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Biomedical subjects

R Morgan

Publications and source records attributed to R Morgan.

At least 109 records · Page 6Linked to original sources
PubMed1995

Plasma cobalamin levels affect information processing speed in a longitudinal study of HIV-1 disease.

OBJECTIVE: To determine whether information processing speed is influenced by change in plasma cobalamin status in human immunodeficiency virus type 1 disease. DESIGN: A longitudinal study, using autoregression, to evaluate the relationship between plasma cobalamin status and change in information processing speed assessed by Posner Letter Matching, Sternberg Short-Term Memory Search, Figure Visual Scanning and Discrimination of Pictures, and continuous paired associates learning tasks. SETTING: University of Miami (Fla) School of Medicine from fall 1987 through summer 1991. PARTICIPANTS: Eighty-four human immunodeficiency virus type 1-infected homosexual men aged 20 to 55 years. None of the subjects displayed acquired immunodeficiency syndrome-defining symptoms at baseline; over the course of the study, 9.5% progressed to acquired immunodeficiency syndrome. MAIN OUTCOME MEASURES: Biochemical measurement of plasma cobalamin; performance on information processing speed tasks. RESULTS: Significant improvement in the Posner Letter Matching NI-PI (Name Identity minus Physical Identity) differential was associated with becoming cobalamin adequate or remaining adequate. Becoming cobalamin deficient, in contrast, was associated with a significant decline in the speed of accessing overlearned name codes. CONCLUSION: Normalization of plasma cobalamin inadequacy in human immunodeficiency virus type 1 disease may provide significant improvement in the speed of retrieving overlearned information from long-term memory.

Adult↗
PubMed1995

Agrin mRNA variants are differentially regulated in developing chick embryo spinal cord and sensory ganglia.

Agrin is a synapse-organizing protein synthesized and externalized by motor neurons in the spinal cord, which organizes the postsynaptic apparatus of the developing neuromuscular junction. Agrin mRNA in the nervous system consists of several alternatively spliced variants. Splicing of agrin gene transcripts at the major site of variability results in four variants: encoding 8 (B8) or 11 (B11) amino acid inserts, both (B19), or predominant variant (B0) without inserts. The insert-containing variants are neuron specific and encode agrin proteins with greater synapse-organizing activity than the B0 variant. Here, we report the localization and developmental regulation of agrin mRNA variants in chick embryo spinal cord and dorsal root ganglia. In situ hybridization using antisense oligodeoxynucleotide (ODN) probes specific for the B8 and B11 sequences shows that the neuron-specific variants are concentrated in ventrolateral cells of the chick embryo spinal cord, presumably motor neurons, beginning at embryonic day 4 (E4). By E14, the insert-containing mRNAs are found almost exclusively in presumptive motor neurons. These variants are also found in dorsal root ganglia and sympathetic ganglia, but not in non-neural tissues. Analysis by polymerase chain reaction showed that the B11 and B19 mRNA variants appeared in spinal cord at E4, whereas the B8 variant was first seen at E14. During development, B11 decreased and disappeared by E20, whereas B8 increased from E14 to E20. A similar time course was seen in dorsal root ganglia. The greatest acetylcholine receptor-aggregating activity in the spinal cord was seen from E6 to E10, coincident with the highest proportion of B11-containing transcripts and with the peak of synaptogenesis in limb muscles. These data provide the first evidence linking appearance of the neuron-specific agrin mRNA variants with expression of the functional protein. The B11 and B19 variants appeared in E2 (stage 15) neural tubes cultured for 2 days with or without notochord and trunk tissues, indicating that there is no peripheral signal required to induce these agrin mRNA variants in developing motor neurons.

Agrin↗
PubMed1995

Effects of storage on the binding of carboplatin to plasma proteins.

Plasma ultrafiltrates are routinely used in pharmacokinetic studies of carboplatin. Experiments were performed to detect and quantitate artifactual decreases in the platinum concentration of ultrafiltrates prepared from plasma samples stored at -20 degrees C and -70 degrees C. Carboplatin was added to anticoagulated, whole human blood to produce a 20 microgram/ml concentration. Plasma produced from the blood was stored frozen at either -20 degrees C or -70 degrees C. Aliquots from each storage condition were thawed and ultrafiltered once a week for up to 100 days. Platinum concentrations in ultrafiltrates and plasma were determined by flameless atomic absorption spectrometry. There was no loss of ultrafilterable platinum in plasma samples stored at -70 degrees C, whereas there was a steady decrease in free platinum concentration in ultrafiltrates prepared from plasma samples stored at -20 degrees C. These results imply that pharmacokinetic studies of carboplatin should use ultrafiltrates prepared immediately or that plasma for such studies should be stored at -70 degrees C. Storage of carboplatin-containing plasma at -20 degrees C and subsequent ultrafiltration is not acceptable, because measurement of platinum in such ultrafiltrates will be artifactually low.

Blood Preservation↗
PubMed1995

Cloning of breakpoints in 3q21 associated with hematologic malignancy.

Rearrangements of band 3q21 have been well documented in leukemia. To analyze the region involved, we have isolated a normal genomic P1 clone that spans the 3q21 breakpoints derived from two leukemia patients carrying t(3;3)(q21;q26). Both breakpoints are contained within a 50-kb NotI restriction fragment, but are not identical. They are separated by 9-11 kb and may disrupt genes associated with either the proximal or distal NotI sites. We further show that one patient carried a small insertion of material from chromosome 2 in the 3q- derivative. The P1 clone will allow isolation of candidate genes for these breakpoints and investigations into the clustering of other 3q21 leukemia breakpoints.

Chromosomes, Human, Pair 3↗
PubMed1995

Influenza vaccination: do the aged reap the benefit?

An audit of 100 elderly in-patients with appropriate medical conditions revealed that 63% had not been vaccinated this winter. 74% would have accepted vaccination if offered. A general practitioner questionnaire found that 42% relied on elderly patients coming forward and requesting vaccination. Unfortunately, many elderly patients are still missing out on influenza vaccination.

Aged↗
PubMed1995

The older driver--a review.

There are differences between elderly drivers and younger drivers in that the elderly are more likely to have cognitive, motor and sensoriperceptual deficits affecting their driving performance. The elderly driver is more likely to have a chronic illness and to be on medication, that might adversely affect driving. The elderly driver requires more study and help either by retraining or provision of adaptations to vehicles. Fitness to drive is of clinical importance to doctors in most specialities and recent studies would suggest that doctors need to be more aware of the current guidelines on driving and be prepared to offer advice.

Accidents, Traffic↗
PubMed1995

The prevalence of drivers in acute geriatric wards.

An audit of 150 patients on five acute geriatric wards found that 28 (19%) still drove. Forty-three (28%) used to drive but had given up, whilst 79 (53%) (76 of whom were female) had never driven. Former drivers gave the main reason for stopping as cost. No driver could recall being advised about driving by a doctor. Twenty-two drivers (79%) had a significant clinical condition that could affect driving, ranging from blackouts to arthritis. It is recommended that all elderly patients should be asked if they drive and any clinical conditions they might have that would adversely affect their driving be sought. Appropriate advice should be given by doctors to their elderly patients in order to safeguard them and the public from road traffic accidents.

Accidents, Traffic↗
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↗