113,605 research outputs found
Increased expression of heme oxygenase (HO)-1 in alveolar spaces and HO-2 in alveolar walls of smokers
It has been suggested that oxidative stress protein heme oxygenase (HO)-1 plays a role in chronic airway diseases including chronic obstructive pulmonary disease (COPD). The inducible isoform HO-1 and the constitutive HO-2 catalyze the same reaction. Their distribution in situ was studied in lungs of 10 nonsmoking subjects, 6 healthy smokers, and 10 smokers with COPD. Paraffin-embedded sections of surgical lung specimens were immunostained with antibodies against HO-1 and HO-2. HO-1 immunoreactivity was observed mainly in alveolar macrophages. HO-1-positive macrophages were increased in smokers with COPD (median: 36%) as compared with nonsmoking subjects (13%; p < 0.02), whereas no differences were observed between patients with COPD and healthy smokers (34%). HO-2 had a more widespread distribution in cells of the alveolar wall, in adventitia of pulmonary arteries and bronchioles, and in vascular smooth muscle. Lower percentages of alveolar macrophages exhibited positive staining for HO-2 without significant differences between the three groups. HO-2(+) cells in the alveolar wall were increased in smokers with (15/mm) and without COPD (12/mm) as compared with nonsmokers (8/mm, p < 0.01). In conclusion, inducible HO-1 and constitutive HO-2 are detectable in human lung tissue and their expression is increased in smokers, suggesting that oxidative stress due to cigarette smoke may increase lung cells expressing HO-1 and HO-2
The 1961 Kampong Bukit Ho Swee fire and the making of modern Singapore
By 1970, Singapore’s urban landscape was dominated by high-rise blocks of planned public housing built by the People’s Action Party government, signifying the establishment of a high modernist nation-state. A decade earlier, the margins of the City had been dominated by kampongs, home to semi-autonomous communities of low-income Chinese families which freely built, and rebuilt, unauthorised wooden houses. This change was not merely one of housing but belied a more fundamental realignment of state-society relations in the 1960s. Relocated in Housing and Development Board flats, urban kampong families were progressively integrated into the social fabric of the emergent nation-state. This study examines the pivotal role of an event, the great Kampong Bukit Ho Swee fire of 1961, in bringing about this transformation. The redevelopment of the fire site in the aftermath of the calamity brought to completion the British colonial regime’s ‘emergency’ programmes of resettling urban kampong dwellers in planned accommodation, in particular, of building emergency public housing on the sites of major fires in the 1950s. The PAP’s far greater political resolve, and the timing of and state of emergency occasioned by the scale of the 1961 disaster, enabled the government to rehouse the Bukit Ho Swee fire victims in emergency housing in record time. This in turn provided the HDB with a strategic platform for clearing other kampongs and for transforming their residents into model citizens of the nation-state. The 1961 fire’s symbolic usefulness extended into the 1980s and beyond, in sanctioning the PAP’s new housing redevelopment schemes. The official account of the inferno has also become politically useful for the government of today for disciplining a new generation of Singaporeans against taking the nation’s progress for granted. Against these exalted claims of the fire’s role in the Singapore Story, this study also examines the degree of actual change and continuity in the social and economic lives of the people of Bukit Ho Swee after the inferno. In some crucial ways, the residents continued to occupy a marginal place in society while pondering, too, over the unresolved question of the cause of the fire. These continuities of everyday life reflect the ambivalence with which the citizenry regarded the high modernist state in contemporary Singapore
HMOX1 gene promoter alleles and high HO-1 levels are associated with severe malaria in Gambian children.
Heme oxygenase 1 (HO-1) is an essential enzyme induced by heme and multiple stimuli associated with critical illness. In humans, polymorphisms in the HMOX1 gene promoter may influence the magnitude of HO-1 expression. In many diseases including murine malaria, HO-1 induction produces protective anti-inflammatory effects, but observations from patients suggest these may be limited to a narrow range of HO-1 induction, prompting us to investigate the role of HO-1 in malaria infection. In 307 Gambian children with either severe or uncomplicated P. falciparum malaria, we characterized the associations of HMOX1 promoter polymorphisms, HMOX1 mRNA inducibility, HO-1 protein levels in leucocytes (flow cytometry), and plasma (ELISA) with disease severity. The (GT)(n) repeat polymorphism in the HMOX1 promoter was associated with HMOX1 mRNA expression in white blood cells in vitro, and with severe disease and death, while high HO-1 levels were associated with severe disease. Neutrophils were the main HO-1-expressing cells in peripheral blood, and HMOX1 mRNA expression was upregulated by heme-moieties of lysed erythrocytes. We provide mechanistic evidence that induction of HMOX1 expression in neutrophils potentiates the respiratory burst, and propose this may be part of the causal pathway explaining the association between short (GT)(n) repeats and increased disease severity in malaria and other critical illnesses. Our findings suggest a genetic predisposition to higher levels of HO-1 is associated with severe illness, and enhances the neutrophil burst leading to oxidative damage of endothelial cells. These add important information to the discussion about possible therapeutic manipulation of HO-1 in critically ill patients
Increased expression of heme oxygenase (HO)-1 in alveolar spaces and HO-2 in alveolar walls of smokers
It has been suggested that oxidative stress protein heme oxygenase (HO)-1 plays a role in chronic airway diseases including chronic obstructive pulmonary disease (COPD). The inducible isoform HO-1 and the constitutive HO-2 catalyze the same reaction. Their distribution in situ was studied in lungs of 10 nonsmoking subjects, 6 healthy smokers, and 10 smokers with COPD. Paraffin-embedded sections of surgical lung specimens were immunostained with antibodies against HO-1 and HO-2. HO-1 immunoreactivity was observed mainly in alveolar macrophages. HO-1-positive macrophages were increased in smokers with COPD (median: 36%) as compared with nonsmoking subjects (13%; p < 0.02), whereas no differences were observed between patients with COPD and healthy smokers (34%). HO-2 had a more widespread distribution in cells of the alveolar wall, in adventitia of pulmonary arteries and bronchioles, and in vascular smooth muscle. Lower percentages of alveolar macrophages exhibited positive staining for HO-2 without significant differences between the three groups. HO-2(+) cells in the alveolar wall were increased in smokers with (15/mm) and without COPD (12/mm) as compared with nonsmokers (8/mm, p < 0.01). In conclusion, inducible HO-1 and constitutive HO-2 are detectable in human lung tissue and their expression is increased in smokers, suggesting that oxidative stress due to cigarette smoke may increase lung cells expressing HO-1 and HO-2
Cooling rates of neutron stars and the young neutron star in the Cassiopeia A supernova remnant
We explore the thermal state of the neutron star in the Cassiopeia A supernova remnant using the recent result of Ho & Heinke that the thermal radiation of this star is well described by a carbon atmosphere model and the emission comes from the entire stellar surface. Starting from neutron star cooling theory, we formulate a robust method to extract neutrino cooling rates of thermally relaxed stars at the neutrino cooling stage from observations of thermal surface radiation. We show how to compare these rates with the rates of standard candles – stars with non-superfluid nucleon cores cooling slowly via the modified Urca process. We find that the internal temperature of standard candles is a well-defined function of the stellar compactness parameter x=rg/R, irrespective of the equation of state of neutron star matter (R and rg are circumferential and gravitational radii, respectively). We demonstrate that the data on the Cassiopeia A neutron star can be explained in terms of three parameters: f?, the neutrino cooling efficiency with respect to the standard candle; the compactness x; and the amount of light elements in the heat-blanketing envelope. For an ordinary (iron) heat-blanketing envelope or a low-mass (? 10?13 M?) carbon envelope, we find the efficiency f?? 1 (standard cooling) for x? 0.5 and f?? 0.02 (slower cooling) for a maximum compactness x? 0.7. A heat blanket containing the maximum mass (?10?8 M?) of light elements increases f? by a factor of 50. We also examine the (unlikely) possibility that the star is still thermally non-relaxe
HO-1 is rapidly increased after haptoglobin and hemopexin infusion.
(A and B) SS-mice (n = 3/group) were infused with vehicle or equimolar (1 μmol/kg) Hb, Hp, Hpx, Hb + Hp, or Hb + Hpx. Livers were removed and flash frozen 1 hour after infusion. Hepatic microsomes were used to assess heme oxygenase (HO) activity (A) via bilirubin production and protein expression (B) via immunoblot. Bars are means ± SD, **p (C and D) SS-mice (n = 3/group) were untreated or infused with Hp or Hpx (1 μmol/kg) at baseline (time 0). Livers were removed and flash frozen 24, 48 or 72 hours after infusion. Hepatic microsomes were used to assess (C) HO activity and (D) HO-1 protein expression via immunoblot. Bars are means ± SD, *p (E and F) SS-mice (n = 3/group) were infused with vehicle or increasing doses (0.0156, 0.0625, 0.25 or 1.0 μmols/kg) of Hp or Hpx at baseline. Livers and kidneys were removed and flash frozen 24 hours after infusion. Hepatic (E) and kidney (F) microsomes were used to assess HO activity. Bars are means ± SD.</p
Chaunax nebulosus Ho & Last 2013
<p> <b> <i>Chaunax nebulosus</i> Ho & Last, 2013</b> </p> <p>(Fig. 4A; Tables 1, 2)</p> <p> <i>Chaunax nebulosus</i> Ho & Last, 2013: 437, figs. 1A, B, 2A–D (type locality: North of Monte Bello Islands, Western Australia, 19°36’S, 115°27’E, depth 245 m).</p> <p> <b>Material.</b> HUMZ 194367 (1, 69), Baruna Jaya IV, st. 126, 5°21.6’N, 94°5.7’E, 5°22.6’N, 94°4.7’E, off Sumatra, 384–426 m, 3 August 2005.</p> <p> <b>Remarks.</b> This species described recently from Western Australia is reported for the first time in Indonesia.</p>Published as part of <i>Ho, Hsuan-Ching, Kawai, Toshio & Satria, Fayakun, 2015, Species of the anglerfish genus Chaunax from Indonesia, with descriptions of two new species (Lophiiformes: Chaunacidae), pp. 301-308 in Raffles Bulletin of Zoology 63</i> on page 306, DOI: <a href="http://zenodo.org/record/4502357">10.5281/zenodo.4502357</a>
Additions to the moss flora of Endau Rompin National Park, Johore State, peninsular Malaysia
In a recent survey of the Endau Rompin National Park (ERNP) in Johore State, 81 species and 4 varieties of mosses were documented. This increases the previous count from 62 species and 3 varieties of mosses in ERNP to 111 species and 5 varieties in total. Of these, 30 species are new records for Johore State. Rhaphidostichum bunodicarpum and Trichosteleum stigmosum are two species new to Peninsular Malaysia. Thuidium assimile is a new record for West Malesia. A new combination, Papillidiopsis aquaticum (Dix.) Boon-Chuan Ho & B.C. Tan is proposed. In terms of species composition, the pan-tropical families of Calymperaceae, Fissidentaceae, Leucobryaceae and Sematophyllaceae predominate the moss flora of ERNP
Influence of Magnetic Field on the Kinetics of Ho(III) Solvent Extraction Using D2EHPA: A Comprehensive Study
The kinetics of Ho(III) extraction using di(2-ethylhexyl)phosphoric acid (D2EHPA) under the influence magnetic field are examined. The methodology for kinetics research is based on spectrophotometric techniques. Initial experiments without a magnetic field assess the influence of Ho(III) concentration (0.00625-0.1 m), pH (1-6), D2EHPA concentration (0.1-2 m), and temperatures (5-35 °C). Subsequent tests (5-35 °C) determine the influence of the magnetic field. Experimental considerations are supplemented with numerical simulations of the magnetic field affecting the extraction system. A white precipitate formed at the phase boundary is characterized using X-ray fluorescence (XRF), X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), and X-ray photoelectron spectroscopy (XPS) techniques. Post-extraction solutions are analyzed with nuclear magnetic resonance (NMR) spectroscopy to investigate the structure and magnetic properties of the D2EHPA-Ho(III) complex. The conducted research indicate that magnetic fields notably enhance kinetics of extraction above 25 °C, suggesting a possible change in the extraction mechanism
HO-1 downregulation favors BRAFV600 melanoma cell death induced by Vemurafenib/PLX4032 and increases NK recognition
Heme oxygenase 1 (HO-1) plays a pivotal role in preventing cell damage. Indeed, through the antioxidant, antiapoptotic and anti-inflammatory properties of its metabolic products, it favors cell adaptation against different stressors. However, HO-1 induction has also been related to the gain of resistance to therapy in different types of cancers and its involvement in cancer immune-escape has been hypothesized. We have investigated the role of HO-1 expression in Vemurafenib-treated BRAF(V600) melanoma cells in modulating their susceptibility to NK cell-mediated recognition. Different cell lines, isolated in house from melanoma patients, have been exposed to 1-10 mu M PLX4032, which efficiently reduced ERK phosphorylation. In three lines, Vemurafenib was able to induce only a limited decrease in cell viability, while HO-1 expression was upregulated. HO-1 silencing/inhibition was able to induce a further significant reduction of Vemurafenib-treated melanoma viability. Moreover, while NK cell degranulation and killing activity were decreased upon interaction with melanoma exposed to Vemurafenib, HO-1 silencing was able to completely restore NK cell ability to degranulate and kill. Furthermore, melanoma cell treatment with Vemurafenib downregulated the expression of ligands of NKp30 and NKG2D activating receptors, and HO-1 silencing/inhibition was able to restore their expression. Our results indicate that HO-1 downregulation can both improve the efficacy of Vemurafenib on melanoma cells and favor melanoma susceptibility to NK cell-mediated recognition and killing
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