A field-effect transistor constitutes a propagation structure along its gate width. Telegraphists equations are solved for this structure. One deduces from this the effect of the propagation on the transistor Z-parameters which can be taken into account in electric simulations and which may improve the use of long transistors at lower frequencies and of short transistors at higher frequencies [1]. New elements have been added to the equivalent circuit in order to take into account the propagation phenomena.

A method for the parameter measurement of a noise-figure meter is proposed. It permits us to perform noise-figure measurement without a tuner. The only assumption lies in the correlation term of the noise model. Variation of the noise source with the temperature is taken into account. (c) 2005 Wiley Periodicals, Inc.

Compression point 1dB (CP1dB) and input 3rd order intercept point (IIP3) are useful parameters to characterize the nonlinear property of RF devices. Automatization methods of CP1dB and IIP3 calculation have been developed and have been realized using LabVlEW software platform. The proposed CP1dB calculation method is based on cubic spline interpolation of a dynamic characteristic of the device under test (DUT). This approach allows the user to reach accuracy about 0.1 dBm. That is comparable with an instrumental accuracy. This result can be reached because of the small procedural error and the algorithm robustness to accidental errors of experimental data. The method of the IIP3 calculation is based on solution of the extrapolation problem when the linear part of the DUT dynamic characteristic is described in analytical form. An automatic correction of the input signal level to preserve the linear regime of the DUT is the feature of methods. The measurement set to measure IIP3 and CP1dB has been assembled and its efficiency has been verified experimentally. For this purpose the CP1dB and IIP3 of pseudo morphic high electron mobility transistors (pHEMT) have been determined. The obtained values of CP1dB and IIP3 are of 6.5dBm and 20dBm respectively in 5Ghz frequency range.

An on-wafer noise parameter measurement method has been developed on a 2.8-18 GHz frequency band. The test bench mainly consists of a probe station, a vector network analyzer and a noise figure meter (NFM). Five noise power measurements and a time- and frequency-domain analysis are used to extract the bench and the device under test (DUT) characterisitics. The method is fitting for any DUT with no assumption on its characteristics and without an impedance-tuner. The aim of this study is to extend the method to a wider frequency band. The main problem is due to the change in the frequency band of the NFM and consists in the incompatibility of the use of direct and inverse Fourier transforms with discontinued characteristics. Discontinuities might provide parasitic additionnal terms, which could invalidate the method. Only a finer analysis of the method can conclude to its accuracy, depending on the kind of discontinuities. In the 0.1-18 GHz frequency band, only our receiver characterics present discontinuities at 1.6 GHz and 2.4 GHz. The problem is easily summarized to the discontinuities of the intercorrelation power sources terms. A deepen study concludes on the effects of these discontinuities and allows an increase of the frequency band. Experimental results on an active two-port are given.

A new resonating mode has been used in a cylindrical cavity to measure the moisture content and the specific mass of cigarettes. A simple theoretic calculation gives the relation between the sample complex permittivity and the characteristics of the cavity. A model is proposed to extract the moisture content and the specific mass from the complex permittivity. An experimental setup has been demonstrated. It uses a servo-controlled oscillator. This setup is ready to be tried on a production machine.

A method is developed that allows the intrinsic parameters of a transistor with a wide gate to be evaluated, taking the effects of propagation into account. It is shown that these parameters are not linearly related to the gate width. The proposed method provides a new transistor model that can be implemented in a circuit simulation.

The neuropeptide neurotensin (NT) elicits hypothermic and naloxone-insensitive analgesic responses after brain injection. Recent pharmacological evidence obtained with NT agonists and antagonists suggests that these effects are mediated by a receptor distinct from the initially cloned high-affinity NT receptor (NTR1). The recent cloning of a second NT receptor (NTR2) prompted us to evaluate its role in NT-induced analgesia. Intracerebroventricular injections in mice of two different antisense oligodeoxynucleotides from the NTR2 markedly decreased NTR2 mRNA and protein and reduced NT-induced analgesia. This effect was specific, because NTR1 levels were unaffected, and sense or scramble oligodeoxynucleotides had no effect. Structure-activity studies revealed a close correlation between the analgesic potency of NT analogs and their affinity for the NTR2 and disclosed potent and selective agonists of this receptor. These data confirm that NTR1 is involved in the NT-elicited turning behavior and demonstrate that the NTR2 mediates NT-induced analgesia.

A cylindrical cavity in TM010 mode is used to measure simultaneously the specific mass and the humidity ratio of cigarettes on a production line. The internal Q-factor and the resonance frequency are related to the complex permittivity of tobacco. Simple relations are proposed between the complex permittivity and the specific mass and the humidity ratio. The cavity is included into a set-up on which the principal voltages are measured in order to calculate the specific mass and the humidity ratio.

An original transistor modeling and synthesis approach, using electromagnetic simulation, is successfully used to describe various FET response. Starting from one single sample, this novel method can predict numerous other device response, which can strongly differ in geometry and gate width. This model shows excellent agreement with experimental data. Other papers have been published on active circuit electromagnetic analysis but, we propose and demonstrate, for the first time, synthesis ability.

We measure transistor noise power density and compute the Fourier's transform. Finally, spectral parametric modeling is used to extract noise waves correlation matrix. Results obtained by this new method has been experimentally compared with a conventional method.

Neurotensin (NT) and neurotensin receptors (NTRs) are widely found in the brain, NT may be considered as a mitogen factor in some tissues. However, no NT-mediated effects on glioma cell proliferation have been reported so far. In our present study we investigated the influence of NT on the proliferation of astrocytic tumor cell lines. To this end we used a synthetic NT agonist (JMV-449), a protease inhibitor which blocks the natural degradation of NT (JMV-531), and NT. The in vitro biological models used in the present study included the low grade SW1088, and the high grade U87, U373 and A172 astrocytic tumor cell lines. The peptide-induced influence on astrocytic tumor cell proliferation was investigated by means of the colorimetric MTT assay. Our results show that the NT and the NT agonist significantly stimulated the proliferation in 2/4 and 3/4 of the astrocytic cell lines respectively. Similarly, compound JMV-531 also induced an increase in the proliferation of 2/4 of the astrocytic cell lines. This marked influence of the NT and NT agonists, or the enzyme-endogenous prevention of its degradation on the regulation of astrocytic tumor growth therefore suggests that NT antagonists might be used to treat certain patients with high grade astrocytic tumors that do not respond to chemotherapy and/or radiotherapy.

Neurotensin (NT) has been shown to be involved in neuroendocrine regulation, and the presence of both the peptide and its receptors has been demonstrated in the hypothalamus. In the present study, we show that hypothalamic neurons in primary cultures express the neurotensin receptor (NTR) and we examined a possible regulation of this receptor by glucocorticoids and activators of adenylate cyclase. In the hypothalamic cultures, 125 I‐NT bound to a single class of binding sites, presenting a selectivity similar to that observed for the high‐affinity NTR previously described in the adult rat brain. Radioautographic studies demonstrated that these 125 I‐NT binding sites were present on 3% of the neurons. A 48‐h treatment with forskolin (fsk) decreased 125 I‐NT binding by 30%. No effect of dexamethasone (dex) alone was found on that parameter. However, a combined treatment with both agents led to a 40% decrease in 125 I‐NT binding, corresponding to a reduced number of binding sites, and to a 68% decrease in the amount of NTR mRNA. In parallel, the dex plus forsk treatment increased NT release in the incubation medium. Moreover, the decreases in 125 I‐NT binding and NTR mRNA induced by this treatment were abolished in the presence of an anti‐NT antibody or SR 48692, a non‐peptidic antagonist of NTR, suggesting that the down‐regulation of NTR observed after dex plus fsk treatment was mediated by the release of endogenous NT. Agonist‐induced down‐regulation of the NTR in this system was confirmed by the application of an exogenous NT analogue, JMV 449. The present findings indicate that, in hypothalamic cultures, dex and fsk indirectly down‐regulate NTR expression via the release of endogenous NT.

A C-terminal cyclic 8–13 neurotensin fragment analog, JMV 1193, a direct agonist of central neurotensin receptors, is able to cross both the cerebrospinal fluid-brain barrier and the blood-brain barrier. When administered intracerebroventricularly (i.c.v.), its hypothermic effect was potentiated by the enkephalinase inhibition induced either by thiorphan (simultaneous intracerebroventricular administration of 10 μg) or by the thiorphan prodrug, acetorphan (intravenous (i.v.) administration of 10 mg/kg). Such a potentiation was not observed when both JMV 1193 and acetorphan were administered intravenously. Therefore it appears that the sensitivity of JMV 1193 to enkephalinase depends on its route of administration. It is exposed to this peptidase after i.c.v. injection (when crossing the cerebrospinal fluid-brain barrier), while it is not after i.v. administration (when crossing the blood-brain barrier).

Selective and mixed inhibitors of the three zinc metallopeptidases that degrade neurotensin (NT), e.g. endopeptidase 24-16 (EC 3.4.24.16), endopeptidase 24-11 (EC 3.4.24.11 or neutral endopeptidase, NEP) and endopeptidase 24-15 (EC 3.4.24.15), and leucine-aminopeptidase (type IV-S), that degrades the NT-related peptides, Neuromedin N (NN), are of great interest. On the structural basis of compound JMV 390-1 (N-[3-[(hydroxyamino)carbonyl]-1-oxo-2(R)-benzylpropyl]-L- isoleucyl-L-leucine), which was a full inhibitor of the major NT degrading enzymes, several hydroxamate inhibitors corresponding to the general formula HONHCO-CH2-CH(CH2-C6H5)CO-X-Y-OH (with X-Y = dipeptide) have been synthesized. Compound 7a (X-Y = Ile-Ala) was nearly 40-times more potent in inhibiting EC 24-16 than NEP and more than 800-times more potent than EC 24-15, with an IC50 (12 nM) almost equivalent to that of compound JMV 390-1. Therefore, this compound is an interesting selective inhibitor of EC 24-16, and should be an interesting probe to explore the physiological involvement of EC 24-16 in the metabolism of neurotensin.

ENSEA has been associated with the microelectronic training actions supported by the European Esprit VLSI Design Action (VDA) project and by the National Microelectronic Committee for Education (CNFM). Since 1990 ENSEA has provided a high level training in the fields of Microwave Monolithic Integrated Circuits (MMIC) on gallium aresenide (GaAs). A presentation of the various aspects of this formation including training programs, and material as well as results are described in this communication.

The synthesis of chiral N-protected tetramic acid derivatives which are important precursors of β-hydroxy γ-amino acid under mild conditions is described. Reaction of urethane-N-carboxyanhydrides (UNCAs) with Meldrum's acid in the presence of a tertiary amine, followed by subsequent cyclisation produced tetramic acid derivatives. This procedure is applicable to Boc-, Fmoc- and Z- N-carboxyanhydrides.

The present study was designed to compare, with respect to structure-activity relationships, the receptors that subserve the hypothermic and analgesic effects of neurotensin (NT) to the receptor that mediates the effects of NT in mesencephalic dopamine (DA) neurons, and to compare these receptors to the cloned adult rat brain NT receptor and to newborn mouse and rat brain NT receptors. The results show that NT receptors in homogenates from newborn mouse and rat brain and from COS 7 cells transfected with the cloned high-affinity NT receptor from the adult rat brain displayed virtually identical structure-activity relationships toward a series of 12 peptide and pseudopeptide NT analogs, as assessed by the ability of the compounds to inhibit the binding of [125I]NT binding in these systems. Furthermore, when eight of these analogs were tested for their ability to inhibit [125I]NT binding and to potentiate K(+)-evoked DA release in primary cultures of rat mesencephalic neurons, it was found that they all behaved as agonists with binding and biological potencies quite similar to those observed in the other binding assays. Finally and strikingly, when seven of these analogs with checked metabolic stability were tested in vivo for their hypothermic and analgesic (tail-flick test) effects after i.c.v. injection in the mouse, they exhibited relative potencies that were completely different from those obtained in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

The synthesis of N-[3-[(hydroxyamino) carbonyl]-1-oxo-2(R)-benzylpropyl]-L-isoleucyl-L-leucine (JMV-390-1, 6a), a multipeptidase inhibitor based on the C-terminal sequence common to neurotensin (NT) and neuromedin N (NN), is described. This compound behaves as a full inhibitor of the major NT/NN degrading enzymes in vitro, e.g. endopeptidase 24.16, endopeptidase 24.15, endopeptidase 24.11, and leucine aminopeptidase (type IV-S), in the nanomolar range (IC50's from 30 to 60 nM). Compound 6a was found to increase endogenous recovery of NT and NN from slices of mice hypothalamus depolarized with potassium. In various assays commonly used to select analgesics, e.g. hot-plate test, tail-flick test, acetic acid-induced writhing test, in mice, compound 6a proved to be potent when intracerebroventricularly (icv) injected. The analgesic effects observed were totally (hot-plate test) or largely (tail-flick test) reversed by the opioid antagonist naltrexone. Furthermore, icv injection of compound 6a (10 micrograms/mouse) was found to significantly potentiate the hypothermic effects of NT or NN.