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Biomedical subjects

M Lieb

Publications and source records attributed to M Lieb.

At least 19 recordsLinked to original sources
PubMed1992

Repetitive behaviors in chronically institutionalized schizophrenic patients.

Repetitive dysfunctional behaviors (e.g., polydipsia, bulimia, hoarding, mannerisms) are frequently observed in chronically institutionalized schizophrenics, cause significant morbidity and are readily reproduced in animal models. The goal of this study was to assess the frequency and severity of these behaviors. Thirty-two chronic schizophrenics on an extended treatment unit were rated on the Elgin Behavioral Rating Scale, which includes eight repetitive behaviors and eight positive and negative symptoms. Forty-seven percent of the patients exhibited at least one severe, or 2 moderate, repetitive behaviors, while 63% exhibited at least one severe or 2 moderate positive or negative symptoms. The mean total score (+/- SD) on the eight repetitive behaviors (10.3 +/- 6.1) was about 2/3 that for the eight positive and negative symptoms (15.3 +/- 8.9, t = 4.1, p = .0001). Interrater reliability for the repetitive behaviors was similar to that for the positive and negative symptoms. Repetitive behaviors were positively related to male gender, white race and total length of hospitalization. Repetitive dysfunctional behaviors are frequently observed and can be reliably rated in chronically institutionalized schizophrenics.

Adult↗
PubMed1991

Spontaneous mutation at a 5-methylcytosine hotspot is prevented by very short patch (VSP) mismatch repair.

In many strains of Escherichia coli, the product of gene dcm methylates the internal cytosines in the sequence 5'CC(A or T)GG. Spontaneous deamination of 5-methylcytosine produces thymine which, if not corrected, can result in a transition mutation. 5-Methylcytosines in the lacI gene are hotspots for spontaneous C to T mutations. dcm is linked to vsr, a gene required for very short patch (VSP) repair. VSP repair corrects T.G mispairs in the following contexts:CTAAGGGGTCC, CTTGGGGACC, TAGGGTCC and CTAGGGTC. I have investigated the relationships between cytosine methylation, mutation, and VSP repair. Spontaneous mutations in the repressor (cI) gene of lambda prophage were isolated in wild-type and mutant lysogens. A hotspot for spontaneous mutation that corresponds with a 5-methylcytosine was observed in wild-type lysogens but was not present in bacteria lacking both methylase and VSP repair activity. Introduction of a plasmid containing dcm+ and vsr+ restored the mutation hotspot. If the added plasmid carried only dcm+, the frequency of spontaneous mutations at the 5-methylcytosine was over 10-fold higher than in Dcm+Vsr+ lysogens. The addition of vsr on a plasmid to a wild-type lysogen resulted in a 4-fold reduction in mutation at the hotspot. These findings support the previously untested hypothesis that VSP repair prevents mutations resulting from deamination of 5-methylcytosine.

5-Methylcytosine↗
PubMed1991

Production of type 5 capsular polysaccharide by Staphylococcus aureus grown in a semi-synthetic medium.

The concentration of the type 5 capsular polysaccharide (CP) antigen of Staphylococcus aureus can be measured directly in cultures or cell suspensions by a two-step inhibition enzyme-linked immunosorbent assay (ELISA), using monoclonal antibodies. CP was synthesized during growth on a variety of carbon substrates and its production was not affected by the nature of the carbon source. High levels of yeast extract inhibited CP formation. CP was synthesized in batch culture at the same rate during exponential growth as in the post-exponential phase. Post-exponential CP production contributed at least half the final amount of CP measured. This phenomenon was observed in different culture media, although the specific yield of polysaccharide varied from one medium to another. Post-exponential CP production was observed in the pH range 6-7, but not at pH 8. Post-exponential production was strictly dependent on oxygen availability and did not occur under anaerobic conditions.

Antigens, Bacterial↗
PubMed1991

Staphylococcus aureus growth and type 5 capsular polysaccharide production in synthetic media.

The production of type 5 capsular polysaccharide by Staphylococcus aureus in synthetic media was investigated. The influence of medium components on capsular polysaccharide synthesis appeared to relate to the presence or absence of the component rather than to concentration gradient. The production of type 5 capsular polysaccharide was linked to energy availability and energy source, but not to carbohydrate concentration or carbon/nitrogen ratio. Regulation of capsular polysaccharide production by S. aureus in response to medium changes would appear to differ from that typically displayed in other organisms that produce polysaccharides.

Bacterial Capsules↗
PubMed1990

A gene required for very short patch repair in Escherichia coli is adjacent to the DNA cytosine methylase gene.

Deamination of 5-methylcytosine in DNA results in T/G mismatches. If unrepaired, these mismatches can lead to C-to-T transition mutations. The very short patch (VSP) repair process in Escherichia coli counteracts the mutagenic process by repairing the mismatches in favor of the G-containing strand. Previously we have shown that a plasmid containing an 11-kilobase fragment from the E. coli chromosome can complement a chromosomal mutation defective in both cytosine methylation and VSP repair. We have now mapped the regions essential for the two phenotypes. In the process, we have constructed plasmids that complement the chromosomal mutation for methylation, but not for repair, and vice versa. The genes responsible for these phenotypes have been identified by DNA sequence analysis. The gene essential for cytosine methylation, dcm, is predicted to code for a 473-amino-acid protein and is not required for VSP repair. It is similar to other DNA cytosine methylases and shares extensive sequence similarity with its isoschizomer, EcoRII methylase. The segment of DNA essential for VSP repair contains a gene that should code for a 156-amino-acid protein. This gene, named vsr, is not essential for DNA methylation. Remarkably, the 5' end of this gene appears to overlap the 3' end of dcm. The two genes appear to be transcribed from a common promoter but are in different translational registers. This gene arrangement may assure that Vsr is produced along with Dcm and may minimize the mutagenic effects of cytosine methylation.

Amino Acid Sequence↗
PubMed1988

Very short patch mismatch repair activity associated with gene dcm is not conferred by a plasmid coding for EcoRII methylase.

The only cytosine methylase in Escherichia coli K-12 methylates the second cytosine in the sequence CC (A/T)GG and is encoded by gene dcm. Methylation and very short patch mismatch repair activities lacking in a dcm mutant of E. coli were restored by a plasmid containing the cloned dcm gene. In contrast, plasmids with the gene for EcoRII methylase, which is a homolog of dcm, restored only cytosine methylase activity and not mismatch repair.

DNA (Cytosine-5-)-Methyltransferases↗
PubMed1987

Amelioration of experimental lipid keratopathy by photochemically induced thrombosis of feeder vessels.

The photochemical interaction between intravenously injected rose bengal dye and 514.5-nm argon laser irradiation was employed to initiate permanent thrombotic occlusions in the corneal neovasculature of rabbit eyes with experimentally induced lipid keratopathy. This photothrombotic procedure did not produce corneal edema or polymorphonuclear leukocyte infiltration, as was found in previous studies employing laser-induced photocoagulation. Thus, by means of the new technique, we avoided the formation of additional neovascularization and lipid deposition. Vascular occlusion by photothrombosis, effected with 8.5 times less incident intensity and 27.5 times less total light exposure than with photocoagulation, yielded an average reduction of corneal cholesterol content of 36% as opposed to an increase of 24% found with previous argon laser photocoagulation.

Animals↗
PubMed1987

Rat brain microvessel extracellular matrix modulates the phenotype of cultured rat type 1 astroglia.

Astroglia from immature rat cerebral white matter which were plated on the insoluble extracellular matrix (ECM) secreted by rat cerebral microvessel endothelial cells (RCMEC) and maintained in a defined medium were induced to become stellate and to express glutamine synthetase. These effects were not elicited by RCMEC-conditioned medium. ECM secreted by rat pleural mesothelium elicited a lesser proportion of stellate astroglia and did not induce glutamine synthetase.

Animals↗
PubMed1987

Bacterial genes mutL, mutS, and dcm participate in repair of mismatches at 5-methylcytosine sites.

Certain amber mutations in the cI gene of bacteriophage lambda appear to recombine very frequently with nearby mutations. The aberrant mutations included C-to-T transitions at the second cytosine in 5'CC(A/T)GG sequences (which are subject to methylation by bacterial cytosine methylase) and in 5'CCAG and 5'CAGG sequences. Excess cI+ recombinants arising in crosses that utilize these mutations are attributable to the correction of mismatches by a bacterial very-short-patch (VSP) mismatch repair system. In the present study I found that two genes required for methyladenine-directed (long-patch) mismatch repair, mutL and mutS, also functioned in VSP mismatch repair; mutH and mutU (uvrD) were dispensable. VSP mismatch repair was greatly reduced in a dcm Escherichia coli mutant, in which 5-methylcytosine was not methylated. However, mismatches in heteroduplexes prepared from lambda DNA lacking 5-methylcytosine were repaired in dcm+ bacteria. These results indicate that the product of gene dcm has a repair function in addition to its methylase activity.

5-Methylcytosine↗
PubMed1986

Characterization of rat schwannoma-Schwann cell hybrids.

Sciatic nerve Schwann cells from strain LEC rats, homozygous for the c form of 6-phosphogluconate dehydrogenase (6-PGD), and RN22 rat Schwannoma cells, a subclone of RN2 deficient in hypoxanthine phosphoribosyltransferase and expressing the s form of 6-PGD, were fused to produce 'RNS' hybrid clones which proliferate rapidly in a medium containing hypoxanthine, aminopterin and thymidine (HAT) and express c, s and c/s heterodimeric forms of 6-PGD. RNS cells, like both parents, maintain a high baseline activity of 2', 3'-cyclic nucleotide 3'-phosphohydrolase and, as in RN22, activity of this enzyme is further inducible by 1 mM N6, O2'-dibutyryl 3', 5'-cyclic AMP. The RNS clones resemble normal Schwann cells in the capacity to bind radioiodinated axolemmal fragments to their plasma membranes.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1986

Recombination between IS5 elements: requirement for homology and recombination functions.

Intermolecular recombination between two IS5 elements was measured, using bacteriophage lambda recombination vectors, and was compared to recombination between two copies of an SV40 segment cloned into the same vectors. Experiments were conducted in the presence and in the absence of RecA and Red functions, and with the recombining inserts in the same or in reversed orientation. Under all conditions, IS5 elements recombined in a manner similar to the SV40 inserts, indicating that IS-encoded functions did not confer measurable additional intermolecular recombination ability to IS5 in E. coli K-12. Bacteriophages containing reversed IS5 inserts, for which the 16 base pair (bp) termini are identical in 15 positions and which display 12 bp of uninterrupted homology, recombined at approximately the same low frequency under Rec+ and Rec- conditions, indicating that these short homologies were not good substrates for the Rec system. Bacteriophages having reversed inserts recombined better under Red+ than under Red- conditions, but the crossovers were located in nonhomologous regions flanking the element termini. This suggests that 12-bp homologies are not good substrates for the Red system.

Bacteriophage lambda↗
PubMed1986

Very short patch mismatch repair in phage lambda: repair sites and length of repair tracts.

Five amber mutations in the repressor (cI) gene of bacteriophage lambda recombine anomalously with nearby cI mutations. When any of these markers is used in four-factor crosses, cI+ recombinants that are expected to require three cross-overs occur at high frequencies. These recombinants are attributable to very-short-patch (VSP) repair of specific mismatches in DNA heteroduplexes formed during recombination between the markers flanking cI. The sites of the repair-prone mutations and the lengths of repair tracts have now been determined. Amber mutations subject to VSP repair are C to T transitions in 5'CCATGG, the sequence methylated by the product of gene dcm, and also in the related 5'CAGG or 5'CCAG sequences. Ambers arising in CAG sequences found in other contexts, or in codons other than CAG, were not subject to VSP repair. Repair tracts rarely, if ever, exceed ten nucleotides in length, and can be as short as two nucleotides. A repair-prone mutation does not stimulate recombination between flanking cI markers.

Bacteriophage lambda↗
PubMed1985

Recombination in the lambda repressor gene: evidence that very short patch (VSP) mismatch correction restores a specific sequence.

The mutation am6 in the cI gene of bacteriophage lambda is identified as a C----T transition in a 5'CCATGG sequence. In four-factor crosses of am6 with nearby mutations in cI, the frequencies of cI+ recombinants are much higher than expected from the physical distances. A very short patch (VSP) mismatch repair system is presumed to recognize am6/am+ mispairs in the heteroduplexes that accompany recombination between the outside markers. Mutation am6 is corrected to am+; correction of am+ to am6 was not detected. Clear-plaque mutation 1-1 in cI is a T----C transition in a 5'CTTGG sequence, resulting in the sequence 5'CCATGG. When 1-1 was crossed with nearby mutations in gene cI, there were no excess cI+ recombinants, which would result from repair of CCTGG (1-1) to CTTGG (cI+). However, in crosses of cI+ phages with mutation 1-1, there was an excess of cI- recombinants, indicating that cI+ was repaired to 1-1. Preferential repair does not require adenine or cytosine methylation: when repairing a mismatch, the VSP repair system apparently identifies specific mispaired bases by sequence alone.

Bacteriophage lambda↗
PubMed1979

Heat-sensitive lambda repressors retain partial activity during bacteriophage induction.

At 43 degrees C, lambda cIts prophages are "induced" and enter the lytic cycle. Lac- lysogens containing heat-inducible lambda N- prophages were superinfected with a lambda trp/lac N+cI- phage containing a lacZ+ gene whose expression is controlled by the lambda cI product (repressor). Lysogens were then heated, and the synthesis of beta-galactosidase and release of progeny phage were measured. In lambda N- cIts2 or lambda N-cIts16 lysogens superinfected with lambda trp/lac N+, beta-galactosidase appeared earlier and was synthesized more rapidly than in superinfected lysogens containing lambda N- cIts857 prophage. Even at 45 degrees C, the cI857 repressor retained some activity. Lysogens containing other N-cIts mutant prophages producing renaturable repressors were also only partially derepressed at 43 degrees C. Partial derepression of lambda "early" transcription is sufficient for induction of lambda N+ prophages.

Bacteriophage lambda↗
PubMed1976

Mapping missense and nonsense mutation in gene cI of bacteriophage lambda: marker effects.

Amber and missense mutations in gene cI of bacteriophage lambda were mapped by reciprocal four-factor crosses, selecting recombinants between the outside markers (N amber and O amber). Distances between cI missense mutations were additive. Several cI amber mutants recombined with other cI mutations with a higher frequency than expected from the map location. Multiple exchanges in the N-O region occurred at a frequency greater than expected by chance. This "high negative interference" was especially marked in crosses with the cI amber mutations that were strong recombiners. A new ind mutation, ind2, was found near tsU51, to the left of the previously-known ind1 mutation, which is located almost in the center of gene cI. The mutation c50 maps to the right of tsU50 and c71. Mutations c60, and ts71, which differ in phenotype, are apparently at the same site.

Chromosome Mapping↗
PubMed1976

LambdacI mutants: intragenic complementation and complementation with a cI promoter mutant.

Complementation for the maintenance of lysogeny was studied by superinfecting lambdacIts lysogens at 34 degrees C. and then heating to 43 degrees C. With certain exceptions, ts mutants with defects in the left half of the repressor complemented ts mutants with defects in the right half to produce a less heat-labile repressor (Fig. 3). All cI amber mutants failed to complement cIts mutants. The cI mutant c50 complements all ts mutants. Mutations in Pre (cy) or genes cII and cIII do not significantly affect the expression of cI by a superinfecting lambda genome in an immune lysogen. Mutants with very heat-labile repressors failed to complement lambdacy42 for the establishment of lysogeny at elevated temperatures, while those with less heat-sensitive repressors apparently did complement cy. According to a suggested model, the left side of the cI product is concerned primarily with subunit aggregation, while operator binding is the function of the right side of the oligomer.

Coliphages↗