Using the demand–control model of job strain to predict caregiver burden and caregiver satisfaction in the informal caregivers of heart failure patients

Objectives The demand–control (D–C) model of job strain has generated a considerable body of empirical support in predicting psychological health outcomes in the context of work. This study aimed to extend previous work using the D–C model of job strain to predict caregiver burden and satisfaction in the informal caregivers of patients with heart failure. Design and method Data were gathered from 60 caregiver/patient dyads in a cross‐sectional design. Patients with chronic stable heart failure were recruited from out‐patient clinics. The dependent variables were caregiver burden and satisfaction. Demand and control were measured using both patient‐ and caregiver‐derived measures. Results The D–C model accounted for 15 and 19% of the variance in caregiver burden, after controlling for age, gender and relationship to the patient. Lower control was associated with higher burden. The D–C model did not predict caregiver satisfaction. Conclusion The D–C model was associated with caregiver burden, but not satisfaction in caregivers, with control being the dominant predictor. Research linking the theory and findings from job strain and informal caregiving studies may elucidate both fields of research. Using the demand–control model of job strain to predict caregiver burden and caregiver satisfaction in the informal caregivers of heart failure patients.     

Regulation of cyclooxygenase-2 by nitric oxide in activated hepatic macrophages during acute endotoxemia

Eicosanoids generated via cyclooxygenase-2 (COX-2) and nitric oxide produced from inducible nitric oxide synthase (NOSII) have been implicated in endotoxin-induced tissue injury. In the present studies, we characterized COX-2 and NOSII activity in rat hepatic macrophages and their interaction during acute endotoxemia. Kupffer cells from control animals were found to constitutively express COX-2 and NOSII mRNA and protein. Whereas treatment of the cells with lipopolysaccharide (LPS) and/or interferon-gamma (IFN-gamma) had no major effect on COX-2, NOSII expression increased. Induction of acute endotoxemia resulted in a rapid and transient increase in constitutive COX-2 expression and prostaglandin E2 (PGE2) production by liver macrophages as well as NOSII expression and nitric oxide release. Cells from endotoxin-treated rats were also sensitized to generate more nitric oxide and express increased NOSII in response to LPS and IFN-gamma. Inhibition of NOSII with aminoguanidine reduced COX-2 mRNA and protein expression as well as PGE2 production by activated macrophages from endotoxemic, but not control animals. In contrast, SC236, a specific COX-2 inhibitor, had no effect on NOSII mRNA or protein levels or on nitric oxide production by hepatic macrophages, even after endotoxin administration. These data suggest that activation of COX-2 may be important in the pathophysiological response of hepatic macrophages to endotoxin. Moreover, nitric oxide is involved in regulating COX-2 in activated liver macrophages during acute endotoxemia.     

The effect of 1-phenylalanine mustard on anti-globulin antibodies in multiple myeloma

An immunochemical and serological study of a patient with rheumatoid arthritis who developed multiple myeloma and was treated with 1-phenylalanine mustard showed a striking difference in the effect of this drug on the rapidly dividing cells, as opposed to the resting plasma cells. The titres of anti-globulin antibodies such as the IgG serum agglutinators and the IgM rheumatoid factors were little altered although the IgG myeloma spike has disappeared following therapy. Fractionation of two different serum samples from 1966 and 1970 showed the IgG paraprotein to be serologically inactive for anti-globulin activity. This paraprotein was also characterized by producing only a single IgG precipitin line with horse anti-human whole serum antibody while the normal IgG globulins always showed a double line.     

A Survey of Laboratory Computers in Psyehophysiology

Since the mid 196O's there has hcen a growing interest in and use of computers in psychophysiology laboratories. There are even a growing number of accepted physiological measures which are fully dependent on computer technology for their derivation. Although minicomputers have been in use for over a decade, recent developments in microcomputer and microprocessor technology have led to rapid acceptance of microcomputers for laboratory work. These rapid advances have produced a need to survey the current state of laboratory computer applications and development. A comprehensive survey was mailed to 301 psychophysiology laboratory groups during the spring and summer of 1979 and completed surveys were received from 61% of the mailing. Sun'ey results are reported on computer hardware and configuration, dependent measures and user satisfaction, and use and cost of engineering and programming support. Developments in computer hardware and user services are also discussed.     

Changes in lymphoid populations of ageing CBA and NZB mice

Changes in subpopulations of lymphoid cells of normal (CBA) and autoimmune (NZB) mice were studied as a function of age, by observing migration patterns of ⁵¹Cr labelled lymph node, spleen and thymus cells from donors aged 8 days to 12 months. The method permits analysis of the proportions and numbers of recirculating and non-recirculating lymphocytes in lymphoid compartments. Changes in the lymphoid populations of CBA mice were found, which could be attributed to the normal processes of maturation and senescence. In NZB mice relative and absolute decreases in the recirculating cell content of lymph node and spleen were observed which coincided with the time of development of autoimmunity. The significance of these results, in relation to altered immunocompetence with age, is discussed.     

Alloactivated long-term cultured human T lymphocytes express both HLA-DR and SB antigens but lack lymphocyte stimulation capacity

Cell populations obtained from mixed leukocyte cultures of 6- or 10-day duration were found specifically to restimulate primed lymphocytes detecting HLA-linked SB as well as HLA-D-associated antigens. After expansion in vitro (9-75 days) with medium containing interleukin 2, the cultured cells expressed the T lymphocyte markers detected in indirect immunofluorescence by monoclonal antibodies Lyt-3, OKT3, OKT4, OKT8, and had high levels of HLA-DR antigens. In addition, they were shown in cell-mediated lymphocytotoxicity specifically to express SB antigens of the donor B cell type. Despite their positivity for DR and SB antigens, such cultured T cells failed to restimulate either SB- or D-specific secondary lymphocyte proliferation. Homogeneous cloned populations of cultured T cells also lacked lymphocyte stimulation capacity. In contrast, B cell lines, which also expressed DR and SB antigens, were potent stimulators of both SB- or D-directed proliferation. These data show that the activated T lymphocytes which express both HLA-DR and SB antigens are by themselves unable to stimulate lymphocyte proliferation.     

Comparison of α-Tocopherol, α-Tocopherol Acetate,and α-Tocopheryl Polyethylene Glycol Succinate 1000 Absorption by Caco-2 TC7 Intestinal Cells

(1) Background: vitamin E is often supplemented in the form of tocopherol acetate, but it has poor bioavailability and can fail to correct blood tocopherol concentrations in some patients with severe cholestasis. In this context, α-tocopheryl polyethylene glycol succinate 1000 (TPGS) has been of value, but very little is known about the mechanisms of its absorption. The aim of our work was to evaluate the mechanisms of absorption/secretion of TPGS compared to tocopherol acetate (TAC) and α-tocopherol by human enterocyte-like Caco-2 TC7 cells. (2) Methods: two weeks post-confluence Caco-2 cells were incubated with tocopherol- or TAC- or TPGS-rich mixed micelles up to 24 h and, following lipid extraction, TAC and tocopherol amounts were measured by high performance liquid chromatography (HPLC) in apical, cellular, and basolateral compartments. (3) Results: at equivalent concentrations of tocopherol in the apical side, the amounts of tocopherol secreted at the basolateral pole of Caco-2 cells are (i) significantly greater when the tocopherol is in the free form in the micelles; (ii) intermediate when it is in the TAC form in the micelles (p < 0.001); and (iii) significantly lower with the TPGS form (p < 0.0001). Interestingly, our results show, for the first time, that Caco-2 cells secrete one or more esterified forms of the vitamin contained in TPGS at the basolateral side.     

Ghrelin as a Biomarker of Stress: A Systematic Review and Meta-Analysis

Introduction: Ghrelin is an orexigenic hormone which favors food-seeking behavior and has been postulated to be a biomarker of stress. We conducted a systematic review and meta-analysis on the evolution of ghrelin levels following acute stress. Methods: The PubMed, Cochrane Library, Embase, and ScienceDirect databases were searched for studies reporting ghrelin levels before and after acute stress in humans. Results: We included ten studies for a total of 348 patients. Acute stress (intervention) was always in a laboratory. Acute stress was psychological (Trier Social Stress Test), physical, or mixed (cold pressure test). The overall meta-analysis demonstrated an increase in ghrelin after the stress intervention (ES = 0.21, 95CI 0.09 to 0.34) compared with baseline levels. Stratification by time demonstrated an acute increase in ghrelin levels in the five minutes immediately following the initiation of stress (0.29, 0.10 to 0.48) but without any difference after. Obese individuals had a more significant (ES = 0.51, 95CI 0.18 to 0.84) and prolonged increase in ghrelin levels for up to 45 min compared with non-obese individuals who had a significant increase only five minutes after stress. Moreover, the ghrelin levels increased in response to stress with BMI (coefficient 0.028, 0.01 to 0.49; p = 0.013) and decreased with the time after the stress intervention (coefficient -0.007, −0.014 to −0.001; p = 0.025). Conclusion: Ghrelin is a biomarker of stress, with a short-term increase following acute stress. Obese individuals have both a higher and prolonged response, emphasizing the link between obesity and stress.