Effects of ocean acidification on invertebrate settlement at volcanic CO<inf>2</inf> vents

We present the first study of the effects of ocean acidification on settlement of benthic invertebrates and microfauna. Artificial collectors were placed for 1 month along pH gradients at CO2 vents off Ischia (Tyrrhenian Sea, Italy). Seventy-nine taxa were identified from six main taxonomic groups (foraminiferans, nematodes, polychaetes, molluscs, crustaceans and chaetognaths). Calcareous foraminiferans, serpulid polychaetes, gastropods and bivalves showed highly significant reductions in recruitment to the collectors as pCO2 rose from normal (336-341 ppm, pH 8.09-8.15) to high levels (886-5,148 ppm) causing acidified conditions near the vents (pH 7.08-7.79). Only the syllid polychaete Syllis prolifera had higher abundances at the most acidified station, although a wide range of polychaetes and small crustaceans was able to settle and survive under these conditions. A few taxa (Amphiglena mediterranea, Leptochelia dubia, Caprella acanthifera) were particularly abundant at stations acidified by intermediate amounts of CO2 (pH 7. 41-7.99). These results show that increased levels of CO2 can profoundly affect the settlement of a wide range of benthic organisms. © 2010 Springer-Verlag

Role of mitochondrial raft-like microdomains in the regulation of cell apoptosis

Lipid rafts are envisaged as lateral assemblies of specific lipids and proteins that dissociate and associate rapidly and form functional clusters in cell membranes. These structural platforms are not confined to the plasma membrane; indeed lipid microdomains are similarly formed at subcellular organelles, which include endoplasmic reticulum, Golgi and mitochondria, named raft-like microdomains. In addition, some components of raft-like microdomains are present within ER-mitochondria associated membranes. This review is focused on the role of mitochondrial raft-like microdomains in the regulation of cell apoptosis, since these microdomains may represent preferential sites where key reactions take place, regulating mitochondria hyperpolarization, fission-associated changes, megapore formation and release of apoptogenic factors. These structural platforms appear to modulate cytoplasmic pathways switching cell fate towards cell survival or death. Main insights on this issue derive from some pathological conditions in which alterations of microdomains structure or function can lead to severe alterations of cell activity and life span. In the light of the role played by raft-like microdomains to integrate apoptotic signals and in regulating mitochondrial dynamics, it is conceivable that these membrane structures may play a role in the mitochondrial alterations observed in some of the most common human neurodegenerative diseases, such as Amyotrophic lateral sclerosis, Huntington's chorea and prion-related diseases. These findings introduce an additional task for identifying new molecular target(s) of pharmacological agents in these pathologies

A systematic review of the diagnostic accuracy of physical examination for the detection of cirrhosis

BACKGROUND: We conducted a review of the diagnostic accuracy of clinical examination for the diagnosis of cirrhosis. The objectives were: to identify studies assessing the accuracy of clinical examination in the detection of cirrhosis; to summarize the diagnostic accuracy of reported physical examination findings; and to define the effects of study characteristics on estimates of diagnostic accuracy. METHODS: Studies were identified through electronic literature search of MEDLINE (1966 to 2000), search of bibliographic references, and contact with authors. Studies that evaluated indicants from physical examination of patients with known or suspected liver disease undergoing liver biopsy were included. Qualitative data on study characteristics were extracted. Two-by-two tables of presence or absence of physical findings for patients with and without cirrhosis were created from study data. Data for physical findings reported in each study were combined using Summary Receiver Operating Characteristic (SROC) curves or random effects modeling, as appropriate. RESULTS: Twelve studies met inclusion criteria, including a total of 1895 patients, ranging in age from 3 to 90 years. Most studies were conducted in referral populations with elevated aminotransferase levels. Ten physical signs were reported in three or more studies and ten signs in only a single study. Signs for which there was more study data were associated with high specificity (range 75–98%), but low sensitivity (range 15–68%) for histologically-proven cirrhosis. CONCLUSIONS: Physical findings are generally of low sensitivity for the diagnosis of cirrhosis, and signs with higher specificity represent decompensated disease. Most studies have been undertaken in highly selected populations

The Effect of SOD1 Mutation on Cellular Bioenergetic Profile and Viability in Response to Oxidative Stress and Influence of Mutation-Type.

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the progressive degeneration of motor neurons. Substantial evidence implicates oxidative stress and mitochondrial dysfunction as early events in disease progression. Our aim was to ascertain whether mutation of the SOD1 protein increases metabolic functional susceptibility to oxidative stress. Here we used a motor neuron-like cell line (NSC34) stably transfected with various human mutant SOD1 transgenes (G93A, G37R, H48Q) to investigate the impact of oxidative stress on cell viability and metabolic function within intact cells. NSC34 cells expressing mutant SOD1 showed a dose dependent reduction in cell viability when exposed to oxidative stress induced by hydrogen peroxide, with variation between mutations. The G93A transfectants showed greater cell death and LDH release compared to cells transfected with the other SOD1 mutations, and H48Q showed an accelerated decline at later time points. Differences in mitochondrial bioenergetics, including mitochondrial respiration, coupling efficiency and proton leak, were identified between the mutations, consistent with the differences observed in viability. NSC34 cells expressing G93A SOD1 displayed reduced coupled respiration and mitochondrial membrane potential compared to controls. Furthermore, the G93A mutation had significantly increased metabolic susceptibility to oxidative stress, with hydrogen peroxide increasing ROS production, reducing both cellular oxygen consumption and glycolytic flux in the cell. This study highlights bioenergetic defects within a cellular model of ALS and suggests that oxidative stress is not only detrimental to oxygen consumption but also glycolytic flux, which could lead to an energy deficit in the cell

Fine needle aspiration cytology of a cutaneous metastasis from an extraadrenal paraganglioma: a case report.

BACKGROUND: Pheochromocytomas/paragangliomas are rare tumors originating from neuroectodermic cells, which metastasize in only 10% of cases. CASE: A case of cutaneous metastasis of an extramedullary paraganglioma was diagnosed by fine needle aspiration cytology (FNAC). A 39-year-old woman complained of a recently arisen subcutaneous nodule located on the scalp. Two years before she had suffered from a sporadic extraadrenal paraganglioma located on the sacrum, and had been evaluated by FNAC. Smears were highly cellular and monomorphous; the cells were uniform and mainly isolated with round or ovoid nuclei, dense chromatin and inconspicuous nucleoli, if any. The cytoplasm was ill defined, clear or granular. Oval-spindle-shaped cells and occasional cells with larger nuclei were also observed. Abundant fibrillar material was present in the background, intermingled with the surrounding cells. The immunocytochemical staining performed on cell block sections showed negativity for CK20, HMB45 and LCA and positivity for chromogranin and S100. The cytologic diagnosis was a neuroendocrine tumor, consistent with a metastasis from the former sacral paraganglioma. CONCLUSION: On conventional samples the cytologic features of paraganglioma are typical enough to allow a cytologic diagnosis of a neuroendocrine tumor; this neoplasm should be considered in the differential diagnosis, even in such unusual locations, because of its unpredictable biologic behavior

Avaliação da ingestão de nutrientes de crianças de uma creche filantrópica: aplicação do Consumo Dietético de Referência Assessment of nutrients intake of children in a charity daycare center: application of Dietary Reference Intake

OBJETIVOS: comparar a adequação aparente da ingestão dos nutrientes utilizando os valores de referência "Consumo Dietético de Referência" (Dietary Reference Intake-DRIs) de 35 crianças de uma creche filantrópica, em dois momentos, no ato da matrícula (momento 1) e após seis meses de freqüência na creche (momento 2). MÉTODOS: A avaliação sócio-demográfica foi realizada através de questionário abordando renda, escolaridade, condições de moradia e saneamento básico. Para avaliação do consumo alimentar, no ato da matrícula, a história dietética foi determinada em entrevista com o responsável, com o propósito de obter informações sobre consumo habitual da criança na sua residência. Após o período de seis meses foi utilizado o método de pesagem direta de alimentos (na creche) complementando com o consumo alimentar da criança na residência. A análise dos nutrientes como proteínas, ferro, cálcio e vitamina C, além das fibras alimentares, foi realizada através um programa computacional. Para comparar a adequação dos nutrientes nos dois momentos do estudo utilizou-se o teste t de Student para dados pareados (p < 0,05). RESULTADOS: observou-se que ocorreu uma melhora significativa no consumo médio de nutrientes e de fibras alimentares das crianças, após seis meses de frequência na creche. Chama atenção que nenhuma criança atingiu o nível de adequação de fibras alimentares nos dois momentos do estudo, apesar da diferença significativa. CONCLUSÕES: os resultados sugerem que as creches podem ter um importante papel na melhora do estado nutricional de crianças de estratos sociais menos favorecidos.<br>OBJECTIVES: to compare nutrients intake apparent adequacy through reference values of Dietary Reference Intake (DRIs) of 35 children of a charity daycare center in two instances, when they enrolled (instance 1) and six months after (instance 2). METHODS: socio-demographic assessment was performed through a questionnaire collecting information pertaining to income, school level, living conditions and basic sanitation. To assess food consumption at enrollment, dietary history was informed through an interview with the parent, family member or guardian on the usual intake of the child at home. Following a six month period the weighed food record method (in the daycare center) was performed complemented by the food intake of the child at home. Nutrient analysis such as proteins, iron, calcium and vitamin C in addition to food fibers was performed by specific software. To compare nutrients' adequacy in the two instances of the study the paired Student test (t) (p < 0.05) was used. RESULTS: a significant improvement in the median intake for all nutrients and fiber six moths after child's attendance to the daycare center was determined. No child reached the level of fiber apparent adequacy of the ingestion at the two moments of the study, despite the significant difference. CONCLUSIONS: results suggest that daycare centers can have an important role in the improvement of lower income children nutritional status

The DNA repair complex Ku70/86 modulates Apaf1 expression upon DNA damage

Apaf1 is a key regulator of the mitochondrial intrinsic pathway of apoptosis, as it activates executioner caspases by forming the apoptotic machinery apoptosome. Its genetic regulation and its post-translational modification are crucial under the various conditions where apoptosis occurs. Here we describe Ku70/86, a mediator of non-homologous end-joining pathway of DNA repair, as a novel regulator of Apaf1 transcription. Through analysing different Apaf1 promoter mutants, we identified an element repressing the Apaf1 promoter. We demonstrated that Ku70/86 is a nuclear factor able to bind this repressing element and downregulating Apaf1 transcription. We also found that Ku70/86 interaction with Apaf1 promoter is dynamically modulated upon DNA damage. The effect of this binding is a downregulation of Apaf1 expression immediately following the damage to DNA; conversely, we observed Apaf1 upregulation and apoptosis activation when Ku70/86 unleashes the Apaf1-repressing element. Therefore, besides regulating DNA repair, our results suggest that Ku70/86 binds to the Apaf1 promoter and represses its activity. This may help to inhibit the apoptosome pathway of cell death and contribute to regulate cell survival