A method is proposed for obtaining the spectrum for noise that causes the phase decoherence of a qubit directly from experimentally available data. The method is based on a simple relationship between the spectrum and the coherence time of the qubit in the presence of a π pulse sequence. The relationship is found to hold for every system of a qubit interacting with the classical-noise, bosonic, and spin baths.

Klotho is a circulating protein, and Klotho deficiency disturbs endothelial integrity, but the molecular mechanism is not fully clarified. We report that vascular endothelium in Klotho-deficient mice showed hyperpermeability with increased apoptosis and down-regulation of vascular endothelial (VE)-cadherin because of an increase in VEGF-mediated internal calcium concentration ([Ca 2+ ]i) influx and hyperactivation of Ca 2+ -dependent proteases. Immunohistochemical analysis, the pull-down assay using Klotho-fixed agarose, and FRET confocal imaging confirmed that Klotho protein binds directly to VEGF receptor 2 (VEGFR-2) and endothelial, transient-receptor potential canonical Ca 2+ channel 1 (TRPC-1) and strengthens the association to promote their cointernalization. An in vitro mutagenesis study revealed that the second hydrolase domain of Klotho interacts with sixth and seventh Ig domains of VEGFR-2 and the third extracellular loop of TRPC-1. In Klotho-deficient endothelial cells, VEGF-mediated internalization of the VEGFR-2/TRPC-1 complex was impaired, and surface TRPC-1 expression increased 2.2-fold; these effects were reversed by supplementation of Klotho protein. VEGF-mediated elevation of [Ca 2+ ]i was sustained at higher levels in an extracellular Ca 2+ -dependent manner, and normalization of TRCP-1 expression restored the abnormal [Ca 2+ ]i handling. These findings provide evidence that Klotho protein is associated with VEGFR-2/TRPC-1 in causing cointernalization, thus regulating TRPC-1–mediated Ca 2+ entry to maintain endothelial integrity.

Uraemic rats made by adenine diet developed severe abnormalities of calcium metabolism in a relatively short period and therefore they may serve as a useful model for the analysis of parathyroid hyperplasia and vascular calcification in chronic renal failure.

Objective: The biological activities of interleukin-17 (IL-17), a newly cloned cytokine, have not been fully elucidated. The present study was designed to assess the in vitro and in vivo effect of transfecting the IL-17 gene into tumor cells. Methods: A complementary DNA (cDNA) encoding human IL-17 (hIL-17) was obtained by polymerase chain reaction amplification from the human CD4+ T cell cDNA library and inserted into the plasmid pRc/cytomegalovirus to construct an expression vector for the hIL-17 gene. Murine Meth-A fibrosarcoma cells were transfected with the hIL-17 gene using the lipofectin method. The hIL-17 gene-expressing clone (Meth-A/IL-17) was selected and analyzed for cytokine expression by Northern blot. Results: There was no significant difference in the in vitro proliferation rate among parent Meth-A, cells transfected with vector alone and Meth-A/IL-17 cells. When the tumor cells were transplanted subcutaneously into BALB/c nude (nu+/nu+) mice, there was no difference in in vivo growth rates among the three cell lines. Challenge with tumor cells in conventional BALB/c mice, however, resulted in the rejection of Meth-A/IL-17 cells, but the other two lines did grow. After immunization with Meth-A/IL-17 cells, the mice were rechallenged by parent Meth-A or syngeneic MOPC-104E plasmacytoma cells; the immunized mice rejected the Meth-A cells, but not the MOPC-104E cells. Injecting the anti-thy 1,2 (CD90), anti-CD4 or anti-CD8 monoclonal antibody into conventional BALB/c mice resulted in the resumption of in vivo growth of Meth-A/IL-17 cells, but injecting the anti-asialo GM1 antibody did not. Furthermore, flow cytometric analysis demonstrated a significant increase in the expression of major histocompatibility complex (MHC) class I and class II antigens and lymphocyte function-associated antigen-1 on Meth-A/IL-17 cells. Conclusion: Meth-A cells transfected with the hIL-17 gene can induce tumor-specific antitumor immunity by augmenting the expression of MHC class I and II antigens, and both CD4+ and CD8+ T cells may play important roles in inducing antitumor immunity, suggesting the possibility of developing a tumor vaccine incorporating IL-17-transfected tumor cells.

The rostra1 ventrolateral medulla (RVLM) has been known to be a major regulating center of sympathetic and cardrovascular acttvtttes An assoctatton between essential hypertension and neurovascular compressron of the RVLM has been reported m clmrcal observattons, mcludmg magnetic resonance tmagmg (MRI) studies To reconfirm this relattonshtp, we performed MRI usmg a high-resolutton 5 12X512 matrix m pattents wtth essential and secondary hypertenston and m normotensrve SubJeCtS The duratton of hypertension and the degree of organ damage by hypertension were not srgmficantly drfferent between the two hypertension groups Neurovascular compressron of the RVLM was observed m 74% of the essential hypertension group, and the incidence of compresston was srgmficantly higher than m the secondary hypertension group (11%) or m the normotenstve group (13%) (P< 01) These results from the clmrcal studies suggest that neurovascular compressron of the RVLM ts, at least m part, causally related to essential hypertension Although blood pressure elevation by pulsatrle compressron of the RVLM m an experimental baboon model has already been reported, tts un-T he rostra1 ventrolateral medulla (RVLM) contams neurons that are considered to be an orlgin of tome sympathetic discharge and a maJor center regulating sympathetic and cardiovascular actrvities 132 Chemical or electrrcal sttmulatron of the RVLM increases sympathetic nerve activities to elevate blood pressure, whrle its destruction causes hypotensron.s-6Since the report by Jannetta and Gendell,T it has been shown that posterior inferior cerebellar artery, anterior inferior cerebellar artery, and vertebral artery occasionally compress the medulla oblongata and that patients with essential hypertension are associated with neurovascular compresston of the ventrolateral medulla at the root-entry zone of glossopharyngeal and vagus nerves (ie, the RVLM) m clnucal observations mcludmg magnetic resonance imagmg (MRI) studtes.a-16 To reconfirm this relationship, we performed MRI using a high-resolution 5 12x5 12 matrix, a newly developed magnetic device, in patients with essential and secondary hypertension and in normotensive SubJects. Jannetta et a110 also reported blood pressure elevation by pulsatile compression of the RVLM m an experimental baboon model However, the mechanism of the development ofFrom the Second Department of Medicine and Department of Radiology (S N , T M ), Kyoto Prefectural Umversny of Medlcme, Kawaramacht-HnokoJt, Kanngyo-ku, Kyoto City, Japan Reprint requests to Dr Satoshr Morrmoto, Second Department of Medicine, Kyoto Prefectural Umversrty of Medtcme, KawaramachtHirokojr, Kamtgyo-ku, Kyoto city 602, Japan 0 1997 American Heart Assocratron, Inc -hypertension was not mvesttgated precisely. Therefore, we performed experimental studies to mvesttgate whether pulsatile compression of the RVLM would increase arterial pressure and to determine the underlying mechanism of the pressor response m rats Clinical Studies MethodsNineteen patients with essential hypert...

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As a means for increasing sympathetic activity, male weanling rats were given 8% sucrose solution to drink instead of water. After 5 weeks, systolic pressures measured with a tail-cuff method became appreciably elevated, and the elevation was verified when phasic pressures were later recorded directly from femoral catheters. Successful induction of sympathetic overactivity was considered a likely explanation because sucrose-ingesting rats, compared with untreated controls, had faster heart rates and larger hypotensive responses to alpha-adrenergic blockade with phentolamine. Upon graded electrical stimulation of the ventromedial hypothalamus under urethane anesthesia, resulting pressor and sympathetic nerve responses were also larger in sucrose-treated rats. By contrast, pressor responses to injections of norepinephrine or tyramine were unaffected, thereby indicating that cardiovascular sensitivity had not been enhanced by sucrose ingestion. During intravenous glucose tolerance tests, increases in plasma insulin were consistently lower in sucrose-treated than control rats even though corresponding increases in plasma glucose were just transiently higher. These results support the interpretation that chronic sucrose ingestion inhibits pancreatic insulin secretion and elevates blood pressure by stimulating the ventromedial hypothalamus to increase sympathetic activity.