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Biomedical subjects

C A Kennedy

Publications and source records attributed to C A Kennedy.

At least 55 records · Page 3Linked to original sources
PubMed1992

Large erythematous patch as the presenting manifestation of meningococcemia.

Meningococcemia commonly presents with a petechial rash and a transient macular or papular rash is sometimes present. This report describes a patient with meningococcemia who presented with an atypical erythematous patch over the right hemithorax, petechial rash, and a normal platelet count. The patient was treated with broad-spectrum antibiotics and his condition rapidly improved. He was discharged showing complete resolution of his rash with no neurologic sequelae.

Adult↗
PubMed1992

Atypical roentgenographic manifestations of Pneumocystis carinii pneumonia.

Although Pneumocystis carinii pneumonia (PCP) usually presents with bilateral interstitial pulmonary infiltrates, many other roentgenographic presentations occur in human immunodeficiency virus-infected patients. To clarify the determinants of atypical presentations of PCP, we evaluated 65 English-language reports that related the roentgenographic manifestations of consecutive cases of PCP. The incidence of PCP-associated upper lobe disease, cysts, and spontaneous pneumothoraxes was increased in human immunodeficiency virus-infected patients receiving aerosolized pentamidine prophylaxis. Normal chest roentgenograms were more common and nodular lesions were less common in human immunodeficiency virus-infected patients than in uninfected patients. However, the roentgenographic manifestations of PCP could not be specifically predicted by a patient's underlying disease. Neither zidovudine therapy nor intravenous drug use apparently affected the roentgenographic presentation of PCP. Unusual pathologic responses to PCP, including granuloma formation, vascular invasion, and microscopic foci of calcification, were present in all patient groups.

HIV Infections↗
PubMed1991

Pneumothorax in AIDS.

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Acquired Immunodeficiency Syndrome↗
PubMed1991

The management of HIV-related illness in the emergency department.

As the AIDS epidemic progresses, the number of ED patients with HIV-related illness will continue to increase. As reviewed in this article, much of the existing clinical research in HIV-related illness has an impact on the diagnostic and management issues that arise in the ED. Many of the patterns of disease, subtleties of diagnosis, and therapies unique to AIDS patients have already been greatly elucidated. However, as the recognition of this disease goes into only its second decade, many questions remain. Further studies are needed, for example, to improve physician assessment of HIV risk, to further identify discriminators of PCP and bacteremia, and to optimize strategies for disposition and outpatient management. In the future, in the areas of research and clinical care, emergency medicine will play an increasing important role in the front-line attack on this modern epidemic.

Bacteremia↗
PubMed1991

Staphylococcal pyomyositis in patients infected by the human immunodeficiency virus.

PURPOSE: We describe the manifestations of spontaneous staphylococcal pyomyositis in patients infected by the human immunodeficiency virus (HIV). PATIENTS AND METHODS: We present the courses of five previously unreported patients infected by HIV who presented to our medical centers with spontaneous staphylococcal pyomyositis. Additionally, we review all previously reported cases of this entity in HIV-infected patients and discuss its possible pathogenesis and importance in the context of HIV infection. RESULTS: All patients presented with gradually developing fever and localized pain and swelling without accompanying leukocytosis. Often only scant evidence of local inflammation was found. None of our patients used intravenous drugs, had a history of trauma, had HIV- or zidovudine-related myositis, or had other conditions known to be associated with serious staphylococcal infections. Two patients studied had normal serum levels of all IgG subclasses. Elevated serum IgE, eosinophilic inflammatory infiltrates, or marked peripheral eosinophilia was observed in two patients. CONCLUSIONS: Staphylococcal pyomyositis in HIV-infected patients presents in an indolent fashion, which may delay appropriate diagnosis and treatment. Since staphylococcal pyomyositis is infrequently reported in the United States, the development of 14 such cases (five in this series and nine previously reported) among the first 140,000 cases of acquired immunodeficiency syndrome in this country implies that this patient population is predisposed to this infectious complication. The pathogenesis of this entity is uncertain, but it is notable that HIV-infected patients are commonly colonized by Staphylococcus aureus and that neutrophils from HIV-infected patients frequently manifest phagocytic, chemotactic, and oxidative defects, diminished expression of Fc tau RIII (CD16) and CR1, and impaired bactericidal activity against S. aureus.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Binding of the T cell activation monoclonal antibody Ta1 to dipeptidyl peptidase IV.

The monoclonal antibodies, Ta1 and IOT15, define T cell activation cell surface markers and have been assigned to the CD26 leukocyte differentiation antigen cluster. Dipeptidyl peptidase IV (DPP IV, EC 3.4.14.5) is an exoaminopeptidase that, among leukocytes, is expressed almost exclusively on activated T cells. Comparative binding studies showed that the Ta1 mAb binds to DPP IV purified from human placenta as well as in extracts of the human YT lymphoid cell line and of CD3 stimulated normal human peripheral blood mononuclear cells. The mAb IOT15 did not bind to DPP IV from any source even upon repeated incubations. Western blot analysis of YT cell extracts revealed that Ta1 and IOT15 bound to distinctly different molecular weight molecules. Immunofluorescent cell surface capping experiments showed that capping of the IOT15 did not alter the surface distribution of the Ta1 fluorescence. The capping results combined with the DPP IV binding results indicate that IOT15 and Ta1 mAb's bind to different, apparently unassociated, molecules on the surface of T cells and that only Ta1 binds the T cell surface enzyme DPP IV.

Antibodies, Monoclonal↗
PubMed1989

Structure of the human CR1 gene. Molecular basis of the structural and quantitative polymorphisms and identification of a new CR1-like allele.

Structural and quantitative polymorphisms have been described in human CR1. In the former, the S allotype is larger than the F allotype by 40-50 kD, the size of a long homologous repeat (LHR). In the latter, homozygotes for a 7.4-kb Hind III fragment express fourfold more CR1 per erythrocyte than do homozygotes for the allelic 6.9-kb restriction fragment. The basis for these genomic polymorphisms has been determined by restriction mapping the entire S allele and part of the F allele. The S allele is 158 kb and contains 5 LHRs of 20-30 kb, designated -A, -B/A, -B, -C, and -D, respectively, 5' to 3'. Extensive homology was found among the LHRs in their restriction maps, exon organization, and the coding and noncoding sequences. The presence of LHR-B/A in the S allele but not in the F allele accounts for the longer transcripts and polypeptide associated with the former allotype. At least 42 exons are present in the S allele, with distinct exons for the leader sequence, the transmembrane and cytoplasmic regions and most of the SCRs comprising the extracellular portion of CR1. Consistent with the mapping of the ligand binding site to the first two SCRs in each LHR, the second SCRs in LHR-A, -B/A, -B, and -C are encoded by two exons, reflecting a specialized function for this unit. The allelic 7.4/6.9-kb Hind III fragments extend from the 3' region of LHR-C to LHR-D. The 6.9-kb restriction fragment is the result of a new Hind III site generated by a single base change in the intron between the exons encoding the second SCR of LHR-D. A second cluster of genomic clones has been identified by hybridization to CR1 probes. Although they contain regions of hybridization to the cDNA and genomic probes derived from CR1, these cannot be overlapped with the structural gene owing to their distinct restriction maps. Three genomic polymorphisms previously identified by CR1 cDNA probes map to this region. These additional clones may represent part of a duplicated allele located nearby within the CR1 locus.

Alleles↗
PubMed1987

Correlation of changes in pulmonary surfactant phospholipids with compliance in bleomycin-induced pulmonary fibrosis in the rat.

Qualitative and quantitative analysis was performed on phospholipids isolated from bronchoalveolar lavage fluid during the development of pulmonary fibrosis in the rat. A single transtracheal injection of 2.0 units of bleomycin was administered to rats to induce lung injury. Animals were killed at 0, 3, 7, 14, 30, and 120 days after bleomycin treatment. Total lipid phosphorus in BAL from animals given bleomycin increased from 1.6 mumol/lung in normal animals to 3.2 mumol/lung at 14 and 30 days. The increase in phospholipids was primarily in phosphatidylcholine with minor increases in phosphatidylinositol and phosphatidylethanolamine. These quantitative changes were accompanied by qualitative changes that included an increase in the percentage of total phosphatidylcholine, disaturated phosphatidylcholine, and phosphatidylinositol. In contrast, the percentage of phosphatidylglycerol was significantly reduced. Plasma phospholipid analysis indicated that these alterations were not due to plasma contamination. The functional significance of the phospholipid changes was assessed by comparing air- and saline-filled compliance measurements at similar times after bleomycin. Abnormal compliance measurements were observed at 3, 7, and 14 days after bleomycin. At 3 and 7 days the predominant compliance defect was at the air-liquid interface; however, at 14 days, when phospholipids were significantly elevated, the defect was primarily due to tissue components.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Analysis of multiple restriction fragment length polymorphisms of the gene for the human complement receptor type I. Duplication of genomic sequences occurs in association with a high molecular mass receptor allotype.

Human CR1 exhibits an unusual form of polymorphism in which allotypic variants differ in the molecular weight of their respective polypeptide chains. To address mechanisms involved in the generation of the CR1 allotypes, DNA from individuals having the F allotype (250,000 Mr), the S allotype (290,000 Mr), and the F' allotype (210,000 Mr) was digested by restriction enzymes, and Southern blots were hybridized with CR1 cDNA and genomic probes. With the use of Bam HI and Sac I, an additional restriction fragment was observed in 20 of 21 individuals having the S allotype with no associated loss of other restriction fragments. Southern blot analysis with a noncoding genomic probe derived from the S allotype-specific Bam HI fragment showed hybridization to this fragment and to two other fragments that were also present in FF individuals. Thus, an intervening sequence may be repeated twice in the F allele and three times in the S allele. A restriction fragment length polymorphism (RFLP) unique to two individuals expressing the F' allotype was seen with Eco RV, but the absence of persons homozygous for this rare allotype prevented further comparisons with the F and S allotypes. Analysis of the CR1 transcripts associated with the three CR1 allotypes indicated that these differed by 1.3-1.5 kb and had the same rank order as the corresponding allotypes. Taken together, these findings suggest that the S allele was generated from the F allele by the acquisition of additional sequences, the coding portion of which may correspond to a long homologous repeat of approximately 1.4 kb that has been identified in CR1 cDNA. We saw two other RFLPs with Hind III and Pvu II that were in linkage dysequilibrium with the Bam HI-Sac I RFLPs associated with the S allotype, and a third polymorphism was seen with Eco RI that was not in linkage dysequilibrium with the other polymorphisms. Thus, 10 commonly occurring CR1 alleles can be defined, making this locus a useful marker for the long arm of chromosome 1 to which the CR1 gene maps.

Alleles↗
PubMed1985

Rapid purification of the human C3b/C4b receptor (CR1) by monoclonal antibody affinity chromatography.

The human C3b/C4b receptor (CR1) is a polymorphic glycoprotein that is expressed on erythrocytes, leukocytes and glomerular podocytes. Further structural analysis and molecular genetic studies would be facilitated by the availability of relatively larger amounts of purified CR1. Milligram quantities of CR1 were purified from erythrocyte membranes 10,000-fold with an average yield of 30-40% by a rapid procedure which utilized sequential chromatography on Matrex Red A and a monoclonal anti-CR1 antibody affinity column. The purified receptor was homogeneous by SDS-PAGE and consisted of the 2 most common alleles of CR1. Purified CR1 also retained its function of serving as a cofactor for the cleavage of C3b to iC3b, C3dg and C3c. The amino acid composition was typical of that of a globular protein and sequence analysis of the N-terminus of the purified CR1 revealed that it was blocked.

Amino Acid Sequence↗
PubMed1984

Infants with birth weights less than 1,001 g. Survival, growth, and development.

Of 56 infants weighing less than 1,001 g who were born in 1980, 30 (54%) survived the neonatal period and 29 (52%) survived the first year. At 12 to 16 months of age, 44% of the measured survivors were below the fifth weight percentile and 32% were below the fifth head circumference percentile for their adjusted ages. Of the first-year survivors, 21 (72%) were developmentally normal, four (14%) were mildly handicapped, and four (14%) were moderately to severely handicapped at 12 to 34 months of age. Handicapped infants differed significantly from normal infants in their neonatal requirements for mechanical ventilation, but did not differ in birth weight, gestational age, route of delivery, Apgar scores, maternal age or marital status, maternal education or income, gender, race, place of birth, or proportions below the tenth percentile in weight or head circumference at birth.

Age Factors↗