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Biomedical subjects

R Morgan

Publications and source records attributed to R Morgan.

At least 127 records · Page 7Linked to original sources
PubMed1995

An audit of echocardiograms in acute left ventricular failure.

All patients with heart failure should have an echocardiogram to establish a diagnosis, both to aid treatment as well as for prognostic reasons. An audit of 100 case notes of patients admitted with acute left ventricular failure over a 12-month period found that 26 patients had not had an echocardiogram. Of the 74 who did have an echocardiogram 68 patients had reduced systolic function (mean ejection fraction 42%). Almost all (93%) were commenced on an angiotension-converting enzyme (ACE) inhibitor. Those who did not receive an ACE inhibitor had no contraindications to these drugs. Seventeen patients had a confirmed myocardial infarction. Of these, 11 had an echocardiogram and 10 were discharged home on an ACE inhibitor. Despite appropriate indications some patients are deprived of echocardiography as well as the benefits of ACE inhibitors.

Acute Disease↗
PubMed1995

Induction of the prospective neural crest of Xenopus.

The earliest sign of the prospective neural crest of Xenopus is the expression of the ectodermal component of Xsna (the Xenopus homologue of snail) in a low arc on the dorsal aspect of stage 11 embryos, which subsequently assumes the horseshoe shape characteristic of the neural folds as the convergence-extension movements shape the neural plate. A related zinc-finger gene called Slug (Xslu) is expressed specifically in this tissue (i.e. the prospective crest) when the convergence extension movements are completed. Subsequently, Xslu is found in pre- and post-migratory cranial and trunk neural crest and also in lateral plate mesoderm after stage 17. Both Xslu and Xsna are induced by mesoderm from the dorsal or lateral marginal zone but not from the ventral marginal zone. From stage 10.5, explants of the prospective neural crest, which is underlain with tissue, are able to express Xslu. However expression of Xsna is not apparently specified until stage 12 and further contact with the inducer is required to raise the level of expression to that seen later in development. Xslu is specified at a later time. Embryos injected with noggin mRNA at the 1-cell stage or with plasmids driving noggin expression after the start of zygotic transcription express Xslu in a ring surrounding the embryo on the ventroposterior side. We suggest this indicates (a) that noggin interacts with another signal that is present throughout the ventral side of the embryo and (b) that Xslu is unable to express in the neural plate either because of the absence of a co-inducer or by a positive prohibition of expression. The ventral co-inducer, in the presence of overexpressed noggin, seems to generate an anterior/posterior pattern in the ventral part of the embryo comparable to that seen in neural crest of normal embryos. We suggest that the prospective neural crest is induced in normal embryos in the ectoderm that overlies the junction of the domains that express noggin and Xwnt-8. In support of this, we show animal cap explants from blastulae and gastrulae, treated with bFGF and noggin express Xslu but not NCAM although the mesoderm marker Xbra is also expressed. Explants treated with noggin alone express NCAM only. An indication that induction of the neural plate border is regulated independently of the neural plate is obtained from experiments using ultraviolet irradiation in the precleavage period. At certain doses, the cranial crest domains are not separated into lateral masses and there is a reduction in the size of the neural plate.

Amino Acid Sequence↗
PubMed1995

Identical fusion transcript associated with different breakpoints in the AML1 gene in simple and variant t(8;21) acute myeloid leukemia.

Fluorescence in situ hybridization (FISH) and/or RNA-based polymerase chain reaction (RT-PCR) were used to analyze the breakpoints within the AML1 gene and the AML1 fusion transcripts in t(8;21) acute myeloid leukemia (AML). Twenty-two patients presented with the simple t(8;21)(q22;q22) and one with a complex variant t(8;2;16;21). In eight cases we used FISH with AML1 cosmid probes on metaphase chromosomes as well as RT-PCR to detect the junctions of MAL1/CDR (ETO,MTG8). Five cases were analyzed by FISH alone and ten cases by RT-PCR alone. By FISH we could identify three groups according to the distribution of the fluorescent signal. Signals were found in group 1 on chromosomes 21 and 21q+, in group 2 on chromosomes 21, 21q+ and 8q- and in group 3 on chromosomes 21 and 8q-. In all groups we could detect an identical AML1/CDR fusion transcript. This transcript showed splicing of AML1 exon 5 onto CDR. Thus regardless of the heterogeneity suggested by FISH, all the breakpoints in the AML1 gene were clustered in the same intro between exons 5 and 6. Our results bring to over one hundred the number of t(8;21) cases in which an identical translocation could be detected at molecular level by RT-PCR. The high sensitivity of the technique makes it suitable for the diagnosis of this translocation in different stages of the disease. The impact of the molecular detection of t(8;21) cells in clinical remission as far as the treatment and the management of the disease are concerned deserves further discussion.

Acute Disease↗
PubMed1994

Mitochondrial gene defects in patients with NIDDM.

Non-insulin-dependent diabetes mellitus (NIDDM) has a strong genetic component and maternal factors have recently been implicated in disease inheritance. The mitochondrial myopathies are a group of diseases which often show maternal inheritance as a result of mtDNA defects; some patients have impaired glucose tolerance. Occasional families with maternally inherited diabetes and deafness associated with a deletion or point mutation of mtDNA have been reported. To assess the importance of mitochondrial gene defects in NIDDM, 150 unrelated diabetic subjects from Wales, UK and 68 unrelated patients with diabetes and at least one affected sibling from England, UK were studied. Southern blot analysis did not show any large mtDNA deletions or duplications. One patient had a mutation in the mitochondrial tRNAleu(UUR) gene at bp 3243. This mutation is commonly associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis and stroke like episodes (MELAS). Study of this patient and his siblings showed a distinct form of late-onset diabetes associated with nerve deafness but no clinical features of the MELAS syndrome. No diabetic subject was shown to have the mtDNA mutation at position 8344 (tRNA(lys)) which has previously been described in the syndrome of mitochondrial encephalomyopathy and red-ragged fibres (MERRF). The role of other mitochondrial gene defects in diabetes and the pathophysiological basis of glucose intolerance in patients with the MELAS mutation requires further elucidation.

Base Sequence↗
PubMed1994

Neural network analysis of the P300 event-related potential in multiple sclerosis.

Neural network analysis is sensitive to subtle changes in patterns of data. We hypothesized that a disease process which can cause impairment of cortical function such as multiple sclerosis (MS) would affect the P300 cognitive evoked potential (P300) in a manner detectable by a feedforward backpropagation neural network. Such a network was trained using a learning data set consisting of 101 P300 wave forms (from 26 MS patients and 26 normal controls). The network was then used to classify a randomly selected test data set of 20 studies (2 studies each of 5 MS patients and 5 controls) to which it had not been previously exposed, with an average accuracy (MS = abnormal, control = normal) of 81% for a single midline electrode, increasing to 90% using 3 midline electrodes in a jury system. Neural network analysis can be of help in distinguishing normal (control) P300 from abnormal (MS) P300.

Acoustic Stimulation↗
PubMed1994

Appreciation of the significance of cytogenetic and FISH analysis of bone marrow in clinical oncology.

Due to some empiric reasons, bone marrow (BM) has never been emphasized and appreciated as a valuable alternative source for metaphases of tumor nature. In the present study, we report the cytogenetic and fluorescence in situ hybridization (FISH) studies of BM in 172 patients with various tumors. Our results indicate that cytogenetic and FISH analyses of BM provide a valuable biologic approach concerning the diagnosis of tumors, evaluation of metastasis, and assessment of secondary hematologic malignancies. Thus, we suggest strongly that these studies become a standard part of clinical pathologic investigations in dealing with clinical oncology.

Bone Marrow↗
PubMed1994

Trisomy 5 in long-term cultures from bone marrow of patients with solid tumors.

Long-term cultures of bone marrow from 15 cases diagnosed previously with primary solid tumors were analyzed cytogenetically. Of these cases, 10 had normal karyotypes and five had chromosomal abnormalities. Trisomy 5 was found in four cases, three with trisomy 5 as the only change and one with trisomy 5 and trisomy 12. These results suggest that trisomy 5 may be a nonrandom change associated with an in vitro or in vivo phenomenon.

Adolescent↗
PubMed1994

X and Y chromosome loss as sole abnormality in acute non-lymphocytic leukemia (ANLL)

Of the 9300 bone marrows and peripheral bloods analyzed for hematologic disease in our laboratory between 1978 and 1990, 240 patients exhibited X or Y loss of chromosomes. Of those 240 patients only two could be positively associated with acute leukemia and no other observable chromosome involvement. The evidence presented here, albeit represented by only two patients, proves that sex chromosome loss as the sole abnormality can be a clonal cytogenetic marker for acute leukemia. One patient was a 48-year-old man with loss of the Y in 93% of his bone marrow metaphases and the other patient was a 53-year-old woman with 100% loss of the X in her bone marrow metaphases (perhaps the first such report of a woman). After therapy, both remission bone marrow analyses showed complete reappearance of the respective sex chromosomes.

Chromosome Aberrations↗
PubMed1994

Identification of complex t(15;17) in APL by FISH.

Fluorescence in situ hybridization (FISH) provides a sensitive and effective approach in identifying the RAR-alpha/PML fusion event in acute promyelocytic leukemia (APL) with the t(15;17). In the present study we describe the use of this assay for the identification of the RAR-alpha/PML fusion in bone marrow (BM) cells from three APL patients with complex t(15;17) translocations.

Adolescent↗
PubMed1994

Psychosocial correlates of illness burden in chronic fatigue syndrome.

We related reported physical symptoms, cognitive appraisals (e.g., negative style of thinking), and coping strategies (e.g., denial/disengagement strategies) with illness burden across several functional domains separately in subsets of chronic fatigue syndrome (CFS) patients with (n = 26) and without (n = 39) concurrently diagnosed major depressive disorder (MDD). In regard to cognitive appraisal measures, automatic thoughts and dysfunctional attitudes were strongly associated with a higher illness burden, as indicated in sickness impact profile (SIP) scores. Active-involvement coping strategies measured on COPE scales (active coping, planning, and positive reinterpretation and growth) were not associated with SIP scores, while other coping strategies (mental disengagement, behavioral disengagement, and denial) were positively correlated with psychosocial and physical SIP scales, especially those pertaining to interpersonal life-style arenas. After we accounted for the number of different CFS-specific physical complaints reported and DSM-III-R depression diagnosis status, cognitive appraisals and coping strategies predicted a substantial proportion of the variance in the severity of illness burden. For the most part, the magnitude of these relationships between our predictor model variables and illness burden severity was similar in the MDD and non-MDD subgroups.

Adaptation, Psychological↗