Helicobacter pylori and peptic ulcer disease.

Medical therapy for duodenal or gastric ulcer disease has traditionally involved gastric acid antisecretory therapy for 4 to 8 weeks to promote initial healing and indefinitely to prevent recurrences of ulcer. The discovery of Helicobacter pylori in most patients with peptic ulcer disease has led to a change in this approach. Therapy designed to eradicate H pylori may facilitate ulcer healing with acid antisecretory agents and, more important, may greatly reduce the incidence of ulcer recurrence, obviating the need for maintenance antisecretory therapy. Regimens designed to eradicate H pylori are difficult to comply with, however, and are associated with adverse effects in some patients. In this article we review the diagnosis and treatment of H pylori infection in patients with peptic ulcer disease and make recommendations regarding the use of conventional ulcer therapies and therapies designed to eradicate H pylori.     

On the probability of loss of new mutations in the presence of linkage disequilibrium

A new selectively neutral mutation occurs in a multilocus genetic background that has achieved a stable equilibrium at which there is a linkage disequilibrium. Perturbation techniques are applied to an extension of the branching process formulation of Fisher in order to address the question of extinction probabilities. We show that under appropriate conditions the probability of extinction of the new mutant is increased by the existence of linkage disequilibrium in the genetic background.Research supported in part by NIH grant GM 28016     

Evidence for the presence of β-lactamase inStreptomyces glaucescens and its inhibition by sodium clavulanate

Streptomyces glaucescens is shown to possess -lactamase activity which is inhibitable by clavulanate. This is important in regard to its use as a cloning host for enzymes of \-lactam biosynthesis.     

The evolutionary consequences of niche construction: a theoretical investigation using two-locus theory

This paper addresses the joint evolution of environment-altering (niche constructing) traits, and traits whose fitness depends on alterable sources of natural selection in environments. We explore the evolutionary consequences of this niche construction using a two-locus population genetic model. The novel conclusions are that niche construction can (1) cause evolutionary inertia and momentum, (2) lead to the fixation of otherwise deleterious alleles, (3) support stable polymorphisms where none are expected, (4) eliminate what would otherwise be stable polymorphisms, and (5) influence disequilibrium. The results suggest that the changes that organisms bring about in their niche can themselves be an important source of natural selection pressures, and imply that evolution may proceed in cycles of selection and niche construction.     

Adenosine(5')tetraphospho(5')adenosine-binding protein of calf thymus

An adenosine(5')tetraphospho(5')adenosine (Ap4A) binding protein has been purified from calf thymus. The protein is comprised of a single polypeptide of Mr 54000 and is capable of high-affinity (Kd = 13 microM) binding of Ap4A with great substrate specificity. The Ap4A binding protein has been isolated in two forms: a 'free', or non-polymerase-bound, form which predominates, and a similar form which copurifies with DNA polymerase alpha, but which can be resolved from it. The free form of Ap4A binding protein contains associated adenosine(5')tetraphospho(5')adenosine phosphohydrolase (Ap4Aase) activity, while the form resolved from DNA polymerase alpha contains no such activity. The Ap4Aase activity, which catalyzes the phosphohydrolysis of Ap4A to ATP and AMP, is strongly inhibited by low levels (50-100 microM) of Zn2+ without any effect on the Ap4A binding protein activity. This difference in associated Ap4Aase activity between free and polymerase-bound forms of the protein, plus the copurification mentioned above, indicate a specific association between Ap4A binding protein and DNA polymerase alpha.     

Estrogen-binding protein from rat preputial gland: purification and characterization.

Cytosol from the rat preputial gland has been shown to contain a protein which binds both estrone and estradiol. The protein, after a 26-fold purification from the cytosol of female Sprague-Dawley rats, migrated as one band during electrophoresis in sodium dodecyl sulfate on acrylamide gel. The electrophoretic mobility indicated a molecular weight of 15,000. The association constant for estrone as determined by equilibrium dialysis was 1.2 X 10(7) M-1, while that for 17beta-estradiol was 3.3 X 10(6) M-1. Progesterone, cortisol, testosterone, or diethylstilbestrol did not bind to the purified protein, whereas 17alpha-estradiol or estriol bound only slightly. In the presence of retinoic acid, but not retinol, the binding of estrone was reduced. Optimum binding for estrone was at pH 6.5 to 8.5.     

T lymphocytes of young and aged rats. II. Functional defects and the role of interleukin-2

Splenic T lymphocytes of aged Lewis rats respond to Con A and PHA with diminished 3H-TdR uptake compared with splenic T lymphocytes of young Lewis rats. After immunization with allogeneic tumor cells, uptake of 3H-TdR in mixed lymphocyte-tumor cultures and T cell cytotoxicity against tumor target cells are significantly lower with spleen cells of aged rats compared with those of young rats. The culture of spleen cells of aged rats with Con A results in a diminished conversion of Ia-positive T cells from Ia-negative precursors compared with similar cultures of spleen cells of young rats. Spleen cells of both young and aged rats produce high amounts of IL-2 in response to Con A stimulation. "Old" T cells, however, bind relatively little IL-2, do not utilize it in culture, and do not respond to exogenous IL-2 with enhanced 3H-TdR uptake as do "young" T cells. In allogeneic MLTC, "old" T lymphocytes produce little IL-2 compared with "young" cells, and both "young" and "old" cells respond to exogenous IL-2 with enhanced 3H-TdR uptake and increased cytotoxic activity. The data suggest defects in the synthesis and/or recognition of IL-2 as well as defects in the regulation of Ia antigen expression may be responsible, in part, for the reduced T cell function in aged animals.