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Biomedical subjects

V L Moore

Publications and source records attributed to V L Moore.

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

Studies on the quantification of proteoglycans by the dimethylmethylene blue dye-binding method. Specificity, quantitation in synovial lavage fluid, and automation.

The dimethylmethylene blue (DMMB) dye-binding technique is widely used for the quantification of sulfated glycosaminoglycans (sGAG) and proteoglycans. We conducted further studies on this technique in our laboratory and found that concentrations of DNA and RNA in excess of 20 micrograms/ml interfered negatively with the detection of sGAGs; interference was eliminated by using DNase and RNase. Hyaluronan at 40 micrograms per ml did not interfere with the detection of sGAG. However, because of the higher concentrations of hyaluronan in synovial lavage fluid, it was necessary to treat this fluid with Streptomyces hyaluronidase in order to quantify sGAG. The DMMB assay was automated with a laboratory work station and compared to the standard method.

Animals↗
PubMed1990

In vivo activity of human recombinant tissue inhibitor of metalloproteinases (TIMP). Activity against human stromelysin in vitro and in the rat pleural cavity.

Recombinant human tissue inhibitor of metalloproteinase (rhTIMP) suppressed the ability of native human stromelysin to degrade [3H]transferrin in vitro. Maximum inhibition occurred at molar ratios (TIMP: stromelysin) of 2:1 and 1:1. Reduced and alkylated tissue inhibitor of metalloproteinases (TIMP) lost its ability to suppress stromelysin activity. rhTIMP also inhibited stromelysin from degrading proteoglycan monomer in vitro. When injected into the rat pleural cavity prior to stromelysin, rhTIMP inhibited the ability of the enzyme to degrade aggregating cartilage proteoglycan monomer. Marked inhibition of stromelysin-mediated proteoglycan degradation in vivo occurred at molar ratios (TIMP: enzyme) of 2:1 and 1:1, with less inhibition at molar ratios of 0.5:1 and 0.25:1. Reduction and alkylation prevented rhTIMP from suppressing stromelysin-mediated degradation of proteoglycan monomer in vivo. By comparison, an equimolar concentration of the serine proteinase inhibitor, alpha 1-proteinase inhibitor (alpha 1-PI), did not inhibit stromelysin activity in the rat pleural cavity. This study demonstrates that rhTIMP is effective in inhibiting native human stromelysin both in vitro and in vivo.

Animals↗
PubMed1990

Surgical intervention in children with human immunodeficiency virus infection.

Twenty-one children with human immunodeficiency virus (HIV) infection required surgical intervention during the course of their disease. There were 11 females and 10 males (age range, 3 months to 6 years). The children underwent 54 operative procedures after diagnosis of their disease. These included placement of central venous catheter (23 patients), open lung biopsy (11), incision and drainage of perirectal abscess (4), incision and drainage of soft tissue abscess (5), myringotomy (2), diverting colostomy (3), Nissen fundoplication (1), and other (5). All 21 patients had clinical AIDS by the Centers for Disease Control CDC classification. To date, there have been 12 deaths in the 21 patients (57%) due to progressive deterioration with the patient's disease. Most procedures were adjuncts for diagnostic and therapeutic intervention in a population of children with a uniformly fatal disease. The knowledge of various high risk groups for AIDS must heighten the surgeon's awareness to the growing and significant pediatric segment of the HIV population, the complications of their disease, and the surgeon's limited role in treating these problems.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Characteristics of pediatric firearm fatalities.

An increase in the awareness of the problem of gunshot fatalities in children has occurred nationwide over the last year. Unintentional firearm deaths are more common among children and young adults. These deaths may be addressed by preventive measures beyond those available for pediatric firearm suicide and homicide. This study focuses on the incidence of fatal gunshot injuries in children under 16 years of age during the years 1979 through 1987 in our state. Over the past 9 years 132 children (0 to 16 years) were shot and killed as a result of firearm injuries (M:F ratio, 3:1). No difference in absolute number in racial distribution existed. Deaths were classified as homicide, 61 (46%); accidental, 33 (25%); suicide, 29 (22%); undetermined, 7 (5%); and other, 2 (1.5%). Over 70% of these fatal injuries occurred in the home environment. Types of weapons involved included handguns (48%), shotguns (22%), rifles (17%), unspecified weapon (12%), and air rifle (1%). In a large number of cases, guns were found in the home unsecured. The perpetrator was known by the victim in 64 instances, while unknown in 27. Thirty-nine self-inflicted wounds and two shotgun blasts in the line of fire accounted for the remaining deaths. The most common anatomical injury and ultimate cause of death was cranial central nervous system (CNS) (62%), followed by chest/mediastinum (20%), abdomen (10%), and other (8%). A child who has sustained a firearm injury is more likely to know the perpetrator, be killed in the home by a readily available unsecured firearm, and die from severe head injury.

Accidents, Traffic↗
PubMed1989

Flow cytometric DNA analysis of primary and concurrent metastatic squamous cell carcinoma of the head and neck.

Adequate flow cytometric DNA analysis comparing primary and concurrent metastatic squamous cell carcinoma of the head and neck has not been done in the past. The purpose of this study was to define any differences between the primary and concurrent metastasis of each patient with respect to flow cytometric parameters and histologic grade. Paraffin-embedded archival specimens from 28 patients with primary and metastatic tumors were prepared into nuclei and analyzed by flow cytometry using human lymphocyte standards. The mean DNA index was 0.82 for primary tumors and 0.83 for the metastases. Aneuploidy was found in 68 percent of primary tumors and in 82 percent of metastases. The percentage of cells in the proliferative fraction was 40.4 in the primary tumors and 24.5 in the metastases. A direct correlation was found between the differentiation of the primary and metastatic tumors. No survival difference was discovered among the flow cytometric parameters and histologic grade. We conclude that there is no difference between the primary and concurrent metastasis in squamous cell carcinoma of the head and neck with regard to DNA index, aneuploidy, or histologic grade.

Aneuploidy↗
PubMed1989

Accessory cell function of human alveolar macrophages in antigen-induced T lymphocyte proliferation.

We compared the accessory cell function of human alveolar macrophages (AM) to that of human blood monocytes (Mo) obtained by bronchoalveolar lavage and venipuncture from normal volunteers. Graded numbers of either AM or Mo were added to autologous peripheral blood T lymphocytes that were stimulated with a purified protein derivative of tuberculin (PPD). Either AM or Mo were cocultured with allogeneic T lymphocytes in mixed lymphocyte reaction (MLR) experiments. Both AM and Mo supported the PPD-induced T lymphocyte proliferation and allogeneic MLR at low ratios of AM or Mo to T lymphocytes with similar efficiency. However, AM showed marked suppressive effects at higher ratios of AM to T lymphocytes (1:1). PPD-pulsed AM, but not AM killed by physical treatments (heat, freeze-thaw, sonication), induced T lymphocyte proliferation. An indirect immunofluorescent study demonstrated that most AM express HLA-DR antigens. Furthermore, AM synthesized DR antigens with molecular weights of 33,000 and 29,000-31,000 daltons. When AM were treated with both anti-DR monoclonal antibody and complement, PPD-induced T lymphocyte proliferation and MLR were diminished. These results suggest that human AM function as accessory cells in the antigen-induced T lymphocyte proliferation and DR antigens on AM play an important role in the accessory cell function.

Antibodies, Monoclonal↗
PubMed1984

Hypersensitivity pneumonitis in rabbits. Modulation of pulmonary inflammation by long-term aerosol challenge with antigen.

Immunized rabbits that were aerosol challenged for 2 to 3 wk with pigeon dropping extract, an etiologic agent of hypersensitivity pneumonitis, developed chronic pulmonary inflammation associated with cell-mediated immunity in bronchoalveolar cells. However, prolonged aerosol challenge for 12 wk resulted in the diminution of pulmonary inflammation (modulation) and the loss of demonstrable cell-mediated immunity. This was probably not due to loss of sensitized lymphocytes that mediated pulmonary inflammation. Furthermore, rabbits undergoing modulation when they were challenged with an unrelated antigen were refractory to the development of pulmonary inflammation for at least 9 wk. After this refractory period, animals reimmunized and aerosol challenged with pigeon dropping extract displayed an anamnestic response and produced pulmonary lesions that were strikingly similar to the histopathology of human hypersensitivity pneumonitis.

Aerosols↗
PubMed1983

Chronic pulmonary inflammation modulates the fate of proteins administered by the respiratory tract. Organ distribution of radiolabeled proteins.

In a previous report we found that, following intrapulmonary administration of radiolabeled albumin, blood concentrations were higher in rabbits with BCG-induced chronic pulmonary inflammation (CPI) than in normal rabbits. The present study demonstrates that this increased blood concentration was not the result of decreased blood clearance by other organs, indicating that increased absorption through the respiratory tract occurred in the inflamed lungs. In addition, rabbits with BCG-induced CPI had larger hilar lymph nodes and larger concentrations of radioactivity in the hilar lymph nodes, suggesting that the pulmonary lymphatics are a route of increased absorption through inflamed lungs.

Animals↗
PubMed1983

Genetic control of BCG-induced granulomatous inflammation in mice.

The genetics of BCG-induced pulmonary granulomatous inflammation (PGI) and splenomegaly was studied by breeding experiments and by the use of BXD recombinant inbred (RI) and allotype-congenic mice. Breeding studies indicated that the genetic control was multifactorial; this observation was confirmed using BXD RI mice. In addition, studies with BXD RI mice suggested that genes linked to the Igh complex influence responsiveness. The influence of the Igh-linked genes was studied further using allotype-congenic mice; SJL mice (Ighb) developed significantly greater PGI than their congenic partner, SJA/9 (Igha). Data from BALB.Igb, CB-20, and BAB-14 mice suggested that Igh-linked genes influencing PGI were a considerable distance from Igh-1. Igh-linked genes that influence BCG-induced splenomegaly were located on the centrometric side of the Igh-1 locus. This was shown by data in which splenomegaly in BALB.Igb and CB-20, but not BAB-14, mice was significantly augmented over BALB/c mice. Further studies are necessary to understand the significance of these observations.

Animals↗
PubMed1983

Immunogenetics of BCG-induced anergy in mice. Control by Igh- and H-2-linked genes.

We previously reported that BCG-induced anergy in mice (evaluated by delayed hypersensitivity to sheep erythrocytes) is unigenic and influenced by genes linked to the immunoglobulin heavy chain allotype (Igh). Using congenic mice (either H-2k or H-2b), we could not detect H-2-linked control of anergy. The current study re-examines this issue by using both BXD (H-2b or H-2d) and BXH (H-2b or H-2k) recombinant inbred (RI) mice as well as H-2 recombinant mice of different haplotypes. BXD RI (H-2b) mice were more anergic than BXD RI (H-2d) animals. Also, BXD RI (Ighb animals were more anergic than BXD RI (Ighc) mice. By evaluating combinations of H-2 haplotypes and Igh allotypes, we found the most anergic animals to be H-2b, Ighb. BCG-induced anergy then appears to be influenced by genes linked to both the H-2 and Igh complexes. BCG-induced anergy developed in H-2 recombinant mice (C57BL/10 background) that were either H-2b or H-2k, but not in H-2d animals. Experiments in the B10.A mouse suggested that genes within the H-2K through H-2I were influential. A more definitive map is presented of Igh-linked genes influencing anergy, suggesting that these genes are approximately 23 recombination units on the centromeric side of Igh-1 between Igh-Src and Lyb-7.

Animals↗
PubMed1982

Development of chronic pulmonary inflammation in immunized guinea pigs by aerosol challenge with antigen: relationship of immune complex disease and cell-mediated hypersensitivity.

Immunized guinea pigs develop immune complex disease (ICD) in the lungs after a single aerosol challenge with specific antigen. In the current study, immunized guinea pigs developed chronic pulmonary inflammation and cellular immunity (CI) in the lungs when aerosol challenged daily with specific antigen for 2 wk. When immune serum was passively transferred to normal recipients that were then aerosol challenged with specific antigen for 2 wk, chronic pulmonary inflammation and CI did not develop. These results suggest that ICD produced by passive transfer of serum and subsequent aerosol exposure to antigen was inadequate to cause chronic pulmonary inflammation and CI. The development of chronic pulmonary inflammation by aerosol challenge with antigen was suppresed with cobra venom factor. However, because of other studies, we attribute this suppression to the diminution of complement (C) factors in the alternative C pathway that affect macrophage mobility rather than to the depletion of C5a, which is important in the development of ICD.

Aerosols↗
PubMed1982

Effect of passive immunization on absorption of antigen through the respiratory tract.

Isolated perfused rabbit lungs were insufflated with 125I-labeled bovine serum albumin (125I-BSA) and the accumulation of radioactive BSA and its breakdown products was measured in the blood. The addition of anti-BSA serum to the blood caused a 4- to 6-fold reduction in the amount of 125I-BSA which appeared in the blood following the insufflation. To determine whether this reduction was the result of inhibition of absorption or the reuptake of 125I-BSA antigen-antibody complexes formed in the blood, we infused the 125I-BSA into the anti-BSA containing blood perfusing the lungs. Virtually none of the radioactivity was taken up by the lungs, indicating that the reduced blood levels following insufflation were the result of reduced absorption through the lung resulting from antigen-antibody interaction within the alveolocapillary membrane or the bronchoalveolar secretions.

Absorption↗
PubMed1982

Elevation of serum chemotactic factor inactivator activity during acute inflammatory reactions in patients with hypersensitivity pneumonitis.

Inflammatory mediators such as the vasoactive and chemotactic factors derived from the activation of the complement system are extremely potent biological peptides that are under rigid control of specific serum-derived regulators, e.g., the anaphylatoxin inactivator (AI) and the chemotactic factor inactivator (CFI). We have previously demonstrated that serum chemotactic factor inactivator concentrations are altered during chronic inflammatory states; here we demonstrate that a rapid elevation of serum CFI activity occurs during acute inflammatory reactions in patients suffering from hypersensitivity pneumonitis. Specifically, serum CFI concentrations were evaluated in patients with hypersensitivity pneumonitis (pigeon breeder's disease) and control subjects (asymptomatic) after aerosol challenge with 2 ml of sterile pigeon serum. At 4 h postchallenge, serum CFI concentrations in the patients with hypersensitivity pneumonitis increased rapidly to 3 times the prechallenge serum concentrations. Asymptomatic (control) subjects showed no increase in serum CFI concentrations after exposure to pigeon serum. In independent studies, we have also demonstrated that serum CFI concentrations are elevated in (1) rabbits with glycogen-induced peritonitis, (2) rabbits after intravenous infusion of C5-derived chemotactic factors, and (3) patients undergoing hemodialysis. These combined data clearly demonstrate that serum CFI activity is rapidly elevated during acute inflammatory reactions within both patient and animal populations, and suggest that serum CFI may represent a "hyperacute" phase reactant that is elevated during inflammation. Possibly, this elevation of CFI may be induced in response to inflammatory mediators produced during inflammation. Thus, the acute elevation of serum CFI concentrations that occurs during acute inflammation may represent the control system that would be responsive to the regulatory needs of the body during inflammatory reactions.

Alveolitis, Extrinsic Allergic↗
PubMed1982

Role of angiotensin-converting enzyme in Bacille Calmette-Guérin-induced granulomatous inflammation. Increased angiotensin-converting enzyme levels in lung lavage and suppression of inflammation with captopril.

Lung lavage levels of angiotensin-converting enzyme (ACE)-like activity were increased in C57BL/6 mice with Bacille Calmette-Guérin (BCG)-induced chronic granulomatous pulmonary inflammation and splenomegaly. Contrariwise, ACE activity was not increased in lung lavage fluids of CBA mice that developed only minimal pulmonary inflammation in response to BCG. ACE-like activity correlated with the intensity of inflammation and Captopril, a specific competitive inhibitor of ACE activity, markedly suppressed the induction and maintenance of the BCG-induced inflammatory response in both lungs and spleen. It was necessary, however, to provide sustained treatment with large doses of Captopril in order to reduce the inflammatory response. After a single intraperitoneal injection of Captopril, ACE levels in lung lavage of BCG-injected mice were reduced but returned to preinjection levels or greater within 24 h. The highest dose of Captopril was more effective in reducing the lung fluid level of ACE in BCG-inflamed lungs. This suggests that sustained daily injections of Captopril were necessary to maintain reduced ACE levels. In vitro studies indicated that high concentrations of Captopril did not affect macrophage mobility or chemotactic activity for macrophages. Thus, ACE may act as a molecular mediator of BCG-induced granulomatous inflammation in the lung.

Animals↗
PubMed1982

Immunogenetics of BCG-induced anergy in mice: control by genes linked to the Igh complex.

The genetics of BCG-induced anergy was studied in mice by evaluating delayed hypersensitivity to sheep erythrocytes. Data obtained using congenic mice and by linkage analysis suggested that genes linked to the H-2 complex do not influence the development of anergy. However, studies in allotype-congenic partners (BALB/c; BALB.Igb) indicated that anergy was influenced by genes linked to the immunoglobulin heavy chain complex (Igh). Breeding studies indicated that the gene influencing anergy is recessive. These studies were extended by using BXD recombinant inbred mice, and verified that anergy is controlled by genes linked to the Igh complex. Because several markers and a tentative map has been constructed for the Igh complex on chromosome 12 in BXD mice, we suggest that the gene that controls BCG-induced anergy is located on the centrometric side of Igh-C approximately 18 to 28 recombination units.

Animals↗