PubMed Health⌕ Search

Biomedical subjects

K Morrison

Publications and source records attributed to K Morrison.

At least 55 records · Page 3Linked to original sources
PubMed1995

The embryonic RNA helicase gene (ERH): a new member of the DEAD box family of RNA helicases.

DEAD box proteins share several highly conserved motifs including the characteristic Asp-Glu-Ala-Asp (D-E-A-D in the amino acid single-letter code) motif and have established or putative ATP-dependent RNA helicase activity. These proteins are implicated in a range of cellular processes that involve regulation of RNA function, including translation initiation, RNA splicing and ribosome assembly. Here we describe the isolation and characterization of an embryonic RNA helicase gene, ERH, which maps to mouse chromosome 1 and encodes a new member of the DEAD box family of proteins. The predicted ERH protein shows high sequence similarity to the testes-specific mouse PL10 and to the maternally acting Xenopus An3 helicase proteins. The ERH expression profile is similar, to that of An3, which localizes to the animal hemisphere of oocytes and is abundantly expressed in the embryo. ERH is expressed in oocytes and is a ubiquitous mRNA in the 9 days-post-conception embryo, and at later stages of development shows a more restricted pattern of expression in brain and kidney. The similarities in sequence and in expression profile suggest that ERH is the murine equivalent of the Xenopus An3 gene, and we propose that ERH plays a role in translational activation of mRNA in the oocyte and early embryo.

Amino Acid Sequence↗
PubMed1994

Prenatal diagnosis of Werdnig-Hoffmann disease: DNA analysis of a mummified umbilical cord using closely linked microsatellite markers.

We present a case of prenatal diagnosis of Werdnig-Hoffmann disease, the most severe type of spinal muscular atrophy (SMA). DNA obtained from a mummified umbilical cord of a decreased affected brother of the index case was analysed with four closely linked microsatellite markers [EF1/2a and EF13/14 (D5S125), MAP1B, and JK53CA (D5S112)], flanking the SMA gene, on chromosome 5q11.2-13.3. The fetus was diagnosed as homozygous for the deleterious SMA gene.

Adult↗
PubMed1994

Detection of tumour necrosis factor alpha in sarcoidosis and tuberculosis granulomas using in situ hybridisation.

AIMS: To determine the site of tumour necrosis factor alpha (TNF alpha) product and mRNA in granulomas. METHOD: In situ hybridisation with digoxigenin labelled or biotinylated oligonucleotide probes was used to demonstrate the presence of total mRNA, and then the presence of TNF alpha mRNA in the biopsy specimens of 37 granulomas (31 sarcoidosis, six tuberculosis). RESULTS: TNF alpha mRNA was detected in epithelioid cells, giant cells, and lymphocytes in the granulomas. Some sarcoidosis specimens did not contain detectable mRNA for TNF, but did contain TNF peptide in the epithelioid or giant cells on immunostaining. This may have been due to stored TNF present in cells in which mRNA for TNF is no longer being produced. CONCLUSION: The results suggest that giant cells should not be regarded as effete cells, as they contain large amounts of mRNA and seem to be actively producing TNF alpha.

Antisense Elements (Genetics)↗
PubMed1993

Applicability of the Greulich and Pyle skeletal age standards to black and white children of today.

OBJECTIVE: The Greulich and Pyle skeletal age atlas was derived from white children of upper socioeconomic level during the 1930s. To our knowledge, the Greulich and Pyle standards have not been reassessed for both black and white children; it was the purpose of this study to reassess the applicability of these standards to today's children. DESIGN: A "blinded" review of hand roentgenograms taken for the evaluation of trauma was performed. Age of the subjects was evenly distributed between 0 and 18 years. The roentgenograms were scored for bone age by five individuals from different disciplines and levels of training. The difference between the median bone age and the child's chronologic age was calculated for each roentgenogram and stratified into four age groups: early childhood (0 to 4 years), middle childhood (4 to 8 years), late childhood (8 to 13 years), and adolescence (13 to 18 years). SETTING: The roentgenograms were obtained from four hospital emergency rooms in the Lake Erie basin area, the same geographic area from which the Greulich and Pyle standards originated. PATIENTS: There were 841 children: 452 boys and 389 girls, 461 black and 380 white children. RESULTS: The bone ages and chronologic ages were similar for white girls of all ages. Black girls were skeletally advanced by 0.4 to 0.7 year (P < .001), except during middle childhood. White boys were skeletally delayed during middle childhood by 0.9 year (P < .001) and during late childhood by 0.4 year (P < .01), but they were advanced during the adolescent years by 0.5 year (P < .01). Black boys showed no difference except for the adolescent group, which was skeletally advanced by 0.4 year (P < .02). CONCLUSIONS: The Greulich and Pyle atlas is not applicable to all children today, especially black girls. We should be aware of this information when making clinical decisions requiring accurate bone ages.

Adolescent↗
PubMed1992

Erythroid expression and DNAaseI-hypersensitive sites of the carbonic anhydrase 1 gene.

The carbonic anhydrase 1 gene is expressed in adult human and mouse erythroid cells and colon epithelia from two distinct promoters. We have explored the erythroid promoter for cis-acting sequences involved in transcription using DNAaseI as a probe. Two DNAaseI-hypersensitive sites (DHS-1 and DHS-2) have been identified in the distal erythroid promoter in CA1-expressing erythroleukaemic cells. These sites are present at low levels in K562 cells, which have a foetal/embryonic phenotype and do not express CA1. DHS-1 and DHS-2 are not present in non-erythroid cells, including colon cells, which express CA1 from the proximal colon promoter. DHS-1 and DHS-2 were also generated in an heterologous CA1 gene containing 5 kb of erythroid promoter sequence after transfection into erythroid cells, including K562 cells. These transfection studies showed that both this fragment, and an abbreviated 817 bp promoter fragment which contains only DHS-1, were sufficient to confer erythroid-specific expression to a reporter gene. These promoters were active in cell lines expressing CA1 and in K562 cells. This latter observation implies that a developmental repressor factor is both present in K562 cells and binds to a cis-acting sequence that is absent from the sequence 5 kb upstream of the erythroid transcription start site.

Base Sequence↗
PubMed1992

Phosphoglucomutase 1: complete human and rabbit mRNA sequences and direct mapping of this highly polymorphic marker on human chromosome 1.

A cDNA clone encoding the mRNA for the highly polymorphic human enzyme phosphoglucomutase 1 (PGM1; EC 5.4.2.2) has been isolated and characterized. This was achieved indirectly by first isolating a rabbit cDNA from an expression library using anti-rabbit PGM antibodies. A comparison of the nucleotide sequences shows that the homologies between human and rabbit PGM1 mRNAs are 92% and 97% for the coding nucleotide sequence and the amino acid sequence, respectively. The derived rabbit amino acid sequence is in complete agreement with the published protein sequence for rabbit muscle PGM. A physical localization of the human PGM1 gene to chromosome 1p31 has been determined by in situ hybridization. Analysis of DNA from a wide variety of vertebrates indicates a high level of PGM1 sequence conservation during evolution.

Animals↗
PubMed1992

Bone mineral density during puberty in western Canadian children.

To assess the influence of puberty and its associated changes in body weight and height on bone mineral density (BMD), lumbar spine (L2-L4) and femoral neck BMD were measured in 74 healthy, active children (9-16 years) using dual-photon absorptiometry. Competitive swimmers were recruited to minimize the potential effect variability in mechanical loading regime may have on bone density of the lumbar spine. Tanner staging was used to assess stage of puberty. Current dietary calcium intake was assessed by analysis of 6-day dietary records. Significant differences in spinal and femoral neck BMD occurred between early (Tanner 1 and 2) and late stages of puberty (Tanner 4 and 5), P < 0.05. A significant correlation was found between bone density and dietary calcium intake. However stepwise regression analyses demonstrated stage of puberty or body weight were the only factors which significantly affected spinal BMD, accounting for 77% and 68% of the variability respectively; while at the femoral neck, body weight accounted for 52% of the variability. These results demonstrate that when potential interacting factors are controlled for through regression analyses, differences in BMD occur mainly as a function of puberty and the associated gains in body weight.

Adolescent↗
PubMed1992

Alpha-1 antitrypsin gene exon use in stimulated lymphocytes.

AIMS: To investigate the expression of mRNA transcripts containing exon A or B in lymphocyte cultures. METHODS: An in situ hybridisation technique, using synthetic, biotinylated oligonucleotide probes was deployed to allow the demonstration of exon A, exon B, or the normal hepatocyte message containing exon C. RESULTS: Lymphocytes used the same alternative splicing technique as monocytes in the generation of their alpha-1 antitrypsin message. They also provided data on the frequency of exon A and B expression in cells from different subjects. Most circulating granulocytes failed to show the alpha-1 antitrypsin message, suggesting that this protein is synthesised in the marrow and represents a stored protein component in polymorph and circulating nuclear lymphocytes. CONCLUSIONS: In situ hybridisation is a sensitive technique for the detection of individual gene exon use in cell populations. Lymphocytes show the same promoter use as that described for monocytes.

Antisense Elements (Genetics)↗
PubMed1991

CAIII a marker for early myogenesis: analysis of expression in cultured myogenic cells.

Carbonic anhydrase III (CAIII) is an abundant muscle protein characteristic of adult type-1, slow-twitch, muscle fibers. We demonstrate that CAIII is not confined to mature muscle but is also expressed in cultured myogenic cells that were originally derived from adult and fetal limb muscle (G8 and C2C12) and by azacytidine treatment of 10T1/2 fibroblasts (23A2). Transcripts may accumulate in these cells to levels that correspond to 6.5% of that found in mature muscle. CAIII is expressed in mononucleate myoblasts and is abundant in those that preferentially fuse to form myotubes, and these findings contrast with those for many other muscle genes whose transcripts only accumulate on or after terminal differentiation. Preliminary promoter-function assays by transfection shows that 2.8 kb of sequence flanking the 5' end of the human CAIII gene efficiently promotes transcription of the bacterial chloramphenicol acetyltransferase gene in myogenic cells. However, none of the sequences within this region are sufficient to confer muscle-specific expression. Removal of sequences 5' to -715 bp leads to a major loss of transcriptional activity of the CAIII promoter. These results imply that the proximal CAIII promoter, which includes a putative CArG box and four potential MyoD binding sites, is not adequate for either myoblast-specific or maximal transcription.

Animals↗
PubMed1990

Chondroitin sulfates in developing mouse tooth germs. An immunohistochemical study with monoclonal antibodies against chondroitin-4 and chondroitin-6 sulfates.

The role of glycosaminoglycans and proteoglycans during ontogenesis is not known. The developing tooth offers a potentially important model for studies of structure-function relationships. In this study, we have analysed the temproal and spatial expression of chondroitins of differing sulfation patterns in embryonic molars and incisors. For this purpose, we have used monoclonal antibodies (Mabs) specific for unsulfated, 4-sulfated, and 6-sulfated forms of chondroitin in conjunction with indirect immunofluorescence or immunoperoxidase labeling. Unsulfated chondroitin was not detected in embryonic teeth. Chondroitin 4- and chondroitin 6-sulfates were present in the stellate reticulum but otherwise they were confined to the dental mesenchyme. The 3B3 and MC21C-epitope, which are markers of 6-sulfated chondroitin, were uniformly distributed in the dental mesenchyme during the bud stage; they disappeared from the dental papilla of the cusps and of the anterior region of the incisor as development proceeded. These epitopes were absent from the basement membrane and from the predentin. In the odontoblastic cell lineage, the 3B3 and MC21C-epitopes were detected only between preodontoblasts at an early stage of differentiation. The monoclonal antibody 2B6 served as a probe to localize chondroitin 4-sulfate. This glycosaminoglycan was detected as early as the dental lamina stage but its expression was restricted to the basement membrane of the teeth until the late bell stage. After the onset of cusp formation, strong staining was also observed over the occlusal region of the dental papilla while the cervical region of the dental papilla remained 2B6-negative. Incisors at the bell stage exhibited a decreasing gradient of immunostaining by 2B6 from their anterior region to their posterior end. The extracellular matrix surrounding preodontoblasts reacted with 2B6 and the predentin, produced by the odontoblasts, was also intensely labeled with this antibody. Comparison between immunostaining with 3B3 and 2B6, on consecutive sections revealed a mutually exclusive pattern of distribution of the corresponding epitopes during odontogenesis. Furthermore, in the continuously growing incisor, a striking positive correlation was found between the immunostaining patterns produced by 3B3 and MC21C and the mitotic indices along the anterior-posterior axis of the tooth. Hence, sulfation of chondroitin seems developmentally regulated. We postulate that changes in the sulfation pattern of chondroitin might play a role in ontogenesis by locally altering the functional properties of the extracellular matrix.

Animals↗
PubMed1990

Tumor necrosis factor alpha and lymphotoxin production in Hodgkin's disease.

It is likely that the characteristic histologic features of Hodgkin's disease reflect cytokine production by the tumor cell population. Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin (tumor necrosis factor beta [TNF-beta]) are important inflammatory mediators with wide-ranging effects within the lymphoreticular system. The aim of the present study was to investigate TNF-alpha and lymphotoxin production in the Hodgkin's disease-derived cell lines L428 and L540. At the product level, both cytokines could be demonstrated by immunostaining with specific monoclonal antibodies. TNF-alpha could be demonstrated by means of an enzyme-linked immunosorbent assay in culture supernatants from both cell lines as well as in cell lysates of L428 and L540 cells. Cytotoxic activity could be achieved only in L428 supernatants. This cytotoxic activity could not be blocked by the addition of a polyclonal antibody against TNF-alpha, but was partially inhibited with the monoclonal antibody against lymphotoxin. Synthesis of TNF-alpha and lymphotoxin in both L428 and L540 was confirmed by demonstrating the intracellular-specific messenger RNA (mRNA) using specific cDNA clones in Northern blot analysis. In situ hybridization studies with the TNF-alpha cDNA probe gave positive hybridization signals in L428 and in L540. These results demonstrate the transcription, translation, and export of TNF-alpha and lymphotoxin in cultured Hodgkin's disease-derived cell lines. In addition, results of preliminary experiments are presented in which we demonstrate Reed-Sternberg cells positive for TNF-alpha protein and mRNA in different Hodgkin's disease tissue biopsies, indicating that, at least for TNF-alpha, our cell line data are relevant to the neoplastic population present in Hodgkin's disease tissue.

Biopsy↗
PubMed1989

The specificity of a mouse monoclonal antibody to human aorta proteoglycans.

Mouse monoclonal antibodies to human aorta proteoglycans have been raised. A sensitive radioimmunoassay which can be employed to measure binding of proteoglycans to these antibodies is described. It offers advantages of simplicity and speed over other immunoassays currently employed for proteoglycan determination. One of the monoclonal antibodies, 6D2/B5, recognizes keratan sulfate-bound antigens (e.g. cartilage proteoglycans). Further work has indicated that this antibody is not specific for keratan sulfate, as brain sulfatide and the seaweed polysaccharide, fucoidan, also possess its epitope. The 6D2/B5 antibody can be of value in localizing and estimating keratan sulfate if additional biochemical criteria for keratan sulfate recognition are utilized.

Antibodies, Monoclonal↗
PubMed1985

Cinderella's stepmother syndrome.

Society, in times and places, has seemed to perceive stepmothers in a negative way. In the past, many of these women have quietly over-compensated in an effort to find acceptance in their new family situation, but they are now coming forward with their psychological distress. On the surface they may present a clinical picture similar to depressive illness (Dysthymic Disorder or Depressive Neurosis 300.40 in DSM III classification). The symptoms include: preoccupation with position in the family, feelings of anxiety, rejection, ineffectiveness, guilt, hostility and exhaustion, loss of self-esteem and overcompensation. With further exploration it becomes clear that the majority of them are experiencing distress that is normal within the context of their adjustment reaction. Clinical findings are based on two separate studies of twelve and ten patients respectively, where two different professionals found remarkably uniform symptoms which have been conceptualized as a new syndrome. An understanding of the normal adjustment reaction of these stepmothers to a very stressful situation can provide the basis for an effective treatment of their problem.

Adult↗
PubMed1984

Characterization of a transitional cell carcinoma line arising from a previously irradiated tumor.

A cell line derived from a poorly differentiated transitional cell carcinoma of the bladder in a patient previously treated with external beam radiation has been established. The line has stable hyperdiploid karyotype which is distinct from other established transitional cell carcinoma lines. Injection of the cells into nude mice induces tumor with histological characteristics similar to the original tumor. This line may serve as a model to study mechanisms of radioresistance in transitional cell carcinoma of the urinary bladder.

Aged↗
PubMed1983

Lymph node mast cells in athymic "nude" (Nu/Nu) and thymus containing (Nu/+ and +/+) Balb/c mice.

Total number of mast cells in popliteal lymph nodes of Balb/c mice is a function of time and Nu gene (complex?) content. The number of mast cells increases with age - in both wild +/+ and in Nu gene (complex?) carriers (Nu/+ and Nu/Nu). The increase in the number of mast cells is faster in the Nu gene carriers than in wild animals +/+ devoid of this gene. In "nude" mice having advanced hepatitis a dramatic increase in the number of lymphoid mast cells was observed. Results obtained deny the importance of thymus in the production of lymphatic mast cells in mice.

Age Factors↗
PubMed1982

Effects of nu gene on the numbers of mast cells in lymph nodes.

The total numbers of mast cells (MC) in popliteal lymph nodes of homozygous nude (nu/nu) and phenotypically normal, heterozygous (+/nu) BALB/c mice are greater than in normal (+/+) BALB/c mice at approximately 6 months of age. The values obtained from 4- to 7-month-old (nu/nu) and (+/nu) mice are twice as high as those from 2- to 3-month-old mice. It is concluded that the thymus does not directly determine the number of MC in lymph nodes, but the presence of the nu gene or another gene closely linked to the nu gene regulates the number of MC. 'Nude' mice infected with hepatitis virus accumulate many more MC than do healthy mice.

Aging↗