Care delivery among refugees and internally displaced persons affected by complex emergencies: a systematic review of the literature

Journal of Public Health - This study reviews the empirical evidence on care delivery in complex emergencies (CEs) to better understand ways of improving care delivery and mitigating inequity in...     

Fluid intake of elderly Europeans

Dehydration is a common fluid disorder which occurs in residents, hospitalised and community-dwelling elderly people. In this study the intake of water and fluids of community-dwelling elderly Europeans is presented in relation to risk factors of dehydration: mental state, ability to perform activities of daily living (ADL), medicine use and body composition. As part of the SENECA-study of 1993, data were collected from a random age-stratified sample (birth cohorts 1913-1918) of inhabitants of small traditional towns in Europe. Food intake data were collected by using the dietary history method. The study population consisted of 629 men and 696 women of the following towns: Hamme/Belgium, Roskilde/Denmark, Haguenau/France, Romans/France, Padua/Italy, Culemborg/the Netherlands, Lisbon/Portugal, Yverdon/Switzerland, Marki/Poland and Ballymoney-Limavady-Portstewart/Northern Ireland/United Kingdom. Fluid intake of elderly people varied between the towns of Europe and between men and women. A high percentage of the female population had a water intake below the cut-off value of 1,700 g. In most towns about 70 percent of daily water intake came from the food groups 'Milk products', 'Alcoholic drinks', 'Juices' and 'Other non-alcoholic drinks'. The consumption of 'Other non-alcoholic drinks' contributed most to daily fluid intake. In the total female population, women with the lowest water intake (first tertile) scored negatively on factors influencing fluid intake (mental state, ADL) in comparison to women of the second and third tertile. However, in the distinct towns no unequivocal relationship emerged between those factors and fluid intake. Yet, women were found to be at higher risk of dehydration because of much lower water intakes than men and because of the overall relationship between a low fluid intake and a poor mental state and ADL problems.     

Regression of rat Dunning R-3327-H prostate carcinoma by treatment with targeted cytotoxic analog of luteinizing hormone-releasing hormone AN-207 containing 2-pyrrolinodoxorubicin

The effects of AN-207, a new targeted cytotoxic analog of LH-RH, were evalued in rats bearing hormone-dependent Dunning R-3327-H prostate carcinomas. AN-207 consists of the agonist [D-Lys(6)]LH-RH linked to 2-pyrrolino-doxorubicin, an intensely potent derivative of doxorubicin. In the first experiment, 2-pyrrolinodoxorubicin was administered at a concentration of 50 nmol/kg, as a single drug (AN-201) and as an unconjugated mixture with [D-Lys(6)]LH-RH or conjugated to the carrier [D-Lys(6)]LH-RH (AN-207). Following the second administration of radical AN-201 alone or mixed with the carrier, all rats died with signs of general toxicity, but all animals treated with the conjugate AN-207, survived. After 5 weeks of treatment with a total dose of 150 nmol/kg AN-207, the tumors regressed from an initial volume of 8.35 +/- 1.7 cm(3) to 4.47 +/- 0.8 cm(3), while tumors in the control group measured 17.84 +/- 2.2 cm(3). The therapy with AN-207 also significantly reduced tumor weight and tumor burden. In the second experiment, we compared the efficacy and toxicity of 3 injections of 25 nmol/kg AN-201 or 25 nmol/kg and 50 nmol/kg AN-207. The initial tumor volume in all groups was between 3.9 and 4.5 cm(3). After 5 weeks of therapy, the tumors of rats treated with 50 nmol/kg AN-207 regressed to 2.3 +/- 0.51 cm(3), whereas 25 nmol/kg AN-201 was still toxic in contrast to 25 nmol/kg AN-207, while the reduction in final tumor volume was similar (6.76 +/- 1.4 cm(3) and 6.74 +/- 1 cm(3), respectively), as compared to 15.6 +/- 2.2 cm(3) for untreated animals. High capacity LH-RH receptors were found in the membranes of untreated Dunning tumor specimens, but after treatment with AN-207, they could no longer be detected. This is the first demonstration that the new targeted cytotoxic LH-RH analog AN-207 is an effective antitumor agent. Our work indicates that the cytotoxic analog AN-207 is much less toxic than the antineoplastic radical (AN-201) incorporated, and significantly more active in inhibiting tumor growth. Further development of approaches based on targeted cytotoxic analog AN-207 may lead to major improvements in current palliative therapy of prostate cancer.     

High maternal body weight and pregnancy outcome

Evidence of adverse perinatal outcomes among infants of obese pregnant women is confirmed by results of a large Swedish, population-based cohort study. Increasing maternal body weight was associated with perinatal mortality, although it protected against the delivery of a small-for-gestational-age infant.     

Myocardial high-energy phosphate metabolism in heart transplant patients is temporarily altered irrespective of rejection

A reliable, sensitive, non-invasive alternative for transvenous endomyocardial biopsy in detecting cardiac allograft rejection is desirable for optimal management of heart transplant patients. To establish whether (31)P magnetic resonance spectroscopy can become a non-invasive tool for detecting cardiac allograft rejection, the cardiac high-energy phosphate metabolism of human heart transplants was serially examined in 13 patients by means of (31)P MRS from post-operative day 13 to day 294, and compared with histologic evaluation of endomyocardial biopsies. Biopsy scores of 2 or higher, according to the Working Formulation criteria of Billingham et al., were considered to indicate rejection. Logistic regression, which was corrected for differences between the individual patients and the time after transplantation, showed no significant correlation between the occurrence of histologically detected rejection and the PCr:ATP ratio. However, using an analysis of variance, the PCr:ATP ratios of non-rejecting cases obtained within 50 days after transplantation (mean: 27 +/- 11 days) appeared to be significantly different from those obtained after post-operative day 50 [0.95 +/- 0.17 (n = 25) vs 1.17 +/- 0.17 (n = 32), mean +/- SD; p < 0.01]. No significant difference was observed between the PCr:ATP ratios obtained 100 days after transplantation (mean: 162 +/- 52 days) and the PCr:ATP ratios in the hearts of healthy volunteers [1.18 +/- 0. 18 (n = 19) and 1.23 +/- 0.17 (n = 6), mean +/- SD, respectively; p = 0.55]. The PCr:ATP ratio in transplanted human hearts is not a sensitive indicator for the detection of early acute human cardiac allograft rejection. This may be due to a temporarily altered high-energy phosphate metabolism early after transplantation irrespective of rejection.     

Microelectrode measurements of the effects of basolateral adenosine in polarized human intestinal epithelial cells in culture

 Activation of the basolateral receptor for adenosine in HT-29cl.19A cells, by 100 μM adenosine, increased the equivalent short-circuit current (ΔI _sc= 24±2 μA/cm²), depolarized the intracellular potential (ΔV _a= 26±2 mV) and decreased the fractional apical membrane resistance (ΔfR _a=–0.48). The changes in all parameters reached their peak values simultaneously. This suggests that the primary action of the adenosine-activated pathway is on only one membrane. Bumetanide inhibited the transepithelial response and repolarized the cell potential. After preincubation with 100 μM forskolin, application of 300 μM adenosine caused a significant further change in V _a, I _sc, the transepithelial potential (V _t) and fR _a. Together with the results from ion-replacement studies, the observations indicate that adenosine activates channels other than the cystic fibrosis transmembrane conductance regulator (CFTR). The rank order of potencies of adenosine and adenosine analogues implies that the receptor is of the A₂ subtype. Preincubation with 4-bromophenacyl bromide (4-BPB) inhibited the effect of an adenosine analogue by 50%, indicating that activation of phospholipase A₂ may be involved in the adenosine-induced response. Received: 5 August 1998 / Received after revision: 12 October 1998 / Accepted: 5 November 1998     

Cytokines associated with amyloid plaques in Alzheimer's disease brain stimulate human glial and neuronal cell cultures to secrete early complement proteins, but not C1-inhibitor

Complement activation products C1q, C4c/d, and C3c/d in amyloid plaques in Alzheimer's disease probably result from direct binding and activation of C1 by amyloid beta peptides. RT-PCR and in situ hybridization studies have shown that several complement factors are produced in the brain parenchyma. In the present study, cytokines that can be detected in amyloid plaques (i.e., interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-alpha) were found to differentially stimulate the expression of C1 subcomponents, C1-Inhibitor (C1-Inh), C4, and C3, by astrocyte and microglial cell cultures derived from postmortem adult, human brain specimens and by neuroblastoma cell lines in culture. C1r and C1s were secreted at low levels by astrocytes and neuroblastoma cell lines. Exposure of cells to IL-1 alpha, IL-1 beta, TNF-alpha and to a far lesser extent IL-6, markedly upregulated C1r, C1s, and C3 production. C4 synthesis increased in response to interferon (IFN)-gamma and IL-6, whereas that of C1-Inh could be stimulated only by IFN-gamma. Thus, C1-Inh production is refractory to stimulation by plaque-associated cytokines, whereas these cytokines do stimulate C1r, C1s, and also C4 and C3 secretion by astrocytes and neuronal cells in culture. In contrast to the amyloid plaque associated cytokines IL-1 beta, IL-1 alpha, and TNF-alpha, the amyloid peptide A beta 1-42 itself did not stimulate C1r and C1s synthesis by astrocytes, microglial cells, or neuroblastoma cell lines. Microglial cells were the only cell type that constitutively expressed C1q. The ability of C1q to reassociate with newly formed C1r and C1s upon activation of C1 and subsequent inactivation by C1-Inh, may enable ongoing complement activation at sites of amyloid deposition, especially when C1-Inh is consumed and not replaced.