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Biomedical subjects

J Hahn

Publications and source records attributed to J Hahn.

At least 145 records · Page 8Linked to original sources
PubMed1982

Translational attenuation of ermC: a deletion analysis.

ermC is a plasmid gene which specifies resistance to macrolide-lincosamide-streptogramin B antibiotics. The product of ermC was previously shown to be an inducible rRNA methylase, which is regulated translationally, and a mechanism for this regulation, termed the translational attenuation model, has been proposed. This model postulates that alternative inactive and active conformational states of the ermC mRNA are modulated by erythromycin-induced ribosome-stalling during translation of a leader peptide. In the present study the translational attenuation model was tested by constructing a series of deletants missing the ermC promoter and portions of the regulatory (leading) region. In these mutants, ermC transcription is dependent on fusion to an upstream promoter. Depending on the terminus of each deletion within the regulatory region, determined by DNA sequencing, ermC expression is observed to be either high level and inducible (like the wild-type), high level and noninducible, or low level and noninducible. The translational attenuation model predicts that as the deletions extend deeper into the leader region, successively masking and unmasking sequences required for translation of the methylase, an alternation of high and low level methylase expression will be observed. These predictions are confirmed. Based on this and other information, the model is refined and extended, and both direct translational activation and kinetic trapping of a metastable active intermediate during transcription are proposed to explain basal synthesis of methylase and to rationalize the effects of certain regulatory mutants.

Bacillus subtilis↗
PubMed1982

Replication and incompatibility properties of plasmid pE194 in Bacillus subtilis.

pE194, a 3.5-kilobase multicopy plasmid, confers resistance to the macrolide-lincosamide-streptogramin B antibiotics in Bacillus subtilis. By molecular cloning and deletion analysis we have identified a replication segment on the physical map of this plasmid, which consists of about 900 to 1,000 base pairs. This segment contains the replication origin. It also specifies a trans-acting function (rep) required for the stable replication of pE194 and a negatively acting copy control function which is the product of the cop gene. The target sites for the rep and cop gene products are also within this region. Two incompatibility determinants have been mapped on the pE194 genome and their properties are described. One (incA) resides within the replication region and may be identical to cop. incB, not located in the replication region, expresses incompatibility toward a copy control mutant (cop-6) but not toward the wild-type replicon.

Bacillus subtilis↗
PubMed1982

Surgical monitoring of spinal cord function: cauda equina stimulation technique.

Spinal cord and subcortical brain stem evoked potentials had an amplitude at least 2 times higher when the cauda equina rather than bilateral peripheral nerves was stimulated. Cauda equina stimulation is indicated when potentials to peripheral nerve stimulation are absent or are too low in amplitude to permit reliable surgical monitoring. The technique is essentially without risks, but should be performed with a small lumbar puncture needle (21 to 22 gauge), and is contraindicated in patients with general infections, increased cerebrospinal fluid pressure, or a hemorrhagic tendency (thrombocytopenia or anticoagulant therapy).

Cauda Equina↗
PubMed1981

Early somatosensory potentials evoked by median nerve stimulation: intraoperative monitoring.

We identified the sites of origin of the somatosensory evoked potentials to median nerve stimulation by recording directly from the cervical cord in the course of intraoperative monitoring. The N9 potential occurred before any potentials recorded from the cord or dorsal roots. Potentials with latencies corresponding to N11 were recorded at the median nerve root entry zone of the lower cervical cord. High-amplitude potentials were recorded at the level of the foramen magnum, with latencies approximating or following P13, suggesting that this potential is generated at the cervicomedullary junction.

Electric Stimulation↗
PubMed1980

Conformational alteration of mRNA structure and the posttranscriptional regulation of erythromycin-induced drug resistance.

The DNA sequence of the ermC gene of plasmid pE194 is presented. This determinant is responsible for erythromycin-induced resistance to the macrolide-lincosamide-streptogramin B group of antibiotics and specifies a 29,000 dalton inducible protein. The locations of the ermC promoter, as well as that of a probable transcriptional terminator, are established both from the sequence and by transcription mapping. The sequence contains an open reading frame sufficient to encode the previously identified 29,000 dalton ermC protein. Between the promoter and the putative ATG start codon is a 141 base pair leader sequence, within which several regulatory (constitutive) mutations have been mapped and sequenced. The leader has a second open reading frame, sufficient to encode a 19 amino acid peptide. It is suggested that induction by erythromycin involves a shift between alternative ribosome-bound mRNA conformations, so that the ribosome binding sequence and the start codon for synthesis of the 29K protein are unmasked in the presence of inducer. Possible active and inactive folded configuration of the leader sequence are presented, as well as the effects on these configurations of regulatory mutations.

Bacillus subtilis↗
PubMed1980

Induction of renin release by exogenous prostaglandins in hyporeninemic hypoaldosteronism.

A deficiency in renal prostaglandin synthesis has been proposed as the cause of the syndrome of hyporeninemic hypoaldosteronism. To determine if renin release could be stimulated by pharmacologic infusions of PGA1, we infused PGA1 0.075 to 0.60 microgram/kg/min to nine patients with the syndrome. Total renal PGE production as measured by urinary PGE excretion was normal (650 +/- 169 vs 400 +/- 55 ng/24hr in normal subjects). Renin (PRA) was markedly depressed in all patients despite stimulation with upright posture and furosemide (1.0 +/- 0.4 vs 9.3 +/- 0.7 ng/ml/hr, p < 0.001). But in two patients PGA1, induced an increase in renin similar to that of normal subjects. PRA increased to a lesser degree in two other patients and plasma aldosterone slightly increased. Five showed no response. Infusions of nitroprusside in doses and duration that mimicked the hypotensive effects of PGA1 failed to increase PRA or aldosterone. The data suggest that total renal PGE production is normal in patients with the syndrome of hyporeninemic hypoaldosteronism. Although orthostasis, furosemide and nitroprusside do not increase renin, prostaglandin A1 infusion appears to be a potent stimulus to renin release in some of the patients.

Aldosterone↗
PubMed1980

In vitro effects of radiographic contrast media on the complement system.

The effect of several radiographic contrast media on the complement system in vitro was examined using quantitative crossed immunoelectrophoresis. Diatrizoate, iothalamate, metrizoate, and methiodal did not cause electrophoretic conversion of C3 or properdin factor B. In fact, the small degree of spontaneous conversion occurring when serum is incubated in polypropylene tubes was inhibited by these contrast media or by hypertonic sodium chloride. Metrizamide caused enhanced conversion of C3 and factor B that was only partially inhibited by ethylene glycol tetracetic acid (EGTA) but completely inhibited by ethylenediaminetetraacetic acid (EDTA). Iodipamide caused a unique electrophoretic alteration of C3 that was not affected by EDTA or several other inhibitors and that was not identical with the usual products of C3 activation. Iodipamide in very low concentrations inhibited complement activation through the classical pathway.

Citrates↗
PubMed1980

Is urinary flow rate a major regulator of prostaglandin E excretion in man?

Urinary PGE2 excretion is enhanced in several polyuric states in man suggesting that PGE2 synthesis could be a mediator of diuresis. To explore the alternate hypothesis that polyuria is the cause of the increased PGE2 excretion, we increased urine flow rate by intravenous administration of dextrose and water with different magnesium, calcium and potassium solutions in four normal males. Urinary PGE excretion rose in parallel with urine volume (r = 0.65 p < 0.01) independently of the electrolyte solution. To determine the effects of chronic alterations in water balance in 5 female subjects, we sequentially regulated oral water intake to induce 1, 2, 4 and 8 liters of urine volume/day. During low (40 mEq) sodium diets, PGE increased from 540 +/- 50 to 4880 +/- 1240 ng/d with increasing urinary volume (r = 0.81, p < 0.01). Similarly, for 200 mEq sodium intake PGE paralleled urinary volume (from 630 +/- 100 to 4740 +/- 800 ng/d, r = 0.61, p < 0.01). In vitro sample dilution studies demonstrated no interference from method blank, and the addition of thin layer chromatography prior to Sephadex chromatography failed to alter assay measurements. We conclude that extreme increases in urinary flow rate may directly enhance PGE excretion in man.

Adult↗