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Biomedical subjects

D Rowley

Publications and source records attributed to D Rowley.

At least 19 recordsLinked to original sources
PubMed1992

Mortality among infants of black as compared with white college-educated parents.

BACKGROUND: In the United States, black infants are twice as likely to die as white infants; this difference reflects both black infants' higher rates of low birth weight and the higher mortality among black infants of normal birth weight. We studied mortality in infants born to college-educated parents in order to investigate this gap while controlling for sociodemographic variables. METHODS: We used the National Linked Birth and Infant Death Files for 1983 through 1985 to calculate infant mortality rates for children born to college-educated parents. The study population consisted of 865, 128 white infants and 42,230 black infants. A separate effect of birth weight was assessed by examining mortality rates before and after the exclusion of infants weighing less than 2500 g at birth (low-birth-weight infants). RESULTS: In this population, the infant mortality rate was 10.2 per 1000 live births for black infants and 5.4 per 1000 live births for white infants; the adjusted odds ratio for death among black infants was 1.82 (95 percent confidence interval, 1.64 to 2.01). The rate of low birth weight was more than twice as high among blacks (7 percent) as among whites (3 percent), although the mortality rate in this group was not higher among blacks than among whites. Black infants were three times as likely as white infants to die of causes attributable to perinatal events, including prematurity. They were no more likely to die of the sudden infant death syndrome. After the exclusion of low-birth-weight infants, the mortality rates for black and white infants were equal. CONCLUSIONS: In contrast to black infants in the general population, black infants born to college-educated parents have higher mortality rates than similar white infants only because of their higher rates of low birth weight. Black and white infants of normal birth weight have equivalent mortality rates.

Black or African American↗
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↗
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↗
PubMed1979

The suppressive effect of circulating specific antibody on the response to oral immunisation with Vibrio cholerae.

Species IgG antibody given intravenously 3-4 hours prior to oral immunisation with Vibrio cholerae led to a specific depression of both the systemic and loca limmune response. One vibriocidal unit of IgG antibody, which itself would given undetectable levels of circulating specific antibody, was significantly immunosuppressive. The suppression is considered to be due to central repression of the antigen-reactive lymphocyte, rather than to antigen exclusion at the gut mucosal surface. The repression appeared less pronounced in some immunoglobulin classes than in others.

Administration, Oral↗