The protein sigma 54 associates with Escherichia coli core RNA polymerase to form a holoenzyme that binds promoters but is inactive in the absence of enhancer activation. Here, mutants of sigma 54 enabled polymerases to transcribe without enhancer protein and adenosine triphosphate. The mutations are in leucines within the NH2-terminal glutamine-rich domain of sigma 54. Multiple leucine substitutions mimicked the effect of enhancer protein, which suggests that the enhancer protein functions to disrupt a leucine patch. The results indicate that sigma 54 acts both as an inhibitor of polymerase activity and as a receptor that interacts with enhancer protein to overcome this inhibition, and that these two activities jointly confer enhancer responsiveness.

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Our study suggests that larger height restoration and solid lump filling cement are risk factors of refracture of cemented vertebral bodies. Symmetric cement distribution and fluid aspiration would be the potential ways to avoid refracture of cemented vertebral bodies.

One hundred and fifty four consecutive adult patients having cardiac surgery for a variety of cardiac lesions were evaluated prospectively for postoperative jaundice, those with a raised preoperative serum bilirubin concentration (greater than 34 ,mol/I or 2 mg/100 ml) being excluded. The incidence of early postoperative jaundice, as defined by a serum bilirubin concentration of 50 ,umoUl (3.0 mg/100 ml) or greater, was 23*4%. The jaundice was mild (bilirubin concentration 51-100 ,umoll (3-.06.0 mg/100 ml)) in 26 patients (16.9%) and moderate to severe (greater than 100 ,umol/I (6.0 mg/100 ml)) in 10 patients (6-5%). Important contributing factors were the preoperative severity of right heart failure (raised right atrial 'pressure at heart catheterisation) and hypotension or hypoxaemia and the amount of blood transfused during or shortly after surgery. Age, sex, underlying cardiac lesion, whether halothane was used, operative procedure, duration of cardiopulmonary bypass, and presence or absence of hepatitis B surface antigen were not predictive of postoperative jaundice.It has long been recognised that transient jaundice could appear after a surgical procedure' and that hepatic damage is particularly liable to follow cardiopulmonary bypass.23 In one retrospective study early jaundice was seen in 13% of 232 patients undergoing open heart operations.4 In a similar study 8.6% of 736 patients undergoing open heart surgery developed postoperative jaundice.5 There have, however, been only a few prospective inquiries into the incidence and causes of postoperative jaundice. The prospective study of Evans et a16 revealed a much higher incidence (21%) of postoperative jaundice in patients having major noncardiac operations. The true incidence of early jaundice after open heart surgery is therefore still unclear and awaits further study.Furthermore, all studies on jaundice after open heart surgery were reported more than 10 years ago, when the medical care of patients undergoing open heart surgery was not as good as today, and when the hepatitis B surface antigen (HBsAg) was not recognised.7 HBsAg carriers are now known to harbour various liver lesions,8 which might contribute to the development of postoperative jaundice.9 It seemed therefore pertinent to investigate this prob-

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Older patients, lung disease, rectal cancer, longer operation duration, and additional pelvic procedure were at greater risk. There is a time-dependent change in postoperative urinary dysfunction. Male gender, American Society of Anesthesiologists' score of 2 or 3, rectal tumor, surgical drain, and pelvic infection can identify patients at risk for prolonged urinary dysfunction.

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ABSTRACT-A4 is a rare bacterial protein that substitutes for 9"m in the case of Escheichia coli genes transcribed by certain activators with encer protein-like properties. It contains a strongly acidic region of previously unknown function. Gel mobility-shift assays using crs4 deletion mutants show that this region is essential for O." to bind the core RNA polymerase and recruit it to the promoter. Multiple-point mutational analysis shows that the acidic amino acids and overlapping periodic hydrophobic amino acids are necessary for this binding. Related sequences are not found within the core biing determinant of aor, which binds the same core RNA polymerase. This comparison suggests that the core RNA polymerase interacts differently with the two a factors, likely contributing to the critical differences in transcription mechanism in the two cases.,54 is a bacterial of factor that directs core RNA polymerase to distinctive promoters for expression of genes involved in diverse metabolic functions (1, 2). aS4 is the only known oa factor that is not a member ofthe ao70 family of proteins (1-3).The transcription mechanism of o54-associated RNA polymerase is unusual in that it is similar to that of eukaryotic polymerase II in several regards (1-5). By contrast with cr70-associated polymerase, promoters transcribed by the o54-associated polymerase all require auxiliary activators, which have enhancer-like properties (2,(5)(6)(7)(8)(9). Core promoter elements can be recognized at the o54 polymerase and polymerase II promoters prior to the association of the RNA polymerases (4, 10-12). The association of the polymerase does not directly trigger transcription; in both cases ATP hydrolysis is required to open the start-site (4, 13, 14). By contrast, there are not yet examples of enhancer-dependent transcription or of ATP-dependent melting among the numerous promoters transcribed by the o70 family of holoenzymes (2). Because the same core RNA polymerase transcribes from both types of bacterial promoters, these differing properties appear to be conferred on the polymerase by the different a factors.These differences may be related to a number of motifs in a54 that are unusual for bacterial transcription factors but are more common in eukaryotic transcription factors (15). These include two hydrophobic heptad repeats; one overlaps a glutamine-rich region and the other overlaps a strongly acidic region. Because neither motif is present in the a70 family of proteins (16) and because similar motifs exist in factors involved in mammalian enhancer-dependent transcription (17), it was suggested that they might be important for the unique function of o54 (15). Previously, we reported that deletions that disrupt either of these motifs destroy the function of o54 at the ginA P2 promoter (15). The deletion mutants continued to protect the ginA P2 promoter against dimethyl sulfate attack in vivo but failed to support open promoter complex formation. On this basis it was suggested that they cooperated to form part of a distinct activati...