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S Davidson

Publications and source records attributed to S Davidson.

At least 145 records · Page 8Linked to original sources
PubMed1986

Family therapy--where are we, and where are we going?

There has been considerable growth and development in the field of family assessment and therapy over the past thirty years. This management approach provides a useful tool in the assessment, management and treatment of children, adolescents and families with various psychiatric disorders and mental health problems. This paper provides a broad overview and a critical evaluation of the present state of the art, paying particular attention to the integration and present status of clinical practice, theoretical models, research, teaching and training programs. Based on the emerging trends, directions for the future are suggested including an exploration of the integration of different therapeutic modalities. Finally, the practical problems associated with the teaching of these approaches in General Psychiatry Training Programs are addressed.

Education, Medical, Graduate↗
PubMed1985

Breast feeding as prophylaxis for atopic eczema: a controlled study of 368 cases.

The present study was undertaken in an attempt to draw data whether breast-feeding is beneficial in prevention of atopic eczema. Three-hundred and sixty-eight babies given different feeding modalities were examined for the presence of atopic eczema at the age of three and six months. Seven percent of breast-fed infants developed eczema compared to 10% of formulae-fed and 6% of mixed breast and formulae-fed infants. No difference in the severity of atopic eczema was recorded in the three study groups. Our experience demonstrates the absence of a protective effect of breast-feeding against the development and severity of atopic eczema.

Breast Feeding↗
PubMed1984

Adherence of Candida albicans to buccal epithelial cells of neonates.

Adherence of Candida albicans to buccal epithelial cells of newborn infants was studied by the visual adherence method. Forty-five samples of buccal epithelial cells were obtained from 21 normal newborns at different times following delivery. In group 1 (mean age 7.5 hr) 367 +/- 51 yeast cells adhered to 100 epithelial cells. In group 2 (mean age 2.3 days) 384 +/- 36 yeast cells adhered to 100 cells. In group 3 (mean age 6.2 days) 488 +/- 57 yeast cells adhered to 100 cells. Differences among the groups were not significant (p greater than 0.1). A significant difference was found in the percentage of epithelial cells binding 10 yeast cells between group 1 (7.25 +/- 0.9) and group 3 (14.9 +/- 2.5), and group 2 (8.0 +/- 2.0) and group 3 (p less than or equal to 0.025). In 12 infants studied twice at mean age of 2.1 and 6.3 days (included in groups 2 and 3) a significant increase was found in the number of adherent yeasts binding to 100 epithelial cells (330 +/- 87 and 485 +/- 52 respectively) (p less than or equal to 0.03), and in the percentage of epithelial cells binding greater than or equal to 10 yeast cells (5.0 +/- 3.0 and 14.7 +/- 3.5 respectively, p less than or equal to 0.004) for each infant. The age-related increased affinity of buccal epithelial cells to Candida albicans may have relevance in the development of oral thrush.

Animals↗
PubMed1984

Infusion cholecystography in the early diagnosis of acute gallbladder disease.

The value of infusion cholecystography 99mTc HIDA cholescintigraphy and ultrasonography was compared in 51 patients presenting with a clinical diagnosis of acute cholecystitis. Of the 35 patients with proven gallbladder disease, the presence of gallstones was correctly predicted in 31 (88 per cent) by infusion cholecystography, 32 (90 per cent) by 99mTc HIDA cholescintigraphy and 27 (77 per cent) by ultrasonography. There were no false positive investigations. Infusion cholecystography may be of particular interest to surgeons with no ready access to isotope scanning techniques.

Acute Disease↗
PubMed1984

Effects of dichloroacetate and glyoxylate on low density lipoprotein uptake and on growth of cultured fibroblasts.

The effects of dichloroacetate, a known hypocholesterolemic agent, were studied in cultured growing and confluent human fibroblast cells. Microscopic examination showed no visible adverse effects of dichloroacetate on confluent cells during exposure to concentrations as high as 5 mM for 96 hr. Higher concentrations resulted in cell death after varying periods of incubation. There were no viable cells after 24 hr of exposure to 100 mM dichloroacetate. In contrast, much lower concentrations proved lethal to growing cells; cell growth, as determined by cell numbers at specified times after splitting, was suppressed by 1 mM dichloroacetate and 5 mM concentrations resulted in cell death. Similar effects were noted with glyoxylate. The hypocholesterolemic effect of dichloroacetate is probably not due to any effect on the low density lipoprotein pathway, since concentrations of up to 1 mM dichloroacetate did not affect the cellular binding and uptake of 125I-labeled low density lipoprotein. It is concluded that growing and rapidly metabolizing cells are much more sensitive to the toxic effects of dichloroacetate and glyoxylate than confluent cells.

Acetates↗
PubMed1983

Mast cell differentiation depends on T cells and granule synthesis on fibroblasts.

Mast cell differentiation was generated in the following three experimental situations: (i) infection of mice with Schistosoma Mansoni or with Nippostrongylus brasiliensis and growth of the lymph node cells in the presence of the corresponding helminth antigen; (ii) immunization with horse serum and growth of blood and lymph node cells in the presence of the horse serum; (iii) exposure of T-cell-depleted suspensions of lymph node cells from unimmunized mice to T-cell factor (TCF) released into medium of the young cultures of (i) and (ii). This differentiation was also obtained when lymph node cells from athymic nude mice were exposed to TCF. The cell suspensions were plated on X-irradiated fibroblast monolayers prepared from embryonic mouse skin. Screening of the suspensions before plating on the fibroblasts in culture revealed no young forms of mast cells, and none were present in culture of nude mice lymph node cells maintained without TCF. Primordial appearance of metachromatic granules generally in the golgi zone was first seen in many 'large lymphoid cells' as early as 18 hr after plating. This was followed by increase in the cytoplasm volume, increase in granule number and mitosis, ending at 10-18 days with homogeneous populations of mature mast cells. When the mesenteric lymph node cells from mice infected with the helminths were grown in the absence of fibroblasts but in the presence of the antigen, homogeneous populations of cells with extended cytoplasm, filled with unstained vacuoles developed during days 7-13. These cells did not contain histamine (or at most 0.2 microgram per 10(6) vacuolated cells). When these cells were plated on fibroblast monolayers clear granule formation in all the vacuoles was seen 2 days later. It increased progressively in size and staining intensity, until the vacuoles transformed into typical mast cell granules. By the fourth day the vacuolated cells attained the typical mast cell morphology and the histamine content greatly increased (from 0.12 microgram per 10(6) vacuolated cells to 3.02 micrograms per 10(6) mast cells). These mast cells were readily degranulated by monoclonal anti-DNP-BSA IgE, and the antigen, releasing 90% of the histamine. The study shows that mucosal mast cells formation from 'large lymphoid-like' cells present in the blood and in the lymph, is stimulated by TCF. The condensation of the metachromatic material and histamine synthesis depends on other cells, presumably fibroblasts which comprise the principal cell in the embryonic skin monolayers. The mechanism of the fibroblast influence is not yet known.

Animals↗
PubMed1983

Murine interleukin-2 generates glycogen-rich and mucus-secreting NK cells.

Colonies of cells termed 'giant granular leucocytes' (GGL) displaying natural killer (NK) activity were generated in cell culture. The prominent feature of these cells was the formation of large cytoplasmic pool--the 'theca'--filled up with glycogen. This was demonstrated by the strong positive red staining of the theca with periodic acid Schiff reagent (PAS) which was abolished by prior treatment with amylase. Two different procedures were employed for obtaining colonies of NK-GGL. In the first, mice were injected either with killed Corynebacterium parvum or with killed Bordetella pertusis preparations and their mesenteric lymph-node cells were grown on syngeneic X-irradiated embryonic skin fibroblast monolayers. At the foci of GGL formation the fibroblasts were killed and the cleared areas thus formed were populated by adherent GGL. In the second procedure, supernates from rat or mouse spleen cultures stimulated with concanavalin A (Con A)--Interleukin-2 (IL-2)--were added to cultures of spleen and lymph-node cells prepared from either ordinary or from athymic nude mice. Richest GGL populations developed when rat IL-2 was added to cells of nude mice. Mouse IL-2 was less consistent. With nude mouse cells it stimulated, either mast cells or GGL, or both; rat IL-2 did not stimulate mast-cell differentiation in nude mouse cultures. In contrast, supernates from lymph-node cell cultures prepared from mice infected with Schistosoma mansoni. Mucosal mast cell-stimulating factor (MMSF) stimulated the formation of colonies of mast cells but not GGL. When MMSF was added as late as 23 days, colonies of young mast cells appeared and mast cells progressively increased in number. When rat IL-2 was added to such mature mast-cell cultures on the 30th day, colonies of cytolytic-GGL appeared. These observations indicate that precursors of mast cells and GGL persist in the cultures and preserve their potential to be stimulated by T-cell factors. GGL-NK cells developed on monolayers prepared from whole embryos released substance that displayed morphology and staining characteristic of mucus. Evidence gathered from in-vitro and in-vivo studies links the in-vitro GGL-NK cells to motile cells that inhabit the mucosal epithelium. Based on the observations, a hypothesis on the function of NK cytotoxicity is brought forward. It proposes the replacement of ordinary epithelial cells, which are killed during a proliferative and differentiative response of other cells at the onset of an infection course.

Amylases↗