Dependence and necessities of non-covered services for the elderly in a health sector of Zaragoza

BACKGROUND: Dependency to carry out the activities of daily living (ADL) and home care needs of older adults depend upon factors which are not well understood. Caregiving is mainly provided by the family. The aim of this study is to estimate the prevalence of ADL dependence and associated factors among older adults and to identify associated factors with unmet home care needs in people over age 75 in Zaragoza (Spain). METHOD: A cross-sectional study was conducted on a representative sample of the community dwelling population over age, 75 in one Health Care District in Saragossa in 1998 (n = 351). Data were collected during a personal interview. ADL dependency was assessed by the Katz index. Home care needs were assessed using prevalent norms for desired frequency of care. Sources of informal care, socio-demographic characteristics, self-rated health and depression (Yesavage Geriatric Depression Scale) were considered independent variables. Logistic regression was used to identify factors associated with both ADL dependency and unmet home care needs. RESULTS: Prevalence of ADL dependence is 37.3%. The variables predicting ADL dependence are the perception of poor health, depression, being a female and being over 85 years of age. The prevalence of unmet care needs among ADL dependent individuals is 22.1%. Sources of help are limited to the families. Being a woman and living alone are the stronger risk factors for unmet needs. CONCLUSIONS: A high percentage of older adults are dependent. Informal support is insufficient and confined to the family. The social and health care system in Spain should provide to the family, emotional, financial and social support and special care for disabled people living alone and with limited material resources.     

Improving the management of waiting lists for elective healthcare services: public perspectives on proposed solutions

An innovative approach to managing waiting lists and access to elective care, and one that is more fair and consistent with the 'guarantee of access' as stipulated in the Canada Health Act, has been developed by a partnership of medical associations, provincial ministries of health, regional health authorities and research centres. Operating as the Western Canada Waiting List Project, this group has developed beta versions of waiting list prioritization tools in five problematic clinical areas: hip and knee joint replacement; cataract removal surgery; general surgery; children's mental health services; and MRI scanning.     

Surgical performance measurement

The need for effective surgical performance measurement has gained an increasingly high profile in recent years, particularly since events at Bristol Royal Infirmary, where apparent poor performance has prompted the UK Department of Health to instigate a major Public Inquiry. This paper describes issues that concern the measuring and monitoring of surgical performance, and methods that have been devised for judging a good surgeon from the less competent. The authors are a collaborative team composed of specialists in Cardiothoracic surgery and Operational Research analysts with experience of monitoring performance in cardiac surgery. This paper describes concrete examples from that knowledge base.     

Great balls of fire and the vicious cycle: a study of the effects of cycling on male fertility

Over the past few years we have been bombarded with publicity telling us to do more exercise in order to reduce our risk of developing heart disease. Also, as commuter traffic increases and petrol prices rise, workers are constantly looking for quicker, cheaper and greener ways of travelling short distances. As a result of this, bicycle sales have risen exponentially. However, as the popularity of cycling increases, so do the fears that spending hours in the saddle every day may not be as beneficial as first thought. For many years now reports in the literature have suggested that exercise in general, and cycling specifically, may actually increase an individual's risk of developing problems in the male reproductive system. In this report I will review the evidence available in the literature, paying special attention to cycling and the risks of developing testicular cancer, secondary impotence and, most importantly, the effects on male fertility.     

Bradykinin potentiation by ACE inhibitors: a matter of metabolism

1. Studies in isolated cells overexpressing ACE and bradykinin type 2 (B(2)) receptors suggest that ACE inhibitors potentiate bradykinin by inhibiting B(2) receptor desensitization, via a mechanism involving protein kinase C (PKC) and phosphatases. Here we investigated, in intact porcine coronary arteries, endothelial ACE/B(2) receptor 'crosstalk' as well as bradykinin potentiation through neutral endopeptidase (NEP) inhibition. 2. NEP inhibition with phosphoramidon did not affect the bradykinin concentration-response curve (CRC), nor did combined NEP/ACE inhibition with omapatrilat exert a further leftward shift on top of the approximately 10 fold leftward shift of the bradykinin CRC observed with ACE inhibition alone. 3. In arteries that, following repeated exposure to 0.1 microM bradykinin, no longer responded to bradykinin ('desensitized' arteries), the ACE inhibitors quinaprilat and angiotensin-(1-7) both induced complete relaxation, without affecting the organ bath fluid levels of bradykinin. This phenomenon was unaffected by inhibition of PKC or phosphatases (with calphostin C and okadaic acid, respectively). 4. When using bradykinin analogues that were either completely or largely ACE-resistant ([Phe(8)psi(CH(2)-NH)Arg(9)]-bradykinin and [deltaPhe(5)]-bradykinin, respectively), the ACE inhibitor-induced shift of the bradykinin CRC was absent, and its ability to reverse desensitization was absent or significantly reduced, respectively. Caveolar disruption with filipin did not affect the quinaprilat-induced effects. Filipin did however reduce the bradykinin-induced relaxation by approximately 25-30%, thereby confirming that B(2) receptor-endothelial NO synthase (eNOS) interaction occurs in caveolae. 5. In conclusion, in porcine arteries, in contrast to transfected cells, bradykinin potentiation by ACE inhibitors is a metabolic process, that can only be explained on the basis of ACE-B(2) receptor co-localization on the endothelial cell membrane. NEP does not appear to affect the bradykinin levels in close proximity to B(2) receptors, and the ACE inhibitor-induced bradykinin potentiation precedes B(2) receptor coupling to eNOS in caveolae.     

Bretylium or 6-OHDA-resistant, action potential-evoked Ca2+ transients in varicosities of the mouse vas deferens

Action potential-evoked calcium transients in varicosities in mouse vas deferens were monitored using laser scanning confocal microscopy. Their significance was examined by comparison with excitatory junction potentials (EJPs) and neurogenic contractions, both indirect measurements of transmitter release. Bretylium abolished EJPs, as well as the ATP and NA-mediated phases of contraction. However, bretylium revealed a prominent late component of contraction that was atropine-sensitive. Bretylium abolished calcium transients in 21%, enhanced in 16% and had no effect in 63% of varicosities examined. Pre-treatment with 6-OHDA reduced NA levels to below detectable levels but many strings of varicosities still responded to nerve impulses with 'normal' calcium transients. Varicosities in which calcium transients were abolished by these agents were sympathetic. The identity of those varicosities in which calcium transients were resistant to bretylium (sympathetic but no uptake-1 sites, parasympathetic, sensory) remains to be established.     

Cyclosporins: structure-activity relationships for the inhibition of the human FPR1 formylpeptide receptor

The human formylpeptide receptor (FPR) is a seven-transmembranous G-protein-coupled receptor (7TM-GPCR) for chemotactic peptides of bacterial origins, possibly involved in the recruitment and activation of neutrophils in various inflammatory diseases of mucosal epithelia. Mutational analyses suggest that interactions of formylated peptides with FPR occur on the outer exoplasmic leaflet/domains of the plasma membrane. The immunosuppressive and antifungal antibiotic cyclic undecapeptide cyclosporin A (CsA; cyclo-[MeBmt(1)-Abu(2)-MeGly(3)-MeLeu(4)-Val(5)-MeLeu(6)-Ala(7)-D-Ala(8)-MeLeu(9)-MeLeu(10)-MeVal(11)]) and some tested analogues such as [Ala(2)]-CsA, [Thr(2)]-CsA, [Val(2)]-CsA, and [Nva(2)]-CsA were able of inhibiting the binding of formylpeptides to the FPR, with [D-MeVal(11)]-CsA (CsH) being much more active than the other analogues. CsH is devoid of immunosuppressive and antifungal activities, and its large potency for human FPR inhibition is of inverse agonism origin. Formylpeptide binding to FPR-expressing cells does not only induce chemotaxis; it also causes a rapid release of granule enzymes in the extracellular medium, allowing the easy monitoring of any inhibition of FPR function "in vivo" (with intact live cells). With such an assay, CsH was confirmed to be the most potent FPR inhibitory cyclosporin, although a far related immunosuppressive cyclosporin analogue, FR901459 ([Thr(2), Leu(5), Leu(10)]-CsA), was found to display a high FPR inhibitory activity (FPR-InhA). To establish structure-activity relationships (SAR) for FPR function inhibition, 59 cyclosporins were now studied by this standardized assay (with differentiated human leukemic cell line HL-60 as FPR-expressing cells and with N-acetyl-beta-D-glucosaminidase release as read-out). These SAR confirmed the low FPR-InhA of classical cyclosporins, where such activity was only seldom found: the most active ones ([Thr(2), Ile(5)]-CsA, [aMeIle(11)]-CsA, and [MeAla(11)]-CsA) remained 3-10-fold less potent than CsH. In contrast, the SAR disclosed that N(10)-desmethylated cyclosporins were particularly prone to display a large FPR-InhA: their most potent one was a [Thr(2), Gly(3), Leu(5), D-Hiv(8), Leu(10)]-CsA, found to be only 2-4-fold less active than [D-MeVal(11)]-CsA (CsH), with which it shows six differences out of 11 residues. Because the free conformations of both CsH and N(10)-desmethylated cyclosporins differ from those of "classical" (N(10)-methylated, [L-MeVal(11)]-using) cyclosporins, these potent FPR inhibitory cyclosporins probably bind to FPR pharmacophores for which classical cyclosporins show little affinity. Moreover, because the conformations of the N(10)-desmethylated cyclosporins widely differ from the CsH one, they probably bind to different pharmacophores on the FPR molecules.     

Comparative study of chronic toxic effects of daunorubicin and doxorubicin in rabbits

This study compares the chronic toxicity of two anthracyclines--daunorubicin and doxorubicin, commonly used for induction of anthracycline cardiomyopathy in the rabbit model. Such a comparative study has not been published until now. Both drugs were administered intravenously to male Chinchilla rabbits in doses at 3 mg/kg (50 mg/m2) once weekly for 10 weeks. Selected biochemical, haematological and cardiovascular parameters and body weights were regularly monitored; additionally, a histological evaluation of heart, kidney and liver was performed at the end of the experiment. In the daunorubicin group, there were marked signs of the progressive development of heart failure, like the significant increases of the pre-ejection period/left ventricular ejection time index values (up to 134%)--and histological changes within the myocardium were also observed. On the other hand, the 10-week doxorubicin administration did not cause these changes that are typical for heart injury. Haematotoxicity, manifested particularly by aplastic anaemia, was apparent in both the experimental groups. Significant body weight loss (by 45.2%) and high premature mortality (100% versus 36.4%) reflected a greater general toxicity, especially nephrotoxicity of doxorubicin in comparison with daunorubicin. Further studies are necessary to find a possible explanation for these findings.     

The caudate nucleus in obsessive-compulsive disorder. Reduced metabolism following treatment with paroxetine: a PET study

Several neuroimaging studies of patients with OCD have pointed to basal ganglia and the frontal cortical regions being relevant for an understanding of the pathophysiology and therapy of OCD. In a search for the neural substrate underlying the therapeutic action of paroxetine in the therapy of OCD we measured regional glucose metabolism in a PET study of 20 OCD patients before and after at least 3 months of treatment. We used 18-fluoro-deoxyglucose PET-scanning to measure regional cerebral glucose metabolic rate (rCMRglc) in 20 non-depressed patients fulfilling DSM-IV criteria for OCD. Patients were studied before and after 12-20 wk of treatment with the serotonin re-uptake inhibitor paroxetine. Clinical assessment rating with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) was performed before the first and after the second study. The PET data was analysed regionally using statistical parametric mapping (SPM-96). A clinical improvement was indicated by a mean decrease of 55% in the Y-BOCS score. There was no difference in global cerebral metabolism before and after treatment whereas a post-treatment reduction in normalized rCMRglc was found in the right caudate nucleus. This finding also showed a significant positive correlation with symptom severity. Our results support hypotheses regarding a malfunction of the cortico-striato-thalamic system in the pathophysiology of OCD and particularly point to the caudate nucleus playing an important role for the therapeutic action of paroxetine in the treatment of OCD.