Extra-endocrine functions of vitamin D.
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Animals↗
Biomedical subjects
D C Anderson
Publications and source records attributed to D C Anderson.
Effect of piliation on interactions of Haemophilus influenzae type b with human polymorphonuclear leukocytes.
Piliated, adherent (P+) and nonpiliated, nonadherent (P-) strains of Haemophilus influenzae type b (Hib) were compared with respect to their ability to induce polymorphonuclear leukocyte (PMN) chemiluminescence (CL) and superoxide (O2-) generation and their susceptibility to phagocytosis by PMNs. P+ strains opsonized in normal human serum (NHS) induced significantly greater CL than did P- strains (500 X 10(5) +/- 112 X 10(5) versus 242 X 10(5) +/- 65 X 10(5) total counts per 60 min; P less than 0.001) when reacted with normal PMNs. Contributions of immunoglobulin and complement to CL activity in these mixtures were shown by findings of lower overall levels of CL when hypogammaglobulinemic serum or heat-inactivated NHS was used to opsonize either P+ or P- organisms. Results obtained with mixtures of hypogammaglobulinemic plus adsorbed heat-inactivated NHS (with P+ or P- organisms) suggested a role for an antipilus antibody in the enhancement of CL by these strains. NHS-opsonized P+ strains also induced significantly greater (P less than 0.002) O2- generation than did P- strains (2.83 +/- 0.08 versus 1.94 +/- 0.14 nmol of ferricytochrome c reduced per 10 min/10(6) PMN). Comparable ingestion of P+ or P- strains opsonized in NHS by PMNs was demonstrated by a radiolabeled uptake technique and transmission electron microscopy, and primary granule release (beta-glucuronidase) was comparable during ingestion of P+ or P- strains. The basis for the observed enhanced capacity of P+ Hib to stimulate PMN oxidative metabolism as compared with P- organisms is uncertain. Possible clinical implications of these findings deserve further study.
Antibodies, Bacterial↗
Clinical experience with the use of two diphosphonates in the treatment of Paget's disease.
The effects of EHDP (20 mg/kd/day) and APD (4.5 mg/kg/day) given for three months to patients with severe symptomatic Paget's disease have been compared in an open trial of 17 patients. Both drugs were equally effective in producing a prompt reduction in pair scores, urine hydroxyproline, and serum alkaline phosphatase levels. The remission was maintained for a variable period after stopping treatment. Both drugs were well tolerated, and a one-month course of either drug was not effective. Comparison with published responses from previous studies indicates that EHDP given at this dose as a relatively short course is more effective than a lower dose for a longer period of time; the present study does not suggest that APD has significant advantages.
Aged↗
Genetics and biochemical variability of variants of 21 hydroxylase deficiency.
In a population and family study we have examined the relationship between HLA types, classical congenital adrenal hyperplasia (CAH), and variants of 21 hydroxylase (21 OH) deficiency detected by increased blood levels of 17 hydroxyprogesterone (17 PO) in response to ACTH after overnight suppression with dexamethasone ('short Synacthen test'). In a non-CAH population, 7.7% of subjects were found to have raised 17 PO response suggesting reduced activity of 21 OH. Such subjects with raised 17 PO levels were designated simply as type 2 responders because the relationship with genotype was unknown. Post-ACTH levels of 17 PO were significantly greater in type 2 responders than in obligate carriers of CAH. A total of 2.5% of the population studied also had raised progesterone (PO) levels in the Synacthen test. HLA-A28 and B14 (in linkage disequilibrium) were significantly increased in frequency and HLA-B12 decreased in the type 2 responders. HLA-Bw47, which is known to be associated with CAH, was found only among obligate carriers of classical CAH. Because type 2 response and classical CAH are linked to HLA but are associated with different antigens, it is likely that they are determined by two (or more) alleles.
17-alpha-Hydroxyprogesterone↗
Startle potentiation and heart rate as affected by fear and hunger.
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Acoustic Stimulation↗
Performance of crosses among Hereford, Angus and Simmental cattle with different levels of Simmental breeding. III. Heifer postweaning growth and early reproductive traits.
Postweaning growth and early reproductive traits in heifers whose potential for milk production differed were studied during the years 1976 through 1979. Data were collected on 230 heifers raised by greater than or equal to 3-yr-old Hereford dams. Heifers were comprised of the following breed groups: Hereford (HH), Angus-Hereford (AH), 25% Simmental-75% Hereford (1S3H) and Simmental-Hereford (SH). Postweaning growth rate during a 140-d period was greatest for SH heifers (.75 kg/d), intermediate for AH and 1S3H groups (.70 and .68 kg/d, respectively) and slowest for HH heifers (.64 kg/d). At 1 yr of age, SH heifers were heavier, taller and had larger pelvic areas than all other groups (P less than .01). Least-squares means for yearling weight, hip height and pelvic area for HH, AH, 1S3H and SH heifers were 283, 303, 298 and 317 kg; 111, 112, 114 and 118 cm, and 132, 136, 139 and 148 cm2, respectively. Ninety-one percent of the heifers reached puberty by the end of the breeding period. Crossbred heifers reached puberty at younger ages and had higher pregnancy rates than HH heifers (P less than .01). Least-squares means for pubertal age, weight and height for HH, AH, 1S3H and SH breed groups were, respectively, 407, 371, 382 and 368 d; 300, 302, 305 and 313 kg, and 115, 114, 117 and 119 cm. Percentage of heifers reaching puberty by 14 mo of age was 64, 99, 85 and 94 for HH, AH, 1S3H and SH, respectively. Respective pregnancy rates were 59, 90, 77 and 86%, but were not significantly different among breed groups when only heifers reaching puberty by the end of the breeding period were studied. No differences among breed groups were found for date of pregnancy.
Animals↗
A model for hospital marketing decision processes and relationships.
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Decision Making↗
Evaluation of the measurement of blood glucose levels on dried filter paper blood spots.
The measurement of blood glucose using discs punched from dried spots on filter paper has been examined as a method to monitor patients' home blood glucose results. We confirm that the method is precise, reproducible, and accurate, but show that impregnation of the filter paper with boric acid leads to an initial false elevation in measured glucose levels and does not improve stability of the sample more than does refrigeration. Degradation of blood glucose is insignificant over 28 days if samples are stored at -20 degrees C, and samples kept at 4 degrees C show minimal falls provided they are analysed within 7 days. The greatest breakdown of glucose was shown to occur during the first 48 hours after application. The filter paper glucose measurements correlated closely with parallel measurements using a Yellow Springs Glucose Analyser.
Blood Glucose↗
Leukocyte LFA-1, OKM1, p150,95 deficiency syndrome: functional and biosynthetic studies of three kindreds.
Three patients (2 female, 1 male) with recurrent infection, granulocytosis, impaired pus formation, and/or delayed umbilical cord separation were identified. Assessments of polymorphonuclear leukocytes (PMN)/monocyte function in each patient revealed profound abnormalities of adherence and adherence-dependent functions. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of their PMN lysates demonstrated a deficient or absent protein(s) of 138 kilodaltons (gp 138). Na3HB4 labeling demonstrated the absence of a major cell surface glycoprotein complex in each patient. Among parental and sibling PMN suspensions, functional assessments revealed no consistent abnormalities, although variably diminished gp138 was identified by SDS-PAGE and Na3HB4 labeling. Analysis by fluorescence-activated cell sorting and monoclonal antibodies (MAb) to LFA-1 alpha, OKM1 alpha, and their common beta subunit demonstrated a severe or total deficiency of PMN/monocyte surface expression of each protein among all patients; intermediate values were observed for parental and affected sibling suspensions, findings consistent with an autosomal recessive mode of inheritance for this disorder. Cell surface labeling (125I) and immunoprecipitation with the same MAb demonstrated the absence of these glycoproteins in addition to a 150-kilodalton protein (p150,95). Identical abnormalities of surface expression of patient lymphocytes blast-transformed with phytohemagglutinin (PHA) or Epstein-Barr virus were demonstrated. Further, significantly diminished natural killer cell cytotoxicity was observed for each patient tested. PHA blast-transformed patient lymphocytes labeled with [35S]methionine demonstrated a total absence of the beta molecule but indicated the presence of an LFA-1 alpha precursor. These findings indicate that LFA-1 alpha synthesis and surface expression require beta association. It is concluded that impaired inflammatory function in this disorder is casually related to a heritable deficiency of critical "adhesive" leukocyte glycoproteins.
Adolescent↗
Heritable lymphocyte function-associated antigen-1 deficiency: abnormalities of cytotoxicity and proliferation associated with abnormal expression of LFA-1.
The effect of heritable LFA-1 deficiency on T lymphocyte function was measured. After primary mixed lymphocyte stimulation, all six patients studied showed diminished allospecific T lymphocyte cytolytic and NK activity as compared with kindred and normal controls. MLR and mitogen-induced proliferative responses were consistently depressed. LFA-1-deficient, EBV-transformed B cell lines were poor stimulators of T cell responses. Primary cytolytic responses by lymphocytes from severely LFA-1-deficient patients (less than 0.2% of normal surface expression) were consistently more profoundly depressed than those by lymphocytes from moderately deficient patients (about 5% of normal surface expression). These results demonstrate the importance of LFA-1 in lymphocyte function. After repeated MLR restimulation, proliferative and cytolytic capacity improved and CTL lines could be established from all patients. Cytolysis by lines from one but not a second severe patient, and by four of four moderate patients, was inhibited by anti-LFA-1 MAb, and at 10-fold lower concentrations than required for inhibition of killing by control CTL lines. The locus of inhibition was on the target cell for the severely deficient CTL line, and on both the target and effector cells for moderately deficient CTL lines. In contrast, the locus of inhibition for normal CTL is on the effector cell. These findings show that LFA-1 can participate bidirectionally in cell interactions. The in vitro results are discussed in terms of the clinical findings in patients.
Antibodies, Monoclonal↗
Rapid radiometric assay used to assess lactoferrin in granulocytes.
We describe a rapid, precise, and sensitive radiometric assay for human lactoferrin. In this typical "sandwich"-type assay, anti-human lactoferrin is adsorbed onto a polystyrene sphere and bound lactoferrin is detected by the subsequent binding of 125I-labeled anti-human lactoferrin. The assay is accurate for lactoferrin concentrations of 5 to 1500 micrograms/L and takes about 2.5 h to complete. The within-assay and interassay variations (CV) are 5% and 13%, respectively. Neither lysozyme nor heparin, substances that form complexes with lactoferrin, interfered with lactoferrin measurement by this method. The assay has been applied to the measurement of lactoferrin in polymorphonuclear leukocytes of both healthy adults and neonates. We found significantly (p less than 0.001) less lactoferrin in the latter, an abnormality that may be related to known functional deficits of polymorphonuclear leukocytes during the newborn period.
Adult↗
Assessment of corpus luteum function by direct radioimmunoassay for progesterone in blood spotted on filter paper.
In this specific, direct RIA for progesterone in capillary blood dried on filter paper, progesterone is eluted, with phosphate buffer containing bovine serum albumin, from 5.9 microL of blood dried on 5.0-mm (diameter) discs of filter paper. The eluate is assayed, with 125I-labeled progesterone-11 alpha-glucuronyl-tyramine as tracer, with separation by a double-antibody solid-phase technique. The sensitivity of the assay is 4.7 pg per tube, corresponding to 2.5 nmol per liter of blood. Within- and between-batch CVs averaged 7.0 and 9.2%, respectively, over the working range of the assay (4.5-64 nmol/L). Concentrations of progesterone in blood spots (y) correlated well with those in serum (x) as measured by an established direct RIA (Clin Chem 28:1314, 1982): y = 0.430x - 2.44 (r = 0.972, n = 104). Progesterone is stable in the blood spots for at least 15 weeks at 25 degrees C. The convenience of multiple sampling of blood by finger prick and the simplicity of the assay make this approach useful in investigating serial progesterone concentrations in outpatients.
Corpus Luteum↗
Evidence that adrenal oestrogens are not involved in benign breast disease.
We have studied 30 women with symptomatic benign breast disease in order to test the hypothesis that in some it might be caused by an enzyme variant leading to excessive adrenal production of oestrone. Synthetic 1-24 ACTH (Synacthen) was given intramuscularly after overnight suppression with dexamethasone, during the early follicular phase of the menstrual cycle. In no subjects did plasma oestrone levels show a consistent and significant response to ACTH despite the expected consistent rises in androstenedione and cortisol. We conclude that it is unlikely that adrenal oestrogens play a significant role in the pathophysiology of even a minority of patients with benign breast disease.
Adult↗
Inherited deficiency of the Mac-1, LFA-1, p150,95 glycoprotein family and its molecular basis.
Leukocyte surface glycoproteins that share a common beta subunit have been found to be congenitally deficient in three unrelated patients with recurring bacterial infection. The glycoproteins, Mac-1, LFA-1, and p150,95, have the subunit compositions alpha M beta, alpha L beta, and alpha X beta, respectively. Using subunit-specific monoclonal antibodies, both the alpha M and beta subunits of Mac-1, the alpha L and beta subunits of LFA-1, and at the least the beta subunit of p150,95, were found to be deficient at the cell surface by the techniques of immunofluorescence flow cytometry, radioimmunoassay, and immunoprecipitation. A latent pool of Mac-1 that can be expressed on granulocyte surfaces in response to secretory stimuli, such as f-Met-Leu-Phe, was also lacking in patients. Deficiency was found on all leukocytes tested, including granulocytes, monocytes, and T and B lymphocytes. Quantitation by immunofluorescence cytometry of subunits on granulocytes from parents of these patients and of a fourth deceased patient showed approximately half-normal surface expression, and, together with data on other siblings and a family with an affected father and children, demonstrate autosomal recessive inheritance. Deficiency appears to be quantitative rather than qualitative, with two patients expressing approximately 0.5% and one patient approximately 5% of normal amounts. The latter patient had alpha beta complexes on the cell surface detectable by immunoprecipitation. Biosynthesis experiments showed the presence of normal amounts of alpha'L intracellular precursor in lymphoid lines of all three patients. Together with surface deficiency of three molecules that share a common beta subunit but have differing alpha subunits, this suggests the primary deficiency is of the beta subunit. The lack of maturation of alpha'L to alpha L and the deficiency of the alpha subunits at the cell surface and in latent pools suggests that association with the beta subunit is required for alpha subunit processing and transport to the cell surface or to latent pools. The molecular basis of this disease is discussed in light of adhesion-related functional abnormalities in patients' leukocytes and the blockade of similar functions in healthy cells by monoclonal antibodies.
Adolescent↗
Dissociation between adrenal androgens and cortisol in Cushing's disease.
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Adrenal Cortex↗
Vitamin D and the lymphomedullary system.
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Animals↗
Multimodality evoked potentials in closed head trauma.
Patients with closed head injuries who had Glasgow coma scale scores of 7 or less were studied with evoked potentials soon after trauma. Of the patients, 39 had brain-stem auditory evoked potentials (BAEPs); 12, stroboscopic visual evoked potentials (VEPs); and 23, short-latency somatosensory evoked potentials (SSEPs). Evoked potential results were graded from 1 (normal) to 4 (most abnormal). Outcomes were categorized by the Glasgow outcome scale, with good outcome and moderate disability further classified as "favorable" and severe disability, vegetative state, and death as "unfavorable." The BAEPs and VEPs were reliable predictors of an unfavorable but not a favorable outcome. The SSEPs reliably predicted both kinds of outcomes. No instances of "false pessimism" were encountered in any modality. Evoked potential results were more reliable than intracranial pressure, pupillary light reaction, or motor findings in predicting outcome. Frequent occurrence of peripheral auditory injuries was shown.
Adolescent↗
Impaired motility of neonatal PMN leukocytes: relationship to abnormalities of cell orientation and assembly of microtubules in chemotactic gradients.
To allow a further understanding of the pathogenesis of impaired stimulated locomotion by polymorphonuclear leukocytes (PMNs) in human neonates, we studied cellular orientation by neonatal PMNs in response to well-defined chemotactic gradients (Zigmond orientation chambers) and characterized the cytoplasmic microtubule (MT) complex of neonatal PMNs during cell orientation and movement. PMN suspensions obtained from 52 neonates demonstrated a diminished capacity to undergo orientation at all time intervals after exposure to gradients of N-formyl-methionyl-leucyl phenylalanine (f-Met-Leu-Phe) or C5a. Among responding (orienting) neonatal PMNs observed, only 70% (f-Met-Leu-Phe) or 59% (C5a) oriented accurately (toward chemotactic gradients) as compared to values of 96% (f-Met-Leu-Phe) or 92% (C5a) for adult controls. Furthermore, neonatal PMNs failed to alter their direction of orientation/migration when chemotactic gradients were reversed. Similar abnormalities were observed when 10-fold gradients of f-Met-Leu-Phe were employed over a concentration range between 10(-7) and 10(-11) M. Employing tubulin immunofluorescence, the cytoplasmic MT complex of-neonatal PMNs was assessed prior to and after cell exposure to uniform concentrations or gradients of chemotactic factors (CFs). MT assembly by neonatal PMNs studied under these experimental conditions was significantly diminished. Neonatal cell suspensions demonstrated 26 +/- 5 (f-Met-Leu-Phe) or 27 +/- 6 (C5a) MT/cell as compared to respective values of 36 +/- 6 or 35 +/- 5 for adult suspensions (P less than .001). MT lengths of neonatal PMNs increased from 6.7 +/- 1 micron (PBS) to 7.5 +/- 1 micron (f-Met-Leu-Phe) or 7.3 +/- 1 micron (C5a) as compared to values of 6.5 +/- 1 micron (PBS), 11.1 +/- 1 micron (f-Met-Leu-Phe), and 10.9 +/- 1 micron (C5a) for adult PMNs exposed to gradients or uniform concentrations of CFs (P less than .01 for both f-Met-Leu-Phe and C5a). Thus, the polymerized tubulin mass product of chemotactically stimulated neonatal PMNs (202 micron) was significantly (P less than .001) diminished as compared to adult PMNs (360 micron). As shown by a [3H]colchicine binding assay, impaired MT assembly could not be attributed to diminished cytoplasmic tubulin content of neonatal PMNs, which was comparable to adult PMNs.
Chemotaxis, Leukocyte↗