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PubMed2004

The nematode-resistance gene, Mi-1, is associated with an inverted chromosomal segment in susceptible compared to resistant tomato.

The gene Mi-1 confers effective resistance in tomato ( Lycopersicon esculentum) against root-knot nematodes and some isolates of potato aphid. This locus was introgressed from L. peruvianum into the corresponding region on chromosome 6 in tomato. In nematode-resistant tomato, Mi-1 and six homologs are grouped into two clusters separated by 300 kb. Analysis of BAC clones revealed that the Mi-1 locus from susceptible tomato carried the same number and distribution of Mi-1 homologs, as did the resistant locus. Molecular markers flanking the resistant and susceptible loci were in the same relative orientation, but markers between the two clusters were in an inverse orientation. The simplest explanation for these observations is that there is an inversion between the two clusters of homologs when comparing the Mi-1 loci from L. esculentum and L. peruvianum. Such an inversion may explain previous observations of severe recombination suppression in the region. Two Mi-1 homologs identified from the BAC library derived from susceptible tomato are not linked to the chromosome 6 locus, but map to chromosome 5 in regions known to contain resistance gene loci in other solanaceous species.

Animals↗
PubMed1998

Genetic and physical localization of the root-knot nematode resistance locus mi in tomato.

As part of a map-based cloning strategy designed to isolate the root-knot nematode resistance gene Mi, tomato F2 populations were analyzed in order to identify recombination points close to this economically important gene. A total of 21,089 F2 progeny plants were screened using morphological markers. An additional 1887 F2 were screened using PCR-based flanking markers. Fine-structure mapping of recombinants with newly developed AFLP markers, and RFLP markers derived from physically mapped cosmid subclones, localized Mi to a genomic region of about 550 kb. The low frequency of recombinants indicated that recombination was generally suppressed in these crosses and that crossovers were restricted to particular regions. To circumvent this problem, a population of Lycopersicon peruvianum, the species from which Mi was originally introgressed, that was segregating for resistance was developed. Screening of this population with PCR, RFLP and AFLP markers identified several plants with crossovers near Mi. Recombination frequency was approximately eight-fold higher in the Mi region of the L. peruvianum cross. However, even within the wild species cross, recombination sites were not uniformly distributed in the region. By combining data from the L. esculentum and L. peruvianum recombinant analyses, it was possible to localize Mi to a region of the genome spanning less than 65 kb.

Animals↗
PubMed2004

Use of Beta Blockers in Patients with Post-MI Left Ventricular Dysfunction.

beta Blockers have been shown to reduce mortality after myocardial infarction (MI) in several large trials. Despite strong evidence supporting the role of beta blockers in treating patients after MI, less than half are prescribed these drugs. The majority of studies demonstrating efficacy of beta blockers in the treatment of the post-MI patients were conducted at a point in time when left ventricular (LV) dysfunction was considered a strong contraindication to their use. In addition, when these studies were carried out a variety of therapies that are known to improve survival were not yet available. In the present era, beta blockers are routinely used to treat patients with heart failure due to systolic dysfunction. Until recently, however, there was uncertainty about their role in the management of patients with LV dysfunction after MI. The recent CAPRICORN (Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction) study demonstrated a significant mortality benefit when carvedilol was added to standard therapy in patients with LV dysfunction after MI. This article reviews information regarding the initiation and maintenance of beta blockers in patients with post-MI LV dysfunction.

Journal Article↗
PubMed1991

Predictors of return to former leisure and social activities in MI patients.

Outcome after myocardial infarction (MI) is commonly conceptualized as exercise tolerance, recurrent infarction and return to work. In the present study a relative measure of return to former leisure and social activities (LSA) was tested in 366 myocardial infarction (MI) patients. Next, the hypothesis that psychosocial factors are more important predictors for return to LSA than medical ones, was tested. It appeared that at baseline (3 weeks after MI) 36%, at post-test (3 months after MI) 51% and at follow-up (1 year after MI) 54%, reached former levels of LSA. It could be shown, both in multiple regression analysis and path analysis, that psychological vulnerability at baseline is the most important predictor of return to former LSA. Females, older patients, single patients and patients with angina pectoris showed an unfavorable psychological profile at baseline. It is suggested that more attention should be given to the improvement of the psychological status soon after MI for the categories of patients mentioned.

Activities of Daily Living↗
PubMed1999

Attentional reactions to an MI: the impact of mood state, worry, and coping style.

This study investigated the possible development of an attentional bias to cardiac-related words in subjects who recently experienced a myocardial infarction (MI). It was hypothesized that cardiac-related stimuli would have attention-capturing characteristics for post-MI subjects, and this bias would be moderated by level of anxiety, degree of cardiac-related worry, and the subject's coping style. Post-MI subjects (n = 33) and matched controls (n = 31) participated in an attentional search task. The post-MI subjects failed to show the predicted group increases in attention allocated to cardiac stimuli, but a difference between groups still occurred as the control group exhibited directed inattention to cardiac stimuli. Subsequent analysis indicated those post-MI subjects who did evince an attentional bias toward cardiac stimuli had higher monitoring scores on a self-report measure of coping style. Level of emotional distress and cardiac-related worry failed to predict attentional bias for the post-MI subjects.

Adaptation, Psychological↗
PubMed2001

Modulation of oxidative stress by a selective inhibition of angiotensin II type 1 receptors in MI rats.

OBJECTIVES: To examine whether blocking of the renin-angiotensin system (RAS) at the angiotensin II type 1 (AT1) receptor site is accompanied by changes in the oxidative stress parameters. BACKGROUND: Congestive heart failure in rats after myocardial infarction (MI) has been shown to correlate with a decrease in antioxidant enzyme activities and an increase in oxidative stress. Inhibition of the RAS with captopril improves cardiac function and survival in MI rats with a reduction in oxidative stress. METHODS: Myocardial infarction in rats was produced by ligation of the left coronary artery. At four weeks after surgery, animals from the sham as well as MI groups were treated with losartan (2 mg/ml in drinking water daily). At 16 weeks after surgery, the animals were examined for hemodynamic function and the hearts were analyzed for antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and catalase) and oxidative stress (lipid hydroperoxides, reduced and oxidized glutathione and redox ratio). RESULTS: Congestive heart failure was characterized by dyspnea, depressed hemodynamic function and presence of lung and liver congestion. This was also associated with a decrease in the myocardial catalase (-25%), glutathione peroxidase (-38%) and superoxide dismutase (-42%) activities. An increase in oxidative stress in these hearts was indicated by an increase in lipid hydroperoxides (+67%) and reduction in the redox ratio (-75%). Hemodynamic function was better maintained and there were no indications of dyspnea or lung or liver congestion in the losartan-treated MI rats. In these animals, myocardial oxidative stress was markedly reduced and glutathione peroxidase and catalase activities were significantly improved compared with the untreated MI group. CONCLUSIONS: Blocking of RAS at the AT1 receptor site without the inhibition of angiotensin-converting enzymes modulates heart failure after MI, and this beneficial effect is associated with a decrease in oxidative stress. This study suggests a newer role for losartan in the treatment of heart failure.

Angiotensin Receptor Antagonists↗
PubMed1994

The alpha-conotoxins GI and MI distinguish between the nicotinic acetylcholine receptor agonist sites while SI does not.

The alpha-conotoxins are paralytic peptide toxins from Indo-Pacific cone snails. This paper presents a detailed analysis of how alpha-conotoxins inhibit [125I]-alpha-bungarotoxin (125I-BTX) equilibrium binding to the acetylcholine receptor (AChR) from electric organ of Torpedo californica and Torpedo nobiliana. All three alpha-conotoxins studied, SI, GI, and MI, completely inhibited 125I-BTX binding with the same order of potency in both species (MI approximately GI > SI approximately d-tubocurarine). BTX-concentration curves showed that this inhibition is competitive. However, while SI appeared to bind to a homogeneous population of sites, both GI and MI displayed curare-like heterogeneous binding. Studies using partially-blocked AChR demonstrated that both GI and MI display different affinities toward the two agonist sites, much like small curariform antagonists do. The high-affinity site for these two alpha-conotoxins is also the high-affinity d-tubocurarine site, which is believed to be located at the alpha gamma-subunit interface. The high-affinity binding of MI and GI was of the same order of magnitude as that of d-tubocurarine; however, their affinity for the other agonist site was somewhat greater than that of dTC, resulting in less site selectivity. Despite being homologous to GI and MI, SI did not distinguish between the two sites. A possible molecular basis for this difference is presented.

Amino Acid Sequence↗
PubMed2002

Association of a polymorphism of the ecNOS gene with myocardial infarction in a subgroup of Turkish MI patients.

In this study we examined a possible association between a 27 base pair (bp)-repeat polymorphism in intron 4 of the ecNOS gene and myocardial infarction (MI) in a subgroup of the Turkish population. We compared MI and control groups for the frequencies of the ecNOS alleles and their genotypes. The frequency of the ecNOS 4a/a and 4a/b genotypes was found to be significantly higher in the MI group than in the control group. Interestingly, the frequency of the ecNOS 4a/b polymorphism was found to be significantly higher in the selected MI group (patients with no known secondary risk factors) than in the control and non-selected MI group. We found that the patients with MI had the frequency of the a/a genotype 4.3%, of the a/b genotype 26.6% and the b/b genotype 69.1%. The controls, however, showed only 0.6% for a/a, 18.0% for a/b and 81.4% for the b/b genotype (P < 0.001; chi2 = 13.626). In this study, we show that myocardial infarction is associated with one subtype of ecNOS gene polymorphism.

Adult↗
PubMed2005

Reduced expression of IL-12 receptor beta2 and IL-18 receptor alpha genes in natural killer cells and macrophages derived from B6-mi/mi mice.

The mi transcriptional factor (MITF) is a basic helix-loop-helix leucine zipper-type transcriptional factor. The mi mutant allele encodes an abnormal MITF, in which one out of four consecutive arginines is deleted in the basic domain. The VGA-9-tg (tg) allele is another mutant allele and considered to be a null mutant allele. C57BL/6 (B6)-mi/mi mice showed abnormal phenotypes of natural killer (NK) cells and macrophages, whereas B6-tg/tg mice did not. The expression levels of the genes for the interleukin-12 receptor (IL-12R) beta2 and IL-18Ralpha were reduced in both the NK cells and macrophages of B6-mi/mi mice, while the expression levels of the corresponding genes in B6-tg/tg mice were unaffected. The B6-mi/mi NK cells and B6-mi/mi macrophages showed impaired responses to stimulation with IL-12, IL-18, and IL-12 plus IL-18 stimulation. The abnormal NK cell and macrophage of B6-mi/mi mice appear to be due to decreased expression of the IL-12Rbeta2 and IL-18Ralpha genes.

Animals↗
PubMed2002

Immunological characterization of anti-Mi(a), a red blood cell alloantibody, in Taiwan.

BACKGROUND AND OBJECTIVES: The red blood cell Mi III phenotype is prevalent in Asia, and its corresponding alloantibody, anti-Mi(a), has been reported to cause haemolytic transfusion reactions and haemolytic disease of the newborn. However, a complete picture of the immunological characteristics of anti-Mi(a) is still lacking. We therefore conducted a systematic study to evaluate the potential clinical significance of this antibody. MATERIALS AND METHODS: From April 1999 to March 2000, we identified 60 sera containing anti-Mi(a) among pretransfusion samples at a teaching hospital in Taiwan. These antibodies were tested for immunoglobulin class, thermal range and activity in a monocyte monolayer assay. RESULTS: Thirty-four (57%) of the antibodies were immunoglobulin M (IgM), and 15 retained their activity at 37 degrees C. Of those that were immunoglobulin G (IgG), 96% were of subclasses IgG1 and/or IgG3. Monocyte monolayer assay studies showed that 69% (18/26) of the IgG anti-Mi(a) sera were reactive. CONCLUSIONS: Our study justifies the implementation of anti-Mi(a) screening in Taiwan.

Erythrocytes↗
PubMed2002

The relationship between MI and SMA afferents and cerebellar and pallidal efferents in the macaque monkey.

The purpose of the present study was to determine the interrelationship between the thalamic afferents arising from the cerebellum (Cb) and the internal segment of the globus pallidus (GPi) with the neurons projecting to the primary motor cortex (MI) and to the supplementary motor area (SMA). We combined fluorescent retrograde tracers with a double anterograde labeling technique. Multiple injections of a combination of Diamidino Yellow and Fast Blue were made into either the MI or SMA hand/arm representation as determined by intracortical microstimulation. In the same animal, biotinylated dextran amine was injected into the GPi and horseradish peroxidase conjugated to wheat germ agglutinin was injected into the contralateral cerebellar nuclei. The results revealed that the cerebellar and pallidal thalamic territories are largely separate. The ventral anterior nucleus (VA) and the ventral lateral nucleus pars oralis (VLo) contained a greater density of pallidal labeling while a greater density of cerebellar label was observed more caudally in the ventral posterior lateral nucleus pars oralis (VPLo) as well as in nucleus X (X). Moreover, we observed that the greatest coincidence of retrograde cell labeling was within the pallidal thalamic territory following the SMA injections and within the cerebellar thalamic territory following the MI injections. However, interdigitating foci of pallidal and cerebellar label were also observed particularly in the ventral lateral nucleus pars oralis (VLo) and the ventral lateral nucleus pars caudalis (VLc). In both VLo and VLc, we additionally observed coincidence between the cerebellar labeling and SMA projection neurons as well as between pallidal labeling and MI projection neurons. These data suggest that while MI primarily receives inputs originating from Cb and SMA primarily receives inputs originating from GPi, it also appears that MI and SMA receive secondary afferents arising from GPi and Cb, respectively.

Animals↗
PubMed2006

Heterologous expression of the Mi-1.2 gene from tomato confers resistance against nematodes but not aphids in eggplant.

The Mi-1.2 gene in tomato (Solanum lycopersicum) is a member of the nucleotide-binding leucine-rich repeat (NBLRR) class of plant resistance genes, and confers resistance against root-knot nematodes (Meloidogyne spp.), the potato aphid (Macrosiphum euphorbiae), and the sweet potato whitefly (Bemisia tabaci). Mi-1.2 mediates a rapid local defensive response at the site of infection, although the signaling and defensive pathways required for resistance are largely unknown. In this study, eggplant (S. melongena) was transformed with Mi-1.2 to determine whether this gene can function in a genetic background other than tomato. Eggplants that carried Mi-1.2 displayed resistance to the root-knot nematode Meloidogyne javanica but were fully susceptible to the potato aphid, whereas a susceptible tomato line transformed with the same transgene was resistant to nematodes and aphids. This study shows that Mi-1.2 can confer nematode resistance in another Solanaceous species. It also indicates that the requirements for Mi-mediated aphid and nematode resistance differ. Potentially, aphid resistance requires additional genes that are not conserved between tomato and eggplant.

Animals↗
PubMed2006

Mi-1-Mediated aphid resistance involves salicylic acid and mitogen-activated protein kinase signaling cascades.

The tomato Mi-1 gene confers resistance to root-knot nematodes (Meloidogyne spp.), potato aphids (Macrosiphum eluphorbiae), and whiteflies (Bemisia tabaci and B. tabaci biotype B). Resistance to potato aphid is developmentally regulated and is not associated with induction of a hypersensitive response. The NahG transgene that eliminates endogenous salicylic acid (SA) was used to test the role of the SA signaling pathway in the resistance mediated by Mi-1 to potato aphids. Aphids survived longer on NahG tomato plants than on wild type. However, aphid reproduction was not affected on NahG tomato. Aphid resistance in Mi-1 NahG plants was completely abolished and the phenotype was successfully rescued by application of BTH (benzo(1,2,3)-thiaiazole-7-carbothioic acid S-methyl ester), indicating that the SA signaling pathway is an important component of Mi-1-mediated aphid resistance. Using virus-induced gene silencing, one or more mitogen-activated protein kinase (MAPK) cascades required for Mi-1-mediated aphid resistance were identified. Silencing plants for MAPK kinase (LeMKK2) and MAPKs (LeMPK2 and LeMPK1, or LeMPK3) resulted in attenuation of Mi-1-mediated aphid resistance. These results further demonstrate that resistance gene-mediated signaling events against piercing-sucking insects are similar to those against other plant pathogens.

Animals↗
PubMed2003

Aphid-induced defense responses in Mi-1-mediated compatible and incompatible tomato interactions.

The tomato Mi-1 gene confers resistance to three species of root-knot nematode and potato aphid. We studied changes in expression of jasmonic acid (JA)- and salicylic acid (SA)-dependent defense genes in response to potato and green peach aphids. We determined changes in three PR proteins, lipoxygenase and proteinase inhibitors I and II transcripts, locally and systemically in both compatible and incompatible interactions in tomato. Transcripts for PR-1 were detected earlier and accumulated to higher levels in the incompatible than in the compatible potato aphid/tomato interactions. The transcript profiles of the other genes were similar in compatible compared with incompatible interactions. Pin1 and Pin2 RNAs were detected early and transiently in both compatible and incompatible interactions. In tomato plants containing Mi-1, systemic expression of PR-1 and GluB was detected in both compatible and incompatible interactions at 48 h after infestations with either aphid. These results suggest that aphid feeding involves both SA and JA/ethylene plant defense signaling pathways and that Mi-1-mediated resistance might involve a SA-dependent signaling pathway. Potato aphid feeding generated reactive oxygen species in both compatible and incompatible interactions. However, a hypersensitive response was absent in the Mi-1-mediated resistance response to potato aphids. Reciprocal grafting experiments revealed that resistance is cell autonomous, and local expression of Mi-1 is required for Mi-1-mediated resistance against the potato aphid.

Animals↗
PubMed2003

Effect of a new 1,3,4-thiadiazolium mesoionic compound (MI-D) on B16-F10 murine melanoma.

The structural characteristics of mesoionic compounds, which contain distinct regions of positive and negative charges associated with a poly-heteroatomic system, enable them to cross cellular membranes and interact strongly with biomolecules. Potential biological applications have been described for mesoionic compounds. In this study we evaluated the antitumour activity of 4-phenyl-5-(4-nitrocinnamoyl)-1,3,4-thiadiazolium-2-phenylamine chloride (MI-D), a new mesoionic compound, against the mouse melanoma B16-F10 cell line. In vitro assays showed that MI-D interferes with both cell viability and proliferation. MI-D was cytotoxic to B16-F10 cells; cell viability, which was determined at various time intervals (1-72 h) and in the presence of different concentrations of the drug (2.5-75 micro M), was reduced by approximately 80% following 24 h exposure at 25 micro M. The proliferation rate evaluated over 72 h using varying subcytotoxic and cytotoxic concentrations (2.5-25 micro M) decreased in a dose-dependent manner. The in vivo antitumour activity of the drug was evaluated using a subcutaneous B16-F10 melanoma tumour in C57BL/6 mice. Animals were given MI-D intraperitoneally at a single dose of 57 micro mol/kg, 24 h after cell inoculation. Positive controls were treated with fotemustine and dacarbazine, which have known effects on melanoma cells. On day 17, tumours were excised and their weights were determined. MI-D inhibited tumour growth by 85%. This is a very encouraging result with regard to the possibility of MI-D becoming a new tool for melanoma research and treatment.

Animals↗
PubMed2002

Establishment and characterization of a new lung cancer cell line (MI-4) producing high levels of granulocyte colony stimulating factor.

We established a human lung cancer cell line, MI-4 from the pleural effusion of a 69-year-old male with advanced large cell undifferentiated carcinoma of the lung complicated by leukocytosis. The culture supernatant of MI-4 contained high levels of granulocyte colony stimulating factor (G-CSF). The intracellular localization of the G-CSF was identified by immunocytochemistry. Reverse transcription-polymerase chain reaction (RT-PCR) revealed G-CSF mRNA expression in this cell line. The cell line was successfully transplanted into nude mice. The transplanted nude mice also showed leukocytosis with a high serum G-CSF level. Southern blot analysis did not show amplification or rearrangement of the G-CSF gene in MI-4 cells. Spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) analyses revealed that this cell line has an additional chromosome 17 attached to a segment of chromosome 10 besides two intact chromosomes 17, and that each of these three chromosomes 17 has a G-CSF gene on chromosome 17q. Inflammatory cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta, significantly enhanced G-CSF expression at both the protein and mRNA levels in MI-4. However, these cytokines did not stimulate the growth of MI-4 cells, regardless of abundant G-CSF production. TNF-alpha rather suppressed it, in a dose-dependent manner. Exogenous recombinant human G-CSF and anti-G-CSF antibody did not promote or inhibit the growth of MI-4 cells at any concentration examined. In addition, RT-PCR analysis did not show G-CSF receptor mRNA expression. These results suggest that this cell line does not have an autocrine growth loop for G-CSF. This cell line should be very useful for understanding the biological activity of G-CSF in G-CSF-overproducing lung cancer.

Aged↗
PubMed1989

Molecular analysis of glycophorin A and B gene structure and expression in homozygous Miltenberger class V (Mi. V) human erythrocytes.

In the Miltenberger class V (Mi. V) condition, red cells lack glycophorin A (GPA) and glycophorin B (GPB) but carry instead an unusual glycoprotein thought to be a hybrid molecule produced by the unequal crossing-over between the closely linked genes encoding for GPA and GPB. By Western blot analysis with rabbit anti-GPA antibodies specific for discrete domains of GPA, it was found that the Mi. V glycoprotein (donor F. M.) contains approximately 60 amino acid residues of GPA at its N-terminus. As a preliminary approach to the molecular analysis of this variant the restriction maps of the GPA and GPB genes were established by Southern blot analysis of genomic DNA and from genomic clones isolated from a human leukocyte library constructed in lambda EMBL4. The GPA and GPB genes cover about 30 kb of DNA and are organized into seven exons (A-1-A-7) and five exons (B-1-B-5), respectively. In addition to the normal genes, a third gene (named inv), closely resembling the GPA and GPB genes, was also identified. In the homozygous Mi. V individual the normal GPA and GPB genes were absent, but an unusual form of gene structure was detected by Southern blot analysis. The Mi. V glycoprotein gene was composed of exon B-1 of the GPB gene followed by exons A-2 and A-3 of the GPA gene and the exons B-3, B-4 and B-5 of the GPB gene. Exon B-1 can be distinguished from exon A-1 of GPA since it is located within a different restriction fragment, but both encode the same amino acid sequence (N-terminal region of the signal peptides). Using the polymerase chain reaction, the junction between exon A-3 and exon B-3 was confirmed by amplification of the DNA region where the putative crossing-over has occurred and it was deduced that the Mi. V glycoprotein is a hybrid molecule composed of amino acid residues 1-58 from GPA fused to amino acid residues 27-72 of GPB. In addition, the finding that part of the signal peptide and the 5'-untranslated region are derived from GPB suggests that the genetic background of the Mi. V variant is rather complex and may involve a cascade of recombination or gene conversion events.

Amino Acid Sequence↗
PubMed2001

Relation of socioeconomic position to the case fatality, prognosis and treatment of myocardial infarction events; the FINMONICA MI Register Study.

OBJECTIVE: To examine socioeconomic differences in case fatality and prognosis of myocardial infarction (MI) events, and to estimate the contributions of incidence and case fatality to socioeconomic differences in coronary heart disease (CHD) mortality. DESIGN: A population-based MI register study. METHODS: The FINMONICA MI Register recorded all MI events among persons aged 35-64 years in three areas of Finland during 1983-1992. A record linkage of the MI Register data with the files of Statistics Finland was performed to obtain information on socioeconomic indicators for each individual registered. First MI events (n=8427) were included in the analyses. MAIN RESULTS: The adjusted risk ratio of prehospital coronary death was 2.11 (95% CI 1.82, 2.46) among men and 1.68 (1.14, 2.48) among women with low income compared with those with high income. Even among persons hospitalised alive the risk of death during the next 12 months was markedly higher in the low income group than in the high income group. Case fatality explained 51% of the CHD mortality difference between the low and the high income groups among men and 38% among women. Incidence contributed 49% and 62%, respectively. CONCLUSIONS: Considerable socioeconomic differences were observed in the case fatality of first coronary events both before hospitalisation and among patients hospitalised alive. Case fatality explained a half of the CHD mortality difference between the low and the high income groups among men and more than a third among women.

Adult↗