Narrowband Signal Detection in OFDM Systems Using Spectral Shaping Techniques

Abstract: Orthogonal Frequency Division Multiplexing (OFDM) allow data to be transmitted efficiently and reliably by using multiple orthogonal subcarriers. It provides robustness against noise and corruption in the channel. The channel can be either wired or wireless depending on the particular application. Due to the close spacing of subcarriers, OFDM is susceptible to corruption caused by various narrowband signals such as Narrowband Interference (NBI). Spectral shaping shapes the Power Spectral Density (PSD) in order to have certain properties. Spectral shaping might improve the effectiveness of OFDM and make it sustainable in the long run for applications beyond the 4th generation of mobile communications (4G) and Long Term Evolution (LTE). We make use of spectral null codes and load them onto OFDM subcarriers. Introducing narrowband signals in the channel degrades the system’s performance and also eliminates the designed spectral properties. From this observation we infer that some narrowband noise is present in the channel. Previously, carriers hit by NBI or other narrowband noise had to be switched off manually. We found that combining OFDM with spectral shaping allows the presence of Narrowband signals in the channel to be detected and conclusions can be drawn over the channel quality. This did not improve the system in terms of bit error rate performance

Angiotensin II and Fever in Rodents

Angiotensin II (ANG II), a bioactive peptide well known to play an important role in blood-pressure and body-fluid regulation, participates in inflammatory responses, too. Recently, we reported results suggesting that ANG II is involved in the development of the fever induced by intravenous (i.v.) injection of lipopolysaccharide (LPS, 2 ?g/kg) in dehydrated rats (in which the secretion of ANG II is elevated). Furthermore, we verified the contributions made by ANG II and its type 1 receptor (AT1 receptor) to the LPS-induced production of interleukin-1β ; (IL-1β) in those rats. It therefore seems likely that in rats, ANG II and its receptors contribute to the induction of this fever at its 1st step (namely, the LPS-induced production of pyrogenic cytokines such as IL-1β). Moreover, we have revealed that intrahypothalamic (i.h.) ANG II and AT2 receptors are involved in the development of the fever induced by i.h. injection of prostaglandin E2 (PGE2), a final fever mediator. ANG II given i.h., which had no effect on the resting body temperature, facilitated PGE2-induced fever. These results suggest that in rats, ANG II and its receptors contribute to the induction of fever at its final step, too (namely, the action of PGE2 to cause fever). Finally, a single i.p. injection of IL-1β results in a weaker IL-1β-induced fever in AT2-receptor-deficient mice than in wild-type mice, suggesting that the brain AT2 receptor is involved in the development of fever (possibly at its final step) in mice as well. Collectively, these results suggest that in rodents, ANG II and its receptors contribute to the development of fever, both at the 1st and final steps in the pathway for fever induction

Gymnemic acids inhibit rabbit glyceraldehyde-3-phosphate dehydrogenase and induce a smearing of its electrophoretic band and dephosphorylation

AbstractGymnemic acids (GA) inhibited rabbit muscle glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity. Binding of GA to GAPDH was observed by surface plasmon resonance measurement. Incubation of GAPDH with GA induced a smearing of the GAPDH band in SDS–PAGE. The GA-induced smearing was diminished by prior incubation of GA with γ-cyclodextrin or by GA treatment with NAD. GA treatment did not affect the electrophoretic mobility of glucose-6-phosphate isomerase and dehydrogenase. GA treatment diminished the GAPDH band detected by an antibody to phosphoserine, but did not affect the phosphoserine bands of glucose-6-phosphate isomerase and dehydrogenase. These results indicated that GA specifically induced dephosphorylation of GAPDH

Angiotensin-Converting-Enzyme Inhibitor, Lisinopril, Reduces Lipopolysaccharide-Induced Expression of Splenic Interleukin-6 mRNA in Dehydrated Rats

Angiotensin II (ANG II) has been shown to have proinflammatory properties. To investigate whether ANG II is involved in the lipopolysaccharide (LPS)-induced production of a pyrogenic/proinflammatory cytokine, interleukin-6 (IL-6), we examined the effects of an angiotensin-converting-enzyme (ACE) inhibitor, lisinopril, on LPS-induced fever and on the expression of IL-6 mRNA in the spleen of dehydrated rats (in which the secretion of ANG II increases). The results showed that the ACE inhibitor significantly inhibited LPS-induced fever as well as the splenic expression of IL-6 mRNA in dehydrated rats. It is suggested that endogenous ANG II may be involved in the production of IL-6 that occurs in response to LPS, and thereby contribute to the LPS-induced febrile response in dehydrated rats

スイヨウエキチュウニオケル5'-AMPニリョウタイノブンシハイコウニカンスルNMR-DESERTホウニヨルケンキュウ

京都大学0048新制・論文博士理学博士乙第3269号論理博第567号新制||理||245(附属図書館)5166UT51-52-L86(主査)教授 波多野 博行, 教授 香月 裕彦, 教授 丸山 和博学位規則第5条第2項該当Kyoto UniversityDA