Search PubMed⌕ Search

Biomedical subjects

V Ferguson

Publications and source records attributed to V Ferguson.

At least 19 recordsLinked to original sources
PubMed1997

Reappearance of the minor alpha-sarcomeric actins in postnatal muscle.

The postnatal expression profiles of alpha-sarcomeric actin transcripts and protein are quantified in mouse striated muscles from birth to postnatal day 56 by Northern and Western blot analyses. alpha-Cardiac actin (alpha-CA) transcripts transiently increase between 12 and 21 days after birth in the quadriceps muscle, reaching approximately 90% that found in the adult mouse heart. Although alpha-CA is the alpha-sarcomeric actin isoform expressed in the immature fiber, the expression profiles of other contractile protein isoforms indicate that this postnatal period is not reflective of an immature phenotype. alpha-Skeletal actin (alpha-SA) transcripts accumulate to approximately 32% of the total alpha-sarcomeric actin transcripts in the adult heart. Our study shows that 1) there is a simultaneous reappearance of alpha-CA and alpha-SA in postnatal skeletal and heart muscles, respectively, and 2) the contractile protein gene expression profile characteristic of adult skeletal muscle is not achieved until after 42 days postnatal in the mouse. We propose there is a previously uncharacterized period of postnatal striated muscle maturation marked by the reappearance of the minor alpha-sarcomeric actins.

Actins↗
PubMed1997

Impact of alpha-skeletal actin but not alpha-cardiac actin on myoblast morphology.

Muscle differentiation involves a profound change in cell cytoarchitecture. This is accompanied by extensive isoform replacement in which the major non-muscle isoforms of the actin filament system are replaced by their muscle isoform counterparts. We have tested whether the sequential expression of the actin isoforms is functionally significant by precociously expressing the two striated muscle actins (alpha-skeletal and alpha-cardiac) in mouse myoblasts. The human alpha-skeletal and alpha-cardiac actin genes were transfected into mouse C2 myoblasts and clones expressing the human genes at the highest level were identified. Expression of the human alpha-skeletal actin gene was low with the highest mRNA level found to be 4% of that in adult human skeletal muscle. Clones expressing alpha-cardiac actin accumulated the mRNA up to 13% of the level of alpha-skeletal actin in adult human skeletal muscle. Despite the low level of alpha-skeletal actin expression, myoblasts transfected with this gene displayed a profound decrease in cell spreading. In contrast, alpha-cardiac actin had no impact on cell spreading. Neither alpha-skeletal actin nor alpha-cardiac actin had any impact on the total actin protein pool nor on the levels of the high molecular weight tropomyosins. The organisation of actin and tropomyosin into stress fibres was similar between transfected and control cells. We conclude that precocious expression of alpha-skeletal actin, but not alpha-cardiac actin, compromises myoblast morphology but not the ability of the cell to assemble stress-fibre-like structures.

Actins↗
PubMed1990

Activated Ki-ras proto-oncogene in spontaneously transformed and chemical tumor-derived cell lines related to the mouse lung alveologenic carcinoma.

An in vitro cell model of mouse lung alveologenic carcinoma consisting of preneoplastic nonmalignant cells, spontaneously transformed cells, and urethane-induced malignant cells was analyzed for phenotypic and genotypic changes associated with the transition to neoplasia. The polymerase chain reaction (PCR) was used to amplify the cDNA derived from the c-Ki-ras mRNA corresponding to exons 1 and 2 of the proto-oncogene. This approach allowed analysis of the gene transcription product rather than potentially unexpressed DNA. Direct sequencing of the PCR product identified a common single point mutation, alone or together with wild-type mRNA for c-Ki-ras, in all of the malignant clones. An A----G transition in the second base position of codon 61 was common to spontaneously malignant and chemical tumor-derived cell lines and to lines selected for lung metastatic behavior. The absence of the mutation in the nonmalignant cells suggests that the Ki-ras mutation may be a factor in onset or maintenance of the malignant phenotype and, at least in vitro, may be a late event in the transformation process.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed1990

Beta-globin gene haplotypes in Polynesians are predominantly southern Chinese in type.

beta-Globin gene haplotypes obtained in Polynesian Samoans were similar to those described in Southern Chinese. An atypical HindIII restriction fragment length polymorphism detected with pRK29, a 3' beta-globin gene probe, was present at a gene frequency of 7% in Samoans. Haplotype patterns suggest that this polymorphism may have arisen by 1 or 2 mutational events. DNA haplotypes derived from the beta-globin gene cluster confirm nuclear and mitochondrial DNA data that Polynesian precursor populations were East Asian in origin.

Chromosomes, Human, Pair 11↗
PubMed1989

A molecular marker associated with mild hemoglobin H disease.

The clinical spectrum of HbH disease varies from a benign disorder to a severe anemia which is blood-transfusion dependent. Heterogeneity at the clinical level is now being understood in terms of the underlying molecular defects. In this study a mild phenotype found in a group of patients with HbH disease is associated with two types of alpha-thalassemia. These are: alpha+-thalassemia (-alpha 3.7/) and alpha 0-thalassemia (--SEA/). In contrast, a second group with more severe HbH disease has a non-deletional alpha-thalassemia defect instead of alpha+-thalassemia (genotype alpha alpha T/--SEA). In the majority of cases, the basis for non-deletional alpha-thalassemia is Hb Constant Spring.

Adolescent↗
PubMed1989

Phenylalanine hydroxylase gene haplotypes in Polynesians: evolutionary origins and absence of alleles associated with severe phenylketonuria.

A total of 630 haplotypes for the phenylalanine hydroxylase (PAH) gene locus were established in five groups of Polynesians comprising Samoans, Tongans, Cook Islanders, Maori, and Niueans. Considerable genetic continuity was demonstrated between these widely dispersed populations, since three common haplotypes (4, 1, and 7) constituted over 95% of alleles. A control group of individuals from Southeast Asia shared the same major haplotypes, 4, 1, and 7, with Polynesians. These data provide further support for the theories of genetic homogeneity and of Asian affinities of the Polynesian precursor populations. The absence of severe phenylketonuria (PKU) in both Polynesians and Southeast Asians is consistent with the lack of PAH haplotypes 2 and 3, on which the severe PKU mutants have arisen among Caucasians.

Biological Evolution↗
PubMed1986

Asthma education by community child health nurses.

A randomised controlled study of an educational programme for children with asthma and their families was carried out by community child health nurses. Three hundred and sixty eight children aged 2 to 14 years were enrolled in the study after admission to hospital for asthma. The intervention group was visited monthly by a nurse for six months. The subjects were assessed six months later by a postal, self administered questionnaire. European children in the intervention group were taking significantly more drugs for the treatment of asthma six months after the index admission to hospital than those in the control group (mean (SD) intake 2.7 (1.1) v 2.1 (1.0), respectively). In particular, they were using more theophylline (56.6% v 37.0%) and inhaled steroids (34.9% v 21.0%). There was no difference between the groups for parental reports of improvement, of missed schooling, and in severe attacks of asthma of not responding to the usual treatment at home. European children in the intervention group used the hospital services for severe attacks of asthma more than controls (34.2% v 10.5%). There were more re-admissions in the European intervention group in the subsequent six months after the index admission than in the control group (mean (SD) 0.51 (0.97) v 0.29 (0.65). Re-admission continued to be higher in the 12 months after the nurse had stopped visiting (0.81 (1.65) v 0.25 (0.65]. There was no difference in the duration of hospital stay between the intervention and control groups. For Polynesian children there was no difference between the groups for any outcome measures.

Adolescent↗
PubMed1985

Cerebrospinal fluid glucose: turnover and metabolism.

The turnover of cerebrospinal fluid (CSF) glucose was studied in cats during steady-state perfusion. In all experiments, the perfusion fluid contained either tracer [14C]glucose alone or tracer glucose along with 4.45 mM unlabeled glucose. In some studies, serum glucose was lowered with insulin. The concentration of glucose and [14C]glucose in the effluent fluid was measured, and the distribution of 14C between glucose and lactate was determined by chromatography. From these values, the extraction of glucose and the metabolism of glucose to lactate were calculated. From the decrease in the specific activity of glucose in the perfusion fluid, the influx of glucose from serum was also determined. During steady-state perfusion, 71% of the radioactivity was recovered in the effluent fluid: 50% in the form of glucose, 6% in the form of lactate, and 15% in forms that were not identified. Thus, 50% of the perfusion fluid glucose was cleared, of which 29% was extracted and 21% metabolized. The influx of glucose was proportional to the serum glucose when the latter was about 2.5 mM or 10.0 mM. During perfusion with tracer glucose only, the concentration of glucose in the effluent fluid was 25% that of serum. The transport of glucose from serum was independent of the glucose concentration gradient between serum and perfusion fluid. However, when perfusion fluid glucose concentration was greater than that of serum, transport was inhibited. These studies suggest that in maintaining CSF glucose at a lower concentration than serum glucose, with equal amounts of glucose entering and leaving the CSF, 50% of CSF glucose concentration cleared is replaced by 25% of serum glucose concentration.

Animals↗