[Perception of kidney transplant patients of the need for information about their donors]. / Percepción de los pacientes trasplantados renales sobre la necesidad de información de sus donantes.

OBJECTIVE: To describe the perceptions of renal transplant patients of the need for information about their donors and the potential influence of their donors' biological sex and age. MATERIALS AND METHODS: Analytical, observational, cross-sectional and prospective study. Kidney transplant patients over 18 years old who had been transplanted, at least, one year before were included. A semi-structured survey was conducted, and data were collected from medical records. RESULTS: 104 patients were analyzed, 58% (n=60) were women; median age: 47 years; and median post-transplantation period: 7 years. Seventy-six percent (n=79) expressed that they were interested in knowing their donors' biological sex and age (p < 0.001). When asked whether they would choose their donors' sex and age, only 13% (n=14) answered that they would (p < 0.001). When asked whether they felt that their donors' sex and age might have an influence on them, 78% (n=81) answered that they did not, while 22% answered that they did (p < 0.001). Of the 79 patients who expressed an interest in knowing their donors' biological sex and age, 62% (n=49) stated that appreciation was the reason for it (p=0.0025). CONCLUSION: The appreciation towards that person about whom only sex and age are known would allow patients to imaginarily construct their donors.

Immune cells subpopulations in cerebrospinal fluid and peripheral blood of patients with Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: There is growing evidence supporting the role of inflammation in aneurysmal subarachnoid hemorrhage (aSAH) pathophysiology and it is of great interest to elucidate which immune mechanisms are involved. METHODS: 12 aSAH patients and 28 healthy controls were enrolled prospectively. We assessed leukocytes subpopulations and their activation status by flow cytometry in cerebrospinal fluid (CSF) and peripheral blood (PB) of SAH patients at the same time and in PB of controls. RESULTS: Monocytes and neutrophils were activated in CSF of aSAH patients. The percentage of CD14(++)CD16(+) monocytes were higher in CSF than in PB of aSAH patients, and were also increased in PB of aSAH patients compared with controls. An enhanced expression of CD69 was shown in CSF neutrophils compared with PB in aSAH patients. PB of aSAH patients showed lower percentage of total lymphocytes compared with controls PB. Additionally, lymphocytes were activated in CSF and PB of aSAH patients. CD4(+) and CD8(+) T cells had a decreased expression on CD3 and higher levels of CD69 in CSF compared with PB in aSAH patients. Moreover, PB CD4(+) and CD8(+) T cells of aSAH patients were activated compared with controls. Additionally, CD28 expression was decreased on CSF T lymphocytes. CONCLUSIONS: Our data suggest an important recruitment of leukocytes to the site of injury in aSAH as well as an increased activation at this level. Overall, these results indicate that aSAH probably stimulates both the innate and adaptive immune responses.

IFNgamma regulates PDGF-receptor alpha expression in macrophages, THP-1 cells, and arterial smooth muscle cells.

The recruitment of monocyte-derived macrophages (MDMs) and arterial smooth muscle cells (ASMCs) contributes to inflammation and development of intimal hyperplasia during atherosclerosis. Platelet-derived growth factor (PDGF) is a potent mitogen for SMC, signalling through PDGF-receptor subunits alpha (Ralpha) and beta (Rbeta). We have previously found that interferon gamma (IFNgamma) upregulates PDGF-Ralpha mRNA expression in human MDM (hMDM) which causes an increased migration towards PDGF. In the present study, we found that IFNgamma mediated an upregulation of PDGF-Ralpha mRNA also in THP-1 cells. The induction of PDGF-Ralpha in both hMDM and THP-1 cells was caused by STAT1 binding to the PDGF-Ralpha promoter. In human ASMCs, IFNgamma again stimulated a transient STAT1-binding to the PDGF-Ralpha promoter. However, this was not followed by an upregulation of PDGF-Ralpha mRNA. IFNgamma-stimulation resulted in augmented expression of PDGF-Ralpha protein in differentiated hMDM. Early hMDM only expressed an immature and not fully glycosylated form of the PDGF-Ralpha protein. In contrast, THP-1 cells did not synthesize PDGF-Ralpha protein, implying further posttranscriptional inhibition. Our results contribute to a better understanding of the complex regulation of PDGF-Ralpha expression and how proinflammatory factors may contribute to PDGF-related hyperplasia in vascular diseases.

Cortical and retinal defects caused by dosage-dependent reductions in VEGF-A paracrine signaling.

To determine the function of VEGF-A in nervous system development, we have utilized the Nestin promoter-driven Cre recombinase transgene, in conjunction with a conditional and hypomorphic VEGF-A allele, to lower VEGF-A activity in neural progenitor cells. Mice with intermediate levels of VEGF-A activity showed decreased blood vessel branching and density in the cortex and retina, resulting in a thinner retina and aberrant structural organization of the cortex. Severe reductions in VEGF-A led to decreases in vascularity and subsequent hypoxia, resulting in the specific degeneration of the cerebral cortex and neonatal lethality. Decreased neuronal proliferation and hypoxia was evident at E11.5, leading to increased neuronal apoptosis in the cortex by E15.5. In order to address whether the observed changes in the structural organization of the nervous system were due to a direct and autocrine role of VEGF-A on the neural population, we conditionally inactivated the main VEGF-A receptor, Flk1, specifically in neuronal lineages, by using the Nestin Cre transgene. The normality of these mice ruled out the possibility that VEGF-A/Flk1 signaling has a significant autocrine role in CNS development. VEGF-A dosage is therefore a critical parameter regulating the density of the vascular plexus in the developing CNS that is in turn a key determinant in the development and architectural organization of the nervous system.

An ecological model of Native Hawaiian well-being.

Native Hawaiian well-being and quality of life can be understood and supported in the distinct arenas in which we live, work and interact. At one level, Native Hawaiian well-being is integrally linked to the vitality and abundance of natural resources relied upon for subsistence and cultural practices. At another level the Native Hawaiian family and 'ohana is the core social unit within which the individual lives and interacts. Historically, there are also socially distinct communities and community organizations within which Native Hawaiians function and work to sustain their well being. The historical Native Hawaiian nation and its recognition and re-establishment within the framework of U.S and international law is another important aspect of Native Hawaiian well-being. This article examines each of these arenas in relation to achieving and sustaining Native Hawaiian well-being.