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Biomedical subjects

R H Rothman

Publications and source records attributed to R H Rothman.

At least 127 records · Page 7Linked to original sources

W-reactivation of phage lambda in recF, recL, uvrA, and uvrB mutants of E. coli K-12.

W-reactivation is reduced by recF143 and recF144 mutations and is undetectable if a second mutation at either the uvrA or uvrB locus is combined with recF143. The uvrA and uvrB mutations alone block W-reactivation partially. A recL152 mutation also partially blocks W-reactivation by itself. In combination with a uvrB5 mutation, recL125 blocks W-reactivation completely but in combination with recF143, significant residual W-reactivation ability remains. We suggest that the phenomenon of W-reactivation is the result of at least two modes or pathways. The observation that recF143 uvrB5 and recF143 uvrA6 strains permit normal levels of mutagenesis (Kato et al., 1977) but completely block all W-reactivation leads us to suggest further that the mechanism(s) of W-reactivation is at least partly different from that of UV mutagenesis.

Coliphages↗

Results of surgical intervention in the symptomatic multiply-operated back patient. Analysis of sixty-seven cases followed for three to seven years.

Sixty-seven of seventy-three patients who had had multiple operations on the back with an initial diagnosis of lumbar-disc disease were reevaluated as to relief of pain two and four years after the most recent operation. More than 80 per cent of the patients had gained enough relief to deem the procedure worth while. A diagnosis of fibrosis, preoperatively or intraoperatively, portended a poor result, while the opposite was true with diagnoses of mechanical compression (disc fragment or stenosis) and instability (pseudarthrosis after fusion or spondylolisthesis). The presence of a pain-free interval lasting one year from the date of the previous operation correlated highly with the presence of a surgically remediable lesion.

Adult↗

Dimer excision and repair replication patch size in recL152 mutant of Escherichia coli K-12.

Dimers are excised slowly in a recL152 mutant. This observation is not an artifact of altered DNA degradation because degradation is the same in recL+ and recL strains. The repair patch size was measured by the bromodeoxyuridine-313 nm radiation photolysis technique. In the recL+ strain, the average patch size was found to be about 30 nucleotides in length, but in the recL mutant, it was about 360.

DNA Repair↗

New concepts in the diagnosis and treatment of infections of the cervical spine.

Of the three major areas of the spinal column, the cervical spine is least commonly infected; approximately 3 to 5 per cent of all spinal infections involve the cervical spine. Tuberculous, pyogenic, fungal, and parasitic infections may involve the cervical spine and occur in this order of decreasing frequency. Difficulty in differential diagnosis most commonly involves tumor. Fungal and parasitic infections of the cervical spine are extremely rare, but fungal infections have been increasing over the past three decades. Clinical suspicion, radiologic examination, and definitive diagnosis via tissue biopsy are necessary so that definitive procedures can be instituted. Specific antibiotic coverage, surgery to facilitate the body's defenses and antibiotic penetration, and stabilization of the spine are the most important therapeutic measures to be instituted.

Adolescent↗

Atlanto-occipital hypermobility.

Hypermobility of the atlanto-occipital joint can be seen following trauma or in a patient with congenital fusion of C1-C2 as a progressive problem. The lateral roentgenogram is the key to the diagnosis, and familiarity with the normal anatomy is necessary. In the trauma setting care should be taken not to increase the dislocation with traction. Treatment by a posterior craniocervical fusion has proved successful in both groups of patients.

Adult↗

Defective excision and postreplication repair of UV-damaged DNA in a recL mutant strain of E. coli K-12.

The mutation recL152 leads to a reduction of excision repair as measured by an increase in the time required to close uvrA uvrB dependent incision breaks, and by a reduction of host cell reactivation ability. Postreplication repair is also delayed when measured in a uvrB5 recL152 double mutant. Such a determination could not be made using the recL152 single mutant because the excision defect led to an accumulation of breaks in the unlabeled high molecular weight DNA to which the labeled DNA synthesized after irradiation must attach in order to achieve normal high molecular weight. Further, the recL gene product seems to be required to rejoin breaks in parental strand DNA which are generated during postreplication repair, since such gaps accumulate in a recL152 uvrB5 double mutant but not in a recL+ uvrB5 single mutant. We have noticed a striking phenotypic similarity between recL152 and polA1 and suggest that recL152 is required for full in vivo activity of DNA polymerase I.

DNA Repair↗

The dependence of postreplication repair on uvrB in a recF mutant of Escherichia coli K-12.

Mutants carrying recF143 or recF144 show wild type levels of host cell reactivation of UV-irradiated lambdavir and wild type rates of excision gap closure in repairing UV damage to their own DNA. The same mutants showed reduced rates of postreplication repair strand joining. When uvrA- recF- or uvrB- recF- strains are tested, postreplication repair strand joining is incomplete or does not occur at fluences above 1 J/m2. We suggest that there may be a UvrAB and a RecF pathway of postreplication repair or that the repair functions controlled or determined by uvrA uvrB and by recF may be similar. An intermediate in postreplication repair may accumulate in the uvr- recF- strain.

DNA Repair↗

Analysis of the role of recombination and repair in mutagenesis of Escherichia coli by UV irradiation.

Multiple mutant strains have been tested or their mimicry of the UV-mutagenesis deficiency of a recA single mutant. Revertants to histidine prototrophy and clear plaque mutants of lambda were scored to determine capacity for UV-mutagenesis. Nearly normal capacity was shown by a uvr+ recB- recF- strain, which shows almost no recA-dependent recombination, by uvr- recB+ recF- strains, which show almost no recA-dependent repair and by a uvrA- recB- recF- strain, which shows neither recA-dependent recombination nor repair. Since the uvr mutants can be assumed to show additionally no excision repair, these results may mean that UV-mutagenesis occurs during processes other than recombination and repair. Alternative hypotheses are discussed. The slight difference in mutagenic capacity was traced to the recF single mutation, which blocks the production of unmixed bursts of clear-plaque lambda mutants. Since this accounts for only about 10% of the mutations leading to clear-plaque mutants, it is suggested that there is more than one UV-mutagenic process.

Coliphages↗

The acute cervical disk.

Acute cervical disk herniations represent one facet of the broad spectrum of cervical disk degeneration. It is productive of symptoms through mechanical compression and biochemical inflammation of the nerve roots and spinal cord. The majority of patients will respond to a conscientiously applied course of conservative treatment. In those individuals who fail to respond to conservative treatment in terms of pain relief or in whom a significant neurologic deficit occurs surgical decompression of the neural elements should be undertaken.

Acute Disease↗