrical current or light illumination). Several papers have described light-induced changes in the shape of polymers and gels, such as contraction, bending or volume changes. Here we report that polymers containing cinnamic groups can be deformed and fixed into pre-determined shapes--such as (but not exclusively) elongated films and tubes, arches or spirals--by ultraviolet light illumination. These new shapes are stable for long time periods, even when heated to 50 degrees C, and they can recover their original shape at ambient temperatures when exposed to ultraviolet light of a different wavelength. The ability of polymers to form different pre-determined temporary shapes and subsequently recover their original shape at ambient temperatures by remote light activation could lead to a variety of potential medical and other applications.

Journal Article↗

PubMed2005

NF-kappaB pathway protects cochlear hair cells from aminoglycoside-induced ototoxicity.

Cell death in outer hair cells of the mammalian inner ear induced by aminoglycoside antibiotics is mediated by reactive oxygen species (ROS) and can be prevented by antioxidants. The current study investigates the role of the nuclear factor (NF)-kappaB pathway in cell death or survival in adult CBA mice. Kanamycin (700 mg/kg subcutaneously, twice per day) progressively destroys hair cells but after 7 days of treatment auditory function and morphology are not yet affected significantly, permitting investigations of early events in drug-induced cell death. Immunostaining for 4-hydroxynonenal, indicative of lipid peroxidation, was elevated in the cochlea, but there was no effect on nitrotyrosine, a marker for peroxynitrite. NF-kappaB was increased at 3 hr, 3 days, and 7 days of treatment, with p50 and p65 proteins as its most abundant subunits. Immunoreactivity for p50 was present in nuclei of inner hair cells and supporting cells that survive the drug treatment. In contrast, nuclei of outer hair cells were devoid of label. Concomitant injections of antioxidants, however, such as 2,3-dihydroxybenzoic acid or salicylate (which prevent cell death induced by kanamycin), promoted the translocation of NF-kappaB into the nuclei of outer hair cells. In addition, kanamycin treatment decreased tyrosine phosphorylation of the inhibitory IkappaBalpha protein, leading to increased IkappaBalpha levels in the cochlea; the effect was reversed by cotreatment with antioxidants. These results suggest that changes in the redox state of the cochlea stimulate the activation of NF-kappaB and that this activation is cell protective.

Aldehydes↗

PubMed2002

[The expression of transforming growth factor alpha, beta 1 in hyperplastic tissue after endoscopic polypectomy and the effect of corticosteroid].

OBJECTIVE: To study the expression of transforming growth factor alpha, beta 1 in hyperplastic tissue after endoscopic polypectomy and the effect of corticosteroid. METHOD: Forty patients with nasal polyps were divided into two groups randomly: corticosteroid group (n = 20) with topical application of Budesonide (BUD, 400 micrograms/d) after endoscopic polypectomy and control group (n = 20) without corticosteroid after surgery. The hyperplastic tissues in operative cavity obtained in the 1st and 8th weeks after operation were studied with HE staining and immunohistochemistry technique respectively. RESULT: Morphological changes of hyperplastic tissue after endoscopic polypectomy included pseudostratified epithelium, highly edematous lamina proper and inflammatory cells infiltration, in which the main infiltrative cells were eosinophils (67.5%). Transforming growth factor alpha(TGF alpha) protein was highly expressed in epithelial cells, grand cells and inflammatory cells in the hyperplastic tissue. Transforming growth factor beta 1 (TGF beta 1) protein was highly expressed in inflammatory cells in the hyperplastic tissue. The expression of TGF alpha and beta 1 was significantly decreased after topical BUD spray (P < 0.01, 0.05). CONCLUSION: Transforming growth factor alpha and beta 1 may play an important role in the formation and recurrence of nasal polyps.

Adult↗

PubMed2002

[Dyspnea analyse and treatment to adult acute epiglottitis].

OBJECTIVE: To discuss the estimation and treatment of adult acute epiglottitis dyspnea. METHOD: 126 adult with acute epiglottitis patients were analyzed. RESULT: None of 30 patients undergone epiglotiotomy had asphyxia, inflammation diffuse or serious hemorrhage. 8 patients undergone tracheotomy, one patient undergone thyroericotomy but died. One of 87 patients with conservative treatment died. CONCLUSION: Gaspping, salivating and dyslogia are symbols of severe larynx obstruction. Fibrous laryngoscope is the best way of examine. Keeping respiratory path open and eliminating epiglottis swelling is the key of treatment.

Acute Disease↗