| 1. |
- Larsson, Bengt, et al.
(författare)
-
Molecular oxygen in the rho Ophiuchi cloud
- 2007
-
Ingår i: Astronomy & Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 466:3, s. 5-
-
Tidskriftsartikel (refereegranskat)abstract
- Context: Molecular oxygen, O2, has been expected historically to be an abundant component of the chemical species in molecular clouds and, as such, an important coolant of the dense interstellar medium. However, a number of attempts from both ground and from space have failed to detect O2 emission.Aims: The work described here uses heterodyne spectroscopy from space to search for molecular oxygen in the interstellar medium. Methods: The Odin satellite carries a 1.1 m sub-millimeter dish and a dedicated 119 GHz receiver for the ground state line of O2. Starting in 2002, the star forming molecular cloud core ρ Oph A was observed with Odin for 34 days during several observing runs.Results: We detect a spectral line at v_LSR =+3.5 km s-1 with Δ v_FWHM=1.5 km s-1, parameters which are also common to other species associated with ρ Oph A. This feature is identified as the O2 (NJ = 11 - 1_0) transition at 118 750.343 MHz.Conclusions: The abundance of molecular oxygen, relative to H{2} , is 5 × 10-8 averaged over the Odin beam. This abundance is consistently lower than previously reported upper limits.Based on observations with Odin, a Swedish-led satellite project funded jointly by the Swedish National Space Board (SNSB), the Canadian Space Agency (CSA), the National Technology Agency of Finland (Tekes) and Centre National d'Étude Spatiale (CNES). The Swedish Space Corporation has been the industrial prime contractor and also is operating the satellite. Appendix A is only available in electronic form at http://www.aanda.org
|
|
| 2. |
|
|
| 3. |
- Bergh, Gösta, et al.
(författare)
-
Altered expression of the retinoblastoma tumor-suppressor gene in leukemic cell lines inhibits induction of differentiation but not G1-accumulation
- 1997
-
Ingår i: Blood. - 1528-0020. ; 89:8, s. 2938-2950
-
Tidskriftsartikel (refereegranskat)abstract
- The retinoblastoma tumor-suppressor gene, RB, has been implicated in tumor suppression, in regulation of the cell cycle, and in mediating cell differentiation. RB is necessary for hematopoiesis in mice, and aberrant RB-expression is associated with the progress and prognosis of leukemia. We have used antisense oligonucleotides, established clones stably expressing an antisense RB construct, and also established clones over expressing the retinoblastoma protein (pRb) to study the role of RB expression in monocytic differentiation induced by all-trans retinoic acid (ATRA) or 1-alpha-25-dihyroxycholecalciferol (Vit D3) in the monoblastic cell line U-937 and erythroid differentiation induced by transforming growth factor beta1 (TGFbeta1) and hemin in the erythroleukemic cell line K562. A reduction in pRb production in antisense RB-transfected U-937 clones was shown. Antisense oligonucleotides as well as expression of the antisense RB construct suppressed differentiation responses to ATRA or Vit D3, as judged by the capability to reduce nitro blue tetrazolium, by the appearance of monocyte-related cell surface antigens and by morphologic criteria. K562 cells showed decreased differentiation response to TGFbeta1, but not to hemin, when incubated with antisense oligonucleotides. U-937 antisense RB-transfected cells were also suppressed in their ability to upregulate levels of hypophosphorylated pRb when induced to differentiate. Although U-937 cells incubated with antisense oligonucleotides and clones expressing the antisense RB construct were hampered in their ability to differentiate on incubation with ATRA or Vit D3, the induced G0/G1-accumulation was similar to differentiating control cells treated with ATRA or Vit D3. Intriguingly, U-937 clones overexpressing RB were also inhibited in their differentiation response to ATRA or Vit D3 but not inhibited in their ability to respond with G0/G1 accumulation when induced with these substances. The results indicate that pRb plays a role in induced differentiation of U-937 cells as well as K562 cells involving mechanisms that, at least partially, are distinct from those inducing G1 accumulation.
|
|
| 4. |
|
|
| 5. |
- Eeg-Olofsson, Måns, 1967, et al.
(författare)
-
Implications for contralateral bone-conducted transmission as measured by cochlear vibrations.
- 2011
-
Ingår i: Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. - : LWW. - 1537-4505 .- 1531-7129. ; 32:2, s. 192-8
-
Tidskriftsartikel (refereegranskat)abstract
- The velocity response at the contralateral cochlea from bone-conducted (BC) stimulation depends on the stimulation position.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
- Eeg-Olofsson, Måns, 1967, et al.
(författare)
-
Transmission of bone-conducted sound in the human skull measured by cochlear vibrations.
- 2008
-
Ingår i: International journal of audiology. - : Informa UK Limited. - 1708-8186 .- 1499-2027. ; 47:12, s. 761-9
-
Tidskriftsartikel (refereegranskat)abstract
- One limitation with the Bone Anchored Hearing Aid (Baha) is too poor amplification for patients with moderate to severe sensorineural hearing losses. Therefore, we investigated if bone conducted (BC) sound transmission improves when the stimulation approaches the cochlea. Also the influence from the squamosal suture on BC sound transmission was investigated. Both sides of the heads on seven human cadavers were used and vibrational stimulation was applied at eight positions on each side with a frequency range of 0.1-10 kHz. A laser Doppler vibrometer was used to measure the resulting velocity of the cochlear promontory. It was found that the velocity of the promontory increases as the stimulation position approaches the cochlea; this was especially apparent at distances within 2.5 cm from the ear canal opening and when the stimulation position was in the opened mastoid. At frequencies above 500 Hz there was on average 10 to 20 dB greater vibrational response at the cochlea when the stimulation was close to the cochlea compared with the normal Baha position. Moreover, even if there were general indications of attenuation of BC sound when passing the squamosal suture, an effect from the suture could not be conclusively determined.
|
|
| 10. |
- Ehinger, Mats, et al.
(författare)
-
Expression of the p53 tumor suppressor gene induces differentiation and promotes induction of differentiation by 1,25-dihydroxycholecalciferol in leukemic U-937 cells
- 1996
-
Ingår i: Blood. - 1528-0020. ; 87:3, s. 1064-1074
-
Tidskriftsartikel (refereegranskat)abstract
- Leukemic U-937 cells, which lack normal p53, were stably transfected with a temperature-sensitive mutant of p53 to investigate the consequences for growth and differentiation. On induction of wild-type p53 activity at the permissive temperature, some of these cells underwent maturation as judged by the capacity for oxidative burst and the appearance of monocyte related cell surface molecules. Moreover, wild-type p53-expressing cells were more sensitive than p53-negative control cells to induction of differentiation by 1,25-dihydroxycholecalciferol; a twofold to fourfold increase of the fraction of cells showing signs of terminal maturation was observed when wild-type p53-expressing cells were incubated with 1,25-dihydroxycholecalciferol at concentrations that only slightly affected control cells. Whereas wild-type p53 activity per se induced maturation of certain cells, other underwent cell death judging from the reduced capability to exclude trypan blue and the appearance of fragmented DNA in flow cytometric analysis. The p53-induced cell death could be inhibited by incubation with 1,25-dihydroxy-cholecalciferol, but not all-trans retinoic acid. Thus, 1,25-dihydroxycholecalciferol, seemed to increase the survival of wild-type p53-expressing cells and to cooperate with wild-type p53 to induce differentiation. The data imply that p53-mediated maturation in U-937 cells depends on optimal regulation of signals for differentiation, survival and proliferation, and suggest a role for p53 in the differentiation induction of leukemic cells.
|
|
