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PubMed2001

Evaluation of motion and realignment for functional magnetic resonance imaging in real time.

Functional magnetic resonance imaging in real time is an emerging tool for the assessment of dynamic changes in brain activation. The short response latency (tens of seconds) renders the technique more sensitive to motion artifacts. Motion correction in real time requires computationally efficient algorithms which can be executed on a complete 3D data set within a single time of repetition cycle. In this study, a method to evaluate motion and realign functional images in real time implemented on standard imaging hardware is introduced. The detection of activity in correlation maps is improved, and artifactual edge enhancements are reduced. As the estimation of large movements is stable, this algorithm is attractive for clinical studies with uncooperative patients. Magn Reson Med 45:167-171, 2001.

Artifacts↗

PubMed2006

Potential of e-health in relation to depression: short survey of previous research.

E-health is developing at a high rate and represents an opportunity for the development and spreading of information and communication channels to interested parties. The aim of this study was to get an overview and comprehension of the e-health field, with special focus on depression. A survey of initiatives and studies regarding e-health and depression was carried out. Relevant articles were found through searches on databases, search engines and reference lists. This paper shows that many different initiators with differing goals and motives are active within the e-health field. In the field of e-health and depression, the following areas show interesting results: studies mapping users' profile and habits, the quality of health-related information and the effectiveness of online therapies and supportive communities. Numerous initiators have launched different kinds of e-health initiatives. The potential of the Internet to be used constructively by health-care professionals and health-care consumers for health-enhancing purposes still needs to be mapped, evaluated and developed.

Attitude to Computers↗

PubMed1998

Effect of within-strain sample size on QTL detection and mapping using recombinant inbred mouse strains.

Increasing the number of mice used to calculate recombinant inbred (RI) strain means increases the accuracy of determining the phenotype associated with each genotype (strain), which in turn enhances quantitative trait locus (QTL) detection and mapping. The purpose of this paper is to examine quantitatively the effect of within-strain sample size (n) on additive QTL mapping efficiency and to make comparisons with F2 and backcross (BC) populations where each genotype is represented by only a single mouse. When 25 RI strains are used, the estimated equivalent number of F2 mice yielding the same power to detect WTLs varies inversely as a function of the heritability of the trait in the RI population (hRI2). For example, testing 25 strains with n = 10 per strain is approximately equivalent to 160 F2 mice when hRI2 = 0.2, but only 55 when hRI2 = 0.6. While increasing n is always beneficial, the gain in power as n increases is greatest when hRI2 is low and is much diminished at high hRI2 values. Thus, hRI2 is high, there is little advantage of large n, even when n approaches infinity. A cost analysis suggested that RI populations are more cost-effective than conventional selectively genotyped F2 populations at hRI2 values likely to be seen in behavioral studies. However, with DNA pooling, this advantage is greatly reduced and may be reversed depending on the values of hRI2 and n.

Animals↗

PubMed1997

Multiecho approaches to spectroscopic imaging of the brain.

Spectroscopic imaging (SI) with nuclear magnetic resonance (NMR) is one of the most powerful tools available for studying brain chemistry in vivo. Both proton (1H) and phosphorus (31P) NMR offer valuable biochemical information that can in principle be mapped throughout the entire brain, thereby enhancing our understanding of brain function. With the exception of protons from tissue water and the triglycerides of adipose tissue, however, nuclei contributing to the NMR signals of living tissue are in relatively small (millimolar) concentrations. The low concentration of metabolite nuclei reduces the overall sensitivity of conventional SI techniques, making high-quality metabolite mapping a lengthy procedure. This problem has led to the development and testing of nonconventional methods for reducing SI scan times, including techniques based on the collection of multiple spin-echoes. The extent to which multiecho methods can be used to decrease SI scan times and maintain high-quality metabolite mapping depends on several factors. These include the spectral transverse relaxation times, the spectral resolution required, and J-coupling interactions. We have discussed these various technical aspects of multiecho SI methods as applied to 1H and 31P spectroscopic imaging of the living brain.

Animals↗

PubMed2006

Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR.

Baroreflex responses to changes in arterial pressure are impaired in spontaneously hypertensive rats (SHR). Mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances were measured before and during electrical stimulation (5-90 Hz) of the left aortic depressor nerve (ADN) in conscious SHR and normotensive control rats (NCR). The protocol was repeated after beta-adrenergic-receptor blockade with atenolol. SHR exhibited higher basal MAP (150 +/- 5 vs. 103 +/- 2 mmHg) and HR (393 +/- 9 vs. 360 +/- 5 beats/min). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (-68 +/- 5 vs. -38 +/- 3 mmHg at 90-Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (-43 +/- 5%) vs. mesenteric (-27 +/- 3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (-33 +/- 7% and -30 +/- 7%). Reflex bradycardia was also preserved in SHR, although its mechanism differed. Atenolol attenuated the bradycardia in SHR (-88 +/- 14 vs. -129 +/- 18 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (-116 +/- 16 vs. -133 +/- 13 beats/min). The residual bradycardia under atenolol (parasympathetic component) was reduced in SHR. MAP and HR responses to ADN stimulation were also preserved or enhanced in SHR vs. NCR after deafferentation of carotid sinuses and contralateral right ADN. The results demonstrate distinct differences in central baroreflex control in conscious SHR vs. NCR. Inhibition of cardiac sympathetic tone maintains reflex bradycardia during ADN stimulation in SHR despite impaired parasympathetic activation, and depressor responses to ADN stimulation are equivalent or even greater in SHR due to augmented hindquarter vasodilation.

Animals↗

PubMedDate not supplied

Angiogenic response of MCF7 human breast cancer to hormonal treatment: assessment by dynamic GdDTPA-enhanced MRI at high spatial resolution.

Dynamic gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced MRI was followed during growth and regression of MCF7 human breast tumors implanted in nude mice in the presence of estrogen and tamoxifen, respectively. Gradient-echo and spin-echo sequences were applied at a temporal resolution of 12 and 100 seconds, respectively, and a spatial resolution of 195 x 390 x 1000 microns. Maps of initial rates of contrast enhancement demonstrated stimulation of local growth of permeable microcapillaries at regions bordering necrotic areas, resulting from tamoxifen treatment. This localized angiogenic stimulation was confirmed by immunohistochemical staining of endothelial cells. After 1 week of tamoxifen treatment, the fraction of tumor pixels exhibiting rapid initial rate of contrast enhancement increased significantly from .28 +/- .05 to .46 +/- .06. In parallel, the fraction of tumor area showing contrast enhancement 3 minutes after Gd-DTPA injection also increased significantly, from .42 +/- .06 to .58 +/- .06. On the basis of these changes, it was possible to assess the response to tamoxifen therapy at an early stage.

Analysis of Variance↗

PubMedDate not supplied

Negative regulation of MAP kinase by diacylglycerol-dependent mechanisms via G protein-coupled receptors in rat basophilic RBL-2H3 (ml) cells.

Carbachol and 5'-(N-ethylcarboxamido)-adenosine (NECA), stimulants of G protein-coupled receptors, induce MAP kinase activation in the muscarinic ml receptor-transfected mast cell line, RBL-2H3 (ml) cells. The phospholipase C inhibitor neomycin and the phosphatidate phosphohydrolase inhibitor propranolol augmented MAP kinase activation induced by carbachol and NECA without affecting the antigen-induced MAP kinase activation. Furthermore, the duration of MAP kinase activation induced by carbachol or NECA was also prolonged by neomycin and propranolol. The specific protein kinase C inhibitor Ro 31-8425 enhanced the carbachol- or NECA-induced MAP kinase activation. These findings suggest that the MAP kinase activation mediated by the G protein-coupled receptors is negatively regulated by diacylglycerol and activated protein kinase C(s).

Adenosine↗

PubMed2000

Comparative genome mapping in the sequence-based era: early experience with human chromosome 7.

The success of the ongoing Human Genome Project has resulted in accelerated plans for completing the human genome sequence and the earlier-than-anticipated initiation of efforts to sequence the mouse genome. As a complement to these efforts, we are utilizing the available human sequence to refine human-mouse comparative maps and to assemble sequence-ready mouse physical maps. Here we describe how the first glimpses of genomic sequence from human chromosome 7 are directly facilitating these activities. Specifically, we are actively enhancing the available human-mouse comparative map by analyzing human chromosome 7 sequence for the presence of orthologs of mapped mouse genes. Such orthologs can then be precisely positioned relative to mapped human STSs and other genes. The chromosome 7 sequence generated to date has allowed us to more than double the number of genes that can be placed on the comparative map. The latter effort reveals that human chromosome 7 is represented by at least 20 orthologous segments of DNA in the mouse genome. A second component of our program involves systematically analyzing the evolving human chromosome 7 sequence for the presence of matching mouse genes and expressed-sequence tags (ESTs). Mouse-specific hybridization probes are designed from such sequences and used to screen a mouse bacterial artificial chromosome (BAC) library, with the resulting data used to assemble BAC contigs based on probe-content data. Nascent contigs are then expanded using probes derived from newly generated BAC-end sequences. This approach produces BAC-based sequence-ready maps that are known to contain a gene(s) and are homologous to segments of the human genome for which sequence is already available. Our ongoing efforts have thus far resulted in the isolation and mapping of >3,800 mouse BACs, which have been assembled into >100 contigs. These contigs include >250 genes and represent approximately 40% of the mouse genome that is homologous to human chromosome 7. Together, these approaches illustrate how the availability of genomic sequence directly facilitates studies in comparative genomics and genome evolution.

Animals↗

PubMed2006

Hybrid therapies for ventricular arrhythmias.

In recent years several trials demonstrated the efficacy of implantable cardioverter-defibrillation (ICD) therapy in reducing cardiac and total mortality in patients affected by rapid ventricular tachycardia (VT) and/or ventricular fibrillation. Nevertheless, ICD do not prevent arrhythmia recurrences, thus being a palliative and not a curative treatment modality. The tolerance to ICD therapy varies greatly, and within individuals, this leading to a nonuniform acceptance of this form of therapy. The very frequent occurrence of VT, defined as an arrhythmic storm, may be a life threatening condition. The majority of ICD patients is under antiarrhythmic drug therapy, to reduce episodes of VT or to make antitachycardia pacing more effective by slowing the tachycardia rate. Drug therapy, however, may cause additional problems, and does not represent the optimal solution. The prevention of VT and/or ventricular fibrillation episodes and excessive ICD therapy, remains a worthwhile goal. Radiofrequency catheter ablation (RFCA) is a curative approach, and can be expected to reduce the frequency of recurrent VT episodes in the majority of patients. The combination of these treatment modalities (ICD and RFCA) is often described as hybrid therapy, implying that the two treatments act providing some form of synergism. In experienced centers, RFCA is now performed, regardless of whether the VT rate is rapid and/or is hemodynamically unstable. Newer mapping and ablation techniques are now available, enhancing the acute success rate of the procedure. In this review the most recent application of VT catheter ablation and the use of advanced mapping and ablation techniques will be discussed.

Body Surface Potential Mapping↗

PubMed1989

Trans-regulation and differential cell specificity of human papillomavirus types 16, 18, and 11 cis-acting elements.

The noncoding region (ncr) of human papillomavirus (HPV) types 16, 18, and 11 contains promoter and/or enhancer function. We have localized the sequence containing the constitutive enhancers of HPV types 16, 18, and 11 to 315, 230, and 213 bp fragments, respectively, for comparative studies. The region of homology shared between the enhancers of the three viruses is limited to the sequence ATTTTTGGCTT, which is also present in the ncr of HPV 6b and 33. We have also examined the enhancer activity of the HPV ncrs in three human cervical carcinoma cell lines, one noncervical human carcinoma cell line, and one monkey kidney established cell line. We observed cell-specific differences in the constitutive expression of the enhancers in the various cell lines. The conditional enhancer activity of the ncr of the viruses is increased in trans by the E2 gene product of HPV 16. Transactivation by E2 is mediated through the E2 binding motif on HPV enhancer plasmids with a heterologous but not with a homologous promoter. Our preliminary studies also indicate a repressor function for the E7 gene of HPV 16.

Base Sequence↗

PubMed2000

The adenovirus E4 ORF6 and E1b 55 kDa proteins cooperate in a p53-independent manner to enhance transduction by recombinant adeno-associated virus vectors.

The observation that exposure of target cells to genotoxic stress or adenovirus infection enhances recombinant adeno-associated virus (rAAV) transduction is an important lead towards defining the rAAV transduction mechanism, and has significant implications for the exploitation of rAAV in gene therapy applications. The adenovirus-mediated enhancement of rAAV transduction has been mapped to the E4 ORF6 gene, and expression of E4 ORF6 alone has been considered necessary and sufficient to mediate this effect. Since p53 subserves an important function in the cellular response to genotoxic stress, and interacts with the E4 ORF6 gene product during adenovirus infection, we hypothesized that p53 function might be essential to the rAAV enhancement resulting from these cellular insults. In the current study, using the p53-null cell lines H1299 and Saos-2, we find that p53 is not essential to either genotoxic stress or adenovirus-mediated enhancement of rAAV transduction. We further demonstrate using HeLa, H1299 and Saos-2 cells that E4 ORF6 expression alone is not sufficient to enhance rAAV transduction and that coexpression of the adenovirus E1b 55 kDa protein is necessary. Together, these observations indicate that the mechanism by which adenovirus infection enhances rAAV transduction involves cooperative and interdependent functions of the E4 ORF6 and E1b 55 kDa proteins that are p53-independent.

Adenoviridae↗

PubMed2006

Activin modulates the transcriptional response of LbetaT2 cells to gonadotropin-releasing hormone and alters cellular proliferation.

Both GnRH and activin are crucial for the correct function of pituitary gonadotrope cells. GnRH regulates LH and FSH synthesis and secretion and gonadotrope proliferation, whereas activin is essential for expression of FSH. Little is known, however, about the interplay of signaling downstream of these two hormones. In this study, we undertook expression profiling to determine how activin pretreatment alters the transcriptional response of LbetaT2 gonadotrope cells to GnRH stimulation. Activin treatment alone altered the transcriptional profile of 303 genes including inducing that of the 17beta-hydroxysteroid dehydrogenase B1 gene that converts estrone to 17beta-estradiol, altering the sensitivity of the cells to estrone. Furthermore, activin had a dramatic effect on the response of LbetaT2 cells to GnRH. Hierarchical clustering of 2453 GnRH-responsive genes identified groups of genes the response of which to GnRH was either enhanced or blunted after activin treatment. Mapping of these genes to gene ontology classifications or signaling pathways highlighted significant differences in the classes of altered genes. In the presence of activin, GnRH regulates genes in pathways controlling cell energetics, cytoskeletal rearrangements, organelle organization, and mitosis in the absence of activin, but genes controlling protein processing, cell differentiation, and secretion. Therefore, we demonstrated that activin enhanced GnRH induction of p38MAPK activity, caused GnRH-dependent phosphorylation of p53, and reduced the ability of GnRH to cause G1 arrest. Thus, although activin alone changes a modest number of transcripts, activin pretreatment dramatically alters the response to GnRH from an antiproliferative response to a more differentiated, synthetic response appropriate for a secretory cell.

Activins↗

PubMed1988

Effects of baroceptor reflex on cardiac and renal sympathetic nerve activity before and after atropinization in awake cats at rest.

The effects of baroceptor reflex on mean cardiac (MCSNA) and renal sympathetic nerve activity (MRNA) were analyzed before and after atropinized (0.1 mg/kg, i.v.) states in conscious cats at rest. Resting values of MCSNA, MRNA, mean aortic pressure (MAP), and heart rate (HR) were 85 +/- 6 imps/s, 76 +/- 11 imps/s, 100 +/- 4 mmHg, and 164 +/- 10 beats/min, respectively. Both MCSNA and MRNA changed almost inversely to changes in the absolute MAP in the range of 90-140 mmHg. Within this pressure range the gain of baroceptor-sympathetic system to the heart and kidney was 2.31 and 1.84, respectively. MCSNA as well as MRNA was reduced to the noise level at the MAP of 142 and 150 mmHg, respectively. With atropine, MCSNA and MRNA were inhibited centrally whereas HR increased to 192 beats/min. The increase in MAP caused by norepinephrine (2.1 micrograms/kg, i.v.) was enhanced to 75 +/- 7 mmHg by atropine from 31 +/- 4 mmHg in control. The piecewise linear MAP-MCSNA and MAP-MRNA relationships changed to a remarkable clockwise hysteresis loop. During the rising MAP period, the gain of the baroceptor-sympathetic system decreased to 0.91 and 0.97 in MCSNA and MRNA, respectively. During the returning MAP period, a delayed activation in MCSNA and MRNA occurred centrally. We conclude that the baroceptor reflex effect on MCSNA is larger than those on MRNA, and that the baroceptor control of MCSNA and MRNA is modified centrally by atropine in the awake cat at rest.

Animals↗

PubMed1995

Treatment of cells with alkaline borate buffer extends the capability of interphase FISH mapping.

Interphase fluorescence in situ hybridization (FISH) has been shown to be a means to map DNA sequences relative to each other in the 100 kb to 1-2 Mb genomic-separation range. At distances below 0.1 Mb, probe sites are infrequently resolved in interphase chromatin. In the 0.1- to 1-Mb range, interphase chromatin can be modeled as a freely flexible chain. The mean square interphase distance between two probes is proportional to the genomic separation between the probes on the linear DNA molecule. Above 1-2 Mb, the relationship between interphase distance and genomic separation changes abruptly and appears to level off. We have used alkaline-borate treatment to expand the capability of interphase FISH mapping. We show here that alkaline-borate treatment increases nuclear diameter, the interphase distance between probes on homologous chromosomes, and the distance between probes on the same chromosome. We also show that the mean square distance between hybridization sites in borate-treated nuclei is proportional to genomic separation up to 4 Mb. Thus, alkaline-borate treatment enhances the capability of interphase FISH mapping by increasing the absolute distance between probes and extending the range of the simple relationship between interphase distance and genomic separation.

Borates↗

PubMed2006

MP-SAGE: A new MP-RAGE sequence with enhanced SNR and CNR for brain imaging utilizing square-spiral phase encoding and variable flip angles.

The magnetization-prepared rapid gradient-echo (MP-RAGE) sequence is well known and widely used for high-resolution, structural brain MRI. Here we present a new version, termed magnetization-prepared spiral acquisition gradient-echo (MP-SAGE), that employs interleaved square-spiral phase-encoding (PE) to take advantage of the 3D nature of the sequence. Resolution loss caused by point-spread function (PSF) blurring is circumvented by the use of variable flip angle (VFA) radiofrequency (RF) pulses. The pulse train is calculated by means of an accurate new signal evolution theory that is derived from the extended phase graph (EPG) description. Phantom results show excellent agreement between theory and experiment for substances with relaxation times similar to those of human brain tissue. Both phantom and in vivo results show a strong enhancement of SNR and CNR compared to the standard MP-RAGE in high-resolution MRI. The benefits for brain tissue segmentation using images obtained with MP-SAGE are shown.

Algorithms↗

PubMed1986

RNA polymerase specificity of mRNA production and enhancer action.

To examine the RNA polymerase (EC 2.7.7.6) specificity of RNA maturation/utilization and transcriptional enhancement, we constructed a chimeric plasmid (pPolI-CAT) in which a promoter for mouse rRNA gene transcription was placed adjacent the coding sequences for chloramphenicol acetyltransferase (CAT; EC 2.3.1.28). A number of other constructs, including plasmids also containing a murine sarcoma virus enhancer or lacking any natural eukaryotic promoter sequences, were also prepared. In apparent agreement with earlier conclusions that an RNA polymerase I transcript can act as a messenger RNA, transient transfection of mouse L cells with pPolI-CAT yielded both high levels of transcription from the RNA polymerase I promoter and enzymatically active CAT protein. However, further examination revealed that CAT protein is not translated from RNA that begins at the normal rRNA transcription initiation site. Polysomal RNA is devoid of such RNA and instead consists of CAT-encoding transcripts that begin elsewhere in the mouse ribosomal DNA (rDNA) region. Since transcription of these aberrant RNAs is stimulated by the addition of a murine sarcoma virus enhancer segment, they are probably transcribed by RNA polymerase II. Transcripts that map to the authentic rRNA start site are not similarly enhanced. Moreover, unlike the RNAs deriving from the rRNA initiation site, these aberrant RNAs are more stable and the level of translatable CAT transcripts is suppressed by inclusion of larger segments of the rDNA promoter regions. Fortuitously initiated mRNAs are also formed in the absence of any natural eukaryotic promoter sequence. From these data we conclude that there is no evidence that normal RNA polymerase I transcription yields functional mRNA and that transcriptional enhancement appears to be RNA polymerase specific.

Acetyltransferases↗

PubMed1997

Nuclear factor I family members regulate the transcription of surfactant protein-C.

Transcription of the surfactant protein-C (SP-C) gene is restricted to Type II epithelial cells in the adult lung. We have shown previously that the 0.32-kilobase pair (kb) mouse SP-C promoter is functional in transient transfection assays of the lung epithelial cell-derived cell line, MLE-15, and that thyroid transcription factor 1 (TTF-1) transactivates promoter activity. The 0.32-kb SP-C promoter can be separated into a proximal promoter region (-230 to +18) and an enhancer region (-318 to -230). Three DNase I footprints were mapped in the promoter region (C1 through C3) and two in the enhancer region (C4 and C5). We now show that nuclear factor I (NFI) family members bind to both individual NFI half-sites in footprints C1, C3, and C5, and to a composite site in footprint C4 by competition gel retardation and antibody supershift analyses. Mutational analysis of the 0.32-kb mouse SP-C promoter and transient transfection of MLE-15 cells demonstrated that the NFI binding sites are required for promoter activity in this cell type. Site-specific mutation of the proximal or distal NFI sites drastically reduced transactivation by a co-transfected NFI-A expression vector in HeLa cells. These data indicate that NFI family member(s), binding to sites in both the promoter and enhancer regions, regulate SP-C gene expression in a process independent of TTF-1.

Animals↗

PubMed1987

Significance of DNase I-hypersensitive sites in the long terminal repeats of a Moloney murine leukemia virus vector.

A Moloney murine leukemia virus-derived retroviral vector (N4) carrying the bacterial neomycin resistance gene (neo) was used to study the chromatin configuration of integrated proviral DNA in NIH 3T3-derived cell lines containing one copy of the vector DNA per cell. Three independently obtained cell lines were examined. In two of these cell lines, the vector was introduced by viral infection, while in the third the construct was introduced by DNA transfection. Such transfected cell lines (including the one examined) usually express 10- to 50-fold less virus-specific RNA than do cell lines obtained by viral infection. All three cell lines exhibited similar patterns of DNase I-hypersensitive (HS) sites. Two strong DNase I HS sites were detected in the 5' long terminal repeat, which contains signals required for proper and efficient initiation of viral transcription. One of these sites was found to overlap the viral enhancer sequences, while the other site mapped very close to the start site for viral transcription. A third HS site was detected in nearby internal viral sequences. Only one HS site was found in the 3' long terminal repeat, which contains the signal(s) required for proper addition of a poly(A) tail to viral transcripts. This HS site was located in the region of the viral enhancer. Several weak DNase I HS sites were also found in the cellular sequences adjacent to the integration sites, at different locations in each cell line analyzed. No common pattern of cellular DNase I HS sites was found. These observations suggest that the 5' and 3' long terminal repeats of integrated retroviral proviruses exhibit different chromatin conformations, possibly reflecting the different functions encoded by the otherwise identical sequences, and the DNase I HS sites detected in these studies reflect only a potential for transcription and are not a reflection of the high transcriptional activity characteristic of retroviruses.

Animals↗