Recovery: revisão sistemática de um conceito / Recovery: systematic review of a concept

O conceito de recovery tem sido descrito em artigos como um estado de recuperação ou restabelecimento de funções psíquicas, físicas e sociais no funcionamento cotidiano. O objetivo do artigo é analisar concepções terminológicas em diferentes metodologias investigativas e a evolução paradigmática da noção de recovery. Pesquisa bibliográfica sistemática na base Pubmed com as palavras "recovery + schizophrenia", limitada a dois anos retrospectivos e a artigos completos gratuitos. Dezenove artigos foram analisados. A maioria destes busca associações entre dada característica e recovery, poucos são aqueles que discutem a sua concepção de forma que se distinga de termos comuns como "cura" e "reabilitação". Recovery como um estado em que o portador de transtorno mental grave possa sentir-se criador de seus caminhos tende a estar presente em estudos com metodologia qualitativa e em revisões bibliográficas, em que a medida de recovery deixa de relacionar-se à ausência de sintomas e passa a priorizar o quão participativa pode ser a vida de um indivíduo apesar da doença. Alguns estudos quantitativos vislumbram essa diferença conceitual. Em pesquisas qualitativas ocorre expansão na concepção de recovery e nas formas de promovê-lo.

The concept of recovery has been described in papers as a state of psychic, physical and social recuperation of day-to-day functions. The scope of this article is to analyze the concepts of the term in different research methodologies and the paradigmatic evolution of the recovery concept. Systematic bibliographical research was conducted in the Pubmed database using the words "recovery + schizophrenia" limited to freely available full papers published in the previous two years. Nineteen papers were analyzed. The majority of the papers sought associations between characteristic data and recovery; few papers discussed the concept in a way to distinguish it from other words like cure or rehabilitation. Recovery as a state in which people with severe mental illness can feel like the creators of their own itinerary tend to be found in qualitative studies and in bibliographic reviews in which the meaning of recovery is not related to the lack of symptoms and tends to prioritize how participative the life of an individual can be despite the disease. Some quantitative studies detect this conceptual difference. In qualitative research there is an increase in the concept of recovery and in ways of promoting it.

Summary of workshop discussions on establishing upper limits for amino acids with specific attention to available data for the essential amino acids leucine and tryptophan.

The morning of the first day of the 8th Amino Acid Assessment Workshop was organized and co-sponsored by the International Council on Amino Acid Science (ICAAS) and the International Life Sciences Institute Research Foundation and was focused on the International Life Sciences Institute Research Foundation's approach to establishing upper limits of nutrients. The remainder of d 1 and all of d 2 were focused on the safety of leucine and tryptophan, with special emphasis on determining the upper level of the safe range of intake. It was recognized that some toxicological frameworks, mainly the key-events dose response framework, might be applicable to amino acids and provide appropriate assistance to regulators in establishing upper limits for amino acids as a group of nutrients used in dietary supplements. ICAAS-funded projects for determining the upper intake limits for the essential amino acid leucine provided the main pool of leucine data discussed at the workshop. The acute clinical study suggests 500 mg/(kg · d) as a possible upper limit for leucine in healthy humans, but the safety margin needed to widen this limit to the general population has not been determined. For tryptophan, the workshop participants found less ground for consensus. Older efficacy studies suggested that tryptophan at 8-15 g/d was well tolerated, but human research was abruptly terminated in the late 1980s and no new data are available. Animal results obtained in pigs and rodents were discussed and 2 possible strategies for applying those outcomes to humans were described.

Alpha-ketoisocaproic acid and leucine provoke mitochondrial bioenergetic dysfunction in rat brain.

Patients affected by maple syrup urine disease (MSUD) present severe neurological symptoms and brain abnormalities, whose pathophysiology is poorly known. In the present study we investigated the in vitro effects of leucine (Leu), alpha-ketoisocaproic acid (KIC) and alpha-hydroxyisovaleric acid (HIV), respectively, the branched-chain amino, keto and hydroxy acids that most accumulate in MSUD, on brain bioenergetic homeostasis, evaluating respiratory parameters obtained by oxygen consumption, membrane potential (Psim), NAD(P)H content, swelling and citric acid cycle enzyme activities in mitochondrial preparations from rat forebrain using glutamate plus malate, succinate or alpha-ketoglutarate as respiratory substrates. KIC increased state 4 and decreased the respiratory control ratio with all substrates, in contrast with Leu and HIV. Furthermore, KIC and Leu, but not HIV, decreased state 3 using alpha-ketoglutarate. A KIC-induced selective inhibition of alpha-ketoglutarate dehydrogenase activity was also verified, with no alteration of the other citric acid cycle activities. The ADP/O ratio and the mitochondrial NAD(P)H levels were also reduced by KIC using glutamate/malate and alpha-ketoglutarate. In addition, KIC caused a reduction in the Psim when alpha-ketoglutarate was the substrate. Finally, KIC was not able to induce mitochondrial swelling. The present data indicate that KIC acts as an uncoupler of oxidative phosphorylation and as a metabolic inhibitor possibly through its inhibitory effect on alpha-ketoglutarate dehydrogenase activity, while Leu acts as a metabolic inhibitor. It is suggested that impairment of mitochondrial homeostasis caused by the major metabolites accumulating in MSUD may be involved in the neuropathology of this disease.

Development of tier-I toxicity assays for Orius insidiosus (Heteroptera: Anthocoridae) for assessing the risk of plant-incorporated protectants to nontarget heteropterans.

A 13-d continuous dietary exposure bioassay using nymphs of the insidious flower bug, Orius insidiosus (Say) (Heteroptera: Anthocoridae), was developed to assess the potential dietary effects of insecticidal substances that have little or no contact toxicity. The nymphs were fed a bee pollen diet treated with different concentrations of an inorganic stomach poison, potassium arsenate, and a cysteine protease inhibitor, E-64. The results showed that the test system was capable of detecting the dietary effects of both substances on the survival and development of O. insidiosus from the nymph to the adult stage in a dose-dependent manner. For the potassium arsenate treatments, approximately 25% of the nymphs survived and developed to the adult stage by 13 d of dietary exposure at 3.8 microg/g of diet, whereas no test nymphs survived to adulthood at or above 15 microg/g of diet. The assay time required for a 75% mortality response ranged from approximately 7 d at 30 microg/g of diet to 13 d at 3.8 microg/g of diet. For the E-64 treatments, no test insects survived to adulthood at any of the concentration tested (75-600 microg/g of diet) by 13 d of dietary exposure, and the assay time required for a 75% mortality response ranged from 5 to 11 d at dietary rates of 600 and 75 microg/g, respectively. The research presented here describes a robust test system that is useful for evaluating potential adverse effects (or toxicity) of plant-incorporated protectants on nontarget heteropteran predators such as O. insidiosus.

Prolonged oral treatment with an essential amino acid L-leucine does not affect female reproductive function and embryo-fetal development in rats.

L-leucine, an essential amino acid, is one of the most popular ingredients in dietary supplements. To investigate a possibility of its embryo-fetal toxicity in rats, 11- to 12-week old dams were orally administered an aqueous solution of L-leucine at doses of 300 or 1000 mg/kg body weight on gestational days 7-17. Body weight and feed intake was evaluated throughout the whole course of pregnancy (days 0-20). L-Leucine did not influence body weight, but at a dose of 1000 mg/kg, slightly enhanced feed intake on days 14 and 18 of pregnancy. Caesarean section (day 20) revealed no influences on the litter size and weight of live-born fetuses, the number of corpora lutea, implantation index or the quality of placenta, and the minor increase in feed intake was considered irrelevant to the pregnancy outcomes. Fetuses were evaluated in a battery of external, visceral and skeletal examinations. No effects of L-leucine on gender ratio and external abnormalities, and no significant treatment-related variations in visceral and skeletal pathologies were observed. These results suggested that L-leucine, administered orally during organogenesis at doses up to 1000 mg/kg body weight, did not affect the outcome of pregnancy and did not cause fetotoxicity in rats.

The effects of a caries-removing gel (Carisolv) on FM3A cell-line in vitro.

OBJECTIVES: The aim of this study was to examine the cytotoxic effects of Carisolv on mouse mammary carcinoma cell line (FM3A) at different application times. METHODS: The FM3A cell line obtained from the European Collection of Animal Cell Cultures was used in the cell culture assays. Exponentially growing cells were seeded in 5x10(5)cells/well in 5 ml of RPMI 1640 medium supplemented with 10(%) fetal calf serum and antibiotics in each well of a six-well plate. Carisolv gel was applied onto the cell culture medium for 1, 5 and 20 min and incubated for 24 h at 37 degrees C in a humidified atmosphere of 5(%) carbon dioxide (CO(2)). After 24 h incubation, the cells were collected by trypsinisation and counted with a hemocytometer. The cytotoxicity of the Carisolv was determined by evaluation of cell growth and viability in comparison to untreated controls (cell growth=100%). For cell viability, the trypane blue exclusion assay was used. Dunnett's t-test was used for statistical analysis. RESULTS: Cell growth was significantly reduced after 20 min application of Carisolv in comparison to the control (p < 0.001) and 1 min treatment groups (p < 0.05) No significant differences were found in cell viability between the study groups. CONCLUSIONS: It can be concluded that prolonged application of Carisolv did not affect cell viability, but had a reducing effect on cell growth in the FM3A cell line.

A randomised, controlled and blinded histological and immunohistochemical investigation of Carisolv on pulp tissue.

OBJECTIVES: This investigation was undertaken to test the hypothesis that Carisolv would show the same safety profile as physiologic saline when in direct contact with pulp tissue for 30 min. Furthermore, the sensory nerve fibre reaction in response to the injury was evaluated. METHODS: Incisors and molars in 40 Sprague-Dawley rats were opened and the pulp tissue randomly exposed to either Carisolv or NaCl for 30 min. Observation periods ranged from I day to I week. RESULTS: Light microscopic examination showed an almost identical cellular response in both test teeth and controls, which consisted of a localised inflammation represented predominantly by macrophages. Immunohistochemistry revealed an accumulation of beaded CGRP-immunoreactive fibres in immediate vicinity of the lesion, suggesting that the nerves had emitted small sprouts. Some fibres at this location were SP-positive, but very few, or no nerve fibres, displayed NPY-immunoreactivity. This innervation pattern was seen in both test and controls in similar distribution and at similar intensity. CONCLUSIONS: Results obtained in this study suggests the hypothesis to be valid, i.e. Carisolv does not seem to add appreciable adverse effects over and beyond what is caused by the experimental procedures. Furthermore, Carisolv does not seem to influence the distribution or neuropeptide expression of sensory nerve fibres in the pulp.