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Biomedical subjects

L Robson

Publications and source records attributed to L Robson.

105 records · Page 6Linked to original sources
PubMed1990

In situ and slot hybridization analysis of RNA in colorectal tumours and normal colon shows distinct distributions of mitochondrial sequences.

cDNA clones of mRNAs with an abnormal abundance in familial adenomatous polyposis were used to examine the levels and distribution of the mRNAs in tissues from 15 patients with colorectal cancer. Of 12 cloned sequences studied by slot hybridization, one was substantially reduced in tumours compared with normal tissue. Sequence analysis showed this to code for IgA. In situ hybridization was consistent with slot hybridization and immunohistochemistry. Two mitochondrially encoded sequences had distinct distributions detected by in situ hybridization but did not have detectable quantitative differences in whole tumour or mucosa extracts.

Adenocarcinoma↗
PubMed1989

Identification of a human ribosomal protein mRNA with increased expression in colorectal tumours.

A human ribosomal protein cDNA was selected from a normal colon cDNA library on the basis of overexpression in familial adenomatous polyposis. Nucleotide sequence analysis was used to identify this cDNA as corresponding to the human equivalent of the rat ribosomal protein L31 (HL31). We have quantified the expression of HL31 mRNA in colorectal tumours and found overexpression in 23 out of 23 cases. Our results indicate that HL31 is associated with a malfunction of normal growth regulatory mechanisms in these tumours, and suggest a role for HL31 in proliferation and neoplasia.

Adenocarcinoma↗
PubMed1989

Primate cytomegalovirus assembly protein: genome location and nucleotide sequence.

A cDNA encoding the 37-kilodalton (kDa) capsid assembly protein of cytomegalovirus (CMV) strain Colburn was isolated from a lambda gt11 library constructed from CMV Colburn-infected human fibroblast RNA. RNA transcribed in vitro from this cDNA was translated in vitro to give a 40-kDa protein whose electrophoretic mobility during sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fragmentation pattern following partial proteolysis were indistinguishable from those of authentic assembly protein precursor. The position of the assembly protein gene was mapped to the EcoRI F, XbaI R, and SalI U restriction fragments, near the middle of the CMV Colburn genome, by Southern hybridizations using the cloned assembly protein cDNA as a probe. Similar sequences were identified by cross-hybridizations in colinear regions of the genomes of human CMV strains Towne and AD169: specifically, in the HindIII H, BamHI V, and EcoRI A fragments of Towne and in the HindIII L and BglII S fragments of AD169. The predominant transcript of the assembly protein gene was determined to be approximately 1 kilobase in size; however, a larger transcript (1.8 kilobases) was also identified. The nucleotide sequence of the assembly protein cDNA was determined and found to contain a single long open reading frame predicted to encode a polypeptide of 36.6 to 37 kDa, close to the 40-kDa size determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis for the assembly protein precursor. The presence of a single cysteine residue at the carboxy-terminal end of this open reading frame is consistent with data from biochemical studies and indicates that processing of the assembly protein precursor includes a proteolytic cleavage that removes its carboxyl end.

Amino Acid Sequence↗
PubMed1987

Myoglobinuria from child abuse.

A child with myoglobinuria following rhabdomyolysis from child abuse is described. The importance of early recognition and treatment of this condition is emphasized.

Adolescent↗
PubMed1986

Inspection time as mental speed in mildly mentally retarded adults: analysis of eye gaze, eye movement, and orientation.

The effect of eye movements away from a target on accuracy of visual discrimination was examined. In Experiment I inspection time was measured for 10 mildly mentally retarded and 10 nonretarded adults under two conditions, with each trial initiated by the subject or under experimental control. Retarded subjects did not gain any advantage from controlling trial onset. Video records of eye movements revealed that retarded subjects glanced off-target more than did nonretarded controls, but this was not sufficient to explain appreciably slower inspection time of the retarded group. Experiment 2 supported this conclusion; the same subjects completed a letter-discrimination task with direction of gaze monitored automatically. Although retarded subjects' eye gaze was more scattered early during a trial, gaze was appropriately directed by the time that the target appeared. Results from both experiments supported the hypothesis that speed of central, perceptual processing is slower among retarded persons, over and above the influence of distractibility. Results from three experiments in Part II were consistent with this interpretation. Experiment 3 was designed to eradicate trials among retarded subjects in which gaze was not properly directed, but results showed that too few such events occurred to influence accuracy. Experiment 4 demonstrated that the preparatory procedure in the previous studies resulted in efficient eye gaze among retarded subjects. Experiment 5 confirmed that lower discriminative accuracy among 10 retarded adults (compared with 10 nonretarded controls) was not due to less-efficient orientation prior to discrimination.

Adolescent↗
PubMed1985

Membranous glomerulonephritis in a patient with Crohn's disease of the small bowel.

A 12-year-old girl presented with concurrent onset of membranous glomerulonephritis and Crohn's disease of the small intestine. Subsequent investigations failed to implicate any other systemic disease as a cause of the glomerulonephritis. Membranous glomerulonephritis is an immune complex--mediated glomerulopathy frequently associated with underlying systemic disease. The association of immune complex phenomenon with Crohn's disease and the variation of renal abnormalities in parallel with activity of bowel disease in this patient suggest that the glomerulonephritis may be due to the underlying Crohn's disease.

Child↗
PubMed1983

Plasma membrane: can its structure and function be modulated by dietary fat?

Compositional analysis of plasma membranes from rats fed nutritionally adequate diets different in fatty acid composition establishes that fundamentally different dietary fat intake results in alteration in structural lipid composition of plasma membranes in brain, liver and the intestinal mucosa. Dietary differences in fatty acid intake altered the fatty acyl tail composition of plasma membrane phospholipids in brain, liver and intestinal mucosa. Diet altered the phospholipid profile observed in brain synaptosomal and liver plasma membrane. Feeding high vs low polyunsaturated to saturated fat diets for 7 days altered the fatty acid composition of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin and monoglucosylceramide isolated from plasma membrane of the intestinal mucosa.

Animals↗
PubMed1979

Age-related changes of the pattern of non-histone chromatin proteins from rat and mouse liver chromatin.

The non-histone chromatin (NHC) proteins which are loosely bound to DNA were extracted from young and old mouse and rat liver chromatin by 0.35 M NaCl and fractionated into three groups: water-soluble, 0.14 M NaCl soluble and 0.35 M NaCl soluble. NHC proteins in each fraction were separated by SDS-disc polyacrylamide gel electrophoresis. Special attempts were made to locate minor high-molecular-weight proteins which develop faint bands. It was found that the aging of liver cells is associated with increase in number and quantities of high-molecular-weight NHC proteins in the water-soluble group. Salt-soluble groups of NHC proteins show fewer changes of pattern.

Aging↗
PubMed1978

The effects of vitamin B6 deficiency on the bone marrow of the rat.

Bone marrow from adult rats fed a vitamin B6 deficient diet for two weeks was found to have reduced numbers of neutrophils, erythroid cells and small lymphocytes. The numbers of transitional cells were not reduced. Since the small lymphocyte population in the bone marrow consists of B cells and null cells in approximately the same proportion, it was concluded that both cell types were reduced as a result of the deficiency. A complete recovery in the cellularity of the bone marrow was brought about by returning the vitamin B6 deficient animals to a normal diet for four weeks. Other effects of the two-week vitamin B6 deficient diet included a failure to gain weight, a decrease in thymus weight and a reduction in the numbers of white blood cells in the peripheral blood. All of these defects were corrected after the animals had been fed a normal diet for four weeks.

Animals↗
PubMed1978

Tissue specificity and age changes for the pattern of the H1 group of histones in chromatin from mouse tissues.

Polyacrylamide gel electrophoresis of the H1 group of histones extracted from different rat and mouse tissues shows a different pattern of fraction (H1, H1 degrees, H1 degrees met) when the two species are compared. Different tissues of each species also have a different pattern of H1 histone fraction and subfraction. However, the age-associated changes of mouse H1 histones from liver and spleen chromatin show the same type of alteration of fraction ratios which had been demonstrated in our earlier research with rat tissues. In both species there is a relative increase of the F1 degree and F1 degree met fractions in tissues from old animals. The presence of the F1 degree fraction in only non-dividing cells suggests that there may be an age-specific type of chromatin condensation.

Aging↗
PubMedDate not supplied

Unbalanced translocation t(15;22) in "severe" Prader-Willi syndrome.

A 13-year-old girl with an unbalanced karyotype 45,XX,-15,der(22)t(15;22)(q13;q13.3) de novo had Prader-Willi syndrome (PWS), (score 13.5), but with features of mental and physical retardation more severe than usually seen in PWS. The clinical diagnosis of PWS was confirmed by methylation analysis that showed absence of the paternal band. With GTG banding, the cytogenetic breakpoint on chromosome 15q13, with 15q14 intact, encompassed the PWS region, while the breakpoint on 22q was terminal. Investigations with FISH utilised ten different probes/combinations, namely SNRPN/PML, TUPLE1/22q13.3, TUPLE/ARSA, GABRB3, three YAC clones and one cosmid for specific regions within chromosome 15q, painting probes for the long arm of chromosomes 15 and 22 and a pantelomere probe. Deletion of SNRPN,TYAC 9 (at 15q11-12), TYAC19 (at 15q13) and GABRB3 (within the PWS locus), was evident on the derivative (22) chromosome, while TYAC10 (at 15q22), cos15-5 (at 15q22) and PML (15q22) were not deleted. On the der(22), 22q13.3 and ARSA were not deleted, but the most distal non specific pantelomeric probe was deleted. Thus, the severe phenotype could be attributable to deletion on chromosome 15q extending beyond q13 to q14, (further than the usual chromosome 15q deletion (q11-13) in PWS), or be related to loss of the very terminal 22q region (from ARSA to the pantelomere) or be due to genetic factors elsewhere in the genome.

Adolescent↗