Biomedical subjects

I Lamont

Publications and source records attributed to I Lamont.

6 recordsLinked to original sources

PubMed1996

Defining the SOS operon of coliphage 186.

We have sequenced the LexA-controlled operon of coliphage 186 that carries the tum gene, whose product is necessary for UV induction of the 186 prophage. The operon consists of orf95 and orf97, and we have identified orf95 as the tum gene. The major translation products from orf95 result from internal initiations and modulate Tum activity. Tum is the product of the full-length Orf95 protein. The second gene of the operon, orf97, is of unknown function but, while it has little effect on prophage induction, its presence in the cell totally blocks infection of that cell by 186.

Amino Acid Sequence↗

PubMed1993

Genes for the establishment and maintenance of lysogeny by the temperate coliphage 186.

To identify the genes in coliphage 186 that are required for lysogeny, we isolated clear-plaque mutants. Complementation studies and DNA sequencing identified two genes, the cI gene for the immunity maintenance repressor and the cII gene, which is required only for the establishment of lysogeny. One mutant carried a change in the LexA-binding site controlling expression of the antirepression protein Tum.

Bacterial Proteins↗

PubMed1992

Chlamydia trachomatis serovar differentiation by direct sequence analysis of the variable segment 4 region of the major outer membrane protein gene.

The polymerase chain reaction method was used to amplify DNA from the fourth variable segment of the gene encoding the major outer membrane protein of Chlamydia trachomatis. Direct sequencing of the amplified DNA from prototype strains confirmed previously identified nucleotide sequence differences that were specific for each serovar. This analysis revealed differences in the DNA sequences of prototype strains C/UW-1 and G/IOL-238 from those of prototype strains C/TW-3 and G/UW-57, sequenced previously. This method was also used to determine the serovar types of C. trachomatis in 125 urogenital specimens from infected patients. The most common serovars were E (38%), F (17%), and G and D (14% each). Serovar D was found significantly more often in specimens from men than in specimens from women (P = 0.004). Conversely, serovar G was found significantly more often in specimens from women than in specimens from men (P = 0.026). Only two serovar G isolates gave sequences identical to that of the prototype strain G/IOL-238, suggesting that this strain may be a serovar variant. Three isolates (D+, G-, and J') gave sequences which have not been reported previously. One isolate had the same sequence as the D- serovar variant. Sequence analysis of amplified DNA reveals subtle differences between C. trachomatis strains and provides a very sensitive method for molecular epidemiological analysis.

Bacterial Outer Membrane Proteins↗

PubMed1989

UV induction of coliphage 186: prophage induction as an SOS function.

Our results show that UV induction of the 186 prophage depends upon the phage function Tum, with the mutant phenotype of turbid plaques on mitomycin plates and the expression of which is controlled by the host LexA protein. Tum function, encoded near the right-hand end of the coliphage 186 chromosome, is under the control of promoter p95. This promoter is overlapped by a sequence closely related to the consensus sequence of the LexA-binding site. It is proposed that inactivation of LexA after UV irradiation (or by genetic means) leads to prophage induction by permitting expression of Tum which, by unknown means, induces prophage. This mechanism is basically different from that seen with the UV-inducible lambdoid coliphages, which are not regulated by LexA.

Base Sequence↗

PubMed1988

Control of gene expression in the P2-related temperate coliphages. V. The use of sequence analysis of 186 Vir mutants to indicate presumptive repressor binding sites.

The prophage of coliphage 186 produces a repressor protein that is required for maintenance of lysogeny and that renders lysogenic cells immune to superinfection by 186. The repressor is likely to be a DNA-binding protein that prevents transcription of the 186 early-lytic genes from promoter pR. To identify the binding site of the repressor, we have isolated virulent mutants that are able to form plaques in the presence of repressor and determined their DNA sequences around pR. The mutants all have mutations in an inverted repeat within pR, and we predict that this repeat is the primary binding site of the repressor. Many of the mutants have second mutations near pR, which allow them to form plaques in the presence of higher concentrations of repressor. The sequences containing these "secondary" mutations show no homology with the putative repressor-binding site, and the role of these mutations in virulence is not clear.

Base Sequence↗

PubMed1977

The experience of a haematemesis and melaena unit: a review of the first 513 consecutive admissions.

This report is of the results of management in a haematemesis and melaena unit at Prince Henry's Hospital, Melbourne. The unit was established in October, 1972, in response to unpublished data for the decades 1950 to 1959 and 1960 to 1969, which showed a mortality of about 15%. In the 39 months to December, 1975, 513 patients were received into a semi-intensive care setting. The unit staff consisted of a group of four surgeons and four physicians working a weekly roster. Primary care and liaison were the responsibility of the gastroenterology registrar. The basic diagnostic measure taken was the routine early use of fibreoptic duodenoscopy. The unit was set up with an agreed policy of management of the common causes of haematemesis and melaena, and data were prospectively recorded in a form suitable for computer analysis in every case. Of the 513 admissions, 378 were of males and 135 were of females. Forty-five patients died, giving an overall admission mortality of 8-8. There were 143 admissions for bleeding duodenal ulceration, 102 for acute peptic ulceration, 47 for chronic gastriculceration, 43 for oesophageal varices, 33 for Mallory-Weiss syndrome and 45 for less common causes of upper gastrintestinal bleeding. In 100 cases the source of bleeding was not discovered. Of the 143 patients admitted for chronic duodenal ulcer, either patients died, giving a mortality of 5-6%; 72 patients underwent operation, with an operative mortality of 9-7%. Of the 47 admitted with bleeding gastric ulcer, nine died (19-1%), while 26 came to operation; the operative mortality was 26-9%. There were 102 admissions for acute peptic ulceration, with an overall mortality of 11-7% (12 patients); 16 patients came to operation, with an operative mortality of 43-7%. Eleven deaths occurred in the 43 patients admitted for bleeding oesophageal varices (25-6%), with 10 patients coming to operation; the operative mortality was 30-0%. An age of greater than 50 years and shock on admission were the most significant factors for poor prognosis in this group of patients.

Adolescent↗