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At least 127 records · Page 7Linked to original sources

AFLP maps of Petunia hybrida: building maps when markers cluster.

AFLP mapping in Petunia hybrida was undertaken with the intention of building a high-density genetic map suitable for applications such as map-based gene cloning. In total five maps were constructed from two mapping populations, with placement of more than 800 markers. Despite the large number of markers the resulting map is roughly ten-fold smaller than those of other plant species, including the closely related tomato. Low levels of recombination are reflected in clusters of tightly linked markers, both AFLPs and RFLPs, in all the maps. Clustering patterns vary between mapping populations, however, such that loci tightly linked in one population may be separable in another. Combined with earlier reports of aberrant meiotic pairing and recombination, our results suggest that, for species like petunia, map-based cloning may be more complex than in model species such as arabidopsis and tomato.

Journal Article↗

The role of visuo-spatial working memory in map learning: new findings from a map drawing paradigm.

Recently, increasing attention has been devoted to the study of the role of visuo-spatial working memory (VSWM) in environmental learning and spatial navigation. The present research was aimed at investigating the role of VSWM in map learning using a map drawing paradigm. In the first study, a dual task methodology was used. Results showed that map drawing was selectively impaired by a spatial tapping task that was executed during the map learning phase, hence supporting the hypothesis that VSWM plays an essential role in learning from maps. In the second study, using a correlational methodology, it was shown that performance in simultaneous VSWM tasks, but not in sequential VSWM tasks, predicted map drawing skills. These skills "in turn" correlated with map learning abilities. Finally, in the third study, we replicated the results of the second study, by using a different map. To our knowledge, the present study is the first to find evidence that the simultaneous aspects of VSWM play a fundamental role in learning from maps.

Adult↗

Epicardial isopotential mapping from body surface isopotential mapping in myocardial infarction.

It is useful to construct the epicardial isopotential mapping (the Ep Map) from the body surface isopotential mapping (the Body Map) for clinical diagnosis of cardiac disease, even though there are many unsolved problems in using the inverse solution. Yamashita et al. carried out this solution by using the finite element technique. In the present study, the clinical value of that method has been investigated in cases of myocardial infarction. The Ep Maps at 20, 25 and 30 msec. from the beginning of the QRS complex were obtained from the Body Map at the same time by using that method; the infarcted areas on the Ep Map were determined by using Toyama's method which was reported in a previous study. The infarcted area at 30 msec. on the Ep Map was located at the anterior wall along the ventricular septum in anterior infarction and at the posterior wall of the left ventricle in inferoposterior infarction. Patients were independently examined with the scintigram with thallium-201 and the infarcted area was coincident to the location of the abnormal findings of the scintigram. Moreover, the size of the infarcted area on the Ep Map and the size of the abnormal findings of the scintigram were parallel in most cases except one.

Electrocardiography↗

Multi atrial maco-re-entry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping.

OBJECTIVES: We sought to characterize re-entry circuits causing intra-atrial re-entrant tachycardias (IARTs) late after the repair of congenital heart disease (CHD) and to define an approach for mapping and ablation, combining anatomy, activation sequence data and entrainment mapping. BACKGROUND: The development of IARTs after repair of CHD is difficult to manage and ablate due to complex anatomy, variable re-entry circuit locations and the frequent co-existence of multiple circuits. METHODS: Forty-seven re-entry circuits were mapped in 20 patients with recurrent IARTs refractory to medical therapy. In the first group (n = 7), ablation was guided by entrainment mapping. In the second group (n = 13), entrainment mapping was combined with a three-dimensional electroanatomic mapping system to precisely localize the scar-related boundaries of re-entry circuits and to reconstruct the activation pattern. RESULTS: Three types of right atrial macro-re-entrant circuits were identified: those related to a lateral right atriotomy scar (19 IARTs), the Eustachian isthmus (18 IARTs) or an atrial septal patch (8 IARTs). Two IARTs originated in the left atrium. Radiofrequency (RF) lesions were applied to transect critical isthmuses in the right atrium. In three patients, the combined mapping approach identified a narrow isthmuses in the lateral atrium, where the first RF lesion interrupted the circuit; the remaining circuits were interrupted by a series of RF lesions across a broader path. Overall, 38 (81%) of 47 IARTs were successfully ablated. During follow-up ranging from 3 to 46 months, 16 (80%) of 20 patients remained free of recurrence. Success was similar in the first 7 (group 1) and last 13 patients (group 2), but fluoroscopy time decreased from 60 +/- 30 to 24 +/- 9 min/procedure, probably related to the increasing experience and ability to monitor catheter position non-fluoroscopically. CONCLUSIONS: Entrainment mapping combined with three-dimensional electroanatomic mapping allows delineation of complex re-entry circuits and critical isthmuses as targets for ablation. Radiofrequency catheter ablation is a reasonable option for treatment of IARTs related to repair of CHD.

Adult↗

A stepwise mapping approach for localization and ablation of ectopic right, left, and septal atrial foci using electroanatomic mapping.

AIMS: We describe a new strategic stepwise mapping approach for fast and accurate identification and ablation of ectopic atrial foci using an electroanatomic mapping system. METHODS AND RESULTS: Mapping procedures started with the acquisition of four points at the superior/septal part of the tricuspid annulus. According to this activation sequence, maps were continued towards the right atrial free wall if relatively early activation was shown at the superior part of the initial map or towards the triangle of Koch and, if necessary, to the left atrium, in cases of relatively early activation at the septum. High density mapping and detailed electrogram analysis only of the target area allowed identification and ablation of 34 foci in 30 of the 32 studied consecutive patients. A small number of mapping points were sufficient within a procedure time of 90 +/- 41 min for right 148 +/- 68 min and for left sided foci and a total fluoroscopy time of 9.6 +/- 7.2 min and 24.8 +/- 16.4 min respectively. Sixteen foci were located at the right free wall, eight at the left free wall, and 10 at the right or left side of the septum. CONCLUSION: Strategic electroanatomic mapping with fast identification of the area of tachycardia origin and high density mapping only of this target area allowed fast and successful localization and ablation of right and left free wall and septal ectopic atrial foci.

Adolescent↗

Microtubule-associated proteins (MAPs): a monoclonal antibody to MAP 1 decorates microtubules in vitro but stains stress fibers and not microtubules in vivo.

A monoclonal antibody (mAb 7-1.1) was produced against a bovine brain microtubule-associated protein (MAP) preparation that had been separated from tubulin after initial purification by cycles of microtubule assembly and disassembly in vitro. The antibody reacted specifically with two high molecular weight polypeptides of the MAP 1 class, designated MAP 1.1 and MAP 1.2, and also with the surfaces of MAP 1-containing microtubules that had been assembled in vitro. Double immunofluorescence microscopy using mAb 7-1.1 and a well-characterized rabbit anti-tubulin antibody revealed that mAb 7-1.1 stained stress fibers in fixed and permeabilized cultured mammalian cells rather than microtubules. The antibody also stained cell nuclei in a punctate fashion. mAb 7-1.1 is one of a number of monoclonal antibodies that react with presumptive MAP 1 polypeptides. Some of the MAP 1 antibodies have been found to bind specifically to microtubules in fixed and permeabilized cells, while others have been reported to react with nonmicrotubule structures. Our results, together with the results of other investigations, indicate that "MAP 1" may be a family of several high molecular weight polypeptides that adventitiously behave as MAPs by the criterion of in vitro coassembly with tubulin through cycles of polymerization and depolymerization but whose cellular distributions, and perhaps functions, are varied.

Animals↗

Mitogen-activated protein (MAP) kinase is regulated by the MAP kinase phosphatase (MKP-1) in vascular smooth muscle cells. Effect of actinomycin D and antisense oligonucleotides.

Angiotensin II stimulates hypertrophic growth of vascular smooth muscle cells (VSMC) and activates many growth-promoting kinases such as mitogen-activated protein (MAP) kinase. A novel transcriptionally regulated phosphatase, MAP kinase phosphatase-1 (MKP-1), is induced by angiotensin II in VSMC and selectively dephosphorylates MAP kinase in vitro. Using actinomycin D and antisense oligonucleotides targeted to MKP-1, we demonstrate that MKP-1 regulates MAP kinase in VSMC. Both actinomycin D and MKP-1 antisense oligonucleotides inhibited MKP-1 mRNA expression and caused prolonged activation of the p42 and p44 MAP kinases as measured by in-gel-kinase assays and Western blot. For example, MAP kinase activity 120 min after angiotensin II treatment was 30% (range 25-35%), 79%, and 74% of maximum in control, actinomycin D-treated (3 micrograms/ml, 30 min), and antisense oligonucleotide-treated (300 nM, 6 h) cells, respectively. A sense oligonucleotide was without effect (34%). MKP-1 antisense oligonucleotides did not affect the activity of MEK indicating that sustained activation of MAP kinase was due to inhibition of MKP-1 expression. These findings demonstrate that inactivation of MAP kinase by angiotensin II is mediated predominantly by MKP-1, suggesting an important role for MKP-1 and other related phosphatases in the regulation of MAP kinases in VSMC.

Angiotensin II↗

Identification of a 34-kD polypeptide as a light chain of microtubule-associated protein-1 (MAP-1) and its association with a MAP-1 peptide that binds to microtubules.

We examined the association of a 34-kD light chain component to the heavy chains of MAP-1 using a monoclonal antibody that specifically binds the 34-kD component and labels neuronal microtubules in a specific and saturable manner. Immunoprecipitation of MAP-1 heavy chains together with the 34-kD component by the antibody indicates that the 34-kD polypeptide forms a complex with MAP-1 heavy chains. Both major isoforms of MAP-1 heavy chains (MAP-1A and MAP-1B) were found in the immunoprecipitate. Digestion of MAP-1 with alpha-chymotrypsin and analysis of the chymotryptic peptides reveals a 120-kD fragment of the MAP-1 heavy chain that binds to microtubules and is precipitable with the 34-kD light chain antibody, suggesting that the 34-kD light chain also binds to this domain of the molecule. Since microtubules that contain the 120-kD fragment lack the long lateral projections characteristic of microtubules with intact MAP-1, the 34-kD light chains may be localized at or near the microtubule surface.

Animals↗

Comparison of endocardial catheter mapping with intraoperative mapping of ventricular tachycardia.

To validate the accuracy of catheter endocardial mapping to localize the origin of ventricular tachycardia (VT), we compared cathether endocardial mapping with intraoperative epicardial and endocardial mapping of 24 morphologically distinct VTs in 18 patients undergoing surgery. Twelve had VT with left bundle branch block morphology and 12 had VT with right bundle branch block morphology. Catheter endocardial mapping localized 23 VT morphologies to the border of a left ventricular aneurysm or myocardial infarction and one VT to a right ventriculotomy scar. Intraoperative epicardial mapping showed epicardial breakthrough on the right ventricle in 10 VTs with left bundle branch block morphology and on the left ventricle in two. In 12 VTs with right bundle branch block morphology, intraoperative epicardial mapping revealed the earliest site of VT with left bundle branch block morphology (11 patients) and VT with right bundle branch block morphology (12 patients) at the border of a left ventricular aneurysm, and one VT with left bundle branch block morphology in the right ventricle. Catheter endocardial mapping predicted the origin of VT within 4--8 cm2 of that determined by intraoperative endocardial mapping, which always identified the earliest site. These data validate the accuracy of catheter endocardial mapping in localizing the origin of VT.

Adult↗

Diesel exhaust particles activate p38 MAP kinase to produce interleukin 8 and RANTES by human bronchial epithelial cells and N-acetylcysteine attenuates p38 MAP kinase activation.

Air pollutants including diesel exhaust particles (DEPs) have been shown to enhance allergic responses. DEPs stimulate airway epithelial cells to produce various cytokines; however, the intracellular signal transduction pathway and the involvement of reduction and oxidation (redox) control in DEP-activated signaling have not been determined. In the present study, we therefore examined the role of p38 mitogen-activated protein (MAP) kinase in DEP-induced interleukin 8 (IL-8) and RANTES production by human bronchial epithelial cells (BECs) in order to clarify the intracellular signal transduction pathway that regulates IL-8 and RANTES production. In addition, we also examined the effect of a thiol-reducing agent, N-acetylcysteine (NAC), on DEP-induced p38 MAP kinase activation and cytokine production in order to clarify the redox control mechanism in DEP-induced p38 MAP kinase activation and IL-8 and RANTES production. The results showed that DEP induced IL-8 and RANTES production and the threonine and tyrosine phosphorylation of p38 MAP kinase, reflecting the activation of p38 MAP kinase in BECs. SB 203580, as the specific inhibitor of p38 MAP kinase activity, inhibited DEP-induced IL-8 and RANTES production. NAC inhibited DEP-induced p38 MAP kinase activation and IL-8 and RANTES production. These results indicate that p38 MAP kinase plays an important role in the DEP-activated signaling pathway that regulates IL-8 and RANTES production by BECs and that the cellular redox state is critical for DEP-induced p38 MAP kinase activation leading to IL-8 and RANTES production.

Acetylcysteine↗

Isolation of Mycobacterium avium subsp paratuberculosis (Map) from feral cats on a dairy farm with Map-infected cattle.

Paratuberculosis is an economically important disease of dairy cattle caused by Mycobacterium avium subsp. paratuberculosis (Map). The role of nonruminant, nondomestic animals in the epidemiology of paratuberculosis in cattle is unclear. To examine nonruminant, nondomestic animals for the presence of Map, 25 feral cats, nine mice (species unknown), eight rabbits (Sylvilagus floridanus), six raccoons (Procyon lotor), and three opossums (Didelphis virginiana) were collected from a mid-western dairy with known Map-infected cattle. Mycobacterium avium subsp. paratuberculosis was isolated from the mesenteric lymph node from seven of 25 (28%) feral cats. Ileum was culture-positive for three of these seven cats, and an isolation of Map was also made from the ileum of one of nine (11%) mice. Tissue samples from other species were negative as determined by Map culture; microscopic lesions consistent with paratuberculosis were not seen in any animal. Restriction fragment polymorphism analysis of isolates from cats and dairy cattle suggest interspecies transmission. The means by which interspecies transmission occurred may be through ingestion of Map-contaminated feces or waste milk or through ingestion of Map-infected prey. Shedding of Map from infected cats was not evaluated. The epidemiologic role of Map-infected feral cats on dairy farms requires further investigation.

Animals↗

Effect of MAP 1, MAP 2, and tau-proteins on structural parameters of tubulin assemblies.

When temperature-dependent recycling procedures for purification were used, tubulin is usually accompanied by a mixture of microtubule-associated proteins (MAPs) primarily comprising MAP 1, MAP 2, and the tau-proteins. Formerly we reported that microtubules formed from tubulin in the presence of these MAPs have more protofilaments than those formed without MAPs. Furthermore, these MAPs suppress the formation of aberrant assemblies (Böhm et al., BBA 800, 119, 1984). Now, we report that each single MAP fraction is able to influence the protofilament number of microtubules and the ratio between aberrant assemblies and microtubules in the same manner as the MAP mixture. This implies that all the MAPs investigated play a certain role in lateral association of tubulin dimers.

Animals↗

Physical mapping of the yeast mitochondrial genome: derivation of the fine structure and gene map of strain D273-10B and comparison with a strain (MH41-7B) differing in genome size.

(1) We have derived a fine-structure map of the 70 kb mitochondrial genome of the yeast S. cerevisiae, strain D273-10B, and compared it with our previous maps for strain MH41-7B. Restriction fragment maps for 56 enzyme recognition sites for 13 endonucleases, Eco RI, Hpa I, Bam HI, Hha I, Hinc II, Xba I, Hind III, Bgl II, Pvu II, Sal I, Pst I, Sst I, and Xho I, have been derived. We have used several methods to obtain these maps: (a) Four enzymes (Sal I, Sst I, Xho I, Pst I), each of which cuts D273-10B mtDNA at a single site, were employed to localize and orient fragments from multi-site enzyme digests that are cleaved by the single-site enzyme. (b) Radioactively labeled probes (rRNA or copy RNA [cRNA] transcribed from simple-sequence petite mtDNA) were hybridized to restriction fragments from different digests for identification of fragments which share common sequences. (c) The products of double or triple enzyme digests were identified for mapping and confirmation of the localization of restriction sites. (2) The antibiotic-resistant (antR) loci for erythromycin (E), chloramphenicol (C), paromomycin (P), and oligomycin (OI, OII) were positioned on the physical restriction map by hybridization of 3H-labeled cRNA transcribed from simple-sequence petite mtDNAs that retain a single genetic antR marker to appropriate restriction fragments bound to nitrocellulose filters. (3) Mitochondrial transcripts (21s rRNA, 14s rRNA, and tRNAs) labeled with 125I were hybridized to restriction fragments for identification of the corresponding coding sequence. (4) The gene order and localization of the antR loci and mitochondrial transcripts are as follows: C(0-1.5u)-tRNA I(0-21.5u)-P(29-36.6u)-tRNA II(29-46.4u)-14s rRNA(36-38.3u)-OII(60.3-62.5u) - tRNA III(73-76u) - OI(78.6-83.0u) - tRNA IV(82.5-83.0u) - E(94.2-98.6u) - 21s rRNA (94.2-99.4u). (5) The DNA fine structure and gene map of the 70 kb D273-10B mtDNA were compared to the map of the larger MH41-7B (76 kb) mtDNA. There are 56 restriction sites on D273-10B and 67 sites on MH41-7B for the 13 enzymes studied. The additional restriction sites are largely accounted for by the presence, in MH41-7B, of two sets of sequences, "A" (2.7 kb) and "B" (3.0 kb), located on either side of the OII marker. The remainder of the fragments map is remarkably similar for the two strains. The distances separating the antR loci and the mitochondrial transcripts are very similar except in the two regions surrounding OII.

DNA Restriction Enzymes↗

Sequential activation of Raf-1 kinase, mitogen-activated protein (MAP) kinase kinase, MAP kinase, and S6 kinase by hyperosmolality in renal cells.

In the renal medulla during antidiuresis, the extracellular fluid becomes hyperosmotic. Madin-Darby canine kidney (MDCK) epithelial cells adapt in hyperosmotic conditions and serve as a useful tissue culture model for cellular responses to hyperosmolality. We demonstrate that hyperosmolality stimulates phospholipase C, Raf-1 kinase mitogen-activated protein (MAP) kinase kinase, MAP kinase, and S6 kinase activities and that it increases phosphorylation of Raf-1 kinase, and p42 MAP kinase in MDCK cells. Stimulation of these kinases is osmolality-dependent (from 300 to 600 mosm/kg H2O). The time course of activation is sequential; the peak stimulation for Raf-1 kinase is at 5 min, at 10 min for MAP kinase kinase and MAP kinase, and at 20 min for S6 kinase. The activation of Raf-1 kinase and MAP kinase is inhibited by phorbol 12-myristate 13-acetate pretreatment in the presence of calphostin C or H-7. Tyrosine kinase inhibitors (genistein, herbimycin) do not significantly suppress hyperosmolality-induced MAP kinase activity. The increase of Ins-1,4,5-P3 levels by hyperosmolality suggests that activation of these kinases is mediated at least partially via activation of phospholipase C. Thus, hyperosmolality stimulates the serine/threonine kinases, Raf-1 kinase, MAP kinase kinase, MAP kinase, and S6 kinase, via predominantly protein kinase C-dependent, tyrosine kinase-independent pathways in MDCK cells.

Amino Acid Sequence↗

Correlations between the spread of ventricular activation and map patterns of measured and difference maps.

Three kinds of torso surface isopotential maps (measured, simulated, and difference maps) were delineated at every 1.5 (or 3) msec. during the QRS duration from the 85 unipolar lead ECG's led from the surface of a cylindrical torso model filled with perfusate and containing a canine heart undergoing Langendorff's perfusion. These three maps were compared as to the propagation process of ventricular activation obtained from the same heart and close correlations were found between the spread of ventricular activation and the map patterns of measured and difference maps. The difference map mainly reflected the proximity potential at each instant of ventricular activation in QRS duration and, when used in combination with the measured map, it was useful to estimate the spread of ventricular activation, especially around the stage of epicardial breakthrough of the activation front. It was confirmed that the interpretation of the difference map expressed in the present paper would not be misleading even if applied to a difference map obtained in a human torso model experiment.

Action Potentials↗

High-resolution physical mapping of human 5q31-q33 using three methods: radiation hybrid mapping, interphase fluorescence in situ hybridization, and pulsed-field gel electrophoresis.

Three physical mapping methods, radiation hybrid (RH) mapping, pulsed-field gel electrophoresis (PFGE), and fluorescence in situ hybridization (FISH) of interphase nuclei, were used to determine the order and relative distances between 12 loci in the q31-q33 region of human chromosome 5. The information obtained by each of the methods was compared to determine whether they gave consistent results. Based upon a combination of data, the predicted order of the 12 loci is cen-ADRB2-PDEA-CSF1R-RPS14-ANX6-SPARC++ +-GLRA1-GLUR1-ADRA1B-IL12- GABRG2-GABRA1-tel. Over the 5-Mb region spanned by these loci, we determined that an RH mapping unit (centiray, cR6500) is equivalent to 21 kb, in good agreement with previous estimates of 27-34 kb/cR6500 using the same set of radiation hybrids to map other regions. Of the three methods, RH mapping was by far the easiest and most efficient method for determining both order and distances. In addition, the range of resolution of RH mapping was the broadest, ranging from approximately 200 kb to several megabasepairs. Interphase FISH was the most informative method for clarifying the order of closely linked markers. The FISH distances obtained in this study will be useful as an internal reference for high-resolution mapping studies of other regions on the long arm of human chromosome 5. In contrast to RH mapping and FISH, PFGE was the least reliable of the three methods, producing some data that were inconsistent with the distances determined by the other two methods.

Chromosome Mapping↗

Map-based cloning in crop plants. Tomato as a model system: I. Genetic and physical mapping of jointless.

A map-based cloning scheme is being used to isolate the jointless (j) gene of tomato. The jointless locus is defined by a single recessive mutation that completely suppresses the formation of the fruit and flower pedicel and peduncle abscission zone jointless was mapped in an F2 population of an interspecific cross between Lycopersicon esculentum and Lycopersicon pennellii to a 7.1 cM interval between two restriction fragment length polymorphism (RFLP) markers TG523 and TG194. Isogenic DNA pools were then constructed from a subset of the mapping population and screened with 800 random decamers for random amplification of polymorphic DNA (RAPD) polymorphisms. Five new RAPD markers were isolated and mapped to chromosome 11, two of which were mapped within the targeted interval. One marker, RPD158, was mapped 1.5 cM to the opposite side of jointless relative to TG523 and thus narrowed the interval between the closest flanking markers to 3.0 cM. Physical mapping by pulse-field gel electrophoresis using TG523 and RPD158 as probes demonstrated that both markers hybridize to a common 600 kb SmaI restriction fragment. This provided an estimate of 200 kb/cM for the relationship between physical and genetic distances in the region of chromosome 11 containing the j locus. The combined results provide evidence for the feasibility of the next step toward isolation of the jointless gene by map-based cloning--a chromosome walk or jump to jointless.

Base Sequence↗

Maps from two interspecific backcross DNA panels available as a community genetic mapping resource.

We established two mouse interspecific backcross DNA panels, one containing 94 N2 animals from the cross (C57BL/6J x Mus spretus)F1 x C57BL/6J, and another from 94 N2 animals from the reciprocal backcross (C57BL/6J x SPRET/Ei)F1 x SPRET/Ei. We prepared large quantities of DNA from most tissues of each animal to create a community resource of interspecific backcross DNA for use by laboratories interested in mapping loci in the mouse. Initial characterization of the genetic maps of both panels has been completed. We used MIT SSLP markers, proviral loci, and several other sequence-defined genes to anchor our maps to other published maps. The BSB panel map (from the backcross to C57BL/6J) contains 215 loci and is anchored by 45 SSLP and 32 gene sequence loci. The BSS panel map (from the backcross to SPRET/Ei) contains 451 loci and is anchored by 49 SSLP loci, 43 proviral loci, and 60 gene sequence loci. To obtain a high density of markers, we used motif-primed PCR to "fingerprint" the panel DNAs. We constructed two maps, each representing one of the two panels. All new loci can be located with a high degree of certainty on the maps at current marker density. Segregation patterns in these data reveal several examples of transmission ratio distortion and permit analysis of the distribution of crossovers on individual chromosomes.

Animals↗