| 1. |
- Gustafsson, Claes G. R., 1965, et al.
(författare)
-
Phylogenetic relationships among species of the neotropical genus Randia (Rubiaceae, Gardenieae) inferred from molecular and morphological data.
- 2002
-
Ingår i: Taxon. ; 51:4, s. 661-674
-
Tidskriftsartikel (refereegranskat)abstract
- Relationships among 38 taxa of Randia (Rubiaceae, Gardenieae) are estimated using nuclear ribosomal internal transcribed spacers (ITS), the 5S non-transcribed spacer (5S-NTS), and six morphological characters. In addition to Randia, 13 species from eight related genera in Gardenieae (four African, four neotropical) formed the ingroup. Three species from three more distantly related genera in Gardenieae (one African, two neotropical) were chosen as the outgroup. Representatives of the African ingroup genera Calochone, Macrosphyra, Oligocodon and Preussiodora formed a well supported monophyletic group as did the neotropical genera Rosenbergiodendron, Sphinctanthus and Tocoyena. Only when including morphological characters did Randia form a monophyletic group corresponding approximately to contemporary circumscription of the genus, but in this analysis Casasia appears sister to a group of Mexican, Central American, and Antillean Randia. There is no strong jackknife support, however, for either Randia or Casasia to be monophyletic. It is concluded that Randia is comprised of several distinct groups, each with its own geographical distribution. One group of Mexican, Central American, and Antillean Randia, including the type species, can be recognized as Randia in a strict sense. Two other South American groups can be recognized as separate taxa. One of these groups comprises mainly lowland species, and the second is comprised of strictly Andean species.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
- Bergman, Kerstin, et al.
(författare)
-
Ska vi äta våra döda: Linné mellan tro och nytta
- 2002
-
Ingår i: I ordets smedja: Festskrift till Per Rydén. - 9172034947 ; , s. 182-191
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- About the struggle between faith and utilitarian aspects in the writings of Carl von Linné.
|
|
| 5. |
|
|
| 6. |
- Chagin, A S, et al.
(författare)
-
Estrogen receptor-beta inhibits skeletal growth and has the capacity to mediate growth plate fusion in female mice.
- 2004
-
Ingår i: Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. - 0884-0431 .- 1523-4681. ; 19:1, s. 72-7
-
Tidskriftsartikel (refereegranskat)abstract
- To determine the long-term role of ER beta in the regulation of longitudinal bone growth, appendicular and axial skeletal growth was followed and compared in female ER beta-/-, ER alpha-/-, and ER alpha-/- beta-/- mice. Our results show that ER beta inhibits appendicular and axial skeletal growth and has the capacity to induce fusion of the growth plates. INTRODUCTION: Estrogen affects skeletal growth and promotes growth plate fusion in humans. In rodents, the growth plates do not fuse after sexual maturation, but prolonged treatment with supraphysiological levels of estradiol has the capacity to fuse the growth plates. It should be emphasized that the estrogen receptor (ER) alpha-/- and the ER alpha-/- beta-/-, but not the ER beta-/-, mouse models have clearly increased serum levels of estradiol. MATERIALS AND METHODS: The skeletal growth was monitored by X-ray and dynamic histomorphometry, and the growth plates were analyzed by quantitative histology, calcein double labeling, bromodeoxyuridine (BrdU) incorporation, and TUNEL assay in 4- and 18-month-old female ER beta-/-, ER alpha-/-, and ER alpha-/- beta-/- mice. RESULTS: Young adult (4-month-old) ER beta-/- mice demonstrated an increased axial- and appendicular-skeletal growth, supporting the notion that ER beta inhibits skeletal growth in young adult female mice. Interestingly, the growth plates were consistently fused in the appendicular skeleton of 18-month-old female ER alpha-/- mice. This fusion of growth plates, caused by a prolonged exposure to supraphysiological levels of estradiol in female ER alpha-/- mice, must be mediated through ER beta because old ER alpah-/- beta-/- mice displayed unchanged, unfused growth plates. CONCLUSIONS: Our results confirm that ER beta is a physiological inhibitor of appendicular- and axial-skeletal growth in young adult female mice. Furthermore, we made the novel observation that ER beta, after prolonged supraphysiological estradiol exposure, has the capacity to mediate growth plate fusion in old female mice.
|
|
| 7. |
|
|
| 8. |
- Erlandsson, M C, et al.
(författare)
-
Role of oestrogen receptors alpha and beta in immune organ development and in oestrogen-mediated effects on thymus.
- 2001
-
Ingår i: Immunology. - : Wiley. - 0019-2805 .- 1365-2567. ; 103:1, s. 17-25
-
Tidskriftsartikel (refereegranskat)abstract
- Oestrogens affect the development and regulation of the immune system. To determine the role of oestrogen receptors alpha (ER-alpha) and beta (ER-beta) on the development of the immune system, male ER-alpha (ERKO) and ER-beta (BERKO) mice, as well as alphabeta-double knockout (DERKO) mice, were studied. Deletion of ER-alpha led to hypoplasia of both thymus and spleen. Interestingly, a higher frequency of immature double CD4+ CD8+ thymocytes was found in ER-alpha(-) mice compared with ER-alpha(+) mice. Female oophorectomized BERKO mice given oestradiol (E2) displayed a similar degree of thymic atrophy compared with the wild-type strain but showed only limited involution of thymus cortex and no alteration of thymic CD4/CD8 phenotype expression. Our data demonstrate that expression of ER-alpha, but not ER-beta, is mandatory in males for development of full-size thymus and spleen, whereas expression of ER-beta is required for E2-mediated thymic cortex atrophy and thymocyte phenotype shift in females. A potential background for the above findings may be down-regulated activity in the growth hormone/insulin-like growth factor-1 (GH/IGF-1) axis in males lacking ER-alpha and suppressed sensitivity of females lacking ER-beta to E2-mediated suppression of IGF-1.
|
|
| 9. |
- Gaspari, Martina, et al.
(författare)
-
The mitochondrial RNA polymerase contributes critically to promoter specificity in mammalian cells.
- 2004
-
Ingår i: The EMBO journal. - : Wiley. - 0261-4189 .- 1460-2075. ; 23:23, s. 4606-14
-
Tidskriftsartikel (refereegranskat)abstract
- Initiation of transcription in mammalian mitochondria depends on three proteins: mitochondrial RNA polymerase (POLRMT), mitochondrial transcription factor A (TFAM) and mitochondrial transcription factor B2 (TFB2M). We show here that the recombinant mouse and human transcription machineries are unable to initiate transcription in vitro from the heterologous light-strand promoter (LSP) of mitochondrial DNA. This species specificity is dependent on the interaction of TFAM and POLRMT with specific distal and proximal promoter elements. A sequence element localized from position -1 to -2 relative to the transcription start site in LSP functionally interacts with POLRMT. The POLRMT/TFB2M heterodimer is unable to interact with promoter elements and initiate even abortive transcription in the absence of TFAM. TFAM is thus an integral part of the mammalian transcription machinery, and we propose that TFAM induces a structural change of the promoter that is required for POLRMT-dependent promoter recognition.
|
|
| 10. |
|
|
