scispace - formally typeset
Search or ask a question

Showing papers by "Anders Björklund published in 2001"


Posted Content
TL;DR: This paper showed that the gender log wage gap in Sweden increases throughout the wage distribution and accelerates in the upper tail of the distribution, which they interpret as a glass ceiling effect, and examined whether this pattern can be asribed primarily to gender differences in labor market characteristics or to gender difference in rewards to those characteristics.
Abstract: Using data from 1998, we show that the gender log wage gap in Sweden increases throughout the wage distribution and accelerates in the upper tail of the distribution, which we interpret as a glass ceiling effect. Using earlier data, we show that the same pattern held at the beginning of the 1990's but not in the prior two decades. Further, we do not find this pattern either for the log wage gap between immigrants and non-immigrants in the Swedish labor market or for the gender gap in the U.S. labor market. Our findings suggest that a gender-specific mechanism in the Swedish labor market hinders women from reaching the top of the wage distribution. Using quantile regressions, we examine whether this pattern can be asribed primarily to gender differences in labor market characteristics or to gender differences in rewards to those characteristics. We estimate pooled quantile regressions with gender dummies, as well as separate quantile regressions by gender, and we carry out a decomposition analysis in the spirit of the Oaxaca-Blinder technique. Even after extensive controls for gender differences in age, education (both level and field), sector, industry, and occupation, we find that the glass ceiling effect we see in the raw data persists to a considerable extent.

847 citations


Journal ArticleDOI
TL;DR: The results of the first double-blind placebo-controlled trial using grafts of embryonic tissue to treat Parkinson's disease have aroused widespread interest and debate about the future of cell replacement therapies.
Abstract: The results of the first double-blind placebo-controlled trial using grafts of embryonic tissue to treat Parkinson's disease have aroused widespread interest and debate about the future of cell replacement therapies. What are the key issues that need to be resolved and the directions in which this technology is likely to develop?

248 citations


Journal ArticleDOI
TL;DR: It is concluded that intraventricular GDNF can successfully block the already initiated degenerative process in the substantia nigra, and that the effects achieved via the striatal route, when GDNF is given acutely after the lesion, diminish as the fibre terminal degeneration proceeds.
Abstract: Here we studied the effects of glial cell line-derived neurotrophic factor (GDNF) in a rat model that represents the symptomatic stages of Parkinson's disease. GDNF was infused starting 2 weeks after an intrastriatal 6-hydroxydopamine (6-OHDA) lesion in order to halt the ongoing degeneration of the nigrostriatal dopaminergic neurons. GDNF or vehicle was infused in the striatum or the lateral ventricle via an osmotic minipump over a total 4-week period (2-6 weeks postlesion). Motor function was evaluated by the stepping, paw reaching and drug-induced motor asymmetry tests before the pump infusion was initiated, and was repeated once during (5 weeks postlesion) and twice after the withdrawal of the minipumps (7 and 11 weeks postlesion). We found that within two weeks following the lesion approximately 40% of the nigral TH-positive neurons were lost. In the vehicle infusion groups there was an additional 20% cell loss between 2 and 12 weeks after the lesion. This latter cell loss occurred mainly in the caudal part of the SN whereas the cell loss in the rostral SN was almost complete within the first two weeks. Ventricular GDNF infusion completely blocked the late degenerating neurons in the caudal SN and had long lasting behavioural effects on the stepping test and amphetamine rotation, extending to 6 weeks after withdrawal of the factor. Striatal infusion affected the motor behaviour transiently during the infusion period but the motor performance of these animals returned to baseline upon cessation of the GDNF delivery, and the delayed nigral cell loss was marginally affected. We conclude that intraventricular GDNF can successfully block the already initiated degenerative process in the substantia nigra, and that the effects achieved via the striatal route, when GDNF is given acutely after the lesion, diminish as the fibre terminal degeneration proceeds.

138 citations


Journal ArticleDOI
TL;DR: It is demonstrated that immortalized neural stem cells that have been retrovirally transduced to produce NGF can markedly improve cognitive and neuromotor function and rescue hippocampal CA3 neurons when transplanted into the injured brain during the acute posttraumatic period.
Abstract: Object. Immortalized neural progenitor cells derived from embryonic rat hippocampus (HiB5), were transduced ex vivo with the gene for mouse nerve growth factor (NGF) to secrete NGF (NGF-HiB5) at 2 ng/hr/105 cells in culture. Methods. Fifty-nine male Wistar rats weighing 300 to 370 g each were anesthetized with 60 mg/kg sodium pentobarbital and subjected to lateral fluid-percussion brain injury of moderate severity (2.3–2.4 atm, 34 rats) or sham injury (25 rats). At 24 hours postinjury, 2 µl (150,000 cells/µl) of [3H]thymidine-labeled NGF-HiB5 cells were transplanted stereotactically into three individual sites in the cerebral cortex adjacent to the injury site (14 rats). Separate groups of brain-injured rats received nontransfected (naive [n])-HiB5 cells (12 animals) or cell suspension vehicle (eight animals). One week postinjury, animals underwent neurological evaluation for motor function and cognition (Morris water maze) and were killed for histological, autoradiographic, and immunocytochemical analysi...

121 citations


Journal ArticleDOI
TL;DR: It is reported that the survival, growth, and function of the grafted DA neurons greatly depend on the severity of the lesion of the host nigrostriatal system and this has implications for the optimal use of fetal nigral transplants in Parkinson patients in different stages of the disease.
Abstract: Previous studies have shown that the functional efficacy of intrastriatal transplants of fetal dopamine (DA) neurons in the rat Parkinson model depends on their ability to establish a new functional innervation of the denervated striatum. Here we report that the survival, growth, and function of the grafted DA neurons greatly depend on the severity of the lesion of the host nigrostriatal system. Fiber outgrowth, and to a lesser extent also cell survival, were significantly reduced in animals in which part of the intrinsic DA system was left intact. Moreover, graft-induced functional recovery, as assessed in the stepping, paw-use, and apomorphine rotation tests, was obtained only in severely lesioned animals, i.e., in rats with >70% DA denervation of the host striatum. Functional recovery seen in these animals in which the 6-hydroxydopamine (6-OHDA) lesion was confined to the striatum was more pronounced than that previously obtained in rats with complete lesions of the mesencephalic DA system, indicating that spared portions of the host DA system, particularly those innervating nonstriatal forebrain areas, may be necessary for the grafts to exert their optimal functional effect. These data have implications for the optimal use of fetal nigral transplants in Parkinson patients in different stages of the disease.

111 citations


Journal ArticleDOI
TL;DR: It is concluded that c‐Jun induction and phosphorylation may be involved in the cellular events leading to death of nigral dopaminergic neurons in vivo and that this response can be modulated by glial‐cell‐line‐derived‐neurotrophic factor.
Abstract: This study was designed to determine whether induction and phosphorylation of the transcription factor c-Jun is associated with lesion-induced death of dopaminergic neurons of the substantia nigra pars compacta, and if this cellular response is modulated by glial-cell-line-derived neurotrophic factor. In adult rats, delayed dopaminergic neuron cell death induced by intrastriatal 6-hydroxydopamine injection led to a marked increase in the number of both c-Jun- and phosphorylated c-Jun-immunoreactive nuclei in the substantia nigra pars compacta. The response was maximal before any significant loss of nigral neurons could be detected (on day 7 post lesion) and was confined to the dopaminergic neurons. Similarly, 6-hydroxydopamine lesion of the striatal dopaminergic terminals or excitotoxic lesion of the striatal target neurons in neonatal rats resulted in an increased number of c-Jun- and phosphorylated c-Jun-immunoreactive nigral nuclei that preceded the loss of nigral dopaminergic neurons. By contrast, after an excitotoxic lesion of the striatal target neurons in the adult rat, resulting in atrophy but not cell death of the nigral dopaminergic neurons, no upregulation of either c-Jun or phosphorylated c-Jun was found. A single injection of 10 microg of glial-cell-line-derived-neurotrophic factor given at day 3 after the intrastriatal 6-hydroxydopamine lesion reduced the number of c-Jun- and phosphorylated c-Jun-immunoreactive nuclei in the substantia nigra and protected the dopaminergic neurons from the ensuing cell death. We conclude that c-Jun induction and phosphorylation may be involved in the cellular events leading to death of nigral dopaminergic neurons in vivo and that this response can be modulated by glial-cell-line-derived-neurotrophic factor.

71 citations



Journal ArticleDOI
TL;DR: A critical look at new data that underpin the last of these claims: the chimeric stem cell.

20 citations


Posted Content
TL;DR: In this article, the change in family gross income inequality between 1951 and 1973 was analyzed using two new samples of the Swedish population from 1951 and 1956 containing tax register data, and compared the results with those obtained from the Swedish Level of Living survey from 1967 and 1973.
Abstract: We analyse the change in family gross income inequality between 1951 and 1973. We use two new samples of the Swedish population from 1951 and 1956 containing tax register data, and compare the results with those obtained from the Swedish Level of Living survey from 1967 and 1973. Gini coefficients, four different Generalised entropy measures as well as decile group shares of total income are calculated. We also do two different decompositions: one between different demographic groups and one between the male and female component of family income. Finally, we examine to what extent zero family income records really reflect low economic welfare by using interview data from the 1968 Swedish Level of Living Survey.

5 citations