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Biomedical subjects

B E Stern

Publications and source records attributed to B E Stern.

4 recordsLinked to original sources
PubMed2000

New fimbrial gene cluster of S-fimbrial adhesin family.

Fimbrial adhesins that mediate attachment to host cells are produced by most virulent Escherichia coli isolates. These virulence factors play an important role in the initial stages of bacterial colonization and also in determination of the host and tissue specificity. Isolates belonging to serotype O78 are known to cause a large variety of clinical syndromes in farm animals and humans and have been shown to produce several types of adherence fimbriae. We studied the fimbrial adhesin from an avian septicemic E. coli isolate of serotype O78. Analysis of the genetic organization of the fac (fimbria of avian E. coli) gene cluster indicates that it belongs to the S-fimbrial adhesin family. Seven open reading frames coding for major and minor structural subunits were identified, and most of them showed a high degree of homology to the corresponding Sfa and Foc determinants. The least-conserved open reading frame was facS, encoding a protein known to play an important role in determining adherence specificity in other S-fimbrial gene clusters.

Adhesins, Escherichia coli↗
PubMed1997

Virulence patterns from septicemic Escherichia coli O78 strains.

Several septicemic Escherichia coli O78 strains, isolated from different sources, were characterized phenotypically and genotypically. Two avian isolates, one of which is known to carry the AC/I fimbriae, hybridized with the sfa determinant in colony dot-blot assay. Southern hybridizations with specific sfa probes, following pulsed-field gel electrophoresis (PFGE), showed positive hybridization to the same fragment in each of these strains. Determination of the N-terminal amino acid sequence of the AC/I major subunit gene revealed high similarity to the sequence of the SfaA-II protein. These data suggest that the adhesin gene cluster, coding for AC/I fimbriae, belongs to the S-fimbrial adhesin family.

Adhesins, Bacterial↗
PubMed1984

Hypothalamic function in amenorrheic runners.

We have examined temperature regulation in eight amenorrheic runners and gonadotropin response to an opioid antagonist in seven amenorrheic runners, 18 to 29 years of age, running 20 to 70 miles a week. Following equilibration, oral temperature was measured continuously, first in a cold room at 39 degrees F and then in a sauna at 172 degrees F in eight amenorrheic runners, in eight eumenorrheic runners, and in eight control subjects in the early follicular phase of the menstrual cycle. Studies were terminated if a subject's temperature fell below 94 degrees F or rose above 102 degrees F, and all studies were conducted in the afternoon. The rates of temperature change, calculated from total net temperature change divided by elapsed time in the test chamber, were not significantly different among the three groups of women. Seven other amenorrheic runners failed to have any significant changes in luteinizing hormone or follicle-stimulating hormone levels in response to the opioid receptor antagonist naloxone administered as an intravenous infusion at 1.6 mg/hour for 4 hours. If opioids inhibit gonadotropin secretion in exercise-associated amenorrhea, an increase in gonadotropins in response to naloxone would have been anticipated. Although it is possible that the dose of naloxone selected was inappropriate and that temperature responses under other conditions might differ from those of normal women, these data suggest that endogenous opiates do not play a direct role in the amenorrhea associated with exercise and that temperature regulatory centers in the hypothalamus are intact in this disorder, compared with other causes of amenorrhea such as anorexia nervosa. Further studies of hypothalamic function are warranted to test these possibilities.

Adolescent↗