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Biomedical subjects

D Rowley

Publications and source records attributed to D Rowley.

At least 37 records · Page 2Linked to original sources
PubMed1992

Maternal and perinatal mortality.

Maternal and perinatal mortality are important health problems in the United States. Emerging causes of maternal deaths are embolism, cardiomyopathy, anesthesia complications, adult respiratory distress syndrome, and acquired immunodeficiency syndrome. Maternal deaths continue to be underreported. Active surveillance is needed to better identify maternal deaths and to understand their causes and risk factors. Although perinatal deaths have declined recently--primarily because technologic advances have improved low-birth-weight babies' chances for survival--they remain a problem, particularly among blacks. Clinicians should strive to reduce preventable deaths among black normal-birth-weight babies and to prevent low birth weight and premature birth among black infants. Future research should focus on determining whether early prenatal care and cesarean delivery actually reduce perinatal mortality. A better understanding of prenatal and intrapartum care and their benefits will help in the development of strategies to reduce perinatal and maternal deaths.

Cause of Death↗
PubMed1991

Characterization and immunogenicity of EX880, a Salmonella typhi Ty21a-based clone which produces Vibrio cholerae O antigen.

EX645 is a derivative of Salmonella typhi Ty21a which carries a plasmid specifying production of Vibrio cholerae O antigen. When cultured with exogenous galactose to overcome the galE defect of the vector, EX645 also synthesizes S. typhi O antigen, and this can result in the masking of the shorter V. cholerae O antigen on the bacterial surface. To determine whether the potential for such masking at least partly underlies the inconsistency of anti-V. cholerae responses elicited by EX645, a derivative of this strain has been isolated, characterized, and tested for immunogenicity in human volunteers. EX880 has an rfb defect which prevents synthesis of S. typhi O antigen, and consequently V. cholerae O antigen is still detectable on the surface of the clone following growth in the presence of galactose. Compared with EX645, EX880 more consistently elicited significant rises in serum bactericidal antibody levels, although individual responses within a cohort still varied widely.

Antibodies, Bacterial↗
PubMed1991

Surveillance of postneonatal mortality, United States, 1980-1987.

In the United States, one-third of all infant deaths (deaths of infants ages 0-364 days) occurs in the postneonatal period (28-364 days). A substantial proportion of these deaths potentially could be prevented. To examine recent trends in postneonatal mortality (PNM) in the United States, the investigators analyzed birth and death certificate data for resident infants for the period from 1980 through 1987. Rates of PNM declined 11% from 3.5 to 3.1/1,000 live births among white infants and declined 16% from 7.3 to 6.1/1,000 live births among black infants. Most of the decline resulted from reduced mortality from infectious diseases and injuries. A decreased mortality attributable to sudden infant death syndrome (SIDS) among black infants additionally accounted for the decline. Autopsy rates for SIDS increased from 82% to 92% but did not differ for black infants and white infants. Birth defects-related PNM declined more among white infants than among black infants. The racial gap in PNM (rate ratio (RR) = approximately 2.0) persisted. However, the largest black/white gap occurred in the Northeast (RR = 2.5), the region with the lowest PNM. Black infants were 2.7 and 2.3 times more likely to die of infections and injuries, respectively, than were white infants. Although PNM rates declined during the 1980s, a greater rate of reduction is needed to achieve the Year 2000 objectives, especially among black infants. Such reductions are possible through improved access to comprehensive pediatric care as well as education and community-oriented prevention programs designed to reduce deaths due to infections and injuries. A better understanding of the etiology of SIDS and birth defects is critical for preventing postneonatal deaths.

Congenital Abnormalities↗
PubMed1991

National trends in the incidence of abruptio placentae, 1979-1987.

Premature separation of the normally implanted placenta is a serious complication of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. Using data from the National Hospital Discharge Survey, we estimated rates of abruptio placentae in the United States for the years 1979-1987 and examined the association of this condition with several demographic risk factors and coexisting obstetric conditions. In 1987, the national rate was 11.5 cases per 1000 deliveries. The rate of abruptio placentae increased significantly between the years 1979-1987 among women of all racial groups. The increase in the rate of placental abruption occurred mainly among women under the age of 25, unmarried women, and women on Medicaid compared with those who had private insurance. Women with placental abruption were 54 times more likely to have coagulopathies and 11 times more likely to have stillbirths than those without placental abruption. Twin gestations, preterm premature rupture of membranes, chorioamnionitis, chronic hypertension, and preeclampsia/eclampsia were also associated with placental abruption. Although the cause for the increase in the incidence of abruptio placentae is not known, most of the increase occurred among women likely to be financially and socially disadvantaged.

Abruptio Placentae↗
PubMed1990

Delayed antigen presentation by epidermal Langerhans cells to cloned T h1 and T h2 cells.

Langerhans (LC) cells require incubation with protein antigen for several days before the cells effectively stimulate proliferation of cloned, H-2 restricted, antigen-specific T h cells. In contrast, splenic antigen-presenting cells are immediately effective. LC are immediately competent, however, if an immunogenic peptide rather than the intact protein is the immunogen, indicating that resident or unchallenged LC have the required class II MHC and can provide the signals necessary for T-cell proliferation but may lack the capacity to internalize or cleave protein antigens. We propose that delayed antigen presentation by LC may be intrinsic and advantageous for promoting early systemic immunity. LC stimulate cloned T h1 and T h2 cells equally well, suggesting that LC may not limit or bias the type of immunity that occurs with cutaneous antigenic challenge.

Animals↗
PubMed1990

Safety, immunogenicity, and efficacy against cholera challenge in humans of a typhoid-cholera hybrid vaccine derived from Salmonella typhi Ty21a.

A live oral vaccine consisting of attenuated Salmonella typhi Ty21a expressing Vibrio cholerae O1 Inaba lipopolysaccharide (LPS) O antigen was constructed and tested in volunteers for safety, immunogenicity, and efficacy. Fourteen adults ingested three doses of 10(10) viable organisms with buffer. One month later, 8 vaccinees and 13 unimmunized controls were challenged with 10(6) pathogenic V. cholerae O1 E1 T or Inaba organisms. No significant adverse reactions to vaccination were observed. All volunteers had significant rises in serum immunoglobulin G (IgG) antibody to S. typhi LPS. Only 2 (14%) of 14 had significant rises in serum IgA or IgG antibody to Inaba LPS, and 5 (36%) of 14 had fourfold rises in vibriocidal antibody. In the challenge study, diarrhea occurred in 13 of 13 controls and 6 of 8 vaccinees (vaccine efficacy, 25%; P = 0.13). The vaccine significantly reduced the severity of the clinical illness (P less than 0.05) and caused decreased excretion of challenge vibrios (P less than 0.05). Although the typhoid-cholera hybrid vaccine did not provide significant protection overall against experimental cholera, this study demonstrates the importance of antibody to V. cholerae O antigen in ameliorating clinical illness and illustrates the use of an S. typhi carrier vaccine strain expressing a foreign antigen.

Antibodies, Bacterial↗
PubMed1990

The serum polymeric IgA antibody response to typhoid vaccination; its relationship to the intestinal IgA response.

The relationship between the IgA antibody response in serum (total and polymeric IgA) and intestinal secretions was examined in volunteers subjected to oral and parenteral typhoid vaccination. After oral vaccination (three doses of 10(11) live Ty21a vaccine given at 48-hr intervals), serum pIgA antibody to typhoid lipopolysaccharide (LPS) was detected in seven of the 14 subjects (46.4 +/- 59 U/100 microliters, mean +/- SD). However, all 14 showed a significant intestinal IgA response (993 +/- 2516 and 9349 +/- 6754 U/mg pre- and post-vaccine; t = 5.25, P = 0.0002). The level of pIgA antibody declined rapidly, whereas intestinal IgA antibody levels remained elevated. Serum pIgA antibody was also found after parenteral immunization (two doses of 5 X 10(8) heat-killed bacteria given 14 days apart to six subjects), but an intestinal IgA antibody response was detected in these individuals only after a subsequent course of the oral vaccine given 1 month after initial parenteral immunization. Changes in serum pIgA antibody followed those of total serum IgA antibody rather than those of intestinal antibody. The results indicate that a serum pIgA response can be induced by an antigenic stimulus delivered either orally or parenterally, whereas an intestinal IgA response is induced only by a local antigen stimulus. The regulation of serum pIgA and intestinal IgA appear to be independent.

Adult↗
PubMed1989

Assays for total and antigen-specific polymeric IgA in serum based on binding to secretory component.

Binding assays with secretory component (SC) were used to detect polymeric IgA antibody to E. coli lipopolysaccharide and to estimate total polymeric IgA in sera from 14 patients with alcoholic liver disease and eight normal controls. Radioiodinated human SC was shown to bind to polymeric IgA and IgM but not to monomeric IgA, secretory IgA or IgG. Serum aliquots (0.5 ml) were totally depleted of IgM using 2 ml anti-IgM affinity columns and the effluent sera were titrated in microtitre plates coated with lipopolysaccharide, the binding of polymeric IgA being detected by adding 10 ng radiolabelled SC. Total polymeric IgA was measured via its capacity to inhibit the binding of 5 ng labelled SC to IgM coated wells, quantitation being achieved by comparison with the inhibition produced by purified polymeric IgA. Total lipopolysaccharide-specific IgA antibody was detected by ELISA in sera from both patients and controls, 1185 +/- 793 and 56 +/- 19 U/100 microliters (mean +/- SD), respectively; but polymeric IgA antibody was detected only in patients' sera (131 +/- 214 U/100 microliters). The concentration of total polymeric IgA was higher in patients' sera than in control sera (488 +/- 333 and less than 120 micrograms/ml respectively).

Antibodies, Bacterial↗
PubMed1988

Oral immunization with live, avirulent fla+ strains of Salmonella protects mice against subsequent oral challenge with Salmonella typhimurium.

Some strains of Salmonella, when fed to mice, establish a nonlethal, limited infection in the Peyer's patches of the small intestine. When such mice are later challenged orally with a normally lethal dose of virulent Salmonella typhimurium, a protective effect of the prior vaccination is seen. In an effort to characterize the determinant(s) of the avirulent strains responsible for this protective effect, we examined the cell envelope protein profiles of five such protective strains and of eight strains of Salmonella that were both nonpersistent and nonprotective when fed to mice. The protective strains produced high levels of flagellin. We made otherwise isogenic fla+ and fla- derivatives of two such strains and showed that although the fla- derivatives colonized mice as well as did the fla+ strains, the fla- derivatives given orally showed a much reduced ability to protect mice from S. typhimurium challenge. Both fla+ and fla- strains induced cellular immunity in vaccinated mice.

Administration, Oral↗
PubMed1988

Bacterial lipopolysaccharide-induced intestinal microvascular lesions leading to acute diarrhea.

Subcutaneous challenge of mice with lipopolysaccharide (LPS) from gram negative bacteria, produced an intestinal microvascular lesion causing fluid exudation into the lumen of the intestine and diarrhea. The microvascular lesion was characterized by endothelial cell damage and microthrombi in the venules and capillaries of the intestinal lamina propria. Marker organisms, given orally to challenged mice, grew in the exuded fluid and could invade the mucosa. Intravenous transfer of postchallenge plasma produced the lesion in normal mice and absorption of such plasma by Sepharose coupled to LPS-antibody abolished this effect. Instillation of large quantities of LPS into the lumen of the intestine produced scattered microvascular lesions, although none of these animals developed diarrhea. Since a similar microvascular lesion has been described in the rectal mucosal lamina propria of adults with acute diarrhea, it is suggested that LPS-induced vascular damage may be a novel mechanism in the pathogenesis of acute diarrhea.

Acute Disease↗
PubMed1987

Nonlipopolysaccharide protective antigens shared by classical and El Tor biotypes of Vibrio cholerae.

The prophylactic significance of the nonlipopolysaccharide (non-LPS) antigens of Vibrio cholerae was investigated further with use of the infant mouse cholera model. Of 16 strains examined to date, 12-including eight recent field isolates of both biotypes and both common serotypes-express common non-LPS protective antigens. The exceptional strains are four old isolates of El Tor biotype, the outer membrane proteins of which are not atypical when analyzed by immunoblotting. The protective activities of antibodies to the shared non-LPS components correlated with their capacities to inhibit the in vitro attachment of Vibrio organisms to isolated murine enterocytes.

Animals↗
PubMed1986

The colonization of Peyer's patches by a strain of Salmonella typhimurium cured of the cryptic plasmid.

We cured a strain of Salmonella typhimurium of its cryptic plasmid and confirmed that orally administered cured strains lost virulence for mice. Loss of the cryptic plasmid rendered the S. typhimurium strain sensitive to the bactericidal action of normal human serum. However, loss of the plasmid did not change the ability of the strain to associate with HeLa cells in tissue culture. Furthermore, when administered orally to mice, both the plasmid-containing and plasmid-free strains invaded the Peyer's patches of the small intestine to the same extent, and both were capable of inducing resistance to oral challenge with virulent S. typhimurium. When injected intraperitoneally, the cured strain was eliminated rapidly, whereas the parental strain persisted. We also showed that the cured strain did not contain a plasmid copy in the chromosome. We propose that although the plasmid-cured strain of S. typhimurium is able to colonize Peyer's patches, it cannot survive when administered intraperitoneally because it is susceptible to elimination by macrophages.

Administration, Oral↗
PubMed1986

Molecular cloning and expression in Escherichia coli K-12 of the O antigens of the Inaba and Ogawa serotypes of the Vibrio cholerae O1 lipopolysaccharides and their potential for vaccine development.

The gene clusters that determine the biosynthesis of both the Inaba and Ogawa serotypes of the O antigen of the lipopolysaccharide of Vibrio cholerae were cloned and expressed in Escherichia coli K-12. Restriction analysis of the clones demonstrated that about 15 kilobases were common to all clones and a further 5 kilobases were common to the Ogawa clones. The O antigens expressed by E. coli K-12 had the specificity of V. cholerae. Antibodies raised against E. coli K-12 that harbor one of these clones, pPM1001 (Inaba), were as highly protective in the infant mouse model system as were antibodies to V. cholerae itself. Introduction of such clones into suitable carrier strains could be expected to produce a good oral immunogen against cholera.

Animals↗
PubMed1986

Decreasing trends in Reye syndrome and aspirin use in Michigan, 1979 to 1984.

The incidence of Reye syndrome has been decreasing in Michigan, perhaps as a result of decreased aspirin use among children. To evaluate possible changes in the frequency of aspirin use, 199 families in Tecumseh, MI, with children younger than 18 years of age were interviewed by telephone in February 1981 and again in February 1983. Based on the reported use of medications for colds or influenza between 1981 and 1983, fewer parents gave aspirin (56% v 25%), but acetaminophen use did not change (59% v 55%). Younger parents and parents who had heard of the association between aspirin and Reye syndrome were more likely to stop giving aspirin. More parents chose to use either no medication or medications containing neither aspirin nor acetaminophen (6% v 32%) for the treatment of colds or influenza. Approximately 90% of parents who chose not to give aspirin for fever also gave medications for colds or influenza that did not contain aspirin. These results suggest that fewer children are receiving aspirin during illnesses that may precede Reye syndrome. The associated decrease in the incidence of Reye syndrome tends to support the hypothesis that the use of aspirin increases the risk for the development of Reye syndrome.

Acetaminophen↗