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PubMed2002

Reduced binocular depth inversion in schizophrenic patients.

Binocular depth inversion represents an illusion of visual perception, serving to invert the perception of implausible hollow objects, e.g. a hollow face into a normal face. Such inversion occurs frequently, especially when objects with a high degree of familiarity (e.g. photographs of faces) are displayed. Under normal conditions, cognitive factors apparently override the binocular disparity cues of stereopsis. This internal mechanism--a kind of "censorship" of perception balancing "top-down" and "bottom-up" processes of perception--appears to be disturbed in psychotic states. The clinical and neuropsychological performance of schizophrenic patients was assessed using the Brief Psychiatric Rating Scale (BPRS), the Positive And Negative Symptoms Scale (PANSS), the Clinical Global Impression Scale (CGI), the Mehrfach-Wahlwortschatz Intelligence Test (MWT-B) and the binocular depth inversion test (BDIT) using pictures with a high degree of familiarity. In schizophrenic patients, the performance in the BDIT differed significantly from healthy controls and from patients with major depression. The schizophrenic patients were more veridical in their judgements in the BDIT. During antipsychotic treatment, BPRS and PANSS scores improved and the inversed faces were seen as more illusionary, driven by an increase in top-down processing. At the end of treatment, there was no significant difference between the patient group and the healthy controls in the score of binocular depth inversion. These findings suggest that testing of binocular depth inversion can detect specific dysfunctions in visual perception and might be useful as a state-marker for psychotic states.

Adult↗
PubMed2005

Reagent anions for charge inversion of polypeptide/protein cations in the gas phase.

Various reagent anions capable of converting polypeptide cations to anions via ion/ion reactions have been investigated. The major charge inversion reaction channels include multiple proton transfer and adduct formation. Dianions composed of sulfonate groups as the negative charge carriers show essentially exclusive adduct formation in converting protonated peptides and proteins to anions. Dianions composed of carboxylate groups, on the other hand, show far more charge inversion via multiple proton transfer, with the degree of adduct formation dependent upon both the size of the polypeptide and the spacings between carboxylate groups in the dianion. More highly charged carboxylate-containing anions, such as those derived from carboxylate-terminated polyamidoamine half-generation dendrimers show charge inversion to give anion charges as high in magnitude as -4, with the degree of adduct formation being inversely related to dendrimer generation. All observations can be interpreted on the basis of charge inversion taking place via a long-lived chemical complex. The lifetime of this complex is related to the strengths and numbers of the interactions of the reactants in the complex. Calculations with model systems are fully consistent with sulfonate groups giving rise to more stable complexes. The kinetic stability of the complex can also be affected by the presence of electrostatic repulsion if it is multiply charged. In general, this situation destabilizes the complex and reduces the likelihood for observation of adducts. The findings highlight the characteristics of multiply charged anions that play roles in determining the nature of charge inversion products associated with protonated peptides and proteins.

Algorithms↗
PubMed1990

An inverse face-centered cubic phase formed by diacylglycerol-phosphatidylcholine mixtures.

Fully hydrated unsaturated diacylglycerol-phosphatidylcholine mixtures are found to adopt an inverse face-centered cubic phase, of crystallographic cubic aspect 15. The same behavior is observed for either the 1,2- or 1,3-isomer of the diacylglycerol. This Q15 cubic phase, of probable space group Fd3m (Q227), occurs between an inverse hexagonal (HII) phase and an inverse micellar (L2) solution, with increasing diacylglycerol concentration, which implies that the mean curvature of the interface is more negative than that of the HII phase. This behavior is quite different from that of the more usual bicontinuous inverse cubic phases Pn3m (Q224), Im3m (Q229), and Ia3d (Q230), which normally occur between the lamellar L alpha and the HII phases. One possible structure for the Fd3m cubic phase has recently been proposed (Mariani, P., Luzzati, V., & Delacroix, H. (1988) J. Mol. Biol. 204, 165-189), consisting of tetrahedrally arranged clusters of inverse micelles surrounded by a continuous cage of tetrahedrally connected water/lipid (inverse) channels.

Densitometry↗
PubMed2006

Biarylpyrazole inverse agonists at the cannabinoid CB1 receptor: importance of the C-3 carboxamide oxygen/lysine3.28(192) interaction.

The biarylpyrazole, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (SR141716; 1) has been shown to act as an inverse agonist/antagonist at the cannabinoid CB1 receptor. Our previous mutant cycle study suggested that K3.28(192) is involved in a direct interaction with the C-3 substituent of 1 in wild-type (WT) CB1.(1) However, these results did not establish what part of the C-3 substituent of 1 is involved in the K3.28(192) hydrogen bond, the carboxamide oxygen or the piperidine nitrogen. Furthermore, our previous calcium channel assay results for 5-(4- chlorophenyl)-3-[(E)-2-cyclohexylethenyl]-1-(2,4-dichlorophenyl)-4- methyl-1H-pyrazole (VCHSR; 2) (an analogue of 1 that lacks hydrogen-bonding capability in its C-3 substituent) showed that this compound acts as a neutral antagonist, a result that is in contrast to 1, which acts as an inverse agonist in this same assay.(1) These results suggested a relationship between biarylpyrazole interaction with K3.28(192) at CB1 and inverse agonism, but these results were for a single pair of compounds (1 and 2). The work presented here was designed to test two hypotheses derived from our modeling and mutant cycle results. The hypotheses are as follows: (1) it is the carboxamide oxygen of the C-3 substituent of 1 that interacts directly with K3.28(192) and (2) the interaction with K3.28(192) is crucial for the production of inverse agonism for biarylpyrazoles such as 1. To determine whether the carboxamide oxygen or the piperidine nitrogen of the C-3 substituent may be the interaction site for K3.28(192), we designed, synthesized, and evaluated a new set of analogues of 1 (3-6, Chart 1) in which modifications only to the C-3 substituent of 1 have been made. In each case, the modifications that were made preserved the geometry of this substituent in 1. The absence of the piperidine nitrogen was not found to affect affinity, whereas the absence of the carboxamide oxygen resulted in a reduction in affinity. CB1 docking studies in an inactive state model of CB1 resulted in the trend, 3,1<5,4<2<6 for ligand/CB1 interaction energies. This trend was consistent with the trend in WT CB1 Ki values versus [3H]CP55,940 reported here. In calcium channel assays, all analogues with carboxamide oxygens (1, 3, and 4) were found to be inverse agonists, whereas those that lacked this group (2, 5, and 6) were found to be neutral antagonists. Taken together, these results support the hypothesis that it is the carboxamide oxygen of the C-3 substituent of 1 that engages in a hydrogen bond with K3.28(192) in WT CB1. Furthermore, functional results for 1-6 support the hypothesis that the interaction of 1 with K3.28(192) may be key to its inverse agonism.

Amides↗
PubMed1998

Chiral inversion and hydrolysis of thalidomide: mechanisms and catalysis by bases and serum albumin, and chiral stability of teratogenic metabolites.

The chiral inversion and hydrolysis of thalidomide and the catalysis by bases and human serum albumin were investigated by using a stereoselective HPLC assay. Chiral inversion was catalyzed by albumin, hydroxyl ions, phosphate, and amino acids. Basic amino acids (Arg and Lys) had a superior potency in catalyzing chiral inversion compared to acid and neutral ones. The chiral inversion of thalidomide is thus subject to specific and general base catalysis, and it is suggested that the ability of HSA to catalyze the reaction is due to the basic groups of the amino acids Arg and Lys and not to a single catalytic site on the macromolecule. The hydrolysis of thalidomide was also base-catalyzed. However, albumin had no effect on hydrolysis, and there was no difference between the catalytic potencies of acidic, neutral, and basic amino acids. This may be explained by different reaction mechanisms of the chiral inversion and hydrolysis of thalidomide. Chiral inversion is deduced to occur by electrophilic substitution involving specific and general base catalysis, whereas hydrolysis is thought to occur by nucleophilic substitution involving specific and general base as well as nucleophilic catalysis. As nucleophilic attack is sensitive to steric properties of the catalyst, steric hindrance might be the reason albumin is not able to catalyze hydrolysis. 1H NMR experiments revealed that the three teratogenic metabolites of thalidomide, in sharp contrast to the drug itself, had complete chiral stability. This leads to the speculation that, were some enantioselectivity to exist in the teratogenicity of thalidomide, it could result from fast hydrolysis to chirally stable teratogenic metabolites.

Algorithms↗
PubMed1988

Pharmacokinetic analysis of the enantiomeric inversion of chiral nonsteroidal antiinflammatory drugs.

Equations describing plasma concentration-time courses of the individual enantiomers of chiral 2-arylpropionic acid nonsteroidal antiinflammatory drugs were derived from a general model. The model assumes first-order absorption and elimination of the enantiomers with presystemic and/or systemic R-to-S enantiomeric inversion. Utilizing reported pharmacokinetic parameters, plasma concentrations of the enantiomers of ibuprofen (IB) were simulated. In the case of presystemic inversion, S:R plasma concentration ratios remained constant after an initial rise; the ratio progressively increased with time, however, when systemic inversion was assumed. Under the assumption of simultaneous systemic and presystemic inversion, the increase in the ratio in the postabsorptive phase was preceded by a steeper increase during absorption. Furthermore, it was shown that perturbation of IB absorption from the gastrointestinal tract may serve as an important discriminative measure for identification of the inversion site. For systemic and presystemic inversions, negative and positive sigmoidal relationships, respectively, were observed between the S:R concentration ratio 5 hr after drug administration and the time to reach the maximum plasma concentration. The applicability of the model to previously reported IB data is discussed.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Treatment with inverse agonists enhances baseline atrial contractility in transgenic mice with chronic beta2-adrenoceptor activation.

In this study, we investigate whether chronic treatment with beta-adrenoceptor (betaAR) ligands with inverse agonist activity enhances myocardial beta2AR-mediated atrial tension more than neutral antagonists in transgenic mice (TG35). These mice exhibit chronic adrenoceptor activation because they possess a greater number of constitutively active receptors than wild type mice due to cardiac-specific overexpression of human betaARs. TG35 and wild type mice were chronically treated for 90 h with three inverse agonists, ICI-118,551, propranolol, and carvedilol, and one neutral antagonist, alprenolol. After 96 h, we compared the basal and isoprenaline-stimulated (10 microM) increase in atrial tension in treated or untreated TG35 mice and wild type mice. In parallel, to determine the effect of chronic betaAR ligand treatment on the amounts of G protein receptor kinase-2 (GRK-2) and G proteins, we performed Western blotting on myocardial cytosolic and membrane proteins. Atria from the TG35 mice treated with inverse agonists showed increases in the baseline tension compared to those from alprenolol/vehicle-treated mice. ICI-118,551 and propranolol treatment restored the elevated myocardial G-inhibitory protein (Gialpha) levels to that of wild type. Also, treatment with inverse agonists upregulated G-stimulatory protein (Gsalpha) levels and GRK2 above those levels in vehicle-treated TG35 or wild type mice. The increased baseline atrial tension was reversed by the addition of ICI-118,551. Overall, our data suggests that inverse agonists enhance baseline atrial tension more than neutral antagonists. Based on this, we propose that upregulation of the active conformation of the beta2ARs, Gsalpha protein and restoration of Gialpha as three possible mechanisms to explain this enhanced receptor activity. Therefore, the favourable effects of some ligands used in pathological conditions involving chronic adrenoceptor activation may be due to the inverse agonist activity of the ligand.

Adrenergic beta-Agonists↗
PubMed2000

Chiral inversion of R(-) fenoprofen and ketoprofen enantiomers in cats.

The chiral inversion process is a characteristic metabolic pathway for different aryl-2-propionic acids or profens. Important variations have been observed between these individual compounds as well as between animal species. In this study, R(-) fenoprofen [R(-)FPF] and R(-) ketoprofen [R(-) KTF] were used to investigate their comparative stereoconversion in cats. After intravenous (i.v.) administration of R(-) FPF, the percentage of chiral inversion was 93.20+/-13.70%. A highly significant correlation (r: 0.978) was observed between the clearance of R(-) FPF and the chiral inversion process. After i.v. administration of R(-) KTF, the percentage of inversion was only 36.73+/-2.8%. No correlation between the clearance of R(-) KTF and this process was observed. R(-) FPF was metabolized by the pathways of thioesterification - chiral inversion processes. For R(-) KTF, the competitive metabolic pathways, glucuronidation and hydroxylation may be involved. However, these metabolic steps are saturable or less functional in cats. Moreover, the thioesterification of R(-) KTF in in vitro studies has been shown to be important in carnivores. The lack of correlation between clearance and chiral inversion process of R(-) KTF may be finally explained by deviation of thioesterification to other metabolic pathways of lipids and/or aminoacid conjugation, particulary glicine derivatives.

Animals↗
PubMed2000

Mechanisms of agonism and inverse agonism at serotonin 5-HT1A receptors.

Mechanisms of agonist and inverse agonist action at the serotonin 5-HT1A receptor have been studied using the modulation of guanosine 5'-O-(3-[35S]thiotriphosphate) ([35S]GTPgammaS) binding in membranes of Chinese hamster ovary (CHO) cells expressing the receptor (CHO-5-HTA1A cells). A range of agonists increased [35S]GTPgammaS binding with different potencies and to different maximal extents, whereas two compounds, methiothepin and spiperone, inhibited both agonist-stimulated and basal [5S]GTPgammaS binding, thus exhibiting inverse agonism. Potencies of agonists to stimulate [35S]GTPgammaS binding in membranes from CHO-5-HT1A cells were reduced by adding increasing concentrations of GDP to assays, whereas changes in sodium ion concentration did not affect agonist potency. The maximal effect of the agonists was increased by increasing sodium ion concentrations. The affinities of agonists in ligand binding assays were unaffected by changes in sodium ion concentration. Increasing GDP in the assays of the inverse agonists increased potency for spiperone to inhibit [35S]GTPgammaS binding and had no effect for methiothepin, in agreement with the sensitivity of these compounds to guanine nucleotides in ligand binding assays. Potencies for these inverse agonists were unaffected by changes in sodium ion concentration. These data were simulated using the extended ternary complex model. These simulations showed that the data obtained with agonists were consistent with these compounds achieving agonism by stabilising the ternary complex. For inverse agonists, the simulations showed that the mechanism for spiperone may be to stabilise forms of the receptor uncoupled from G proteins. Methiothepin, however, probably does not alter the equilibrium distribution of different receptor species; rather, this inverse agonist may stabilise an inactive form of the receptor that can still couple to G protein.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2002

Multielectrode venous catheter mapping as a high quality constraint for electrocardiographic inverse solution.

A persistent challenge in solving inverse problems in electrocardiography is the application of suitable constraints to the calculation of cardiac sources. Whether one formulates the inverse problem in terms of epicardial potentials or activation wavefronts, the problem is physically ill-posed and hence results in numerically unstable computations. Suitable physiological constraints applied with appropriate weighting can recover useful inverse solutions. However, it is often difficult to determine the best possible constraints and their optimal weighting. We have recently begun to use multielectrode catheters as a means of mapping epicardial signals in animal models. To accommodate the sparse sampling of this venous catheter based approach, we have applied statistical signal processing methods to estimate complete epicardial maps of activation time and epicardial potentials. Such measurements--and the estimated maps from them--also have the potential to provide high quality constraints for electrocardiographic inverse problems because they provide direct--albeit sparse--access to the desired solution. In this presentation we describe several approaches we have applied to extract useful constraints from sparsely sampled epicardial signals as well as a training set of epicardial maps, and use them to improve the quality of computed inverse solutions. Results suggest that combining various information sources provides valuable constraint information. Such a multimodal approach to cardiac mapping is clinically and technically viable and offers a possible means to overcome a major remaining limitation of inverse electrocardiography.

Animals↗
PubMed2006

Inversion vibration of PH3+(X2A2") studied by zero kinetic energy photoelectron spectroscopy.

We report the first rotationally resolved spectroscopic studies on PH3+(X2A2") using zero kinetic energy photoelectron spectroscopy and coherent VUV radiation. The spectra about 8000 cm(-1) above the ground vibrational state of PH3+(X2A2") have been recorded. We observed the vibrational energy level splittings of PH3+(X2A2") due to the tunneling effect in the inversion (symmetric bending) vibration (nu2+). The energy splitting for the first inversion vibrational state (0+/0-) is 5.8 cm(-1). The inversion vibrational energy levels, rotational constants, and adiabatic ionization energies (IEs) for nu2+ = 0-16 have been determined. The bond angles between the neighboring P-H bonds and the P-H bond lengths are also obtained using the experimentally determined rotational constants. With the increasing of the inversion vibrational excitations (nu2+), the bond lengths (P-H) increase a little and the bond angles (H-P-H) decrease a lot. The inversion vibrational energy levels have also been calculated by using one dimensional potential model and the results are in good agreement with the experimental data for the first several vibrational levels. In addition to inversion vibration, we also observed firstly the other two vibrational modes: the symmetric P-H stretching vibration (nu1+) and the degenerate bending vibration (nu4+). The fundamental frequencies for nu1+ and nu4+ are 2461.6 (+/-2) and 1043.9 (+/-2) cm(-1), respectively. The first IE for PH3 was determined as 79670.9 (+/-1) cm(-1).

Journal Article↗
PubMed1998

Rump white inversion in the mouse disrupts dipeptidyl aminopeptidase-like protein 6 and causes dysregulation of Kit expression.

The mouse rump white (Rw) mutation causes a pigmentation defect in heterozygotes and embryonic lethality in homozygotes. At embryonic day (E) 7.5, Rw/Rw embryos are retarded in growth, fail to complete neurulation and die around E 9.5. The Rw mutation is associated with a chromosomal inversion spanning 30 cM of the proximal portion of mouse chromosome 5. The Rw embryonic lethality is complemented by the W19H deletion, which spans the distal boundary of the Rw inversion, suggesting that the Rw lethality is not caused by the disruption of a gene at the distal end of the inversion. Here, we report the molecular characterization of sequences disrupted by both inversion breakpoints. These studies indicate that the distal breakpoint of the inversion is associated with ectopic Kit expression and therefore may be responsible for the dominant pigmentation defect in Rw/+ mice; whereas the recessive lethality of Rw is probably due to the disruption of the gene encoding dipeptidyl aminopeptidase-like protein 6, Dpp6 [Wada, K., Yokotani, N., Hunter, C., Doi, K., Wenthold, R. J. & Shimasaki, S. (1992) Proc. Natl. Acad. Sci. USA 89, 197-201] located at the proximal inversion breakpoint.

Amino Acid Sequence↗
PubMed2006

Molecular mechanism underlying inverse agonist of angiotensin II type 1 receptor.

To delineate the molecular mechanism underlying the inverse agonist activity of olmesartan, a potent angiotensin II type 1 (AT1) receptor antagonist, we performed binding affinity studies and an inositol phosphate production assay. Binding affinity of olmesartan and its related compounds to wild-type and mutant AT1 receptors demonstrated that interactions between olmesartan and Tyr113, Lys199, His256, and Gln257 in the AT1 receptor were important. The inositol phosphate production assay of olmesartan and related compounds using mutant receptors indicated that the inverse agonist activity required two interactions, that between the hydroxyl group of olmesartan and Tyr113 in the receptor and that between the carboxyl group of olmesartan and Lys199 and His256 in the receptor. Gln257 was found to be important for the interaction with olmesartan but not for the inverse agonist activity. Based on these results, we constructed a model for the interaction between olmesartan and the AT1 receptor. Although the activation of G protein-coupled receptors is initiated by anti-clockwise rotation of transmembrane (TM) III and TM VI followed by changes in the conformation of the receptor, in this model, cooperative interactions between the hydroxyl group and Tyr113 in TM III and between the carboxyl group and His256 in TM VI were essential for the potent inverse agonist activity of olmesartan. We speculate that the specific interaction of olmesartan with these two TMs is essential for stabilizing the AT1 receptor in an inactive conformation. A better understanding of the molecular mechanisms of the inverse agonism could be useful for the development of new G protein-coupled receptor antagonists with inverse agonist activity.

Amino Acid Sequence↗
PubMed1987

The role of model and computational experiments in the biomagnetic inverse problem.

This is a review of the role of model and computational experiments in studies of the part of the biomagnetic inverse problem that deals with the determination of electrical sources in the body using magnetic measurements around the body. Results from modelling studies of the forward problem that are important for the inverse problem are also reviewed. An evaluation is made of the adequacy of various models of the body for use in the biomagnetic inverse problem. This evaluation indicates that simple torso models, e.g. a semi-infinite volume or sphere, are probably inadequate. The review of the modelling studies of the inverse problem includes the effects of noise, source modelling errors, body modelling errors and measurement errors on the accuracy of source localisation methods using magnetic measurements. Source modelling errors are caused by differences between an actual complex source in the body and the simple model of it used in most source localisation methods; body modelling errors are caused by differences between the actual body and a simple model of it. The review indicates that typical experimental noise will only cause significant source localisation errors for inverse solutions calculated using fewer than approximately ten measurement points; it also indicates that source modelling errors must be rather large to be detectable when typical experimental noise is present. In addition, the review indicates that many experimental measurement errors will not cause significant localisation errors. The effects of body modelling errors are largely unknown. Suggestions for further biomagnetic inverse problem research are given. These include the development of more realistic models of the body, the experimental verification of such models and source localisation methods, and the development of methods for detecting and localising distributed or multiple discrete sources.

Electric Conductivity↗
PubMed2002

Analysis of an exact inversion algorithm for spiral cone-beam CT.

In this paper we continue studying a theoretically exact filtered backprojection inversion formula for cone beam spiral CT proposed earlier by the author. Our results show that if the phantom f is constant along the axial direction, the formula is equivalent to the 2D Radon transform inversion. Also, the inversion formula remains exact as spiral pitch goes to zero and in the limit becomes again the 2D Radon transform inversion formula. Finally, we show that according to the formula the processed cone beam projections should be backprojected using both the inverse distance squared law and the inverse distance law.

Algorithms↗
PubMed2003

A comparison of truncated total least squares with Tikhonov regularization in imaging by ultrasound inverse scattering.

For good image quality using ultrasound inverse scattering, one alternately solves the well-posed forward scattering equation for an estimated total field and the ill-posed inverse scattering equation for the desired object property function. In estimating the total field, error or noise contaminates the coefficients of both matrix and data of the inverse scattering equation. Previous work on ill-posed inverse ultrasonic scattering commonly used Tikhonov regularization, which considers error only in the data. The solution so obtained is not precise enough to reconstruct the quantitative internal structure of a large or high-contrast object. This paper adopts the truncated total least squares method, simultaneously considering error and noise on both sides of the inverse scattering equation, and compares it with the classical Tikhonov regularization. We show that it can substantially improve reconstruction fit and image quality when the inverse scattering equation system is strongly ill-posed.

Algorithms↗
PubMed1994

Endpoint bias in large Tn10-catalyzed inversions in Salmonella typhimurium.

A genetic strategy identified Salmonella typhimurium strains carrying large (> 40 kb) Tn 10-catalyzed inversions; the inverted segments were characterized by XbaI digestion and pulsed field gel electrophoresis. Two size classes of large inversions were found. More than half of the inversions extended 40-80 kb either clockwise or counterclockwise of the original Tn10 site. The remaining inversions extended up to 1620 kb (33% of the genome), but the distal endpoints of these inversions were not randomly scattered throughout the chromosome. Rather, each Tn10 repeatedly yielded similar (though not identical) inversions. The biased endpoint selection may reflect the limited search for target DNA sequences by the Tn10 transposase, and the spatial proximity of the donor and target regions in the folded S. typhimurium nucleoid. Using this interpretation, the data suggest that DNA sequences 40-80 kb clockwise and counterclockwise of the insertion site are in spatial proximity with the insertion, perhaps reflecting the organization of DNA into approximately 120-kb nucleoid domains. In addition, the data predict the spatial proximity of several distant DNA regions, including DNA sequences equidistant from the origin of DNA replication.

Base Sequence↗
PubMed1974

Nineteen paracentric chromosomal inversions in mice.

Using mutagens on sperm and spermatids we have produced nineteen chromosomal inversions in mice. The levels of radiation and chemical mutagen we used induced inversions in about one per cent of the animals screened. Nine inversions have been transmitted through successive generations, and the particular frequency of first meiotic anaphase bridges manifested by each inversion remained constant. The cytological properties of first meiotic anaphases varied considerably among the inversions. Chromosomal locations of five inversions are known. Four of the five are fully viable in homozygous condition.

Animals↗