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Biomedical subjects

D C Anderson

Publications and source records attributed to D C Anderson.

At least 307 records · Page 17Linked to original sources
PubMed1989

Volume therapy in orthostatic transient ischemic attacks.

We report the case of an 83-year-old man with recurrent orthostatic transient ischemic attacks despite anticoagulation and crystalloid therapy. An initial cerebral angiogram revealed a nearly occluded right carotid artery with a string sign. Following aggressive volume expansion with albumin, the patient became asymptomatic. A second angiogram demonstrated the resolution of the carotid string sign and unmasked a high-grade, very tight, surgically approachable stenosis. The role of a high intravascular volume status is discussed.

Aged↗
PubMed1989

Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family.

The process of neutrophil adhesion to and migration through the microvascular endothelium, an early event in the induction of the acute inflammatory response, has been attributed to the generation of extravascular chemoattractants. Although both chemotactic peptides and lipid mediators enhance neutrophil adherence in vitro and in vivo, the mechanism(s) involved in the interaction between circulating neutrophils and microvascular endothelial cells is still not completely understood. In a microtiter well adherence assay, the chemotactic peptides, FMLP and C5a, and the lipid mediators, leukotriene B4 (LTB4) and platelet activating factor (PAF), enhanced human neutrophil adherence to cultured human microvascular endothelial cells as well as to human umbilical vein endothelial cells in a dose-dependent manner with a rapid time course. This stimulated adhesive interaction between neutrophils and cultured human endothelial cells was dependent on the expression of the Mac-1, LFA-1, p150,95 glycoprotein family on the neutrophil surface since neutrophils from patients with leukocyte adhesion deficiency, lacking surface expression of the adhesive glycoproteins, exhibited markedly diminished adherence to human endothelial cells in response to stimulation with chemotactic factors compared to normal control neutrophils. All four mediators enhanced expression of the glycoprotein family on the surface of normal neutrophils as determined by flow cytofluorimetry using a monoclonal antibody (TS1/18) to the glycoprotein common beta subunit. In addition, TS1/18 inhibited up to 100% the adherence of normal neutrophils to endothelial cells stimulated by maximal concentrations of FMLP, C5a, LTB4, or PAF. Moreover, HL-60 cells, human promyelocytic leukemia cells, neither increased glycoprotein surface expression nor adherence in response to stimulation. Thus, peptide and lipid mediators of the acute inflammatory response appear to enhance adherence of circulating neutrophils to the microvascular endothelium by a mechanism dependent on expression of the Mac-1, LFA-1, p150,95 glycoprotein family on the neutrophil surface.

Antigens, Differentiation↗
PubMed1989

Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophils in vitro.

The adherence of human neutrophils to human umbilical vein endothelial cells (HUVEC) is partially dependent on the CD11/CD18 family of glycoproteins on the neutrophil and ICAM-1 on the HUVEC. The CD18 heterodimer involved in this adherence was evaluated in vitro using subunit-specific monoclonal antibodies (MAbs). The adherence of unstimulated neutrophils to IL-1-stimulated HUVEC was significantly inhibited by anti-CD11a but not CD11b MAbs, while the adherence of fMLP-stimulated neutrophils was significantly inhibited by both anti-CD11a and -CD11b. Anti-CD11a, but not anti-CD11b MAbs, reduced the adherence of unstimulated neutrophils on purified ICAM-1 to the same low level untreated neutrophils exhibited on a control protein, glycophorin. Stimulation with fMLP significantly increased neutrophil attachment to purified ICAM-1, but not to the control protein. Anti-CD11b MAbs reduced this chemotactically augmented adherence to that of unstimulated neutrophils, and in combination with anti-CD11a MAbs reduced adherence to that on the control protein. The results in this report indicate that unstimulated neutrophils exhibit LFA-1-dependent attachment to ICAM-1, and chemotactic stimulation enhances the attachment of human neutrophils to ICAM-1 by a Mac-1-dependent process.

Adult↗
PubMed1989

HIV-1-stimulated expression of CD11/CD18 integrins and ICAM-1: a possible mechanism for extravascular dissemination of HIV-1-infected cells.

To identify mechanisms which might facilitate emigration of HIV-1-infected cells from the circulation, we studied the effect of HIV-1 infection on T lymphocyte and monocytoid cell expression of molecules involved in adherence and translocation of leukocytes across endothelial cell barriers. CD11a, CD18, and ICAM-1 were demonstrated on up to 80% of HIV-1-infected H9 T cells by flow cytometry; these molecules were not evident on uninfected H9. CD18 mRNA was detected in HIV-infected, but not in uninfected H9 T cells. Cell surface expression of CD11a and CD18, but not ICAM-1, was increased on HIV-infected, as compared to uninfected U937 and THP1 monocytoid cells. Increased cell surface expression of the leukocyte integrins was associated with a significantly increased tendency of HIV-infected monocytoid cells to adhere to human umbilical vein endothelial cell monolayers or aggregate homotypically. Preincubating the monocytoid cells with anti-CD18 or anti-CD11a or preincubating endothelial cells with anti-ICAM-1 suppressed these cell to cell interactions. These studies suggest that HIV-1 infection stimulates cell surface expression of molecules involved in leukocyte adherence and transendothelial migration in vitro. Similar mechanisms may influence leukocyte trafficking, in vivo, and may play a role in the localization of HIV-1 infected cells in the central nervous system and other tissues.

Antigens, Differentiation↗
PubMed1989

The prevalence of hyperlipidaemia and related clinical features in insulin-dependent diabetes mellitus.

The prevalence of hyperlipidaemia and related clinical features was examined in 205 individuals with insulin-dependent diabetes mellitus. Overall, 40 per cent (82) of the individuals had hyperlipidaemia. Whilst the prevalence of hypertriglyceridaemia and combined hyperlipidaemia was greater in patients with insulin-dependent diabetes mellitus than non-diabetics, this was not the case for hypercholesterolaemia. Hyperlipidaemia was present in older patients, and the daily insulin dose and levels of HbA1 were highest in those with combined hyperlipidaemia. In addition normolipidaemic subjects had the lowest levels of serum creatinine. Triglyceride levels were predicted (in order of importance) by insulin dose, age at diagnosis, HbA1 and body mass index, whilst cholesterol levels were predicted by the age at the time of study, body mass index, urinary protein excretion, and levels of fasting blood glucose and HbA1. Hyperlipidaemia is common in insulin-dependent diabetes mellitus, and may be particularly apparent in older patients and/or those with early renal dysfunction or poor glycaemic control.

Adult↗
PubMed1989

Neonatal neutrophil dysfunction.

Functional as well as quantitative abnormalities of neutrophilic granulocytes have been implicated in the pathogenesis of neonatal septicemia and other infectious complications in human neonates. Despite considerable previous investigation, the molecular basis for observed abnormalities of inflammatory functions of neonatal neutrophils is not well understood. The development of novel preventative or therapeutic strategies for high-risk neonatal populations will depend upon further investigations to delineate the fundamental basis of abnormal cellular events.

Chemotaxis, Leukocyte↗
PubMed1988

A Mycobacterium leprae-specific human T cell epitope cross-reactive with an HLA-DR2 peptide.

Mycobacterium leprae induces T cell reactivity and protective immunity in the majority of exposed individuals, but the minority that develop leprosy exhibit various types of immunopathology. Thus, the definition of epitopes on M. leprae antigens that are recognized by T cells from different individuals might result in the development of an effective vaccine against leprosy. A sequence from the 65-kD protein of this organism was recognized by two HLA-DR2-restricted, M. leprae-specific helper T cell clones that were derived from a tuberculoid leprosy patient. Synthetic peptides were used to define this epitope as Leu-Gln-Ala-Ala-Pro-Ala-Leu-Asp-Lys-Leu. A similar peptide that was derived from the third hypervariable region of the HLA-DR2 chain, Glu-Gln-Ala-Arg-Ala-Ala-Val-Asp-Thr-Tyr, also activated the same clones. The unexpected cross-reactivity of this M. leprae-specific DR2-restricted T cell epitope with a DR2 peptide may have to be considered in the design of subunit vaccines against leprosy.

Amino Acid Sequence↗
PubMed1988

Exact definition of species-specific and cross-reactive epitopes of the 65-kilodalton protein of Mycobacterium leprae using synthetic peptides.

With the use of solid phase synthesis of peptides corresponding to major and minor peaks in a Hopp-Woods hydrophilicity plot, the epitopes for 10 of 14 known different mAb to the Mycobacterium leprae 65-kDa protein, a prominent T and B cell Ag of this bacillus, have been located in the primary structure. Five epitopes have been precisely mapped by using the synthetic peptides in inhibition ELISA experiments, and five others have been located on peptides of 22 amino acids or less in length. The epitope of an important species-specific antibody, IIIE9, which may be useful for seriodiagnosis of leprosy, appears to be distinguished from the epitope of the antibody IVD2, widely cross-reactive among mycobacteria, not by its sequence, but only by its critical residues. All epitopes studied appear continuous insofar as can be determined by this approach.

Amino Acid Sequence↗
PubMed1988

Primates.

Nonhuman primates demonstrate marked similarities to humans in almost all aspects of their anatomy, endocrinology, and physiology. These similarities underlie the value of these animals for appropriate studies in neurobiology, immunology, pathology, reproductive biology, teratology, neonatology, endocrinology, cardiology, and psychology. Investigations with nonhuman primates has made, and continues to make, significant contributions to biomedical and behavioral research. This review provides an overview of basic and applied studies for which primates are appropriate subjects and a summary of the advantages and problems of using nonhuman primates in research.

Aging↗
PubMed1988

Single dose versus daily intravenous aminohydroxypropylidene biphosphonate (APD) for the hypercalcaemia of malignancy.

Thirty patients with hypercalcaemia and known malignant disease were randomly allocated to receive 60 mg 3-amino-1-hydroxypropylidene-1,1-bisphosphonate (APD) intravenously as a single dose or as consecutive daily doses of 30 mg (two days) or 15 mg (four days). The rate of infusion was the same for each regimen (7.5 mg/hour). Calcium concentrations fell in all patients and returned to normal in all but two. Relapse of hypercalcaemia occurred after a mean of 21 days in each group. Urinary calcium excretion fell in all groups and symptoms were greatly improved. After relapse patients were retreated with APD (30 mg as a single infusion) and normocalcaemia maintained by regular infusions at two to three week intervals. APD given as a single 60 mg infusion over eight hours together with rehydration is recommended as the initial management of the hypercalcaemia of malignancy, followed by 30 mg APD roughly every two to three weeks to maintain normal or near normal serum calcium concentrations.

Calcium↗
PubMed1988

Delayed traumatic midbrain syrinx. Clinical, pathologic, and electrophysiologic features.

Seven months following severe crushing closed-head trauma with initial excellent recovery, neurologic deficits referable to the right mesencephalon abruptly developed in a 28-year-old man. Computed tomography demonstrated a cystic midbrain lesion with apparent communication with the aqueduct (later confirmed at autopsy). Brain-stem auditory evoked potentials after the clinical deterioration showed depression of amplitude of wave V, compared with predeficit records, only when the ear contralateral to the brain-stem lesion was stimulated.

Adult↗
PubMed1988

Quantitation of intracellular Mac-1 (CD11b/CD18) pools in human neutrophils.

The adhesive glycoprotein Mac-1 (CD11b/CD18) of the CD11/CD18 complex contributes to multiple neutrophil inflammatory functions. Activation of neutrophils by chemotactic stimuli results in a rapid, protein synthesis-independent increase in surface Mac-1 derived from incompletely defined intracellular compartments. Therefore, we developed a novel quantitative lectin immunoblot technique to define intracellular pools of Mac-1 in subcellular neutrophil fractions resolved on discontinuous Percoll gradients. In cavitates of unstimulated neutrophils, 30% and 26% of total Mac-1 was identified in beta [1.10 gm/ml; vitamin B12 binding protein (vit B12 B.P.)-rich] or pre-gamma (1.07 gm/ml; vit B12 B.P.-poor) granular fractions, respectively, whereas 24% was associated with the plasma membrane-rich gamma (1.06 gm/ml) fractions. N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation (10(-8) M, 15 min, 37 degrees C) significantly diminished Mac-1 in pre-gamma (-18% of total, P less than 0.05) but not beta fractions (+6% of total). Under these conditions, the content of Mac-1 in gamma fractions increased 13% in association with four- to eightfold increase in surface Mac-1 expression (OKM-1 binding). These findings suggest that chemotactic stimuli increase plasma membrane and/or surface Mac-1 on human neutrophils by mobilizing a novel intracellular granule pool.

Adult↗
PubMed1988

A quantitative cytochemical assay for osteoclast acid phosphatase activity in foetal rat calvaria.

Acid phosphatase activity is prominent in osteoclasts (bone resorbing cells) and has been implicated in the process of bone resorption, although its precise role is not understood. To study the distribution and activity of this enzyme, a quantitative cytochemical method has been developed using undecalcified fresh frozen sections of foetal rat calvariae. Sections were allowed to react with 3 mM naphthol ASBI phosphate at pH 5.0, and the reaction was stopped by rinsing in ice-cold tap water containing 50 mM sodium fluoride. The reaction product was post-coupled to Fast Garnet at 4 degrees C. The absorbance of areas of reaction product in the cytoplasm was measured using scanning and integrating microdensitometry. The initial velocity rate was maintained for up to 2 min at pH 5.0 with a substrate concentration of 3 mM and a section thickness of 5 micron. Under these conditions reaction product was localized to osteoclasts and the surface of bone matrix beneath these cells. Activities in osteoblasts and chondrocytes were negligible. Osteoclastic acid phosphatase was almost totally inhibited by 10 mM fluoride and reduced by 70% by 100 mM tartrate.

Acid Phosphatase↗
PubMed1988

Residents' perceptions of the effects of a practice plan on their training.

Residents were surveyed about the characteristics and quality of their education before and twice after a new practice plan for faculty members was implemented at a county medical center. The residents assessed the impact of the practice plan on their training programs. Compared with the ratings before the plan began (1984), the responses one and two years (1985 and 1986) after institution of the plan were significantly more positive on three of nine characteristics: quality of staff, quality of supervision, and heterogeneity of patients. Contrary to concerns expressed by faculty members and residents prior to the plan, the 1985 and 1986 residents did not identify significant decline in the level of their patient care responsibility and opportunities for independent decision-making. One-third of the residents in 1985 and 1986, however, commented (usually negatively) about increased time required for attending rounds due to involvement of faculty members in ward care and documentation activities. These results suggest that changes in faculty organization to increase patient care reimbursement are not necessarily incompatible with maintaining and even improving graduate education.

Attitude of Health Personnel↗
PubMed1988

Bioactive LH in women with polycystic ovaries and the effect of gonadotrophin suppression.

Discrepancies between levels of bioactive LH (B-LH) and immunoreactive LH (I-LH) in polycystic ovarian syndrome (PCO) have been reported previously. Serum levels of I-LH, B-LH (by dispersed Leydig cell assay), FSH, oestradiol (E2) and progesterone (Prog) were measured once to three times weekly over 4 weeks in 13 women with classical clinical, ultrasound and endocrine features of PCO. Eleven women attending for infertility but whose profiles when studied three times weekly by combined endocrine and ultrasound assessment were normal and ovulatory served as controls. Seven of the women with PCO were evaluated during and after 3 weeks suppression with ethinyloestradiol (30 micrograms) plus 150 micrograms either of desogestrel or levonorgestrel; two were given both treatments. Both I-LH and B-LH levels were higher in PCO patients (20 +/- SD 5 U/l and 46 +/- 9 U/l respectively, P less than 0.0001), compared with all phases of the normal cycles except the mid-cycle peak. The B-LH to I-LH (B:I LH) ratio in PCO patients (2.5 +/- 0.7) was higher than in all the control cycle phases (P less than 0.05). I-LH, B-LH, B:I LH ratio, FSH and E2 were all suppressed from the second week of oestrogen-progestogen treatment (P less than 0.01) and returned gradually to pretreatment levels by the third or fourth week after suppression. The LH and FSH levels and B:I LH ratio in PCO patients during suppression were comparable with levels in the early and mid-follicular phases of control cycles but the LH/FSH ratio remained significantly raised (P less than 0.01) at 2.3 +/- 0.7.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Recognition of an endothelial determinant for CD 18-dependent human neutrophil adherence and transendothelial migration.

Human neutrophil (PMN) attachment to human umbilical vein endothelial cells (HUVEC) was evaluated in vitro using two MAbs, R6-5-D6 and RR1/1, that recognize intercellular adhesion molecule-1 (ICAM-1), and one MAb, TS1/18, that recognizes CD18. Pretreatment of the HUVEC with anti-ICAM-1 MAbs produced greater than 50% inhibition of attachment to HUVEC, and IL-1 (0.5 U/ml)- or lipopolysaccharide (LPS) (10 ng/ml)-stimulated HUVEC, and greater than 99% inhibition of f-Met-Leu-Phe (0.5 nM) enhanced adherence. Anti-ICAM-1 MAbs also inhibited by greater than 85% the transendothelial migration induced by 4-h IL-1 (0.5 U/ml) and LPS (10 ng/ml) activation of the HUVEC. That these effects involved a CD18-dependent mechanism is supported by the following results: pretreatment of PMN with TS1/18 produced the same degree of inhibition of attachment and migration as seen with R6-5-D6. In addition, the use of both MAbs together did not further increase the inhibition of cell attachment to stimulated HUVEC. The attachment of PMN from patients with CD18 deficiency to stimulated HUVEC was not reduced by R6-5-D6, and both R6-5-D6 and TS1/18 revealed the same time course for appearance and disappearance of an adherence component on stimulated HUVEC not blocked by either MAb. These results demonstrate that attachment and transendothelial migration of PMN in vitro depend substantially on both CD18 on the PMN and ICAM-1 on the endothelial cell.

Antibodies, Monoclonal↗