Low heat transfer oxidizer heat exchanger design and analysis

The RL10-IIB engine, a derivative of the RLIO, is capable of multi-mode thrust operation. This engine operates at two low thrust levels: tank head idle (THI), which is approximately 1 to 2 percent of full thrust, and pumped idle (PI), which is 10 percent of full thrust. Operation at THI provides vehicle propellant settling thrust and efficient engine thermal conditioning; PI operation provides vehicle tank pre-pressurization and maneuver thrust for log-g deployment. Stable combustion of the RL10-IIB engine at THI and PI thrust levels can be accomplished by providing gaseous oxygen at the propellant injector. Using gaseous hydrogen from the thrust chamber jacket as an energy source, a heat exchanger can be used to vaporize liquid oxygen without creating flow instability. This report summarizes the design and analysis of a United Aircraft Products (UAP) low-rate heat transfer heat exchanger concept for the RL10-IIB rocket engine. The design represents a second iteration of the RL10-IIB heat exchanger investigation program. The design and analysis of the first heat exchanger effort is presented in more detail in NASA CR-174857. Testing of the previous design is detailed in NASA CR-179487

Design and analysis report for the RL10-2B breadboard low thrust engine

The breadboard low thrust RL10-2B engine is described. A summary of the analysis and design effort to define the multimode thrust concept applicable to the requirements for the upper stage vehicles is provided. Baseline requirements were established for operation of the RL10-2B engine under the following conditions: (1) tank head idle at low propellant tank pressures without vehicle propellant conditioning or settling thrust; (2) pumped idle at a ten percent thrust level for low G deployment and/or vehicle tank pressurization; and (3) full thrust (15,000 lb.). Several variations of the engine configuration were investigated and results of the analyses are included

Non-muscle myosins 2A and 2B drive changes in cell morphology that occur as myoblasts align and fuse

The interaction of non-muscle myosins 2A and 2B with actin may drive changes in cell movement, shape and adhesion. To investigate this, we used cultured myoblasts as a model system. These cells characteristically change shape from triangular to bipolar when they form groups of aligned cells. Antisense oligonucleotide knockdown of nonmuscle myosin 2A, but not non-muscle myosin 2B, inhibited this shape change, interfered with cell-cell adhesion, had a minor effect on tail retraction and prevented myoblast fusion. By contrast, non-muscle myosin 2B knockdown markedly inhibited tail retraction, increasing cell length by over 200% by 72 hours compared with controls. In addition it interfered with nuclei redistribution in myotubes. Nonmuscle myosin 2C is not involved as western analysis showed that it is not expressed in myoblasts, but only in myotubes. To understand why non-muscle myosins 2A and 2B have such different roles, we analysed their distributions by immuno-electron microscopy, and found that nonmuscle myosin 2A was more tightly associated with the plasma membrane than non-muscle myosin 2B. This suggests that non-muscle myosin 2A is more important for bipolar shape formation and adhesion owing to its preferential interaction with membrane-associated actin, whereas the role of non-muscle myosin 2B in retraction prevents over-elongation of myoblasts

Current and future management of non-tuberculous mycobacterial pulmonary disease (NTM-PD) in the UK

A rising number of non-tuberculous mycobacterial (NTM) isolates are being identified in UK clinical practice. There are many uncertainties around the management of non-tuberculous mycobacterial pulmonary disease (NTM-PD), including its epidemiology, diagnosis, treatment and prevention. Regional variations in how patients with NTM-PD are managed reflects the lack of standardised pathways in the UK. Service optimisation and multidisciplinary working can improve the quality of care for patients with NTM-PD, including (1) better identification of patients at risk of NTM-PD and modification of risk factors where applicable; (2) standardisation of reference laboratory testing to offer clinicians access to accurate and prompt information on NTM species and drug sensitivities; (3) development of recognised specialist NTM nursing care; (4) standardisation of NTM-PD imaging strategies for monitoring of treatment and disease progression; (5) establishment of a hub-and-spoke model of care, including clear referral and management pathways, dedicated NTM-PD multidisciplinary teams, and long-term patient follow-up; (6) formation of clinical networks to link experts who manage diseases associated with NTM; (7) enabling patients to access relevant support groups that can provide information and support for their condition; and (8) development of NTM research groups to allow patient participation in clinical trials and to facilitate professional education