Flavonoids from the Amazon plant Brosimum acutifolium induce C6 glioma cell line apoptosis by disrupting mitochondrial membrane potential and reducing AKT phosphorylation.

Glioblastoma, which is highly invasive and has a poor patient prognosis, is the most common type of brain tumor. Flavonoids have known antiproliferative and antineoplastic effects, such as apoptosis induction and tumor growth inhibition. We investigated the effects of treatment with three flavonoids (BAS-1, BAS-4, and BAS-6) isolated from the Amazon plant Brosimum acutifolium on the proliferation and migration of the C6 glioma cell line. Cytotoxicity was evaluated by MTT assay, and morphological changes were evaluated by phase-contrast microscopy and by transmission electron microscopy. Apoptosis was determined using Annexin V-FITC-propidium iodide (PI) staining. A hemolysis assay was used to evaluate plasma membrane injury. Antiproliferative effects were assessed by wound migration and colony formation assays. Mitochondrial transmembrane potential (ΔΨm) was determined using JC-1 dye and flow cytometry. To identify the flavonoid targets, western blotting was performed. BAS-1 and BAS-4 reduced C6 cell proliferation in a dose-dependent manner. BAS-6 showed no effect. Due to its high toxicity toward primary glial cells and its high hemolytic index, BAS-1 was not used in the remaining experiments. BAS-4 treatment did not induce cytotoxicity in primary glial cells; however, in glioma cells, it suppressed migration and invasion and led to apoptosis through mitochondrial damage, ΔΨm loss, cell cycle arrest, and reduced AKT phosphorylation, which is a component of the main cell survival pathway. We conclude that BAS-4 showed potential activity against glioma by inducing apoptosis mediated by ΔΨm loss and AKT pathway disruption, and future studies should further evaluate BAS-4 as a promising antineoplastic agent against glioblastoma.

Equity-focused health impact assessment of Portuguese tobacco control legislation.

The World Health Organization recommend the Equity-Focused Health Impact Assessment (HIA) as a means to assess the impact of social and economic policies on the health of populations, and acknowledges their contribution to health inequality. We describe the application of the Equity-focused Impact Assessment methodology on the Portuguese law on Smoking Prevention and Tobacco Control (Law No. 37/2007). A rapid assessment was carried out to issue recommendations which could be incorporated into the law during a revision in 2014. Quantitative (consumption and health status indicators; equity analysis) and qualitative (Focus Group) approaches were taken to evaluate the impact of the law and formulate recommendations. Young people, men and women of low socioeconomic status, and pregnant women were identified as requiring specific and appropriate interventions to prevent smoking and support smoking cessation.

Long-term globular adiponectin administration improves adipose tissue dysmetabolism in high-fat diet-fed Wistar rats.

Adiponectin administration to obese or type 2 diabetic patients is still far off, due to its expensive costs and absence of studies demonstrating the effectiveness of its chronic administration. We performed long-term globular adiponectin administration, testing its usefulness in improving adipose tissue metabolism. Adiponectin (98 υg/day) was administered through a subcutaneous minipump with continued release (28 days) to Wistar rats fed a high-fat diet. Adiponectin decreased body weight and adipocyte size, while decreasing circulating leptin levels. More, adiponectin was able to increase IkappaBalpha and PPARgamma levels and to prevent high-fat diet-induced impairment of insulin signalling, especially in epididymal adipose tissue. This resulted in improved glucose profile. High-fat diet caused an impairment of lipolysis in epididymal adipose tissue, which was partially restored by adiponectin treatment. Long-term globular adiponectin administration was able to improve pathways of insulin signalling and lipid storage in adipose tissue of high-fat diet-fed rats, contributing to a better metabolic profile.

Effects of atorvastatin and insulin in vascular dysfunction associated with type 2 diabetes.

Atorvastatin and insulin have distinct mechanisms of action to improve endothelial function. Therefore, we hypothesized that atorvastatin and insulin therapies alone or in combination could have beneficial effects on endothelium-dependent vascular reactivity, oxidative stress, inflammation and metabolic parameters in Goto-Kakizaki (GK) rats, a model of type 2 diabetes fed with atherogenic diet (GKAD). In parallel with the development of diabetes and lipid profile, the generation of oxidative stress was determined by measurement of lipid peroxides and oxidized proteins and the presence of inflammation was evaluated by assessing C-reactive protein (CRP). Additionally, endothelial dependent and independent vascular sensitivity to acetylcholine and sodium nitroprusside were evaluated. GKAD showed increased carbonyl stress, inflammation, fasting glycemia, dyslipidemia and endothelial dysfunction when compared to control GK rats. Noteworthy, supplementation with insulin deteriorated endothelial dysfunction while atorvastatin induced an improvement. Atorvastatin and insulin therapies in combination improved metabolic parameters, CRP levels and insulin resistance indexes and ameliorated endothelial dysfunction in GKAD rats while they were unable to reduce urinary 8-isoprostranes and plasma carbonyl compounds. The therapeutic association of atorvastatin and insulin provided a better metabolic control with a reduction in endothelial dysfunction in GKAD rats by a mechanism that involves an improvement in systemic inflammation.

Methylglyoxal chronic administration promotes diabetes-like cardiac ischaemia disease in Wistar normal rats.

BACKGROUND AND AIMS: The influence of lifestyle is well documented, especially the diet regime, in the development of type 2 diabetes (T2D) and associated cardiovascular diseases. Diabetic patients have increased risk of suffering cardiac ischemia and impaired response to such accidents. Methylglyoxal (MG) circulates at high concentration in diabetics' blood and is linked to the development of diabetes chronic complications. We propose that besides promoting the cardiovascular disease, MG may also negatively regulate the endogenous cardioprotection pathways after ischemia. METHODS AND RESULTS: We performed a comparative study between three animal groups: normal Wistar (W), type 2 diabetic non-obese Goto-Kakizaki (GK) and normal rats submitted to MG chronic administration (3 months) with gradually enhanced concentration, up to 75 mg/Kg (WMG). Hearts were submitted to different experimental conditions: control, ischemia and ischemia-reperfusion. Levels of oxidative stress markers, advanced glycation end-products (AGEs) and their receptors (RAGEs) were evaluated. The serine/threonine protein kinase Akt (Akt), crucial for cardiomyocytes recovery after ischemia, and apoptosis markers were also assessed. Levels of MG, systemic and cardiac oxidative stress markers, AGEs and RAGEs were similar in GK and WMG groups. Akt protein was negatively regulated by MG, leading to impaired apoptotic markers. CONCLUSION: Chronic MG administration to normal rodents mimicked most diabetic alterations, being associated with the development of cardiovascular disease and the impairment of survival pathways. Our results demonstrate the negative effect of MG rich diet in healthy animals and suggest the potential of methylglyoxal as a therapeutic target in diabetes.

Common mechanisms of dysfunctional adipose tissue and obesity-related cancers.

The relation between cancer and metabolic disorders was recognized several decades ago, but the underlying mechanisms involved in cancer development and progression remain obscure. In the last years, many groups have been studying systemic adipose tissue markers in cancer patients. However, few consistent results were obtained. On the other hand, several studies revealed many aspects of adipose tissue physiology in obesity. Nowadays, it is recognized that excessive lipid uptake in adipocytes leads to hypertrophy and consequently to metabolic dysregulation, hypoxia, inflammation, impaired adipocytokine expression and angiogenesis, insulin resistance and macrophage recruitment. In obese patients, tumours commonly colocalize with excessive adipose tissue accumulation, and most of the features of hypertrophic adipose tissue are observed in cancer patients, namely breast and colon. This review aimed to summarize pathological adipose tissue alterations that may contribute to cancer aetiology and development.

Methylglyoxal causes structural and functional alterations in adipose tissue independently of obesity.

CONTEXT: Adipose tissue is one of the first organs to develop insulin resistance even with moderate BMI. However, the contribution of developing hyperglycaemia and concomitant methylglyoxal increment to tissue dysfunction during type 2 diabetes progression was not addressed before. METHODS: Young and aged Wistar and Goto-Kakizaki rats (non-obese model of type 2 diabetes) and a group of MG-treated W rats were used to investigate the chronic effects of hyperglycaemia and ageing and specifically MG-induced mechanisms. RESULTS: Diabetic and aged rats showed decreased adipose tissue irrigation and interstitial hypoxia. Hyperglycaemia of diabetic rats leaded to fibrosis and accumulation of PAS-positive components, exacerbated in aged animals, which also showed decreased hipoadiponectinemia, increased MCP-1 expression and macrophage infiltration to glycated fibrotic regions. MG leaded to increased free fatty acids, hipoadiponectinemia, decreased irrigation, hypoxia and macrophage recruitment for glycated fibrotic regions. CONCLUSIONS: MG contributes to dysfunction of adipose tissue during type 2 diabetes progression.

Study of neurinomas with ultrasound contrast media: review of a case series to identify characteristic imaging patterns.

PURPOSE: The aim of this study was to evaluate whether there exists a characteristic distribution pattern of vessels within neurinomas that may be used to characterise this type of lesion by employing a contrast-specific ultrasound technique. MATERIALS AND METHODS: Between January 2003 and May 2010, 66 suspected neurinomas were evaluated according to their sonographic features (solid fusiform mass with well-defined margins located in direct continuity with the nerve that was not always discernible and heterogeneous as a result of the presence of small cystic areas or calcifications). The lesions were examined using a sonographic contrast medium consisting of sulphur hexafluoride microbubbles and equipment with dedicated contrast-specific software [contrast tuned imaging (CnTI)]. Of these lesions, five were excluded from the analysis because the definitive diagnosis was not available (in two cases, the follow-up was still in progress, whereas in the remaining three, there was no follow-up). Our study, therefore, is based on 61 surgically excised lesions that were confirmed to be neurinomas by histology, which is regarded as the gold standard. RESULTS: In 41/61 cases (67.2%), we identified an enhancement pattern that we termed reticular owing to the interweaving of blood vessels, of which two subtypes were identified depending on whether the interwoven vessels were densely or sparsely packed: loose-knit reticular in 18/41, and tight-knit reticular in 23/41. In 20/61 (32.8%) cases, we observed a vascular pattern of diffuse heterogeneous enhancement, which was divided into two subtypes based on the presence of one (7/20) or more (13/20) avascular areas. CONCLUSIONS: Results showed that all neurinomas studied could be divided into two groups according to the type of enhancement pattern observed: reticular or diffuse heterogeneous.

Free-standing urethane/urea elastomer films undoped and doped with ferro-nano-particles.

We report on an experimental study of the structures presented by urethane/urea elastomeric films without and with ferromagnetic nanoparticles incorporated. The study is made by using the X-ray diffraction, nuclear magnetic resonance (NMR), optical, atomic and magnetic force (MFM) microscopy techniques, and mechanical assays. The structure of the elastomeric matrix is characterized by a distance of 0.46 nm between neighboring molecular segments, almost independent on the stretching applied. The shear casting performed in order to obtain the elastomeric films tends to orient the molecules parallel to the flow direction thus introducing anisotropy in the molecular network which is reflected on the values obtained for the orientational order parameter and its increase for the stretched films. In the case of nanoparticles-doped samples, the structure remains nearly unchanged although the local order parameter is clearly larger for the undoped films. NMR experiments evidence modifications in the molecular network local ordering. Micrometer size clusters were observed by MFM for even small concentration of magnetic particles.

Methylglyoxal-induced imbalance in the ratio of vascular endothelial growth factor to angiopoietin 2 secreted by retinal pigment epithelial cells leads to endothelial dysfunction.

Progressive microvascular complications are a main feature of diabetes and are associated with impairment of the angiogenic response. Methylglyoxal (MGO) has been implicated in the molecular events that lead to endothelial dysfunction in diabetes. In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells. Indeed, we show that MGO increases the levels of Ang 2 and dramatically decreases the levels of VEGF secreted by RPE cells in response to hypoxia. Downregulation of VEGF is likely to be related to decreased hypoxia-inducible factor-1alpha (HIF-1alpha) protein levels and HIF-1 transcriptional activity. Data further show that MGO-induced imbalance in the VEGF/Ang II ratio significantly changes the levels of BAX and Bcl-2 in endothelial cells. Moreover, this imbalance is accompanied by an increase in the activity of caspase-3 and decreased proliferation of endothelial cells. Data obtained in cell culture systems are consistent with observations in retinas of diabetic animals, where increased availability of MGO is associated with changes in distribution and levels of HIF-1alpha, VEGF and Ang 2 and increased microvascular permeability. In conclusion, the MGO-induced imbalance in the VEGF/Ang 2 ratio secreted by retinal epithelial cells activates apoptosis and decreases proliferation of retinal endothelial cells, which are likely to contribute to endothelial dysfunction in diabetic retinopathy.

Antioxidant and vascular effects of gliclazide in type 2 diabetic rats fed high-fat diet.

Diabetes mellitus is characterized by oxidative stress, which in turn determines endothelial dysfunction. Gliclazide is a sulphonylurea antidiabetic drug with antioxidant effects due to its azabicyclo-octyl ring. It has been reported to potentially protect the vasculature through improvements in plasma lipid levels and platelet function. We hypothesized that gliclazide has a beneficial effect on endothelial function in Goto-Kakizaki rats (GK), an animal model of type 2 diabetes fed an atherogenic diet for 4 months. We evaluated the influence of gliclazide on both metabolic and oxidative status and NO-mediated vasodilation. GKAD rats showed increased oxidative stress and impaired endothelium-dependent vasodilation. GKAD rats treated with gliclazide showed increased sensitivity to NO-mediated vasodilation, a significant decrease in fasting glycemia and insulinemia, and a significant decrease in systemic oxidative stress. In conclusion, our results suggest that gliclazide treatment improves NO-mediated vasodilation in diabetic GK rats with dyslipidemia probably due to its antioxidant effects, although we cannot rule out substantial benefits due to a reduction in fasting blood glucose. The availability of a compound that simultaneously decreases hyperglycemia, hyperinsulinemia, and inhibits oxidative stress is a promising therapeutic candidate for the prevention of vascular complications of diabetes.

Effects of alpha-lipoic acid on endothelial function in aged diabetic and high-fat fed rats.

BACKGROUND AND PURPOSE: This study was conducted to investigate the effects of alpha-lipoic acid (alpha-LA) on endothelial function in diabetic and high-fat fed animal models and elucidate the potential mechanism underlying the benefits of alpha-LA. EXPERIMENTAL APPROACH: Plasma metabolites reflecting glucose and lipid metabolism, endothelial function, urinary albumin excretion (UAE), plasma and aortic malondialdehyde (MDA) and urinary 8-hydroxydeoxyguanosine (8-OHdG) were assessed in non-diabetic controls (Wistar rats), untreated Goto-Kakizaki (GK) diabetic and high-fat fed GK rats (fed with atherogenic diet only, treated with alpha-LA and treated with vehicle, for 3 months). Vascular eNOS, nitrotyrosine, carbonyl groups and superoxide anion were also assessed in the different groups. KEY RESULTS: alpha-LA and soybean oil significantly reduced both total and non-HDL serum cholesterol and triglycerides induced by atherogenic diet. MDA, carbonyl groups, vascular superoxide and 8-OHdG levels were higher in GK and high-fat fed GK groups and fully reversed with alpha-LA treatment. High-fat fed GK diabetic rats showed significantly reduced endothelial function and increased UAE, effects ameliorated with alpha-LA. This endothelial dysfunction was associated with decreased NO production, decreased expression of eNOS and increased vascular superoxide production and nitrotyrosine expression. CONCLUSIONS AND IMPLICATIONS: alpha-LA restores endothelial function and significantly improves systemic and local oxidative stress in high-fat fed GK diabetic rats. Improved endothelial function due to alpha-LA was at least partially attributed to recoupling of eNOS and increased NO bioavailability and represents a pharmacological approach to prevent major complications associated with type 2 diabetes.

Soybean oil treatment impairs glucose-stimulated insulin secretion and changes fatty acid composition of normal and diabetic islets.

We investigated the effect of sub-chronic soybean oil (SO) treatment on the insulin secretion and fatty acid composition of islets of Langerhans obtained from Goto-Kakizaki (GK), a model of type 2 diabetes, and normal Wistar rats. We observed that soybean-treated Wistar rats present insulin resistance and defective islet insulin secretion when compared with untreated Wistar rats. The decrease in insulin secretion occurred at all concentrations of glucose and arginine tested. Furthermore we observed that soybean-treated normal islets present a significant decrease in two saturated fatty acids, myristic and heneicosanoic acids, and one monounsaturated eicosenoic acid, and the appearance of the monounsaturated erucic acid. Concerning diabetic animals, we observed that soybean-treated diabetic rats, when compared with untreated GK rats, present an increase in plasma non-fasting free fatty acids, an exacerbation of islet insulin secretion impairment in all conditions tested and a significant decrease in the monounsaturated palmitoleic acid. Altogether our results show that SO treatment results in a decrease of insulin secretion and alterations on fatty acid composition in normal and diabetic islets. Furthermore, the impairment of insulin secretion, islet erucic acid and fasting plasma insulin levels are similar in treated normal and untreated diabetic rats, suggesting that SO could have a deleterious effect on beta-cell function and insulin sensitivity.

Sources of endogenous glucose production in the Goto-Kakizaki diabetic rat.

Plasma glucose, insulin and glucose tolerance were quantified in diabetic Goto-Kakizaki (GK) rats (342+/-45 g, n = 5) and compared with weight-matched non-diabetic Wistars (307+/-30 g, n = 8). Compared to Wistars, GK rats had higher fasting plasma insulin (219+/-50 versus 44+/-14 pmol/l, P<0.002) and glucose (9.2+/-2.3 versus 5.5+/-0.5 mmol/l, P<0.025). GK rats showed impaired glucose tolerance (IPGTT 2 h plasma glucose=14+/-1.5 versus 6.4+/-0.1 mmol/l, P<0.001). Endogenous glucose production (EGP) from glycogenolysis, phosphoenolpyruvate (PEP) and glycerol after 6 hours of fasting was quantified by a primed infusion of [U-(13)C]glucose and (2)H(2)O tracers and (2)H/(13)C NMR analysis of plasma glucose. EGP was higher in GK compared to Wistar rats (191+/-16 versus 104+/-27 mumol/kg per min, P<0.005). This was sustained by increased gluconeogenesis from PEP (85+/-12 versus 35+/-4 mumol/kg per min, P<0.02). Gluconeogenesis from glycerol was not different (20+/-3 in Wistar versus 30+/-6 mumol/kg per min for GK), and glycogenolysis fluxes were also not significantly different (76+/-23 mumol/kg per min for GK versus 52+/-19 mumol/kg per min for Wistar). The Cori cycle accounted for most of PEP gluconeogenesis in both Wistar and GK rats (85+/-15% and 77+/-10%, respectively). Therefore, increased gluconeogenesis in GK rats is largely sustained by increased Cori cycling while the maintenance of glycogenolysis indicates a failure in hepatic autoregulation of EGP.

Insulin attenuates diabetes-related mitochondrial alterations: a comparative study.

This study evaluated and compared the effect of insulin treatment on the status of brain, heart and kidney mitochondria isolated from 12-week streptozotocin (STZ)-induced diabetic rats versus STZ-diabetic animals treated with insulin during a period of 4 weeks. Mitochondria isolated from 12-week citrate (vehicle)-treated rats were used as control. Several mitochondrial parameters were evaluated: respiratory indexes (state 3 and 4 of respiration, respiratory control and ADP/O ratios), transmembrane potential, depolarization and repolarization levels, ATP, glutathione and coenzyme Q contents, production of hydrogen peroxide, superoxide dismutase, glutathione peroxidase and glutathione reductase activities and the ability of mitochondria to accumulate calcium. We observed that diabetes promoted a significant decrease in kidney and brain mitochondrial coenzyme Q9 content while this parameter was increased in heart mitochondria. Furthermore, diabetes induced a significant increase in hydrogen peroxide production in kidney mitochondria this effect being accompanied by a significant increase in glutathione peroxidase and reductase activities. Furthermore, brain mitochondria isolated from diabetic animals presented a lower ATP content and ability to accumulate calcium. In contrast, heart and kidney mitochondria presented a slight higher capacity to accumulate calcium. Insulin treatment normalized the levels of coenzyme Q9 and glutathione peroxidase and reductase activities and increased ATP content and the ability to accumulate calcium. Altogether these results suggest that insulin treatment attenuates diabetes-induced mitochondrial alterations protecting against the increase in oxidative stress and improving oxidative phosphorylation efficiency. In this line, insulin therapy, besides its well-known importance in the maintenance of glycemic control, may help to protect against mitochondrial dysfunction associated to several age-related disorders such as diabetes.

Bienestar psicológico en envejecientes de la República Dominicana / Psychological well being in elderly from the Dominican Republic

En este trabajo presentamos una investigación sobre bienestar psicológico con envejecientes dominicanos. Para ello se partió de la escala de bienestar psicológico de Ryff, consiguiendo mediante análisis factorial y con índices de fiabilidad adecuados una versión reducida de la misma. Además y a partir de los resultados obtenidos se puede observar como el bienestar psicológico no solo depende de factores internos sino que los elementos externos también tienen un peso importante para su logro. Respecto a las diferentes variables utilizadas se pudo evidenciar como esta medida parece disminuir según aumenta la edad, aunque los resultados encontrados no fueron estadísticamente significativos. En cambio sí que se encontraron diferencias estadísticamente significativas en el estado civil y entre los sujetos institucionalizados y no institucionalizados

In this document, an investigation on psychological well-being with Dominican elderly was performed. For this, we ran from the Ryff’ scale of psychological well-being, obtaining a reduced version of the same by factorial analysis and reliability indexes Going by the results obtained, we can observe how psychological well-being not only depends on internal factors but how the external factors also have an important role. With respect to the different variables used, it is possible to view as this measurement seems to diminish according to age increase, although the results found were not statistically significant. However, there were statistically meaninful differences found in the civil state and between the institutionalized and non-institutionalized subjects

A preliminary validation of the Positive and Negative Suicide Ideation (PANSI) inventory with normal adolescent samples.

The present study evaluated the factor structure, reliability, and validity of the Positive and Negative Suicide Ideation (PANSI; Osman, Gutierrez, Kopper, Barrios, & Chiros, 1998) inventory in a sample of high-school youths. The PANSI is designed as a measure of risk and protective factors related to suicidal behavior. Participants (114 boys and 103 girls) completed the PANSI and other self-report instruments. Results of the confirmatory factor analyses supported adequate fit of the 2-factor oblique model to the sample data. Both factor scales attained adequate levels of reliability. Boys and girls did not differ in their responses to the PANSI scales. The PANSI scale scores were associated with scores from related measures. Logistic-regression analyses were used to evaluate the contributions of the PANSI scale scores to differentiate between the study groups. Receiver Operating Characteristic (ROC) analyses, using data from the psychiatric suicide risk and high-school control youths, were used to identify cutoff scores of 1.63 and 3.33 for the PANSI-negative and PANSI-positive scales, respectively.

The Positive and Negative Suicide Ideation (PANSI) inventory: psychometric evaluation with adolescent psychiatric inpatient samples.

In this study, we evaluated the factor structure of the Positive and Negative Suicide Ideation (PANSI) Inventory (Osman, Gutierrez, Kopper, Barrios, & Chiros, 1998) using confirmatory factor analysis (CFA). The PANSI assesses the frequency of negative risk and protective factors that are related to suicidal behavior. Participants (n = 195) were adolescent psychiatric inpatients, ages 14 to 17 years, in the CFA. Results of the CFA supported the fit for the 2-factor oblique model as the best fitting model. The internal consistency reliability estimates of the 2 subscales, the PANSI-Negative (alpha = .96) and the PANSI-Positive (alpha = .89) were high. Scores on the PANSI scales differentiated between suicide attempters and controls and those at severe risk for suicide and controls. Correlational analyses provide strong support for the concurrent validity of the scales. The results of the logistic regression analyses provide support for the use of this new inventory as a risk measure of suicide-related behaviors: Scores on the PANSI scales (n = 54) also showed satisfactory evidence for test-retest reliability over a 2-week period.

Isoform-specific inhibition of voltage-sensitive Ca(2+) channels by protein kinase C in adrenal chromaffin cells.

Selective protein kinase C (PKC) activators and inhibitors were used to investigate the involvement of specific PKC isoforms in the modulation of voltage-sensitive Ca(2+) channels (VSCCs) in bovine adrenal chromaffin cells. Exposure to the phorbol ester phorbol-12,13-dibutyrate (PDBu) inhibited the Ca(2+) currents elicited by depolarizing voltage steps. This inhibition was occluded by the PKC-specific inhibitor Ro 31-8220 but remained unaffected by Gö 6976, a selective inhibitor of conventional PKC isoforms. PDBu treatment caused the translocation of PKC-alpha and -epsilon isoforms from cytosol to membranes. PKC-iota and -zeta showed no signs of translocation. It is concluded that VSCCs are specifically inhibited by the activation of PKC-epsilon in chromaffin cells. This may be relevant to the action of phospholipase-linked receptors involved in the control of Ca(2+) influx, both in catecholaminergic cells and other cell types.

[Implementation strategies of nursing processes for an HIV-positive patient]. / Estratégias de implementação do processo de enfermagem para uma pessoa infectada pelo HIV.

Aiming at valuing the use of strategies such as teaching and learning methods, the relaxation technique and coping are described in a case study concerning a hospitalized HIV-positive person presenting the Acquired Immuno-Defficiency Syndrome (AIDS). The Conceptual Model proposed by Dorothéia Orem (OREM, 1985), Risner's proposal for the conduction of diagnostic thinking and the Nursing Diagnostic Unifying System proposed by NANDA (NANDA, 1996) were use as theoretical framework. Among the identified diagnoses, three were selected in order to exemplify the planning, implementation and process evaluation phases.