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We studied the seroprevalence of three viruses (mouse cytomegalovirus (MCMV), minute virus of mice (MVM), and mouse parvovirus (MPV)) in house mice (Mus domesticus) in 1995–7. In the first year average mouse density was less than 1 mouse/ha. From November 1995 to May 1996 the population increased at an average rate of 7% per week, a doubling time of about 10 weeks. From August 1996 to May 1997 the population increased at an average rate of 10% per week, a doubling time of about 7·5 weeks. From a peak around 250 mice/ha in May 1997, the mouse population fell 19% per week to 5 mice/ha in October 1997. The seroprevalence for all three viruses varied dramatically over time. MCMV had the highest seroprevalence (61·7%), followed by MVM (8·5%) and MPV (18·4%). Time series data indicated that MCMV spread rapidly through the population of mice once trap success was greater than 14% (40–100 mice/ha). By contrast MVM and MPV seroprevalence occurred with a 2–3 month and 3–4 month time lag, respectively. The current study supports the contention that MCMV would be a good carrier for an immunocontraceptive vaccine for controlling field populations of mice.

Treponema pallidum, the causative agent of venereal syphilis, is a microaerophilic obligate pathogen of humans. As it disseminates hematogenously and invades a wide range of tissues, T. pallidum presumably must tolerate substantial oxidative stress. Analysis of the T. pallidum genome indicates that the syphilis spirochete lacks most of the iron-binding proteins present in many other bacterial pathogens, including the oxidative defense enzymes superoxide dismutase, catalase, and peroxidase, but does possess an orthologue (TP0823) for neelaredoxin, an enzyme of hyperthermophilic and sulfate-reducing anaerobes shown to possess superoxide reductase activity. To analyze the potential role of neelaredoxin in treponemal oxidative defense, we examined the biochemical, spectroscopic, and antioxidant properties of recombinant T. pallidum neelaredoxin. Neelaredoxin was shown to be expressed in T. pallidum by reverse transcriptase-polymerase chain reaction and Western blot analysis. Recombinant neelaredoxin is a 26-kDa alpha(2) homodimer containing, on average, 0.7 iron atoms/subunit. Mössbauer and EPR analysis of the purified protein indicates that the iron atom exists as a mononuclear center in a mixture of high spin ferrous and ferric oxidation states. The fully oxidized form, obtained by the addition of K(3)(Fe(CN)(6)), exhibits an optical spectrum with absorbances at 280, 320, and 656 nm; the last feature is responsible for the protein's blue color, which disappears upon ascorbate reduction. The fully oxidized protein has a A(280)/A(656) ratio of 10.3. Enzymatic studies revealed that T. pallidum neelaredoxin is able to catalyze a redox equilibrium between superoxide and hydrogen peroxide, a result consistent with it being a superoxide reductase. This finding, the first description of a T. pallidum iron-binding protein, indicates that the syphilis spirochete copes with oxidative stress via a primitive mechanism, which, thus far, has not been described in pathogenic bacteria.

Because of the dismal condition of United States exports, many state and federal government programs are being developed to encourage exports. Some state programs are described. Some programs include assistance in advertising. Many states are cooperating together in promoting exports. Some states are offering limited amounts of financing for companies interested in exporting. With the increased interest in expanding exports, will come a demand for experienced international markets.

The abnormal umbilical artery Doppler waveform represented by absent enddiastolic flow velocity (AEDFC) identifies a group of preterm fetuses with intrauterine growth restriction (IUGR) at high risk of perinatal death due chronic hypoxia from compromised umbilical artery blood flow. Initial studies of AEDFV placentae suggested a loss of small stem arterioles, though by immunohistochemical localization with an antibody to @a-smooth muscle actin, we were unable to demonstrate any selective loss of even the smallest vessels in the 10-25 @mM post-fixation diameter range. Further studies of villous ultrastructure and immunohistochemical localization of matrix molecules (laminin and collagens I, III and IV) demonstrated evidence of villous fibrosis and trophoblast aging. Parallel scanning electron microscopy studies demonstrated reduced numbers of malformed peripheral villi, whose capillaries were elongated and only poorly branched. Several of the structural differences in the terminal villi of this IUGR group, such as reduced cytotrophoblast proliferation and stromal fibrosis, are incompatible with the prevailing view of placental hypoxia in preterm IUGR with AEDFV. Reduced numbers of malformed terminal vili would be predicted to both increase capillary vascular impedance, and compromise placental gas exchange. Despite the known reduction in uteroplacental arterial blood flow in IUGR with AEDFV in the umbilical arteries, there is a greater fall in extraction of oxygen from the intervillous space: as such that maternal blood leaving the placenta has a higher content than under normal circumstances. Our data challenge the presumption of ''placental hypoxia'' in this subset of preterm IUGR pregnancies complicated by AEDFV in the umbilical arteries, which has both scientific and clinical implications.