Sensor systems testbed for telerobotic navigation

A testbed has been developed for the study of sensor systems to be used in telerobotic operations. The program, conducted in conjunction with Johnson Space Center of NASA, addresses the navigational problems associated with target acquisition and rendezvous for teleoperated robotic work stations. The program will utilize a mobile platform which will support various sensor systems during their development and testing in an earth-based environment. The testbed has been developed in support of a program to develop sensor systems that will aid in rendezvous and docking operations to be conducted as a part of the space station program. A mobile platform has been used to permit testing of these components in a conventional laboratory environment with consequent savings in cost and complexity. The sensor systems, while representative of devices currently in use for robotic applications, are not considered prototypical of the ones that will be used in the final applications. The test program provided information that will support the design of system augmentations and will lead to a comprehensive test program for sensor development

Nup358 integrates nuclear envelope breakdown with kinetochore assembly

Nuclear envelope breakdown (NEBD) and release of condensed chromosomes into the cytoplasm are key events in the early stages of mitosis in metazoans. NEBD involves the disassembly of all major structural elements of the nuclear envelope, including nuclear pore complexes (NPCs), and the dispersal of nuclear membrane components. The breakdown process is facilitated by microtubules of the mitotic spindle. After NEBD, engagement of spindle microtubules with chromosome-associated kinetochores leads to chromatid segregation. Several NPC subunits relocate to kinetochores after NEBD. siRNA-mediated depletion of one of these proteins, Nup358, reveals that it is essential for kinetochore function. In the absence of Nup358, chromosome congression and segregation are severely perturbed. At the same time, the assembly of other kinetochore components is strongly inhibited, leading to aberrant kinetochore structure. The implication is that Nup358 plays an essential role in integrating NEBD with kinetochore maturation and function. Mitotic arrest associated with Nup358 depletion further suggests that mitotic checkpoint complexes may remain active at nonkinetochore sites

Saúde Brasil 2011 : uma análise da situação de saúde e a vigilância da saúde da mulher

Introdução: No Brasil, ocorrem cerca de 3 milhões de nascimentos ao ano, sendo grande parte deles por meio de cesarianas. Entender como se distribui esse procedimento no País é relevante para a reflexão sobre o papel das políticas públicas nesse contexto. Objetivos: a) Descrever: magnitude e tendência da taxa de cesáreas*1 no País; morbimortalidade materna e neonatal associada a tipo de parto; e características dos hospitais; b) analisar o preenchimento das variáveis da nova versão da Declaração de Nascido Vivo (DNV) que permitirão monitoramento das indicações de cesárea; c) descrever as respostas institucionais para o enfrentamento do problema. Métodos: Estudo descritivo de série histórica da taxa de cesarianas, no País e macrorregiões, segundo características sociodemográficas, morbimortalidade e tipo de provedor, com fonte em bancos de dados oficiais. Analisou-se a completitude de variáveis da versão da DNV de 2010 para monitoramento das indicações de cirurgia. Foram pesquisados documentos oficiais, visando identificar iniciativas para qualificar a atenção a partos e nascimentos e reduzir cesarianas desnecessárias. Resultados: A taxa de cesarianas foi de 32%, em 1994, e de 52%, em 2010, sendo menor no Norte e Nordeste. Mulheres submetidas a cesáreas tiveram 3,5 vezes mais probabilidade de morrer (entre 1992–2010) e 5 vezes mais de ter infecção puerperal (entre 2000–2011) que as de parto normal. No período, a proporção de prematuros se elevou, mais nas cesáreas (7,8%, sendo 6,4% nos partos normais em 2010). Em 2010, hospitais não públicos apresentaram taxas maiores (63,6%) e maior aumento no período de 2006 a 2010 (14,0%); para os públicos, as taxas foram de 47,8% (federais), de 39,6% (estaduais) e de 34,0% (municipais). Conclusão: A cesariana é frequente e sua proporção ascende no País, sendo muito elevada no setor de Saúde Suplementar. Para reverter essa tendência, serão necessárias várias medidas, incluindo a qualificação da informação para monitorar a efetividade das medidas propostas

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

Comparative Toxicity of Diphacinone to Northern Bobwhite (\u3ci\u3eColinus virginianus\u3c/i\u3e) and American Kestrels (\u3ci\u3eFalco sparverius\u3c/i\u3e)

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be about 20 times greater to American kestrels (LD50=97 mg/kg) than to northern bobwhite (LD50=2,014 mg/kg). Several precise and sensitive clotting assays (prothrombin time, Russell’s Viper venom time, thrombin clotting time) were adapted for use in these species, and this combination of assays is recommended to detect effects of diphacinone and other rodenticides on coagulation. Oral administration of diphacinone over a range of doses (sublethal to the extrapolated LD15) prolonged prothrombin time and Russell’s Viper venom time within 24 to 48 hrs post-exposure. Prolongation of in vitro clotting time reflects impaired coagulation complex activity and was detected before or at the onset of overt signs of toxicity and lethality. These data will assist in the development of a pharmacodynamic model to assess and predict rodenticide toxicity to non-target avian species

Coupling of the nucleus and cytoplasm: role of the LINC complex

The nuclear envelope defines the barrier between the nucleus and cytoplasm and features inner and outer membranes separated by a perinuclear space (PNS). The inner nuclear membrane contains specific integral proteins that include Sun1 and Sun2. Although the outer nuclear membrane (ONM) is continuous with the endoplasmic reticulum, it is nevertheless enriched in several integral membrane proteins, including nesprin 2 Giant (nesp2G), an 800-kD protein featuring an NH2-terminal actin-binding domain. A recent study (Padmakumar, V.C., T. Libotte, W. Lu, H. Zaim, S. Abraham, A.A. Noegel, J. Gotzmann, R. Foisner, and I. Karakesisoglou. 2005. J. Cell Sci. 118:3419–3430) has shown that localization of nesp2G to the ONM is dependent upon an interaction with Sun1. In this study, we confirm and extend these results by demonstrating that both Sun1 and Sun2 contribute to nesp2G localization. Codepletion of both of these proteins in HeLa cells leads to the loss of ONM-associated nesp2G, as does overexpression of the Sun1 lumenal domain. Both treatments result in the expansion of the PNS. These data, together with those of Padmakumar et al. (2005), support a model in which Sun proteins tether nesprins in the ONM via interactions spanning the PNS. In this way, Sun proteins and nesprins form a complex that links the nucleoskeleton and cytoskeleton (the LINC complex)

The “invisible cholecystectomy”: A transumbilical laparoscopic operation without a scar

Background Looking to further reduce the operative trauma of laparoscopic cholecystectomy, we developed, in patients with no history of cholecystitis and a normal BMI, a scarless operation through the umbilicus. The operative technique, along with the results of the first 10 patients operated in this way, are fully described. Methods 10 female patients underwent transumbilical scarless laparoscopic cholecystectomy. Through the umbilicus, two trocars of 5 mm were introduced parallel to another with a bridge of fascia between them (one for the 5-mm laparoscope and the other for the grasper). With the help of one 1-mm Kirschner wire, introduced at the subcostal line and bent with a special designed device, the gallbladder was pulled up and the triangle of Callot was dissected free, clipped, cut, and the gallbladder was subsequently resected. Finally the gallbladder was taken out through the umbilicus and the umbilicus reconstructed. Results 10 female patients, mean age 36 years (range: 31–49), mean body mass index (BMI) 23 (range: 20–26), after one attack (six patients) or a second attack (four patients) and cholelithiasis confirmed by ultrasonography with no suspicion of inflammation were included in this preliminary study. Mean operative time was 70 minutes (range: 65–85) with no conversions; hospital stay was less than 24 hours with no complications. Conclusion Looking to reduce operative trauma and improve the cosmetic result following laparoscopic cholecystectomy, a transumbilical operative technique has been developed. Results of the operative procedure in a selected group of patients are encouraging with no signs of inflammation and normal BMI. The umbilicus can be developed as a natural port for performing various operative procedures with the help of the traction produced by thin Kirschner wires

Dose Dependent Effects on Cell Cycle Checkpoints and DNA Repair by Bendamustine

Bendamustine (BDM) is an active chemotherapeutic agent approved in the U. S. for treating chronic lymphocytic leukemia and non-Hodgkin lymphoma. Its chemical structure suggests it may have alkylator and anti-metabolite activities; however the precise mechanism of action is not well understood. Here we report the concentration-dependent effects of BDM on cell cycle, DNA damage, checkpoint response and cell death in HeLa cells. Low concentrations of BDM transiently arrested cells in G2, while a 4-fold higher concentration arrested cells in S phase. DNA damage at 50, but not 200 µM, was efficiently repaired after 48 h treatment, suggesting a difference in DNA repair efficiency at the two concentrations. Indeed, perturbing base-excision repair sensitized cells to lower concentrations of BDM. Timelapse studies of the checkpoint response to BDM showed that inhibiting Chk1 caused both the S- and G2-arrested cells to prematurely enter mitosis. However, whereas the cells arrested in G2 (low dose BDM) entered mitosis, segregated their chromosomes and divided normally, the S-phase arrested cells (high dose BDM) exhibited a highly aberrant mitosis, whereby EM images showed highly fragmented chromosomes. The vast majority of these cells died without ever exiting mitosis. Inhibiting the Chk1-dependent DNA damage checkpoint accelerated the time of killing by BDM. Our studies suggest that BDM may affect different biological processes depending on drug concentration. Sensitizing cells to killing by BDM can be achieved by inhibiting base-excision repair or disrupting the DNA damage checkpoint pathway