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Biomedical subjects

X Zhou

Publications and source records attributed to X Zhou.

At least 181 records · Page 10Linked to original sources

[Gentamicin for the transtympanic treatment of Menière's disease].

OBJECTIVE: This study described the method and efficacy of intratympanic gentamicin injection for obstinated, incapacitated Meniere's disease. METHOD: It is a prospective study. Patients selected had classic unilateral Meniere's disease. All had preinjection audiometric and electronystagmography. Injection was accepted every two or three days. It is important to direct the therapy by observing the symptoms closely and checking the audiometric and electronystagmography whenever necessary. RESULT: All the 12 cases undergone the treatment were followed up from 2 to 9 years. According to the criterion of Chinese Medical Association of ENT, the vertigo of Meniere's disease was evaluated. A (completed control): 10 cases; B (largely control): 2 cases. 4 cases said their tinnitus disappeared and 3 cases felt it improved. Hearing loss and vibration illusion vision are two complications. CONCLUSION: The methods is simple, useful and safe, the effect of which is similar to vestibular neurectomy. It is the first choice therapy suitable to Meniere's disease patients, which symptoms keep unchanged after medical treatment or failed in surgery.

Adult↗

[The effects of adenosine, interleukin-1 and theophylline on the expression of A2 adenosine receptor mRNAs in peripheral blood mononuclear cells from asthmatic patients].

OBJECTIVE: To explore the roles of A2a and A2b adenosine receptors(A2aAR and A2bAR) in the pathogenesis of bronchial asthma. METHODS: Eleven asthmatics and 11 healthy subjects were included in this investigation. Peripheral blood mononuclear cells(PBMCs) were obtained after density centrifugation on Ficoll-Hypaque. The expression of A2aAR and A2bAR mRNAs in PBMCs was examined by use of the reverse transcription-polymerase chain reaction (RT-PCR) and image pattern analysis semiquantitation method. RESULTS: The expression of A2aAR mRNA in PBMCs from asthmatics was not enhanced, compared with that of healthy subjects(P > 0.05). Adenosine or IL-1 or theophylline was not observed to have effect on A2aAR mRNA (P > 0.05). A2bAR gene expression in PBMCs was more markedly in patients with asthma than in normal individuals (P < 0.05). Adenosine and IL-1 significantly increased A2bAR mRNAs in asthmatics. Theophylline inhibited A2bAR gene expressions. The expression of A2bAR mRNA in PBMCs was positively correlated to serum total immunoglobulin E (TIgE) level in asthmatics (r = 0.72, P < 0.01). The expressions of A2bAR mRNA elevated by adenosine or IL-1 were correlated positively with serum TIgE(r = 0.78 or r = 0.61; P < 0.05) and negatively with the forced expiratory volume in first second to predicted value ratio (FEV1%) (r = -0.62 or r = -0.81; P < 0.05) in asthmatics. CONCLUSION: These results indicated that the expression of A2bAR mRNAs in PBMCs was more remarkable in asthmatics than in healthy subjects; that adenosine or IL-1 potentiated the mRNA expression of A2bAR in PBMCs in asthmatic patients, which was correlated with allergy state and the degree of airway obstruction; and that theophylline might antagonize adenosine by inhibiting A2bAR mRNA.

Adenosine↗

[Measurement of nerve growth factor in the nasal mucosa of experimental allergic rhinitis].

OBJECTIVE: To investigate the role of nerve growth factor in the development of allergic rhinitis. METHODS: Animal model of allergic rhinitis was established in rat, the content of nerve growth factor in the nasal mucosa was measured using enzyme-linked immunosorbent assay (ELISA) technique. RESULTS: The content of nerve growth factor significantly (P < 0.001) increased in the nasal mucosa of experimental allergic rhinitis (6.65 +/- 0.42) ng/g wet weight, compared with that in control animals (3.51 +/- 0.29) ng/g wet weight. CONCLUSION: Nerve growth factor may play an important role in the development of allergic rhinitis by regulating expression and release of neuropeptides and/or by activating immune cells such as mast cells.

Animals↗

[Synthesis and ultraviolet-visible spectrum of two new symmetrical porphyrins].

Meso-tetra(p-benzoylaminophenyl) porphyrin or meso-tetra (o-benzoylaminophenyl) porphyrin are synthesized by condensation of meso-tetra (p-aminophenyl) porphyrin or meso-tetra (o-aminophenyl) porphyrin and benzoyl chloride in DMF using NaOH as catalyst, these porphyrins and the method have not been reported previously. Their structures are ascertained by elemental analysis, ultraviolet-visible spectrum, IR and 1H-NMR measurements. The ultraviolet-visible spectrum of the two porphyrins is discussed in detail.

Molecular Structure↗

[Pulmonary surfactant impairment in the development of ventilator-induced lung injury in rats].

OBJECTIVE: To evaluate whether pulmonary surfactant (PS) impairment plays a role in the development of ventilator-induced lung injury (VILI). METHODS: Thirty-two healthy adult Sprague-Dawley rats were randomly allocated to four groups ( n = 8, each group ) and mechanically ventilated (MV). (1) P7 group: with settings [expressed as peak inspiratory pressure (PIP, cm H2O)/frequency (cpm)/inspiratory:expiratory ratio/positive end expiratory pressure (PEEP, cm H2O)] of 7/40/1:1/0, (2) P45 group: with settings of 45/ 20/1:1/0, (3) PS group: 100 mg/kg of a porcine PS administered intra-tracheally and with the same settings as P45 group, (4) PEEP group: with settings of 45/20/1: 1/10. After 20 minutes of MV, all animals were killed. Another 8 animals were killed immediately after surgical procedure to serve as nonventilated controls (CON group). Arterial blood O2 partial pressure (PaO2) and maximum thorax-lung compliance (C(max)) were measured, and total proteins (TP), total phospholipids (TPL), small and large aggregates (SA, LA), and minimum surface tension (ST min) of bronchoalveolar lavage fluid (BALF) were analyzed. RESULTS: P45 group had decreased PaO2, C(max), TPL/TP all P < 0.01), increased TP, SA/LA and ST min of ABLF (all P < 0.01) as compared with P7 group. Both PS group and PEEP group had improved PaO2, C(max), BALF analyses as compared with P45 group (P < 0.05 or P < 0.01). There was no significant difference between P7 group and CON group in any parameter described above. CONCLUSIONS: A short period of mechanical ventilation with high PIP alone can cause VILI in rats that is associated with PS impairment; both exogenous PS and PEEP can restore or preserve alveolar space PS composition and function, attenuate abnormalities of lung oxygenation and mechanics, indicating PS impairment may play an important role in the development of VILI.

Animals↗

[A clinical trial of oxymatrine in treating chronic viral hepatitis type B].

OBJECTIVE: To investigate the therapeutic effect of oxymatrine on chronic viral hepatitis type B. METHODS: 303 patients were randomly allocated either to a treatment group or a control group. The treatment group consisted of 253 patients treated with intravenous or intra-muscular injection of oxymatrine and oral oxymatrine capsule. Oral tiopronin was used in the control group. RESULTS: At the end of treatment, the rate of normal ALT was similar among the different groups. The rate of normal ALT was 53.3% - 58.3% in the three oxymatrine groups six months after the end of treatment. It was higher than that of the tiopronin group (P < 0.05). After a follow up of six months, the rate of negative HBeAg was 30.0% - 40.9% in the three oxymatrine groups. It was higher than that of the tiopronin group (16.7%). The rate of negative HBV DNA was 39.2% - 49.5% in the three oxymatrine groups. It was also higher than that of the tiopronin group. CONCLUSION: Oxymatrine can improve the liver function and increase the negative rate of HBeAg and HBV DNA in the patients with chronic hepatitis B. The therapeutic effect of oxymatrine will persist after the cessation of administration.

Adolescent↗

Histone deacetylase 4 associates with extracellular signal-regulated kinases 1 and 2, and its cellular localization is regulated by oncogenic Ras.

Histone deacetylase 4 (HDAC4) is a member of a family of enzymes that catalyze the removal of acetyl groups from core histones, resulting in a compact chromatin structure that is generally associated with repressed gene transcription. Protein phosphorylation has been implicated in the regulation of the corepressor activity of the deacetylase. Here we report that serine/threonine kinases are found in association with HDAC4 and phosphorylate HDAC4 in vitro, and HDAC4 is phosphorylated in cells. The extracellular signal-regulated kinases 1 and 2 (ERK1/2), also known as p44(MAPK) and p42(MAPK), respectively, are two of the kinases associated with HDAC4. ERK1/2 are components of the Ras-mitogen-activated protein kinase (MAPK) signal transduction pathway. Activation of the Ras-MAPK pathway by expression of oncogenic Ras or constitutively active MAPK/ERK kinase 1 results in an increased percentage of cells (from approximately 10% to approximately 70%) that express HDAC4 in the nucleus in C2C12 myoblast cells. In cells transfected with oncogenic Ras, nuclear HDAC4 is associated with kinase activity. Our results provide evidence that protein kinase activity is present in a protein complex with HDAC4 and directly links the Ras-MAPK signal transduction pathway to a mechanism for chromatin remodeling (i.e., histone deacetylation).

Animals↗

A role for CD21/CD35 and CD19 in responses to acute septic peritonitis: a potential mechanism for mast cell activation.

Although it is now appreciated that mast cell-mediated release of TNF-alpha is critical for resolution of acute septic peritonitis, questions remain as to how mast cells are activated upon peritoneal bacterial infection. Clues to how this may occur have been derived from earlier studies by Prodeus et al. in which complement proteins C3 and C4 were shown to be required for survival following cecal ligation and puncture (CLP), a model for acute septic peritonitis. To evaluate the mechanism for mast cell activation in the CLP model, complement receptor CD21/CD35-deficient mice (Cr2(null)) were examined in the present study. Along with CD19-deficient (CD19(null)) mice, these animals exhibit decreased survival following CLP compared with wild-type littermates. Injection of IgM before CLP does not change survival rates for Cr2(null) mice and only partially improves survival of CD19(null) mice, implicating CD21/CD35 and CD19 in mast cell activation. Interestingly, early TNF-alpha release is also impaired in Cr2(null) and CD19(null) animals, suggesting that these molecules directly affect mast cell activation. Cr2(null) and CD19(null) mice demonstrate an impairment in neutrophil recruitment and a corresponding increase in bacterial load. Examination of peritoneal mast cells by flow cytometry and confocal microscopy reveals the expression and colocalization of CD21/CD35 and CD19. Taken together, these findings suggest that the engagement of complement receptors CD21/CD35 along with CD19 on the mast cell surface by C3 fragments may be necessary for the full expression of mast cell activation in the CLP model.

Acute Disease↗

Transfer of CD4(+) T cells aggravates atherosclerosis in immunodeficient apolipoprotein E knockout mice.

BACKGROUND: Atherosclerosis is associated with immune responses to oxidized lipoproteins and certain microorganisms, but the role of specific immunity has remained unclear. METHODS AND RESULTS: To study the role of immunity in atherosclerosis, we crossed atherosclerosis-prone apoE(-/-) mice with immunodeficient scid/scid mice. The offspring showed a 73% reduction in aortic fatty streak lesions when compared with immunocompetent apoE(-/-) mice. Transfer of CD4(+) T cells from apoE(-/-) to immunodeficient apoE(-/-)/scid/scid mice increased lesions by 164%. This was associated with the infiltration of transferred T cells into lesions, increased circulating interferon-gamma levels, and increased I-A expression in lesions. CONCLUSIONS: CD4(+) T cells carry disease-promoting immunity in atherosclerosis.

Animals↗

An analysis of the helix-to-strand transition between peptides with identical sequence.

An analysis of peptide segments with identical sequence but that differ significantly in structure was performed over non-redundant databases of protein structures. We focus on those peptides, which fold into an alpha-helix in one protein but a beta-strand in another. While the study shows that many such structurally ambivalent peptides contain amino acids with a strong helical preference collocated with amino acids with a strong strand preference, the results overwhelmingly indicate that the peptide's environment ultimately dictates its structure. Furthermore, the first naturally occurring structurally ambivalent nonapeptide from evolutionary unrelated proteins is described, highlighting the intrinsic plasticity of peptide sequences. We even find seven proteins that show structural ambivalence under different conditions. Finally, a computer algorithm has been implemented to identify regions in a given sequence where secondary structure prediction programs are likely to make serious mispredictions.

Algorithms↗

Pax6 activity in the lens primordium is required for lens formation and for correct placement of a single retina in the eye.

The Pax6 transcription factor plays a key role in ocular development of vertebrates and invertebrates. Homozygosity of the Pax6 null mutation in human and mice results in arrest of optic vesicle development and failure to initiate lens formation. This phenotype obscures the understanding of autonomous function of Pax6 in these tissue components and during later developmental stages. We employed the Cre/loxP approach to inactivate Pax6 specifically in the eye surface ectoderm concomitantly with lens induction. Although lens induction occurred in the mutant, as indicated by Sox2 up-regulation in the surface ectoderm, further development of the lens was arrested. Hence, Pax6 activity was found to be essential in the specified ectoderm for lens placode formation. Furthermore, this mutant model allowed us for the first time to address in vivo the development of a completely normal retina in the absence of early lens structures. Remarkably, several independent, fully differentiated neuroretinas developed in a single optic vesicle in the absence of a lens, demonstrating that the developing lens is not necessary to instruct the differentiation of the neuroretina but is, rather, required for the correct placement of a single retina in the eye.

Animals↗

Corticofugal inhibition compresses all types of rate-intensity functions of inferior collicular neurons in the big brown bat.

Recent studies have shown that the auditory corticofugal system modulates and improves signal processing in the frequency, time and spatial domains. In this study, we examine corticofugal modulation of rate-intensity functions of inferior collicular (IC) neurons of the big brown bat, Eptesicus fuscus, by electrical stimulation in the primary auditory cortex (AC). Cortical electrical stimulation compressed all types of rate-intensity functions so as to increase the slope but decrease the dynamic range of IC neurons. Cortical electrical stimulation also shifts the responsive intensity of IC neurons to higher levels. These data indicate that corticofugal modulation also improves subcortical signal processing in intensity domain. The implication of these findings to bat echolocation is discussed.

Acoustic Stimulation↗

Measurements of the mass, total width, and two-photon partial width of the eta(c) meson.

Using 13.4 fb(-1) of data collected with the CLEO detector at the Cornell Electron Storage Ring, we have observed 300 events for the two-photon production of ground-state pseudoscalar charmonium in the decay eta(c)-->K(0)(S)K-/+pi(+/-). We have measured the eta(c) mass to be [2980.4+/-2.3 (stat)+/-0.6 (syst)] MeV and its full width as [27.0+/-5.8 (stat)+/-1.4 (syst)] MeV. We have determined the two-photon partial width of the eta(c) meson to be [7.6+/-0.8 (stat)+/-0.4 (syst)+/-2.3 (br)] keV, with the last uncertainty associated with the decay branching fraction.

Journal Article↗

Study of charmless hadronic B meson decays to pseudoscalar-vector final states.

We report results of searches for charmless hadronic B meson decays to pseudoscalar( pi(+/-), K+/-, pi(0), or K(0)(S))-vector( rho, K(*), or omega) final states. By using 9.7x10(6) BB pairs collected with the CLEO detector, we report the first observation of B(-)--->pi(-)rho(0), B(0)-->pi(+/-)rho(-/+), and B(-)-->pi(-)omega, which are expected to be dominated by hadronic b-->u transitions. The measured branching fractions are (10.4(+3.3)(-3.4)+/-2.1)x10(-6), (27.6(+8.4)(-7.4)+/-4.2)x10(-6), and (11.3(+3.3)(-2.9)+/-1. 4)x10(-6), respectively. Branching fraction upper limits are set for all of the other decay modes investigated.

Journal Article↗

The serpin alpha1-proteinase inhibitor is a critical substrate for gelatinase B/MMP-9 in vivo.

We have identified the key protein substrate of gelatinase B/MMP-9 (GB) that is cleaved in vivo during dermal-epidermal separation triggered by antibodies to the hemidesmosomal protein BP180 (collagen XVII, BPAG2). Mice deficient in either GB or neutrophil elastase (NE) are resistant to blister formation in response to these antibodies in a mouse model of the autoimmune disease bullous pemphigoid. Disease develops upon complementation of GB -/- mice with NE -/- neutrophils or NE -/- mice with GB -/- neutrophils. Only NE degrades BP180 and produces dermal-epidermal separation in vivo and in culture. Instead, GB acts upstream to regulates NE activity by inactivating alpha1-proteinase inhibitor (alpha1-PI). Excess NE produces lesions in GB -/- mice without cleaving alpha1-PI. Excess alpha1-PI phenocopies GB and NE deficiency in wild-type mice.

Animals↗

3,5-Bis(trifluoromethyl)pyrazoles: a novel class of NFAT transcription factor regulator.

A series of bis(trifluoromethyl)pyrazoles (BTPs) has been found to be a novel inhibitor of cytokine production. Identified initially as inhibitors of IL-2 synthesis, the BTPs have been optimized in this regard and even inhibit IL-2 production with a 10-fold enhancement over cyclosporine in an ex vivo assay. Additionally, the BTPs show inhibition of IL-4, IL-5, IL-8, and eotaxin production. Unlike the IL-2 inhibitors, cyclosporine and FK506, the BTPs do not directly inhibit the dephosphorylation of NFAT by calcineurin.

Animals↗

Nitric oxide induces thymocyte apoptosis via a caspase-1-dependent mechanism.

We previously showed that NO induces apoptosis in thymocytes via a p53-dependent pathway. In the present study, we investigated the role of caspases in this process. The pan-caspase inhibitor, ZVAD-fmk, and the caspase-1 inhibitor, Ac-YVAD-cho, both inhibited NO-induced thymocyte apoptosis in a dose-dependent manner, whereas the caspase-3 inhibitor, Ac-DEVD-cho, had little effect even at concentrations up to 500 microM. ZVAD-fmk and Ac-YVAD-cho were able to inhibit apoptosis when added up to 12 h, but not 16 h, after treatment with the NO donor S-nitroso-N-acetyl penicillamine (SNAP). Caspase-1 activity was up-regulated at 4 h and 8 h and returned to baseline by 24 h; caspase-3 activity was not detected. Cytosolic fractions from SNAP-treated thymocytes cleaved the inhibitor of caspase-activated deoxyribonuclease. Such cleavage was completely blocked by Ac-YVAD-cho, but not by Ac-DEVD-cho or DEVD-fmk. Poly(ADP-ribose) polymerase (PARP) was also cleaved in thymocytes 8 h and 12 h after SNAP treatment; addition of Ac-YVAD-cho to the cultures blocked PARP cleavage. Furthermore, SNAP induced apoptosis in 44% of thymocytes from wild-type mice; thymocytes from caspase-1 knockout mice were more resistant to NO-induced apoptosis. These data suggest that NO induces apoptosis in thymocytes via a caspase-1-dependent but not caspase-3-dependent pathway. Caspase-1 alone can cleave inhibitor of caspase-activated deoxyribonuclease and lead to DNA fragmentation, thus providing a novel pathway for NO-induced thymocyte apoptosis.

Animals↗

State-dependent cross-inhibition between transmitter-gated cation channels.

Transmitter-gated cation channels are detectors of excitatory chemical signals at synapses in the nervous system. Here we show that structurally distinct alpha3beta4 nicotinic and P2X2 channels influence each other when co-activated. The activation of one channel type affects distinct kinetic and conductance states of the other, and co-activation results in non-additive responses owing to inhibition of both channel types. State-dependent inhibition of nicotinic channels is revealed most clearly with mutant P2X2 channels, and inhibition is decreased at lower densities of channel expression. In synaptically coupled myenteric neurons, nicotinic fast excitatory postsynaptic currents are occluded during activation of endogenously co-expressed P2X channels. Our data provide a molecular basis and a synaptic context for cross-inhibition between transmitter-gated channels.

Acetylcholine↗