Multi-objective optimization in systematic conservation planning and the representation of genetic variability among populations.

Biodiversity crises have led scientists to develop strategies for achieving conservation goals. The underlying principle of these strategies lies in systematic conservation planning (SCP), in which there are at least 2 conflicting objectives, making it a good candidate for multi-objective optimization. Although SCP is typically applied at the species level (or hierarchically higher), it can be used at lower hierarchical levels, such as using alleles as basic units for analysis, for conservation genetics. Here, we propose a method of SCP using a multi-objective approach. We used non-dominated sorting genetic algorithm II in order to identify the smallest set of local populations of Dipteryx alata (baru) (a Brazilian Cerrado species) for conservation, representing the known genetic diversity and using allele frequency information associated with heterozygosity and Hardy-Weinberg equilibrium. We worked in 3 variations for the problem. First, we reproduced a previous experiment, but using a multi-objective approach. We found that the smallest set of populations needed to represent all alleles under study was 7, corroborating the results of the previous study, but with more distinct solutions. In the 2nd and 3rd variations, we performed simultaneous optimization of 4 and 5 objectives, respectively. We found similar but refined results for 7 populations, and a larger portfolio considering intra-specific diversity and persistence with populations ranging from 8-22. This is the first study to apply multi-objective algorithms to an SCP problem using alleles at the population level as basic units for analysis.

Serum levels of selenium in patients with breast cancer before and after treatment of external beam radiotherapy.

BACKGROUND: To evaluate the influence of radiotherapy on the selenium serum levels of breast cancer patients. PATIENTS AND METHODS: This prospective study includes 209 breast cancer patients treated by external beam radiotherapy from December 2007 until August 2008. Plasma selenium concentrations were determined before and at the end of the radiotherapeutic treatment. Age, clinical stage, prior chemotherapy, body mass index (BMI) and personal habits (smoking and alcoholism) were recorded for each patient. RESULTS: The mean age was 61 years; the mean BMI was 28.7. One hundred and seventy-four patients (83.3%) were nonsmokers. One hundred and eighty-nine patients (90.4%) showed no drinking habits and 110 (52.6%) have no prior chemotherapy. Sixty patients (28.7%) were in clinical stage I, 141 (67.5%) in clinical stage II and 8 (3.8%) in clinical stage III. At the beginning of radiotherapy, the mean selenium value for all patients was 86.4 µg/l and after radiation this value dropped to 47.8 µg/l. Multivariate analysis showed statistically significant difference in the plasma selenium concentration before and after radiotherapy for age (P > 0.001), BMI (P > 0.001), smoking (P > 0.001), alcoholism (P > 0.001), chemotherapy (P > 0.001) and clinical stage (P > 0.001). CONCLUSIONS: Significant reduction in plasma levels of selenium is recorded in patients undergoing radiotherapy, suggesting attention to the nutritional status of this micronutrient and other antioxidant agents.

Endoplasmic reticulum calcium release engages Bax translocation in cortical astrocytes.

Apoptosis is a highly complex form of cell death that can be triggered by alterations in Ca(2+) homeostasis. Members of the Bcl-2 family may regulate apoptosis and modulate Ca(2+) distribution within intracellular compartments. Bax, a proapoptotic member of the family, is constitutively expressed and soluble in the cytosol and, under apoptotic induction, translocates to mitochondrial membranes. However, it is not clear if the intracellular Ca(2+) stores and selective Ca(2+) releases can modulate or control Bax translocation. The aim of this study was to investigate the relation of intracellular Ca(2+) stores with Bax translocation in rat cortical astrocytes. Results show that the classical apoptotic inducer, staurosporine, caused high elevations of cytosolic Ca(2+) that precede Bax translocation. On the other hand, agents that mobilize Ca(2+) from endoplasmic reticulum such as noradrenaline or thapsigargin, induced Bax translocation, while mitochondrial Ca(2+) release evoked by carbonyl cyanide-p-(trifluoromethoxyphenyl) hydrazone was not able to cause Bax punctation. In addition, microinjection of inositol 1,4,5- trisphosphate induced Bax translocation. Taken together, our results show that in Bax overexpressing cortical astrocytes, endoplasmic reticulum-Ca(2+) release may induce Bax transactivation and specifically control apoptosis.

A comparative study between cone-beam computed tomography and periapical radiographs in the diagnosis of simulated endodontic complications.

AIM: To compare cone-beam computed tomography (CBCT) with periapical radiography for the identification of simulated endodontic complications. METHODOLOGY: Sixteen human teeth, in three mandibles, were submitted to the following simulated endodontic complications: G1) fractured endodontic file; G2) root perforation; G3) cast post with deviation; G4) external root resorption. Periapical radiographs were taken of each tooth at three different angles, and CBCT scan was taken. One calibrated examiner who was specialized in dental radiology interpreted the images. The results were analysed using the following scoring system: 0 - unidentified alteration; 1 - alteration identified with inaccurate diagnosis; and 2 - alteration identified with accurate diagnosis. Data were analysed using McNemar and Wilcoxon tests (alfa=0.05). RESULTS: In the overall assessment, CBCT was superior when compared with periapical radiographs (P<0.05). When individual results on each complication were evaluated, CBCT was superior only in the identification of external root resorption (100% Score 2) (P<0.05). CONCLUSION: Cone-beam computed tomography could be an alternative to periapical radiographs especially in the detection and assessment of external root resorption.

Semitendinosus and patellar tendons shear modulus evaluation by supersonic shearwave imaging elastography.

PURPOSE: Shear modulus (µ) is directly correlated to the tissue stiffness and can predict the tendon ultimate force to failure. With the knee extended 0° (K0), semitendinosus tendon (ST) is tensioned while patellar tendon (PT) is relaxed. At 80o , knee flexion (K80) tendons present an opposite stress pattern; however, the relation between ST and PT µ in both situations was not studied yet. METHOD: We accessed the µ of the ST and PT at 0o and 80o knee flexion by supersonic shear wave imaging (SSI) elastography from 18 healthy males. Relative µ indexes were calculated for relaxed and tensioned conditions. RESULT: The average µ for ST was µST-K0  = 197·62 ± 31·93 kPa and µST-K80  = 77·76 ± 30·08. For TP, values were µTP-K0  = 23·45 ± 5·89 and µTP-K80  = 113·92 ± 57·23 kPa. Relative µ indexes were calculated for relaxed (IR = µST-K80 /µTP-K0 ) and tensioned conditions (IT = µST-K0 /µPT-K80 ). The relative µ indexes were IR = 3·63 ± 1·50 and IT = 2·00 ± 0·96 (P<0·05). CONCLUSION: Semitendinosus tendon µ was significantly higher than PT µ in both tensioned and relaxed positions. This can predict a higher ultimate force to failure and a less elastic behaviour in ST grafts when compared to PT grafts. This new parameter could aid physicians in graft choice previous to anterior cruciate ligament reconstruction.

Evaluation of 1000 lacrimal ducts by dacryocystography.

AIM: To establish the association between the obstruction site, whether it is unilateral or bilateral, age group, and sex. METHODS: A retrospective observational study of 1000 lacrimal ducts of 500 consecutive patients seen in the Emílio Amorim Radiological Clinic, who were suspected of having lacrimal duct obstructions, was performed. RESULTS: Of the studied patients, 121 were men and 379 were women. Their ages varied between 2 years and 93 years. 148 of the examinations were normal; in 298 the obstructions were unilateral and in 54 they were bilateral. The majority of the obstructions occurred at the valve of Krause. There was a significant difference in the correlation of the obstruction site with sex. The obstruction was total in 378 valves and partial in 28. Other findings included sinusitis, osteomas, bone fractures, fistulae, diverticulum, and lacrimal stones. CONCLUSION: Obstruction of the lacrimal ducts is normally total, unilateral, and sited at the valve of Krause. The obstruction of this valve predominantly affects women, whereas obstruction of the valve of Hasner mainly affects men. There was no significant difference in the distribution of obstructions by age group.

Bax affects intracellular Ca2+ stores and induces Ca2+ wave propagation.

In the present study, we evaluated proapoptotic protein Bax on mitochondria and Ca2+ homeostasis in primary cultured astrocytes. We found that recombinant Bax (rBax, 10 and 100 ng/ml) induces a loss in mitochondrial membrane potential (Delta Psi m). This effect might be related to the inhibition of respiratory rates and a partial release of cytochrome c, which may change mitochondrial morphology. The loss of Delta Psi m and a selective permeabilization of mitochondrial membranes contribute to the release of Ca2+ from the mitochondria. This was inhibited by cyclosporin A (5 microM) and Ruthenium Red (1 microg/ml), indicating the involvement of mitochondrial Ca2+ transport mechanisms. Bax-induced mitochondrial Ca2+ release evokes Ca2+ waves and wave propagation between cells. Our results show that Bax induces mitochondrial alteration that affects Ca2+ homeostasis and signaling. These changes show that Ca2+ signals might be correlated with the proapoptotic activities of Bax.

Transmission of wireless neural signals through a 0.18 µm CMOS low-power amplifier.

In the field of Brain Machine Interfaces (BMI) researchers still are not able to produce clinically viable solutions that meet the requirements of long-term operation without the use of wires or batteries. Another problem is neural compatibility with the electrode probes. One of the possible ways of approaching these problems is the use of semiconductor biocompatible materials (silicon carbide) combined with an integrated circuit designed to operate with low power consumption. This paper describes a low-power neural signal amplifier chip, named Cortex, fabricated using 0.18 µm CMOS process technology with all electronics integrated in an area of 0.40 mm(2). The chip has 4 channels, total power consumption of only 144 µW, and is impedance matched to silicon carbide biocompatible electrodes.

Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling.

Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death through the regulation of a number of Ca2+-dependent enzymes such as phospholipases, proteases, and nucleases. Mitochondria along with the endoplasmic reticulum play pivotal roles in regulating intracellular Ca2+ content. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. During cellular Ca2+ overload, mitochondria take up cytosolic Ca2+, which in turn induces opening of permeability transition pores and disrupts the mitochondrial membrane potential (deltapsim). The collapse of deltapsim along with the release of cytochrome c from mitochondria is followed by the activation of caspases, nuclear fragmentation and cell death. Members of the Bcl-2 family are a group of proteins that play important roles in apoptosis regulation. Members of this family appear to differentially regulate intracellular Ca2+ level. Translocation of Bax, an apoptotic signaling protein, from the cytosol to the mitochondrial membrane is another step in this apoptosis signaling pathway.

Mitochondrial calcium, oxidative stress and apoptosis in a neurodegenerative disease model induced by 3-nitropropionic acid.

Intracellular calcium homeostasis is important for cell survival. However, increase in mitochondrial calcium (Ca2+m) induces opening of permeability transition pore (PTP), mitochondrial dysfunction and apoptosis. Since alterations of intracellular Ca2+ and reactive oxygen species (ROS) generation are involved in cell death, they might be involved in neurodegenerative processes such as Huntington's disease (HD). HD is characterized by the inhibition of complex II of respiratory chain and increase in ROS production. In this report, we studied the correlation between the inhibitor of the complex II, 3-nitropropionic acid (3NP), Ca2+ metabolism, apoptosis and behavioural alterations. We showed that 3NP (1 mm) is able to release Ca2+m, as neither Thapsigargin (TAP, 2 microm) nor free-calcium medium affected its effect. PTP inhibitors and antioxidants inhibited this process, suggesting an increase in ROS generation and PTP opening. In addition, 3NP (0.1 mm) also induces apoptotic cell death. Behavioural changes in animals treated with 3NP (20 mg/kg/day for 4 days) were also attenuated by pre- and co-treatment with vitamin E (VE, 20 mg/kg/day). Taken together, our results show that complex II inhibition could involve Ca2+m release, oxidative stress and cell death that may precede motor alterations in neurodegenerative processes such as HD.

Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling

Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death through the regulation of a number of Ca2+-dependent enzymes such as phospholipases, proteases, and nucleases. Mitochondria along with the endoplasmic reticulum play pivotal roles in regulating intracellular Ca2+ content. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. During cellular Ca2+ overload, mitochondria take up cytosolic Ca2+, which in turn induces opening of permeability transition pores and disrupts the mitochondrial membrane potential (Dym). The collapse of Dym along with the release of cytochrome c from mitochondria is followed by the activation of caspases, nuclear fragmentation and cell death. Members of the Bcl-2 family are a group of proteins that play important roles in apoptosis regulation. Members of this family appear to differentially regulate intracellular Ca2+ level. Translocation of Bax, an apoptotic signaling protein, from the cytosol to the mitochondrial membrane is another step in this apoptosis signaling pathway