Synergistically enhanced ultraviolet emission of Yb doped ZnO films by using a capping of ultrathin Al and SiO2 microspheres.

We studied the enhancement effects of ultraviolet (UV) emission from rare earth ytterbium (Yb) doped ZnO films, by using capping layers of Al and SiO2 micro-spheres. The films were deposited on Si substrates with magnetron sputtering followed by high temperature (∼1000°C) heat treatment, and then capped with a nanoscale ultrathin aluminum (Al) layer and/or SiO2 micro-spheres on the surface of the films. The photoluminescence (PL) results indicate that compared to the case without any capping, the UV emission is enhanced by a factor ranging from several to dozens times, the films capped with 2.0 nm Al layer and 5.0 µm SiO2 microspheres have the longest highest PL intensity among the samples. The PL enhancements are discussed in terms of increased optical (or electrical) fields around the surface of the films combined with defect passivation after the capping. Our work has proposed a strategy to enhance the UV emissions of ZnO, which will broaden the application potential of ZnO in UV photonics.

Wnt3 knockdown sensitizes human non-small cell type lung cancer (NSCLC) cells to cisplatin via regulating the cell proliferation and apoptosis.

OBJECTIVE: Aberrant activation of (Wingless and mouse homolog Int-1) Wnt/ß-catenin signaling pathways closely involved in the occurrence and progression of several types of human malignancies. This research was undertaken to elucidate the important role of (Wingless and mouse homolog Int-1) in lung cancer. PATIENTS AND METHODS: Wnt3 expression in lung cancers and their respective normal tissues were examined by immunoblotting and immunohistochemistry. Then, Wnt3 was regulated with RNA interference (RNAi) technology in human lung cancer A549 cells, and the cell proliferation, cell cycle, cell invasion/metastasis, and apoptosis were evaluated. RESULTS: In all cases, Wnt3 expression was significantly elevated in lung cancers compared with normal tissues. Knocking down Wnt3 in A549 lung cancer cells by small interfering RNAs transfection led to a distinct reduction of Wnt3 in both transcript and protein levels. Knockdown of Wnt3 expression in lung cancer cells inhibited the expression of ß-catenin and cyclin D1 genes in Wnt/ß-catenin pathway. It also significantly blocked cellular proliferation, delayed cell cycle and suppressed cell invasion/metastasis, accompanied by a higher apoptosis rate. CONCLUSIONS: We conclude that the upregulation of Wnt3 plays a crucial role in lung tumorigenesis by inducing proliferation, migration, and invasion and inhibiting apoptosis of cancer cells. Wnt3 might be a potential target for the treatment of lung cancer.

Gametocidal chromosomes enhancing chromosome aberration in common wheat induced by 5-azacytidine.

The gametocidal (Gc) chromosome from Aegilops spp induces chromosome mutation, which is introduced into common wheat as a tool of chromosome manipulation for genetic improvement. The Gc chromosome functions similar to a restriction-modification system in bacteria, in which DNA methylation is an important regulator. We treated root tips of wheat carrying Gc chromosomes with the hypomethylation agent 5-azacytidine; chromosome breakage and micronuclei were observed in these root tips. The frequency of aberrations differed in wheat containing different Gc chromosomes, suggesting different functions inducing chromosome breakage. Gc chromosome 3C caused the greatest degree of chromosome aberration, while Gc chromosome 3C(SAT) and 2C caused only slight chromosome aberration. Gc chromosome 3C induced different degrees of chromosome aberration in wheat varieties Triticum aestivum var. Chinese Spring and Norin 26, demonstrating an inhibition function in common wheat.

RAPD and ISSR-assisted identification and development of three new SCAR markers specific for the Thinopyrum elongatum E (Poaceae) genome.

Diploid Thinopyrum elongatum, a wild relative of wheat, contains many agronomically desirable traits and has potential for increasing genetic variability and introducing desirable characters in this crop. Few molecular markers are available for rapid screening of T. elongatum genome segments in the wheat genetic background. We used 36 RAPD primers and 33 ISSR primers to screen for polymorphisms in the common wheat variety Chinese Spring and in T. elongatum. Two RAPD markers and one ISSR marker, designated OPF03(1407), LW10(1487) and UBC841(701), were identified and were specific for the T. elongatum E genome. Three pairs of primers flanking these specific sequences were designed to produce SCAR markers. All three SCAR markers were T. elongatum E genome-specific. Two of these SCAR markers, SCAR(807) and SCAR(577), were present in all seven T. elongatum chromosomes, while SCAR(839) was specific for T. elongatum chromosomes 2E and 3E. These newly developed SCAR markers should be useful for detecting alien genome chromatin or chromosome segments in the genetic background of common wheat.

Optimal phenotypic testing of AmpC beta-lactamases using boronic acid solutions.

Plasmid-mediated class C ß-lactamases are reported from Escherichia coli and Klebsiella pneumoniae with increasing frequency. No screening and confirmatory tests have been uniformly established for these strains. We investigated for the presence of plasmid-mediated AmpC production in 51 clinical isolates of Enterobacteriaceae, comparing two different boronic acid formulations, phenylboronic acid (PB) and 3-(N-Boc-amino)phenylboronic acid (APB), using polymerase chain reaction (PCR). PB performed better than APB.

Induction of pulmonary matrilysin expression by combustion and ambient air particles.

The molecular mechanism(s) by which chemically complex air pollution particles mediate their adverse health effects is not known. We have examined the ability of combustion and ambient air particles to induce pulmonary matrilysin expression due to the well-documented role of matrix metalloproteinases in tissue injury and repair responses. Rats were exposed to saline, residual oil fly ash (2.5 mg/rat), or ambient air particles (2.5 mg/rat) via intratracheal instillation and examined 3-72 h after exposure. Saline-exposed animals had low levels of matrilysin mRNA, whereas the animals exposed to either complex particle showed an early induction of pulmonary matrilysin gene expression as well as of the 19-kDa activated form of matrilysin. Immunocytochemistry and in situ hybridization analyses identified the alveolar macrophages and monocytes as primary sources of air pollution particle-induced matrilysin expression. Matrilysin gene induction and protein activation by combustion and ambient air particles correlated with the early histopathological changes produced by these particles. These results demonstrate the ability of combustion and ambient air particles to induce pulmonary matrilysin expression and suggest a role for this matrix metalloproteinase in the initiation of lung injury produced by these particles.

Particulate Matter Induction of Pulmonary Gelatinase A, Gelatinase B, and Tissue Inhibitor of Metalloproteinase Expression.

Gelatinase A and gelatinase B are matrix metalloproteinases (MMPs) that are capable of degrading type IV collagen as well as other major components of basement membranes. These MMPs are also involved in modulating inflammation and tissue remodeling. Previous studies have shown the induction of pulmonary matrilysin, another MMP, following exposure to either combustion or ambient particulate matter (PM). In the present study, we examined whether gelatinase A, gelatinase B, or tissue inhibitor of metalloproteinase (TIMP) was affected following exposure to PM. Sprague-Dawley rats were exposed to a combustion PM (residual oil fly ash, ROTA, 2.5 mg/rat) or saline by intratracheal instillation and examined at 6 to 72 h postexposure. Changes in gelatinase A, gelatinase B, and TIMP-1 and -2 m RNA levels were determined using reverse transcription (RT) polymerase chain reaction (PCR). ROTA exposure increased the mRNA levels of gelatinase A and TIMP-1. However, gelatinase B mRNA, not expressed in control animals, was significantly induced from 6 to 24 h following ROFA exposure. Western blot analysis confirmed the presence of gelatinase A and B protein in lung tissue following ROFA exposure. Immunocytochemical analysis revealed that alveolar epithelial cells and inflammatory cells were major cellular sources for the pulmonary gelatinase A and B expression. To compare the effects of ambient PM with that of combustion PM and to further examine effects of ambient PM size on MMP induction, animals were treated with the same dose of the size-fractionated ambient PM [PM1.7, PM1.7-3.7, PM37.20 (size indicated in micrometers) collected from Washington, DC], Gelatinase A, gelatinase B, and TIMP gene expression and cellular distributions were assessed using RT-PCR and immunocytochemistry, respectively. Interestingly, gelatinase B was significantly induced to the same extent by all three size-fractionated ambient PM. Celatinase A and TIMP-1 expression were not changed, while TIMP-2 expression was slightly decreased by PM1.7 and PM1.7-3.7. Immunocytochemically, gelatinase A, gelatinase B, and TIMP-2 expression were localized mainly to the terminal bronchiole region and associated with inflammatory cells in ambient PM exposed animals. Thus, we have provided further evidence that MMP and TIMP expression are altered following exposure to either combustion or ambient PM supporting the hypothesis that MMP may be involved in pathogenesis of PM-induced lung injury.

In vivo exposure to ozone produces an increase in a 72-kDa heat shock protein in guinea pigs.

Although several lines of evidence have suggested that oxidizing agents can induce heat shock proteins (HSPs) in vitro, little is known about the induction of HSPs during in vivo exposure to oxidants. Guinea pigs were exposed to ozone for 6 h and euthanized up to 72 h later. Proteins from lavage cells and lung tissue were characterized by immunoblotting with 72- and 73/72-kDa HSP monoclonal antibodies. Although 73-kDa HSP was expressed constituitively in lung tissue, it was not affected by ozone. In contrast, 72-kDa HSP was significantly increased in lavage cells and lung tissue of animals exposed to 0.4 and 0.66 parts/million of ozone. Both heat treatment and arsenite induced 72-kDa HSP in cultured alveolar macrophages. The increase in 72-kDa HSP in the lavage cell pellet peaked at 24 h after ozone, whereas the influx of polymorphonuclear leukocytes peaked at 4 h. Examination of the induction of HSPs by ozone may provide clues to the development of ozone tolerance in humans and animals.

Late-onset life-threatening angioedema and upper airway obstruction caused by angiotensin-converting enzyme inhibitor: report of a case.

Angioedema is a rare but potentially lethal adverse effect when associated with upper airway obstruction. Sporadic cases of angioedema secondary to angiotensin converting enzyme inhibitors (ACEI) have been reported in the literature. The overall incidence is around 0.1% to 0.2%, and the time of onset is usually during the first week of ACEI therapy. Late-onset angioedema secondary to treatment with ACEIs is much more frequent than appreciated, and is largely unrecognized because of the absence of temporal correlation between ACEI therapy and the development of angioedema. Since angioedema may progress to upper airway obstruction, otolaryngologists must be aware of this association. Most importantly, late-onset angioedema should alert the clinician to discontinue the ACEI immediately to prevent further morbidity. This report presents an example of late-onset angioedema which was precipitated by taking a double dose of captopril incidentally. The case is discussed, and the literature, pathophysiology and treatment of angioedema are reviewed.

Genetic variability in combustion particle-induced chronic lung injury.

Occupational exposure to anthropogenic particles is associated with lung injury in humans. We hypothesized that residual oil fly ash (ROFA), an emission source particulate, may induce acute lung injury and fibrosis in sensitive rat strains and that fibronectin (Fn) gene expression will correspond to the development of fibrosis. Male Sprague-Dawley (SD), Wistar (WIS), and Fischer 344 (F-344) rats (60 days old) were exposed to saline or ROFA (8.3 mg/kg) by intratracheal instillation and examined for up to 12 wk. Histology indicated focal areas of lung damage showing inflammatory cell infiltration as well as alveolar, airway, and interstitial thickening in all three rat strains during 1-7 days postexposure. Trichrome staining of the lung sections indicated a sporadic incidence of focal alveolar fibrosis at 1, 3, and 12 wk in SD rats, whereas WIS and F-344 rats showed only a modest increase in trichrome staining in the septal areas. Of all Fn mRNA isoforms examined by polymerase chain reaction, only EIIIA(+) was upregulated during 6 h-1 wk in ROFA-exposed SD and WIS rats but not in F-344 rats. In situ hybridization analysis in SD rats revealed Fn mRNA expression by macrophage and alveolar and airway epithelium and within fibrotic areas. Immunohistochemical analysis revealed increased presence of Fn EIIIA(+) protein in the areas of fibrotic injury and basally to the airway epithelium. In summary, Fn EIIIA(+) increases early in the course of particle-induced lung injury and remodeling, which may or may not result in discernible alveolar fibrosis. There is a rat strain variation in ROFA-induced fibrosis and associated Fn EIIIA(+) expression.

Extracellular superoxide dismutase mRNA expressions in the human lung by in situ hybridization.

The extracellular form of superoxide dismutase (EC-SOD), SOD3, is contained in the human lung in relatively high amounts when compared to other organs. It has not been previously shown whether or not EC-SOD is synthesized and secreted by specific lung cells. We examined the expression of EC-SOD mRNA in human lung cells by in situ hybridization using a digoxigenin-labeled EC-SOD cRNA probe. Strong signals of EC-SOD synthesis were found in the epithelium of all airways. Secretory and basal cells, but not ciliated cells, were labeled for EC-SOD mRNA. Expression of EC-SOD mRNA was found in endothelial cells lining both arteries and veins. Many cells in the alveolar septum exhibited strong expression of EC-SOD mRNA. In addition, epithelial cells lining the outer wall of intrapulmonary airways and vessels were heavily labeled for EC-SOD mRNA. The lung parenchymal epithelial cells containing EC-SOD mRNA were identified as alveolar type II cells by colocalization with surfactant protein-A. Human alveolar macrophages were found to contain a substantial amount of EC-SOD mRNA expression. Alveolar type I epithelial cells and capillary endothelial cells did not display detectable signals of EC-SOD mRNA. Smooth muscle cells in muscular arteries were not labeled by the EC-SOD mRNA probe. These results show that airway epithelial cells and alveolar type II cells are the major cell types that synthesize fibroblasts EC-SOD in the human lung. EC-SOD has been shown by immunocytochemistry to be associated with the extracellular matrix around airway epithelium and in the walls of intrapulmonary arterioles. The site of EC-SOD localization, therefore, is closely related to the site of its synthesis.

Lung epithelial cell-released nitric oxide protects against PMN-mediated cell injury.

A calcium-independent type II nitric oxide (NO) synthase has been localized in lung epithelial cells; however, the function of NO. released by epithelial cells is unclear. We hypothesized that epithelial-derived NO may affect the interactions between polymorphonuclear neutrophils (PMN) and the alveolar epithelium and studied PMN adhesion and cytotoxicity to lung epithelial cells. A dose- and time-dependent production of NO. by L2 cells can be induced by a mixture of inflammatory mediators (cytomix) containing lipopolysaccharide, tumor necrosis factor-alpha, and interferon-gamma. Increased NO. production by L2 cells was associated with decreased 51Cr release by the epithelial cells after they were incubated with activated PMN. Addition of NG-monomethyl-L-arginine or oxyhemoglobin reversed the protective effects of cytomix, suggesting that increased NO. production by L2 cells was responsible for the decreased 51Cr release. However, PMN adhesion and intercellular adhesion molecule-1, a major adhesion molecule involved in PMN adhesion to epithelium, were increased by cytomix. We conclude that NO. released by lung epithelial cells was involved in protecting epithelial cells from PMN-mediated cytotoxicity. NO.-mediated protection of lung epithelial cells occurred in spite of PMN adhesion being increased, suggesting that reduced adhesion is not required for NO.-mediated inhibition of PMN cytotoxicity.

Alterations in surfactant protein A after acute exposure to ozone.

The surfactant layer covering the gas-exchange region of the lung serves as the initial site of interaction with inhaled oxidant gases. Among the endogenous compounds potentially vulnerable to oxidative injury are surfactant proteins. This study focused on the effect of ozone on surfactant protein A (SP-A) function, content, and gene expression. To determine the time course of response to ozone, guinea pigs were exposed to 0.2-0.8 parts/million (ppm) ozone for 6 h and were killed up to 120 h postexposure. To determine the effect of repeated exposure, animals were exposed to 0.8 ppm ozone for 6 h/day and were killed on days 3 and 5. A significant increase in surfactant's ability to modulate the respiratory burst induced by phorbol 12-myristate 13-acetate in naive macrophages was observed at 24 h after a single 0.8 ppm ozone exposure. Because neutralizing antibodies to SP-A blunted this stimulatory effect, we hypothesized that ozone enhanced the modulatory role of SP-A in macrophage function. This alteration in function was accompanied by an influx of inflammatory cells and only marginal changes in SP-A levels as determined by an enzyme-linked immunosorbent assay. No significant changes in steady-state levels of SP-A mRNA were observed after single or repeated exposure to ozone. Thus the inflammation that accompanies in vivo ozone exposure may result in a change in the structure and thus functional role of SP-A in modulating macrophage activity.

Noradrenergic innervation of nasal polyps and polypoid mucosae.

In order to study the sympathetic innervation of nasal polyps and polypoid mucosae, the glyoxylic catecholaminergic histofluorescence method was employed in the examination of specimens taken from patients who had nasal disorders with polyps or polypoid mucosae. One percent neutral red was used as a counterstain. Abundant sympathetic fibers were present around the vessels of the pedicle of nasal polyps. However, no sympathetic innervation was found in the body and apex of the polyps. In the microscopical views of polypoid formations, there were no obvious differences between non-diseased nasal mucosa and polypoid mucosa in the distribution of sympathetic innervation. Based on these results, the following conclusions were drawn: (1) The loss of the sympathetic innervation was suggested to an important role in the pathogenesis of nasal polyps. (2) During polypectomy, the polyp had better be removed along with the pedicle for there is abundant sympathetic innervation and it will result in reduced bleeding.

Effects of amphetamine on human nasal mucosa.

The present study was devised to determine the effects of amphetamine on the sympathetic function of human nasal mucosa. A tissue bath method was employed on the vitro preparations of nasal turbinate mucosa from adult patients with nasal allergies or hypertrophic rhinitis. The effects of amphetamine on the contractile response of isolated human nasal mucosal blood vessels were investigated following electrical field stimulation and methoxamine. The results showed that amphetamine inhibited field stimulation and antagonized the effects on mucosal contraction induced by methoxamine. Likewise, the drug increased mucosal basal tension but had local drug toxicity when a 10(-4) M solution was used. Amphetamine could potentiate mucosal contraction induced by norepinephrine or epinephrine. The study indicated that amphetamine may increase sympathetic function by potentiating the effect of norepinephrine and that high concentration of amphetamine may actually antagonize alpha-adrenoceptors.

Temporal expression and cellular distribution of pulmonary fibronectin gene induction following exposure to an emission source particle.

This study examines the ability of an emission source particle, residual oil fly ash (ROFA), to influence pulmonary fibronectin (Fn) gene expression. Fn is an extracellular matrix (ECM) protein involved in a variety of cellular functions, including inflammation, cell proliferation, and fibrosis. Temporal expression and spatial distribution of Fn gene induction were assessed by in situ hybridization in rat lung during acute phase of lung injury occurring 6 to 72 h following intratracheal instillation of ROFA. Fn mRNA was not detected in rat lungs treated with either saline or at 6 h after ROFA treatment. However, Fn mRNA was induced in airway epithelial cells 24 h after ROFA instillation. Histopathology showed peribronchial inflammation and focal edema. Diffuse inflammation in alveolar region with limited expression of Fn mRNA was evident 48 h after ROFA exposure, occurring mainly in proliferating epithelial cells. Extensive Fn mRNA expression was seen in proliferating fibroblasts and in hyperplastic epithelial cells within incipient fibrotic lesions 72 h after exposure, while the intensity of expression in the airway epithelial cells was decreased. Therefore, Fn mRNA induction was associated with inflammatory and incipient fibrotic lesions, indicating its possible involvement in airway hyperreactivity and initiation of fibrogenesis.

Noradrenergic innervation of juvenile nasopharyngeal angiofibroma.

The glyoxylic catecholaminergic histofluorescence method was employed on tissues from five cases of juvenile nasopharyngeal angiofibroma in order to study the sympathetic innervation present. There was no sympathetic innervation identified in tumor parenchyma while some scant noradrenergic fibers were found in the tumor border. These findings indicate that keeping a dissection surface out of tumor during planned excisions may be very important, as vessels there have more sympathetic innervation which will then result in good vessel contraction in controlling bleeding. Non-diseased nasal mucosa from each patient was used as control tissue, with its submucosa seen to be filled with noradrenergic innervation. Some noradrenergic fibers were also found to innervate the muscle layers of arterioles or venules adjacent to the sphenopalatine foramen.

[Psychogenic dizziness].

Psychogenic dizziness is defined as recurring or persistent symptoms of balance dysfunction, inconsistent with organic vestibular disease as determined by history, clinical examination and pertinent investigations, and consistent with emotional origin. Of 1,335 patients seen in our dizziness clinic between January 1988 and August 1991, psychogenic dizziness was diagnosed in 180 (13.5%) patients. There were 67 men and 113 women aged from 12 to 77 years (mean age 40.2 years). The characteristics of psychogenic dizziness are: (1) continuous dizziness for long periods of time; (2) younger patients; (3) predominant female; (4) associated symptoms of panic attack, such as headache, breathlessness, nausea, sleep disturbance, paresthesias, anxiety and palpitation; (5) symptoms of aggravation due to stressful life events; (6) normal neurotological bedside examination; (7) hyperventilation reproduced accurately. The electronystagmographic results of 74 patients show normal bithermal caloric responses in 47 patients (63.5%), caloric hyperactivity in 21 patients (28.4%), canal paresis in four patients (5.4%), canal paresis with directional preponderance in two patients (2.7%), large random voluntary eye swings or severe blinking in 35 patients (47.3%), and spontaneous nystagmus (slow phase velocity < 6.5 degrees/s) in four patients (5.4%). There were 31 patients who consulted psychiatrists with diagnoses of anxiety (51.6%), depression (16.1%), insomnia (12.9%), psychosomatic disorder and adjustment disorder. Treatment of patients with psychogenic dizziness must be directed at the underlying anxiety. Psychiatric consultation is necessary.