Biomedical subjects
Publications and source records attributed to J R Scott.
The coupling sequences of conjugative transposons are short variable sequences derived from the DNA flanking the transposon insertion site. We show here that for Tn916 the left coupling sequence is 6 bases long. The right-hand end of the transposon can excise with either four or five T's, but integration occurs to restore the five T's at the transposon's right end.
Attachment of enterotoxigenic Escherichia coli to the human gut is considered an important early step in infection that leads to diarrhea. This attachment is mediated by pili, which belong to a limited number of serologically distinguishable types. Many of these pili require the product of rns, or a closely related gene, for their expression. We have located the major promoter for rns and found that although its sequence diverges significantly from a sigma-70 promoter consensus sequence, it is very strong. Transcription of rns is negatively regulated both at a region upstream of this promoter and at a region internal to the rns open reading frame. In addition, rns positively regulates its own transcription, probably by counteracting these two negative effects.
UNLABELLED: We investigated whether acute weight gain between the weigh-in and competition was associated with success in a collegiate wrestling tournament. Wrestlers at the NCAA championships were weighed at the official weigh-in and again just before the first round of the tournament (20 h later). Weight gain and the weight discrepancy between first-round opponents were calculated (N = 607 excluding heavyweights). Indices of success included season record (% wins in total matches), tournament seeding, the sum of the advancement and placement points scored during the tournament (team points), and final placement in the tournament. ANOVA showed no differences in weight variation between placewinners and non-placewinners, or across placewinners only. Correlation coefficients among weight variables and indices of success were also low (P > 0.05). Multiple logistic regression, used to determine whether weight gain or weight discrepancy between opponents contributed to success in the first round of the tournament, revealed that neither variables was predictive of first-round outcome even after attempting to account for differences in ability (e.g., forcing team points into the regression first). CONCLUSION: neither acute weight gain after the weight-in or the weight discrepancy between opponents in the first round influenced success in a collegiate wrestling tournament.
UNLABELLED: The purpose of this study was to determine the magnitude of weight gained in collegiate wrestlers between the weigh-in and beginning of tournament competition. Body weight of the qualifiers for the NCAA Division I, II, and III wrestling finals (N = 668) was recorded at the official weigh-in and again approximately 20 h later, before the first round of competition in the tournament. The results showed that on average (+/- SD), wrestlers gained 4.9 +/- 2.4% (3.3 +/- 1.5 kg) of body weight before competing. An inverse relationship was found such that wrestlers in the lightest weight classes gained the most weight (kg) compared with heavier wrestlers (r = -0.45, P < 0.05). Despite the large mean weight gain, the mean discrepancy between first round opponents was 2.1 +/- 3.0 kg and even less when heavyweight wrestlers were excluded from the analyses (1.5 +/- 1.2 kg, N = 607). A significant correlation between weight gain and weight discrepancy of opponents was found (r = 0.65, P < 0.05). CONCLUSION: collegiate wrestlers, excluding heavyweights, gained significant amounts of weight (3.7 kg average) during the 20-h period prior to tournament competition. The magnitude of weight gain was positively correlated to the degree of weight discrepancy (size advantage) over the opponent; however, because weight gain of some magnitude after the weigh-in was common in most participants, the average discrepancy between opponents was only about 1.5 kg.
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OBJECTIVE: To determine the risk of antiphospholipid antibody-related disorders in women with elevated levels of these antibodies. METHODS: We used an historic cohort study design. Surveys of medical and obstetric histories for the interval from initial antibody testing to the time of patient interview were used to calculate age-adjusted rates for the development of medical disorders associated with antiphospholipid antibodies. The cohort included 130 women with lupus anticoagulant, medium to high levels of immunoglobulin G anticardiolipin antibodies, or both. RESULTS: The median interval of study was 3.2 years (range 0.7-9.5, mean 3.7). Sixty-three subjects (48%) developed at least one new disorder during the study interval. The age-adjusted rates (per 1000 patient-years; +/- standard error) for the development of the disorders studied were as follows: thrombosis (156.8 +/- 30.0), cerebrovascular accident (93.8 +/- 25.1), amaurosis fugax (57.1 +/- 23.2), transient ischemic attack (170.4 +/- 27.6), systemic lupus erythematosus (9.8 +/- 3.8), and autoimmune thrombocytopenia (56.0 +/- 22.2). Of the 34 thrombotic events that occurred during the study interval, eight were associated with pregnancy and eight occurred while the patients were taking anticoagulant medications. CONCLUSIONS: Our subjects developed complications associated with antiphospholipid antibodies at a substantial rate, and almost half suffered at least one new event during the study interval. The high rate of thrombosis in individuals with antiphospholipid antibodies, especially associated with pregnancy, underscores the need to evaluate long-term anticoagulation in these patients.
Mice were infected with one of two strains of scrapie by instilling brain homogenate into the conjunctiva to establish whether infection could be initiated. Of the 55 mice infected with ME7 scrapie, 23 developed clinical disease 323 +/- 8 (mean +/- standard error) days later. Three out of 12 mice infected with 79A scrapie developed disease after 232 +/- 35 days. The ME7 incubation period is similar to that for the oral route of infection. We feel that these results emphasize the need for adequate eye protection when handling tissues infected with spongiform encephalopathies.
OBJECTIVE: We tabulated first-trimester ultrasonography findings in women with recurrent pregnancy loss and determined the rate of subsequent pregnancy loss and live births after demonstration of a live embryo. STUDY DESIGN: Sixty-seven women with three or more recurrent miscarriages underwent first-trimester ultrasonography and were prospectively followed through 101 pregnancies. RESULTS: First-trimester ultrasonography showed a dead embryo in seven pregnancies. Two of gestational sac in 12, and an empty uterus in four. A live embryo was seen in 78 pregnancies. Two of these pregnancies were terminated because of fetal chromosomal abnormalities. Of the remaining 76 pregnancies, 13 (17%) ended in a fetal loss (spontaneous abortion or fetal death) and 63 (83%) resulted in viable live births. CONCLUSIONS: Among women with recurrent pregnancy loss the presence of a live embryo detected by first-trimester ultrasonography is not as encouraging as in normal pregnant women. These findings are useful in counseling patients with recurrent pregnancy loss.
There is no specific marker for scrapie infectivity, and therefore no means other than prolonged bioassay for estimating levels of infection in tissues. Our knowledge of replication dynamics depends on precise rodent models which have enabled us to determine how the disease spreads and in which cells it replicates. We know, firstly, that infection replicates in the lymphoreticular system, and can identify a candidate cell; secondly, the factors which control the length of the disease process, and how difficult it is to influence this; thirdly, that clinical disease depends on access to the nervous system, and that once neuroinvasion has occurred, the spread of infectivity in both PNS and CNS is along neuroanatomical pathways at a similar rate to slow axonal transport in uninfected mice. Infecting the visual pathways of the CNS through the retina has shown that spongiform pathology occurs as a consequence of replication, and that the Sinc gene, which has a major effect on incubation period length in mice, acts by controlling the initiation, but not the rate, of replication. The localisation of PrP, a host protein of unknown function which accumulates in an abnormal form in diseased animals provides an important pointer to pathogenetic mechanisms.
The major virulence factor of the important human pathogen Streptococcus pyogenes is the M protein, which prevents phagocytosis of the bacterium. In different strains of streptococci, there are over 80 serologically different M proteins and there are additional M-like proteins, some of which bind immunoglobulins. Although the sequence of the M molecules differs among different S. pyogenes strains, all M proteins, and some of the immunoglobulin-binding molecules, have at least two copies of the C repeat region. We describe construction of a deletion mutation in S. pyogenes, which has only one C repeat copy, and show that the mutant strain is still resistant to phagocytosis. The mutation was constructed in vitro and used to replace the resident emm allele in an S. pyogenes strain. To facilitate homologous recombination into the streptococcal chromosome, we adapted a shuttle vector which is temperature sensitive for replication in Gram-positive bacteria but not in Gram-negative hosts. This new method for delivery of a homologous DNA fragment to the S. pyogenes chromosome is efficient and reproducible and should be of general use.
The major virulence factor of Streptococcus pyogenes, the M protein, is positively regulated at the transcriptional level by mry in the M type 6 strain studied. We show here that in two S. pyogenes strains isolated from cases of toxic-shock-like syndrome, a type M1 strain and a type M3 strain, an mry-like gene is also required for resistance to phagocytosis.
OBJECTIVE: To determine the outcome of pregnancies in cardiac allograft recipients. METHODS: Thirty women who became pregnant after heart transplantation were identified from cases managed personally, questionnaires sent to all cardiac transplant centers, and review of the literature. Mothers were evaluated for evidence of rejection and for obstetric complications. The infants were observed for congenital abnormalities and perinatal morbidity or mortality. RESULTS: Frequent pregnancy complications included chronic hypertension (48%), preeclampsia (24%), and preterm labor (28%). The rate of cesarean delivery was 32%. Six episodes of rejection required treatment, and three late maternal deaths occurred. Among the 27 live births, 17 infants were born after 36 weeks' gestation and ten were preterm, five were small for gestational age, and four had neonatal complications. There were no congenital anomalies. CONCLUSION: Pregnancies in heart transplant recipients present management problems similar to those seen in patients with other allografts and should be considered high risk.
Prion protein (PrP) is an abundant membrane-associated host protein which accumulates in abnormal, relatively protease-resistant forms in the brains of animals with scrapie and related diseases. Using correlative light and electron microscopy we determined the sites of subcellular localisation of PrP in mice infected with the 87V strain of scrapie. Disease specific accumulation of PrP was observed at light microscopy as amyloid plaques or as diffuse or granular staining within the neuropil, often clearly associated with individual neurons. Serial electron microscopical preparations were immunostained for PrP by the immunogold method. Gold particles were located on amyloid fibrils and on the plasmalemma of neurites at the periphery of plaques and in the neuropil, irrespective of the morphological form of PrP accumulation when viewed by light microscopy. This suggests that amyloid fibrils are formed following the accumulation and aggregation of sub-unit proteins at the plasmalemma and, furthermore, that normal PrP may be converted to its pathological form at this site.
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The ultrastructural neuropathology of mice experimentally inoculated with brain tissue of nyala (Tragelaphus angasi; subfamily Bovinae), or kudu (Tragelaphus strepsiceros; subfamily Bovinae) affected with spongiform encephalopathy was compared with that of mice inoculated with brain tissue from cows (Bos taurus; subfamily Bovinae) with bovine spongiform encephalopathy (BSE). As fresh brain tissue was not available for nyala or kudu, formalin-fixed tissues were used for transmission from these species. The effect of formalin fixation was compared with that of fresh brain in mice inoculated with fixed and unfixed brain tissue from cows with BSE. The nature and distribution of the pathological changes were similar irrespective of the source of inoculum or whether the inoculum was from fresh or previously fixed tissue. Vacuolation caused by loss of organelles and swelling was present in dendrites and axon terminals. Vacuoles were also seen as double-membrane-bound and single-membrane-bound structures within myelinated fibres, axon terminals and dendrites. Vacuoles are considered to have more than one morphogenesis but the structure of vacuoles in this study was nevertheless similar to previous descriptions of spongiform change in naturally occurring and experimental scrapie, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and kuru. Other features of the ultrastructural pathology of the transmissible spongiform encephalopathies including dystrophic neurites and scrapie-associated particles or tubulovesicular bodies were also found in this study. Neuronal autophagy was a conspicuous finding. It is suggested that excess prion protein (PrP) accumulation, or accumulation of the scrapie-associated protease-resistant isoform of PrP, may lead to localised sequestration and phagocytosis of neuronal cytoplasm and ultimately to neuronal loss.
Transfer of fetal red blood cells and platelets to the maternal circulation can stimulate an immune response with production of immunoglobulin that can cross the placenta. Similarly, passage of maternal stem cells to an immunologically incompetent fetus can theoretically produce graft-versus-host disease. disease. Maternal sensitization to red blood cell antigens such as D and Kell can result in anaemia, hydrops, and death in an incompatible fetus. Current assessment of these pregnancies involves serial analysis of amniotic fluid bilirubin concentration, with umbilical cord blood sampling reserved for special circumstances; neither ultrasound or Doppler blood flow analysis are accurate in the prediction of fetal haematocrit. Intravascular transfusion is the treatment of choice for hydropic fetuses. Perinatal survival in non-hydropic fetuses is similar with either intravascular or intraperitoneal transfusion, and the choice of procedures is individualized. Isoimmune fetal thrombocytopenia is usually the result of maternal sensitization to the PlA1 antigen. There is significant risk of intracranial haemorrhage, both antepartum and during labour and delivery. Umbilical cord blood sampling at term can determine fetal platelet count and the need for platelet transfusion, and can aid in deciding the appropriate route of delivery.
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UNLABELLED: The purpose of this study was to characterize anaerobic power and aerobic power (power at peak oxygen uptake, or peak VO2) of elite senior (post-collegiate) wrestlers. Subjects (n = 14) from the U.S. national senior freestyle and Greco Roman wrestling teams were evaluated at separate tests using cycle ergometry for peak VO2 of the arms, peak VO2 of the legs, arm anaerobic peak power, and leg anaerobic peak power. Power output at peak VO2 was recorded for each test and compared to the anaerobic power of the appropriate body segment. The results (mean +/- SD) showed that wrestlers produced 2.3 +/- 0.4 W.kg body weight-1 at arm peak VO2 (43.7 +/- 4.6 ml.kg body weight-1. min-1), 4.2 +/- 0.5 W.kg body weight-1 at leg peak VO2 (50.9 +/- 5.1 ml.kg body weight-1.min-1), arm PP of 7.7 +/- 1.0 W.kg body weight-1, and leg PP of 10.5 +/- 1.7 W.kg body weight-1. Comparing power output during anaerobic and aerobic tests, the subjects performed at 3.4 +/- 0.6 times their peak oxygen uptake during arm anaerobic ergometry, whereas leg anaerobic peak power was 2.7 +/- 0.4 times the power at peak oxygen uptake for the legs (p < 0.05 for difference between ratios). CONCLUSION: relative to aerobic power, elite senior wrestlers may produce power anaerobically in the upper body at significantly higher levels than in the lower body.