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Biomedical subjects

B R Davis

Publications and source records attributed to B R Davis.

At least 127 records · Page 7Linked to original sources
PubMed1987

Standardized physician preparation of death certificates.

One method for determining cause of death in a clinical trial is to use standard nosological coding of death certificates. In order to look at an alternative approach, the Hypertension Detection and Follow-up Program (HDFP) assessed underlying causes of death through the use of three physicians. These physicians were trained and standardized in the proper recording of cause of death on death certificates. Each physician completed a death certificate for each of the 768 deaths in the HDFP, utilizing all available information, including HDFP records, plus any additional hospital and autopsy records. The new standardized death certificates were then transmitted to a panel of three nosologists who coded the cause of death. The physician preparation procedure was compared with a procedure wherein a panel of three nosologists coded the original death certificate for the underlying cause of death. The procedures agreed on the three-digit International Classification of Disease, Adapted code in 60.1% of the cases. The agreement rate improved to 72.5% when disease codes were collapsed into broad disease categories utilized in the HDFP.

Adult↗
PubMed1987

Survival analysis of adverse effects data in the Beta-Blocker Heart Attack Trial.

Monitoring for adverse effects in an integral part of controlled clinical trials. Traditionally the results of monitoring are reported as either cumulative percentages at the end of the study or cross-sectional percentages at a given time in the study. These results are likely to underestimate the true number of complaints because participants may be withdrawn (e.g., deaths, losses to follow-up, and refusals) before they ever complain of an adverse effect. However, survival analysis methods can be used to compare the distributions of "time to first complaint" in the active and placebo treatment groups, taking into account withdrawals. Participants in the Beta-Blocker Heart Attack Trial were monitored for possible adverse effects. On each follow-up visit they were asked whether they had had any of four conditions (blacking out, fatigue, depression, and bronchospasm) since their previous visit about 3 months earlier. The patients were followed for up to 30 months. For fatigue and bronchospasm, the complaint-free time was significantly longer in the placebo vs. active (propranolol) treatment group (P less than 0.005).

Adult↗
PubMed1987

Characterization of a preleukemic state induced by Moloney murine leukemia virus: evidence for two infection events during leukemogenesis.

A preleukemic state in mice inoculated with Moloney murine leukemia virus (Mo-MuLV) was characterized. Six to 10 weeks after neonatal inoculation, animals developed mild splenomegaly and generalized hematopoietic hyperplasia. The hyperplasia was evident from myeloid and erythroid progenitor assays. A nonleukemogenic variant, Mo+PyF101 Mo-MuLV, did not induce the hyperplasia; this suggests that the hyperplasia is a necessary event in Mo-MuLV leukemogenesis. Another variant, MF-MuLV, which contains the long terminal repeat of Friend MuLV and causes erythroid leukemia instead of T-cell lymphoma, also induced the preleukemic hyperplasia. A model for Mo-MuLV leukemogenesis is presented in which two infection events are necessary: the first leads to generalized hematopoietic hyperplasia, and the second results in site-specific insertion and long terminal repeat activation of cellular protooncogenes.

Animals↗
PubMed1987

The association of postural changes in systolic blood pressure and mortality in persons with hypertension: the Hypertension Detection and Follow-up Program experience.

Participants in the Hypertension Detection and Follow-up Program (HDFP) were classified on the basis of baseline standing minus sitting systolic blood pressure into four groups (less than or equal to -20 [group 1], -19 to 0 [group 2], 1 to 20 [group 3], and greater than 20 mm Hg [group 4]) to study 5 year mortality. Group 1, 3.3% of the total, contained those participants who had postural hypotension. The 5 year total and age-adjusted mortality rates for these groups were significantly different (p less than .04), with group 1 having the highest rates. To account for the possible confounding effects of certain baseline risk factors--age, sex, race, prior antihypertensive treatment, randomization group, diabetes, end-organ damage, sitting diastolic and systolic blood pressures, pulse, hematocrit, smoking status, and relative weight (percent of ideal weight)--in assessing group differences in mortality rates, a multiple logistic model was used. Relative weight proved to be a confounding factor for the association of drop in postural systolic blood pressure with mortality. However, there is an interaction between history of diabetes and postural change in systolic blood pressure. Thus, postural hypotension may indicate a poor prognosis in diabetic hypertensive patients.

Actuarial Analysis↗
PubMed1986

Treatment of advanced stage mycosis fungoides with bleomycin, doxorubicin, and methotrexate with topical nitrogen mustard (BAM-M).

Ten patients with advanced stage (TNM IIB-IVB) mycosis fungoides were treated with a combination chemotherapy program consisting of bleomycin and methotrexate weekly, doxorubicin every 3 weeks, and topical nitrogen mustard daily (BAM-M). Seven patients obtained histologically documented complete remissions ranging from 4 to 105+ months in duration. Median survival is 16.5+ months. Three patients in whom splenomegaly was detected during their staging evaluation underwent splenectomy. These three patients have had unmaintained disease-free survivals of 36+, 100+, and 105+ months. This study indicates that BAM-M is effective therapy for advanced stage mycosis fungoides and suggests that the therapeutic role of splenectomy should be evaluated further.

Adult↗
PubMed1986

Effects of nonleukemogenic and wild-type Moloney murine leukemia virus on lymphoid cells in vivo: identification of a preleukemic shift in thymocyte subpopulations.

Infection of mice with Moloney murine leukemia virus (M-MuLV) as well as with a nonpathogenic variant, Mo+PyF101 M-MuLV, was studied. Mo+PyF101 M-MuLV differs from wild-type M-MuLV by the addition of enhancer sequences from polyomavirus in the long terminal repeat. Previous experiments indicated that Mo+PyF101 establishes infection in animals, even though it does not induce disease. In vivo infection studies with particular attention to the thymus were performed, since the thymus is the target organ for M-MuLV leukemogenesis. Mice inoculated at birth with wild-type M-MuLV developed maximal levels of thymic infection by 2 to 3 weeks. Animals inoculated with Mo+PyF101 M-MuLV showed considerably less thymic infection at early times (2 to 4 weeks); nevertheless, by 5 to 6 weeks infection equivalent to wild-type M-MuLV-inoculated animals developed. Therefore the nonpathogenicity of Mo+PyF101 M-MuLV did not simply reflect a lack of thymotropism. Furthermore, thymic infection by itself may not be sufficient to induce leukemia. The relative deficit of Mo+PyF101 M-MuLV thymic infection at early versus late times did not reflect a change in the nature of the cells in the thymus, since in vitro infection of primary thymocytes from 2- and 6-week-old animals was equally efficient. One possible explanation is that infected thymocytes normally arise from progenitor cells which were infected in the bone marrow or spleen, and the cells restricted for Mo+PyF101 M-MuLV are located in those organs. Comparison of wild-type and Mo+PyF101 M-MuLV also allowed identification of important preleukemic changes in the thymus of wild-type M-MuLV-inoculated mice. Flow cytometry with monoclonal antibodies specific for thymocyte subpopulations was used. Staining of cells for Thy-1 or Thy-1.2 antigens indicated a shift toward low or negative cells. A concomitant increase in cells positive for antigen Pgp-1 was also observed. This is consistent with an increase in the relative frequency of immature blastlike cells. Importantly, thymuses from mice inoculated with Mo+PyF101 M-MuLV did not show these shifts in thymocyte subpopulations.

Animals↗
PubMed1986

Generation of infectious Moloney murine leukemia viruses with deletions in the U3 portion of the long terminal repeat.

Deletional analysis within the long terminal repeat (LTR) of Moloney murine leukemia virus (M-MuLV) was performed. By molecular cloning, deletions were made in the vicinity of the XbaI site at -150 base pairs (bp) in the U3 region, between the tandemly repeated enhancers and the TATA box. The effects of the deletions on LTR function were measured in two ways. First, deleted LTRs were fused to the bacterial chloramphenicol acetyltransferase gene and used in transient expression assays. Second, infectious M-MuLVs were generated by transfection of M-MuLV proviruses containing the deleted LTRs, and the relative infectivity of the mutant viruses was assessed by XC-syncytial assay. Most of the deleted LTRs examined showed relatively high promoter activity in the transient chloramphenicol acetyltransferase assays, with values ranging from 20 to 50% of the wild-type M-MuLV LTR. Thus, the sequences between the enhancers and the TATA box were not absolutely required for transient expression. However, infectivity of viruses carrying the same deleted LTRs showed more pronounced effects. Deletion of sequences from -195 to -174 bp reduced infectivity 20- to 100-fold. Deletion of sequences within the region from -174 to -122 bp did not affect infectivity, indicating that this region is dispensable. On the other hand, deletion of sequences from -150 to -40 bp reduced infectivity from 5 to 6 logs, although the magnitude of the reduction partly may have reflected threshold envelope protein requirements for positive XC assays. The reduced infectivity did not appear to result from a failure of proviral DNA synthesis or integration by the mutant. Thus, the infectivity measurements identified three functional domains in the region between the enhancers and the TATA box.

Animals↗
PubMed1985

Cytophagic histiocytic panniculitis. A variant of malignant histiocytosis.

This report describes a patient with cytophagic histiocytic panniculitis in which the aggressive use of chemotherapeutic agents resulted in an apparent remission. The histiocytic nature of the process was confirmed by immunohistochemical techniques. There are many similarities with malignant histiocytosis, and it is believed that this entity should be regarded as a variant of malignant histiocytosis.

Adipose Tissue↗
PubMed1985

Comparative observation of fibroblasts derived from the papillary and reticular dermis of infants and adults: growth kinetics, packing density at confluence and surface morphology.

We have confirmed the reports of Harper and Grove (Science, 204 (1979) 526-527), and Azzarone and Macierira-Coehlo (J. Cell Sci., 57 (1982) 177-187) that fibroblasts derived from the papillary dermis have greater in vitro growth potential and longer replicative lifespans than genomically identical fibroblasts derived from the reticular dermis. In addition we demonstrate that the kinetics of cell replication differ for papillary and reticular fibroblasts derived from infant and adult donors. Infant papillary fibroblasts replicate at faster rates than reticular fibroblasts throughout the growth cycle. Adult papillary and reticular fibroblasts replicate at similar rates at low cell densities, but exponential growth of reticular fibroblasts slows at lower cell densities than papillary fibroblasts suggesting that they are more sensitive to density-dependent inhibition of replication. The surface morphologies of reticular fibroblasts and papillary fibroblasts at confluence correlate with their growth kinetics. The decreased cell yields of reticular fibroblasts appears related to the spreading behaviors of individual cells which stretch and occupy more area of the growth surface than do papillary fibroblasts. These data and the reports cited clearly show that one must account for the presence of at least two distinct populations of dermal fibroblasts when examining their biological properties in vitro.

Adult↗
PubMed1985

Correlation between adherence to HeLa cells and serogroups, serotypes, and bioserotypes of Escherichia coli.

Four hundred fifty Escherichia coli strains of 45 O serogroups and subgroups and 112 serotypes were studied to determine their patterns of adherence to HeLa cells. Adherence was exhibited by strains of 17 O serogroups and subgroups, but within these groups more than one adherence pattern was frequently observed. However, within each serotype, the adherence pattern was highly consistent. Localized adherence (LA) was observed much more frequently in serotypes that we considered to be enteropathogenic E. coli serotypes (93%) than in other serotypes (14%), whereas diffuse adherence (DA) occurred predominantly among nonenteropathogenic E. coli strains. Determination of biochemical characteristics showed that within O serogroups, nonmotile strains tended to have the same behavior as motile strains with the LA adherence pattern, suggesting that they were derived from these motile strains. LA and non-LA strains of the same serotype differed biochemically. LA appears to be a property of most E. coli commonly considered to be enteropathogenic and should assist attempts to determine which E. coli are enteropathogenic and to elucidate their pathogenic mechanisms.

Adhesiveness↗
PubMed1985

Addition of three new serotypes of Shigella boydii to the Shigella schema.

No new serotypes have been added to the Shigella schema since 1958, although several provisional serotypes have been described. We conducted biochemical and serological studies on three provisional Shigella boydii serotypes. Four strains of serotype 2710-54 from four widely separated countries, 7 strains of serotype 3615-53 from three different countries, and 31 strains of serotype 1344-78 (E10163) from six different countries were included. Reactions of all three serotypes were consistent with those of S. boydii. On the basis of these results and other published research, we propose that these three provisional serotypes be admitted to the Shigella schema as S. boydii 16, 17, and 18.

Asia↗
PubMed1985

Biochemical identification of new species and biogroups of Enterobacteriaceae isolated from clinical specimens.

In 1972 there were only 11 genera and 26 species in the family Enterobacteriaceae. Today there are 22 genera, 69 species, and 29 biogroups or Enteric Groups. This paper is a review of all of the new organisms. It has a series of differential charts to assist in identification and a large chart with the reactions of 98 different organisms for 47 tests often used in identification. A simplified version of this chart gives the most common species and tests most often used for identification. The sources of the new organisms are listed, and their role in human disease is discussed. Fourteen new groups of Enterobacteriaceae are described for the first time. These new groups are biochemically distinct from previously described species, biogroups, and Enteric Groups of Enterobacteriaceae. The new groups are Citrobacter amalonaticus biogroup 1, Klebsiella group 47 (indole positive, ornithine positive), Serratia marcescens biogroup 1, and unclassified Enteric Groups 17, 45, 57, 58, 59, 60, 63, 64, 68, and 69.

Adult↗
PubMed1985

Escherichia fergusonii and Enterobacter taylorae, two new species of Enterobacteriaceae isolated from clinical specimens.

Escherichia fergusonii (formerly known as Enteric Group 10) and Enterobacter taylorae (formerly known as Enteric Group 19) are proposed as new species in the family Enterobacteriaceae. By DNA hybridization (32P, 60 degrees C, hydroxyapatite), strains of E. fergusonii were 90 to 97% related to the type strain (holotype) ATCC 35469. They were most closely related to Escherichia coli and more distantly related to species in other genera. E. fergusonii strains are positive for indole production, methyl red, lysine decarboxylase, ornithine decarboxylase, and motility. They ferment D-glucose with gas production and also ferment adonitol, L-arabinose, L-rhamnose, maltose, D-xylose, trehalose, cellobiose, and D-arabitol. They are negative for Voges-Proskauer, citrate utilization (17% positive), urea hydrolysis, phenylalanine deamination, arginine dihydrolase, growth in KCN, and fermentation of lactose, sucrose, myo-inositol, D-sorbitol, raffinose, and alpha-methyl-D-glucoside. By DNA hybridization (32P, 60 degrees C, hydroxyapatite), strains of E. taylorae were 84 to 95% related to the type strain (holotype) ATCC 35317. Their nearest relative was E. cloacae, to which they were 61% related. Other named species were more distantly related. Strains of E. taylorae are positive for Voges-Proskauer, citrate utilization, arginine dihydrolase, ornithine decarboxylase, motility, growth in KCN medium, and malonate utilization. They ferment D-glucose with gas production and also ferment D-mannitol, L-arabinose, L-rhamnose, maltose, D-xylose, trehalose, and cellobiose. They are negative for indole production, methyl red, H2S production on triple sugar-iron agar, urea hydrolysis, phenylalanine deamination, lysine decarboxylase, gelatin hydrolysis, and fermentation of adonitol, i-inositol, D-sorbitol, and raffinose. Both new species occur in human clinical specimens. Two strains of E. fergusonii were isolated from blood. Five stains of E. taylorae were isolated from blood, and one was from spinal fluid. These blood and spinal fluid isolates suggest possible clinical significance, but this point requires further study.

Aged↗
PubMed1985

H7 antiserum-sorbitol fermentation medium: a single tube screening medium for detecting Escherichia coli O157:H7 associated with hemorrhagic colitis.

Escherichia coli serotype O157:H7 has been isolated from outbreaks and sporadic cases of hemorrhagic colitis. There is convincing evidence that it can cause this diarrheal disease. Because of the interest in hemorrhagic colitis, it has become desirable to detect this particular strain in human feces, which usually contains many other strains of E. coli. Two characteristics of the incriminated E. coli O157:H7 strain have made its isolation and identification easier. It does not ferment D-sorbitol rapidly, in contrast to about 95% of other E. coli strains. In addition, the strain has H antigen 7, but only about 10% of other E. coli strains have this particular antigen. To screen for E. coli O157:H7 we devised H7 antiserum-sorbitol fermentation medium (18 g of enteric fermentation base, 10 g of D-sorbitol, 4 g of agar, 10 ml of Andrade indicator, 989 ml of water; all ingredients were mixed, autoclaved, and cooled; 1 ml of E. coli H7 antiserum was then added). Colonies to be screened were inoculated into this medium. Strains of E. coli O157:H7 gave a characteristic pattern; they did not ferment sorbitol and were immobilized in the semisolid medium because of the reaction of their flagella with the flagella antiserum. Almost all other strains of E. coli gave a different pattern; they fermented sorbitol or were not immobilized by the H7 serum or both. Strains which were presumptive positives (sorbitol negative, H7 positive) were then tested in E. coli O157 serum by slide or tube agglutination. The number of strains which were presumptive positive by H7-sorbitol medium but then were not found to be O157 was less than 1%. A second approach has been helpful in deciding which colonies to screen in H7-sorbitol medium. MacConkey-sorbitol agar (22.2 g MacConkey agar base [which contains no sugar], 10 g of D-sorbitol, 1,000 ml of water) was designed as a plating medium. Stools were plated on MacConkey agar to estimate the number of E. coli colonies and also plated on MacConkey-sorbitol agar to estimate the number of sorbitol-negative colonies of E. coli. These two approaches have proved useful for isolating and identifying E. coli O157:H7 form human feces and from feces of animals infected in the laboratory with this strain. The results suggest that media may be formulated in a similar fashion for detecting other specific strains of E. coli.

Agglutination Tests↗
PubMed1985

Generation of a recombinant Moloney murine leukemia virus carrying the v-src gene of avian sarcoma virus: transformation in vitro and pathogenesis in vivo.

A Moloney murine leukemia virus (M-MuLV) recombinant carrying the v-src gene of avian sarcoma virus was generated by the introduction of a cloned portion of v-src from Schmidt-Ruppin A avian sarcoma virus into a molecular clone of M-MuLV provirus at the recombinant DNA level. The v-src sequences (lacking a portion of the 5' end of v-src) were inserted into the p30 region of the M-MulV gag gene so that M-MuLV gag and v-src were in the same reading frame. Transfection of this chimeric clone, pMLV(src), into NIH 3T3 cells which were constitutively producing M-MuLV gag and pol protein resulted in the formation of foci of transformed cells. Infectious and transforming virus could be recovered from the transformed cells. This virus was designated M-MuLV(src). M-MuLV(src)-transformed cells contained two novel proteins of 78 and 90 kilodaltons. The 78-kilodalton protein, p78gag-src, contained both gag and src determinants, exhibited kinase activity in an immune kinase assay, and is probably a fusion of Pr65gag and src. The 90-kilodalton protein, which is of the appropriate size to be the gPr80gag fused to src, contained gag determinants as well as a V8 protease cleavage fragment typical of the carboxy terminus of avian sarcoma virus pp60src. However, it could not be immunoprecipitated with an anti-v-src serum. M-MuLV(src)-transformed cells showed elevated levels of intracellular phosphotyrosine in proteins, although the elevation was intermediate compared with cells transformed with wild-type v-src. M-MuLV and amphotropic murine leukemia virus pseudotypes of M-MuLV(src) were inoculated into newborn NIH Swiss mice. Inoculated mice developed solid tumors at the site of inoculation after 3 to 6 weeks, with most animals dying by 14 weeks. Histopathological analysis indicated that the solid tumors were mesenchymally derived fibrosarcomas that were both invasive and metastatic.

Amino Acids↗
PubMed1984

A multistate outbreak of infections caused by Yersinia enterocolitica transmitted by pasteurized milk.

In June and July 1982, a large interstate outbreak of Yersinia enterocolitica infections caused by an unusual serotype occurred in Tennessee, Arkansas, and Mississippi. Eighty-six percent of cases had enteritis characterized by fever, abdominal pain, and diarrhea. In three separate case-control studies, drinking milk pasteurized by plant A was statistically associated with illness. In a survey of randomly chosen households, 8.3% of persons who recalled having drunk milk from plant A during the suspect period experienced a yersiniosislike illness. Inspection of the plant and cultures of the available raw and pasteurized milk did not reveal the source or mechanism of contamination or a breach in normal pasteurizing technique. Although outbreaks of enteric disease caused by pasteurized milk are rare in the United States, the ability of Y enterocolitica to grow in milk at refrigeration temperatures makes pasteurized milk a possible vehicle for virulent Y enterocolitica. The extent to which milk is responsible for sporadic cases of yersiniosis is unknown.

Adolescent↗
PubMed1984

Sporadic cases of hemorrhagic colitis associated with Escherichia coli O157:H7.

After two outbreaks of hemorrhagic colitis associated with a previously unrecognized pathogen, Escherichia coli O157:H7, a surveillance system was established to identify and study sporadic cases of this distinct clinical illness in the United States. Between August 1982 and April 1984, we identified 28 persons from 11 states who met our case definition and whose stool specimens yielded E. coli O157:H7. Patients ranged in age from 1 to 80 years. Seventeen patients required hospitalization. All patients recovered, although one developed hemolytic-uremic syndrome 7 days after the onset of bloody diarrhea. Detection of E. coli O157:H7 in stools from persons with hemorrhagic colitis was highly associated with collection of stool specimens within the first 6 days after onset of illness. All E. coli O157:H7 isolates produced a Vero cytotoxin. Hemorrhagic colitis caused by E. coli O157:H7 is widely distributed in the United States as a sporadic illness; clinicians should be aware of its distinctive clinical presentation, and should collect specimens promptly when the diagnosis is suspected.

Adolescent↗