| 1. |
- Haneda, Katsuyuki, et al.
(author)
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Comparison of angular and delay spreads between channel measurements and the COST channel model
- 2010
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In: ; , s. 477-480
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Conference paper (peer-reviewed)abstract
- The COST2100 channel model is a reference channel model which provides dynamic multiple-input multiple-output channel responses for radio system simulations. In this paper, channels created by the COST2100 model were compared to channel measurements in order to understand behaviours of the model. Model parameters of the COST2100 model were derived by dynamic double-directional channel measurements with which the channel realizations from the COST2100 model were compared. Delay and angular spreads were used as a simple but important metric for the comparison. Despite a fundamental difference that the COST2100 model is a geometry- based stochastic model while the channel measurements are ob- tained in deterministic environments, the comparison revealed an acceptable level of agreement for practical channel simulations.
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| 2. |
- Haneda, Katsuyuki, et al.
(author)
-
Comparison of delay and angular spreads between channel measurements and the COST2100 channel model
- 2010
-
In: 2010 Loughborough Antennas and Propagation Conference, LAPC 2010. - 9781424473052 ; , s. 477-480
-
Conference paper (peer-reviewed)abstract
- The COST2100 channel model is a reference channel model which provides dynamic multiple-input multiple-output channel responses for radio system simulations. In this paper, channels created by the COST2100 model were compared to channel measurements in order to understand behaviours of the model. Model parameters of the COST2100 model were derived by dynamic double-directional channel measurements with which the channel realizations from the COST2100 model were compared. Delay and angular spreads were used as a simple but important metric for the comparison. Despite a fundamental difference that the COST2100 model is a geometry-based stochastic model while the channel measurements are obtained in deterministic environments, the comparison revealed an acceptable level of agreement for practical channel simulations
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| 3. |
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| 4. |
- Junnila, Arttu, et al.
(author)
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HSD17B1 Compensates for HSD17B3 Deficiency in Fetal Mouse Testis but Not in Adults.
- 2024
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In: Endocrinology. - 0013-7227 .- 1945-7170. ; 165:6
-
Journal article (peer-reviewed)abstract
- Hydroxysteroid (17β) dehydrogenase (HSD17B) enzymes convert 17-ketosteroids to 17beta-hydroxysteroids, an essential step in testosterone biosynthesis. Human XY individuals with inactivating HSD17B3 mutations are born with female-appearing external genitalia due to testosterone deficiency. However, at puberty their testosterone production reactivates, indicating HSD17B3-independent testosterone synthesis. We have recently shown that Hsd17b3 knockout (3-KO) male mice display a similar endocrine imbalance, with high serum androstenedione and testosterone in adulthood, but milder undermasculinization than humans. Here, we studied whether HSD17B1 is responsible for the remaining HSD17B activity in the 3-KO male mice by generating a Ser134Ala point mutation that disrupted the enzymatic activity of HSD17B1 (1-KO) followed by breeding Hsd17b1/Hsd17b3 double-KO (DKO) mice. In contrast to 3-KO, inactivation of both HSD17B3 and HSD17B1 in mice results in a dramatic drop in testosterone synthesis during the fetal period. This resulted in a female-like anogenital distance at birth, and adult DKO males displayed more severe undermasculinization than 3-KO, including more strongly reduced weight of seminal vesicles, levator ani, epididymis, and testis. However, qualitatively normal spermatogenesis was detected in adult DKO males. Furthermore, similar to 3-KO mice, high serum testosterone was still detected in adult DKO mice, accompanied by upregulation of various steroidogenic enzymes. The data show that HSD17B1 compensates for HSD17B3 deficiency in fetal mouse testis but is not the enzyme responsible for testosterone synthesis in adult mice with inactivated HSD17B3. Therefore, other enzymes are able to convert androstenedione to testosterone in the adult mouse testis and presumably also in the human testis.
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| 5. |
- Liu, Lingfeng, et al.
(author)
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The COST 2100 MIMO Channel Model
- 2012
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In: IEEE Wireless Communications. - 1536-1284. ; 19:6, s. 92-99
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Journal article (peer-reviewed)abstract
- The COST 2100 channel model is a geometry-based stochastic channel model (GSCM) that can reproduce the stochastic properties of multi-link Multiple-Input Mulitple-Output (MIMO) channels over time, frequency and space. By contrast to other popular GSCMs, the COST 2100 approach is generic and flexible, making it suitable to model multi-user or distributed MIMO scenarios. In this paper a concise overview of the COST 2100 channel model is presented. Main concepts are described, together with useful implementation guidelines. Recent developments, including dense multipath components, polarization and multi-link aspects are also discussed.
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| 6. |
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| 7. |
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| 8. |
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| 9. |
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| 10. |
- Poutanen, Juho, et al.
(author)
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Multi-link MIMO channel modeling using geometry-based approach
- 2012
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In: IEEE Transactions on Antennas and Propagation. - 0018-926X. ; 60:2, s. 587-596
-
Journal article (peer-reviewed)abstract
- Geometry-based stochastic channel models (GSCMs) are extended to support multi-link simulations by applying the concept of common clusters. This novel approach aims to control the correlation between different links, inter-link correlation, by adjusting the amount of power simultaneously propagating via the same clusters in the different links. The behavior of common clusters is analyzed based on dual-link channel measurements, and a multi-link GSCM is developed based on common clusters. In addition, the effects that the common clusters have on inter-link correlation and on sum rate capacity are investigated based on simulations. Finally, comparison between simulations and measurements is done in order to indicate the validity of the proposed multi-link GSCM.
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