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Biomedical subjects

E M Johnson

Publications and source records attributed to E M Johnson.

At least 343 records · Page 19Linked to original sources
PubMed1981

Genetic regulation of variable Vi antigen expression in a strain of Citrobacter freundii.

Certain strains of the genus Citrobacter exhibit a variable expression of the Vi surface antigen that appears to involve a special mechanism for regulation of gene expression. Two nonlinked chromosomal loci, viaA and viaB, are known to determine nonvariable Vi antigen expression in strains of Salmonella. To confirm the presence of analogous loci in Citrobacter and to ascertain whether either of them is involved in variable Vi antigen expression in this organism, donor strains were constructed from Citrobacter freundii WR7004 and used to transfer their Vi antigen-determining genes to ViaA- and ViaB- Salmonella typhi recipient strains. Vi antigen expression in C. freundii was found to be controlled by loci analogous to the Salmonella via genes. S. typhi recipients of the C. freundii viaA+ genes were restored to the full, continuous expression of the Vi antigen normally seen in S. typhi. Thus, the C. freundii viaA genes appeared to play no role in the variable expression of the Vi antigen. In contrast, S. typhi recipients of the C. freundii viaB+ genes exhibited the rapid, reversible alternation between full Vi antigen expression and markedly reduced Vi antigen expression that was seen to occur in the C. freundii parent. The C. freundii viaB locus was thus identified as the one whose genes are regulated so as to produce variable Vi antigen expression. Genes determining another C. freundii surface antigen, the synthesis of which is not affected by the mechanism regulating Vi expression, were coinherited with the C. freundii viaB+ genes. An invertible, insertion sequence element located within the C. freundii viaB locus is proposed to account for the regulation of variable Vi antigen expression.

Antigens, Bacterial↗
PubMed1981

Screening for teratogenic hazards: nature of the problems.

State of the art teratology is sufficient to develop a screening system of teratogenic hazard potential if one remembers the basic developmental biology underlying teratogenesis. Understanding of teratogenic mechanisms may provide better systems but such knowledge is not yet available. The system described is an interim step and may not prove valid. Hopefully Karnofsky's law will remain in our attention thereby permitting our realization that the question, "Is table salt teratogenic?" is naive and largely irrelevant. The answer is "Yes" from the viewpoint of total well-being of the conceptus. What the question is really asking is: "What is the developmental hazard potential of table salt?" This question can be answered quantitatively and it is, "No, it is not a developmental hazard because it is a coeffective teratogen with a developmental hazard index of less than 0.1." If we could all understand these basics, we could realistically proceed to safeguard your grandchildren and mine.

Animals↗
PubMed1981

Factors related to the successful performance of psychiatric aides.

Psychiatric aides play a vital role in providing daily care for the mentally ill. Yet despite their importance in the mental health system, little research has been done into the selection, hiring, training, and retention of aides. In the first phase of a two-phase study of aides in psychiatric centers in New York State, the authors used several data instruments on four major populations of aides and supervisors. The authors isolated several characteristics, notably sex of the aide and relationship with the supervisor, that seem to be associated with tenure in the position. The implications of the study for the training of aides and for future research are briefly discussed.

Adult↗
PubMed1981

Characterization of increased plasma dopamine-beta-hydroxylase activity in rats with experimental diabetes.

Plasma dopamine-beta-hydroxylase (pDBH) activity is markedly elevated in chronic experimental streptozotocin (STZ) diabetes in the rat. Several possible explanations, all potentially relevant to the pathophysiology of diabetes, could explain this observation. The objective of this paper was to further delineate the behavior of pDBH in diabetes and examine several possible mechanisms fot the increase. Plasma DBH increases within 1 day of STZ administration, is fivefold elevated within 1 wk, and slowly reaches ninefold control values after several months. Similar changes result from alloxan-induced diabetes. The increase in pDBH activity correlates well with the severity of diabetes as assessed by plasma glucose levels. Reversal of the diabetic state with insulin administration or islet cell transplantation results in the decrease of pDBH activity toward normal values. Plasma DBH is not increased in hyperglycemic obese (ob/ob) mice, suggesting a primary dependence of pDBH elevation on reduced levels of insulin and not hyperglycemia per se. Guanethidine-sympathectomized and sympathectomized/adrenal demedullated animals, with 60% and 25% of control levels of pDBH, respectively, show the same percentage increase in pDBH activity with induction of diabetes, thus, the increase in pDBH does not result from a selective activation or dysfunction of the sympathetic nervous system or adrenal medulla in diabetic animals. No evidence is found for the alteration of the kinetic parameters, molecular size, or charge of pDBH in diabetes. Several mechanisms for the increase are considered.

Adrenal Gland Neoplasms↗
PubMed1981

Use of an experimental autoimmune model to define nerve growth factor dependency of peripheral and central substance P-containing neurons in the rat.

Rats exposed to maternal antibodies against nerve growth factor (NGF) in utero and in milk have been used to investigate the developmental dependency of various substance P-containing neurons on NGF. Substance P and other peptides were measured by radioimmunoassays. The substance P content of sensory ganglia, spinal cord, and skin was depleted 40 to 60% in anti-NGF-treated rats. These results demonstrate the NGF dependence of substance P-containing neurons in sensory ganglia. Opiate binding in the spinal cord was not changed despite the large depletion in substance P: the Bmax and KD were the same in control and treated animals. The results suggest that opiate receptors may not be located presynaptically on substance P-containing primary afferents. Among the peripheral tissues which were assayed (ileum, submaxillary gland, retina, and adrenal), substance P decreased only in the adrenal, suggesting innervation by a NGF-dependent substance P-containing neuron. No changes were detected in the substance P content of nine different brain regions, in agreement with previous observations on the lack of effect of NGF on central neurons.

Animals↗
PubMed1981

Experimental diabetic autonomic neuropathy.

The regular occurrence of autonomic neuropathy, colonic dilatation, and loss of fecal consistency was investigated in streptozotocin-diabetic, age-matched control, and pancreatic-islet--transplanted rats using ultrastructural, histochemical, and biochemical methods. Degenerating unmyelinated axons were observed by electron microscopy in the colonic submucosa and muscularis, ileal mesentery, and splenic pedicle in 5--7 months diabetic animals; similar changes were not found in control rats or animals subjected to islet transplantation three weeks after induction of diabetes and sacrificed 4--6 months later (colon only). Regenerative changes, including axons with identifiable growth cones, were demonstrated in the mesenteric nerves of chronically diabetic animals. Formaldehyde-induced catecholamine fluorescence and cholinesterase histochemistry suggested deficiencies in colonic adrenergic and cholinergic innervation; histochemical findings in islet-transplanted animals were comparable to those of untreated control animals. Biochemical measurements of the adrenergic and cholinergic nervous system marker enzymes dopamine-beta-hydroxylase and choline acetyltransferase, respectively, in colon and spleen confirm a deficit in adrenergic (colon and spleen) and cholinergic (colon) innervation in chronically diabetic animals.

Animals↗
PubMed1980

Dorsal root ganglion neurons are destroyed by exposure in utero to maternal antibody to nerve growth factor.

Rats and guinea pigs, when immunized with mouse nerve growth factor, produce antibodies that cross-react with their own nerve growth factor. The antibodies reach developing offspring of these animals both prenatally (rats and guinea pigs) and postnatally (rats). Depriving the fetus of nerve growth factor in this way results in the destruction of up to 85 percent of dorsal root ganglion neurons as well as destruction of sympathetic neurons. Sensory neurons of placodal origin in the nodose ganglion were not affected. These data demonstrate that dorsal root ganglion neurons go through a phase of nerve growth factor dependence in vivo.

Animals↗
PubMed1980

Effects of long-term nerve growth factor deprivation on the nervous system of the adult rat: an experimental autoimmune approach.

Adult rats immunized with 2.5S mouse nerve growth factor (NGF) produced antibodies which cross-reacted with rat NGF. By the criterion of ammonium sulfate precipitation followed by Sephadex G-200 chromatography, all serum anti-NGF activity was retained in the IgG fraction. Animals which developed and maintained chronic (5-6 months) serum titers of anti-NGF demonstrated a pronounced biochemical and morphological atrophy of the superior cervical ganglion which was accompanied by a 35-40% reduction in neuronal number. Norepinephrine was reduced by approximately 90% in heart and brown fat. The extent of biochemical atrophy correlated well with serum titers of anti-NGF. No effects were observed on the short adrenergic neurons of the vas deferens, adrenal medullary chromaffin cells, central adrenergic neurons, of peripheral sensory neurons. These results strongly suggest that mature peripheral sympathetic neurons remain dependent on NGF for survival as well as for maintenance.

Animals↗
PubMed1980

Incorporation of exogenous pyrene-labeled histone into Physarum chromatin: a system for studying changes in nucleosomes assembled in vivo.

Treatment of Physarum histone with iodoacetoxypyrene selectively derivatizes a single H3 cysteine with acetoxypyrene. Microplasmodia can incorporate this AP-H3 into nucleosomes. The distinction between blue monomeric pyrene fluorescence and green excimer pyrene fluorescence allows detection of changes in distance between the closely positioned H3 cysteines in nucleosomes. Fluorescence of nucleosomes labeled in vivo with AP-H3 is almost exclusively of the excimer form, indicating that H3 cysteines are within a few angstroms of each other in the nucleosome core. In histones recovered from these nucleosomes all detectable pyrene is covalently bound to H3. When Physarum is exposed sequentially to labeled followed by unlabeled histone, there is a rapid appearance of green excimer emission in nucleosomes after addition of labeled histone and no apparent switch from excimer to monomer fluorescence after several replications of the genome in the presence of unlabeled histone. These experiments provide evidence in favor of a model for conservative distribution of nucleosomal histones during chromatin replication.

Biological Transport↗
PubMed1980

A family of inverted repeat sequences and specific single-strand gaps at the termini of the Physarum rDNA palindrome.

Ribosomal genes of Physarum polycephalum are located on multiple copies of an extrachromosomal, 61 kb rDNA palindrome. Each terminus of the palindrome consists of a nontranscribed spacer, averaging 5.4 kb in length, which includes a region of multiple inverted repeat sequences. Electron microscopy of denatured and reannealed termini reveals foldback segments that are multiples of a unit length of 50 bp, a length confirmed by sizing of restriction fragments from labeled termini. The total length of this inverted repeat region averages 600 bp per terminus, and the region is centered approximately 4 kb from the 3' end of the 26S gene. Restriction fragments containing the termini are heterogeneous, varying in length by +/- 400 bp. This heterogeneity is due to variability in both the number of 100 bp inverted repeats and the length of additional terminal spacer sequences. The inverted repeat region contains selectively located single-strand discontinuities as revealed by brief incubation with deoxynucleoside alpha-32P-triphosphates and E. coli DNA polymerase I (nick translation). Labelling at the discontinuities begins specifically with the sequence CCCTA. Discontinuities are nonligatable and are most likely gaps one nucleotide long. Each terminus contains 3 to 5 such gaps spaced approximately 200 bp apart. As measured by hybridization with selectively labeled foldback DNA, sequences homologous to the inverted repeats are widely distributed throughout chromosomal DNA.

Base Sequence↗
PubMed1980

A group program for cancer patients and their family members in an acute care teaching hospital.

An open-ended information/support group program for cancer patients and family members is described. The leadership role of the social work authors in developing the program, facilitating the sessions, adapting it to the limitations of an acute care teaching hospital, coordinating and training the multidisciplinary staff, and dealing with problem behaviors within the group sessions are discussed. Consumer satisfaction survey results are presented. The authors believe the program provides a helpful service to patients and families and a valuable opportunity for staff and students to become more sensitive health professionals through increased understanding of the psychosocial aspects of chronic illness.

Cancer Care Facilities↗
PubMed1980

A subvertebrate system for rapid determination of potential teratogenic hazards.

The multiplicity of potential teratogenic mechanisms requires that a practical screening system for developmental hazards simultaneously assess effects on as wide a variety of developmental phenomena as possible. The system also must provide the relevant dose level based on adult toxicity. A fresh water coelenterate fashioned into an artificial "embryo" may provide the former, while exposure of adult polyps may provide the latter. The system appears to separate the two dose levels as adequately as standard laboratory rodents but as significantly lower cost in time and effort.

Animals↗
PubMed1979

Reduction by reserpine of the accumulation of retrogradely transported [125I]nerve growth factor in sympathetic neurons.

Experiments were carried out to determine if stimuli which augment preganglionic nerve activity to sympathetic neurons, and thereby cause trans-synaptic induction, increase the retrograde transport of nerve growth factor (NGF). It was found that nerve activity had no effect on retrograde transport of [125I]NGF. It was found, however, that reserpine decreased retrograde transport of [125I]NGF and this inhibition was characterized. Reserpine decreased the maximal accumulation of intravenously administered [125I]NGF in superior cervical ganglia (SCG) by about 60%. It also caused a distinct shift in the time course of accumulation so that maximal accumulation was seen 12 h after [125I]NGF injection rather than at 9 h as in control animals. Reserpine had no effect on retrograde transport in sensory neurons. Dose--response curves showed that maximal inhibition occurred with doses of reserpine of 2.5 mg/kg i.p. and that reserpine was not able to completely block transport at any dose. The maximal inhibition of retrograde transport was achieved within 30 min of reserpine administration and inhibitory activity was unchanged for 36 h. The ability of sympathetic neurons to transport [125I]NGF subsequently recovered and was normal 96 h after reserpine administration. The inhibitory effect of reserpine appears to be due to an action at or very near to the nerve terminal since it was effective at reducing NGF transport at very low doses (0.33 microgram) when co-administered directly into the eye with [125I]NGF. An action of reserpine at the nerve terminal was further suggested by the inability of reserpine to affect transport if the drug was given 4 h after [125I]NGF administration. Based upon these data, it is suggested that there may be two pools of retrogradely transported NGF and that only more rapidly turning over pool is reserpine-sensitive. This pool may represent the retrogradely moving synaptic vesicles or some derivative of the vesicles.

Animals↗