Performance of joints in reinforced concrete slabs for two-way spanning action

A series of tests on filigree slab joints was performed with the aim of assessing whether such joints can be reliably used in the construction of two-way spanning reinforced concrete slabs. The test results were compared with code requirements. Adequate joint performance is shown to be achievable when the joints are appropriately detailed. Further research is recommended for the formulation of a more generic understanding when the design parameters are varied from those studied in this work

Diagenesis in salt dome roof strata: barite - calcite assemblage in Jebel Madar, Oman

Halokinesis causes a dynamic structural evolution with the development of faults and fractures, which can act as either preferential fluid pathways or barriers. Reconstructing reactive fluid flow in salt dome settings remains a challenge. This contribution presents for the first time a spatial distribution map of diagenetic phases in a salt dome in northern Oman. Our study establishes a clear link between structural evolution and fluid flow leading to the formation of diagenetic products (barite and calcite) in the salt dome roof strata. Extensive formation of diagenetic products occurs along NNE-SSW to NE-SW faults and fractures, which initiated during the Santonian (Late Cretaceous) and were reactivated in the Miocene, but not along the E-W fault, which was generated during Early Paleocene time. We propose that the diagenetic products formed by mixing of a warm (100 °C) saline (17 wt% NaCl eq.) 87Sr enriched (87Sr/86Sr: 0.71023) fluid with colder (35 °C) meteoric fluid during Miocene to Pleistocene. The stable sulphur and strontium isotope composition and fluid inclusion data indicate that a saline fluid, with sulfate source derived from the Ara Group evaporite and Haima Supergroup layers, is the source for barite formation at about 100 °C, predominantly at fault conjunctions and minor faults away from the main graben structure in the dome. In the Miocene, the saline fluid probably ascended along a halokinesis-related fault due to fluid overpressure (due to the rising salt and impermeable layers in the overlying stratigraphic sequence), and triggered the formation of barite due mixing with barium-rich fluids, accompanied by a drop in temperature. Subsequently, evolving salt doming with associated fault activity and erosion of the Jebel allows progressively more input of colder meteoric fluids, which mix with the saline warmer fluid, as derived from stable isotope data measured in the progressively younger barite-associated calcite, fault zone calcite and macro-columnar calcite. The reconstructed mixing model indicates a 50/50 to 90/10 meteoric/saline fluid mixing ratio for the formation of fault zone calcite, and a 10 times higher concentration of carbon in the saline fluid end member compared to the meteoric fluid end member. The presented mixing model of salt-derived fluids with meteoric fluids is suggested to be a general model applicable to structural diagenetic evolution of salt domes world wide

The spectrum of resistance in SR/CR mice: the critical role of chemoattraction in the cancer/leukocyte interaction

<p>Abstract</p> <p>Background</p> <p>Spontaneous regression/complete resistance (SR/CR) mice are a unique colony of mice that possess an inheritable, natural cancer resistance mediated primarily by innate cellular immunity. This resistance is effective against sarcoma 180 (S180) at exceptionally high doses and these mice remain healthy.</p> <p>Methods</p> <p>In this study, we challenged SR/CR mice with additional lethal transplantable mouse cancer cell lines to determine their resistance spectrum. The ability of these transplantable cancer cell lines to induce leukocyte infiltration was quantified and the percentage of different populations of responding immune cells was determined using flow cytometry.</p> <p>Results</p> <p>In comparison to wild type (WT) mice, SR/CR mice showed significantly higher resistance to all cancer cell lines tested. However, SR/CR mice were more sensitive to MethA sarcoma (MethA), B16 melanoma (B16), LL/2 lung carcinoma (LL/2) and J774 lymphoma (J774) than to sarcoma 180 (S180) and EL-4 lymphoma (EL-4). Further mechanistic studies revealed that this lower resistance to MethA and LL/2 was due to the inability of these cancer cells to attract SR/CR leukocytes, leading to tumor cell escape from resistance mechanism. This escape mechanism was overcome by co-injection with S180, which could attract SR/CR leukocytes allowing the mice to resist higher doses of MethA and LL/2. S180-induced cell-free ascites fluid (CFAF) co-injection recapitulated the results obtained with live S180 cells, suggesting that this chemoattraction by cancer cells is mediated by diffusible molecules. We also tested for the first time whether SR/CR mice were able to resist additional cancer cell lines prior to S180 exposure. We found that SR/CR mice had an innate resistance against EL-4 and J774.</p> <p>Conclusions</p> <p>Our results suggest that the cancer resistance in SR/CR mice is based on at least two separate processes: leukocyte migration/infiltration to the site of cancer cells and recognition of common surface properties on cancer cells. The infiltration of SR/CR leukocytes was based on both the innate ability of leukocytes to respond to chemotactic signals produced by cancer cells and on whether cancer cells produced these chemotactic signals. We found that some cancer cells could escape from SR/CR resistance because they did not induce infiltration of SR/CR leukocytes. However, if infiltration of leukocytes was induced by co-injection with chemotactic factors, these same cancer cells could be effectively recognized and killed by SR/CR leukocytes.</p

Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements

<p>Abstract</p> <p>Background</p> <p>Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin (Prf^-/-), superoxide (Cybb^-/), or inducible nitric oxide (Nos2^-/).</p> <p>Methods</p> <p>SR/CR mice were bred into individual Prf^-/-, Cybb^-/-, or Nos2^-/-genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined.</p> <p>Results</p> <p>When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of Prf^-/-, Cybb^-/-, or Nos2^-/-did not completely abolish the SR/CR cancer resistant phenotype. However, the Nos2^-/-background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls.</p> <p>Conclusion</p> <p>Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice.</p

Time-dependent Effects in Photospheric-Phase Type II Supernova Spectra

Spectroscopic modeling of Type II supernovae (SNe) generally assumes steady-state. Following the recent suggestion of Utrobin & Chugai, but using the 1D non-LTE line-blanketed model atmosphere code CMFGEN, we investigate the effects of including time-dependent terms that appear in the statistical and radiative equilibrium equations. We base our discussion on the ejecta properties and the spectroscopic signatures obtained from time-dependent simulations, investigating different ejecta configurations, and covering their evolution from one day to six weeks after shock breakout. Compared to equivalent steady-state models, our time-dependent models produce SN ejecta that are systematically over-ionized, affecting helium at one week after explosion, but ultimately affecting all ions after a few weeks. While the continuum remains essentially unchanged, time-dependence effects on observed spectral lines are large. At the recombination epoch, HI lines and NaID are considerably stronger and broader than in equivalent steady-state models, while CaII8500A is weakened. If time dependence is allowed for, the HeI lines at 5875A and 10830A appear about 3 times stronger at one week, and HeI10830A persists as a blue-shifted absorption feature even at 6 weeks after explosion. Time dependence operates through the energy gain from changes in ionization and excitation, and, perhaps more universally across SN types, from the competition between recombination and expansion, which in-turn, can be affected by optical-depth effects. Our time-dependent models compare well with observations of the low-luminosity low-velocity SN 1999br and the more standard SN 1999em, reproducing the Halpha line strength at the recombination epoch, and without the need for setting unphysical requirements on the magnitude of nickel mixing.Comment: 19 pages, 18 figures, accepted for publication in MNRAS, high-resolution of the paper at http://hermes.as.arizona.edu/~luc/pap_ddt/pap_ddt.ps.g

Evidence-Based Recommendations for Optimal Dietary Protein Intake in Older People: A Position Paper From the PROT-AGE Study Group

New evidence shows that older adults need more dietary protein than do younger adults to support good health, promote recovery from illness, and maintain functionality. Older people need to make up for age-related changes in protein metabolism, such as high splanchnic extraction and declining anabolic responses to ingested protein. They also need more protein to offset inflammatory and catabolic conditions associated with chronic and acute diseases that occur commonly with aging. With the goal of developing updated, evidence-based recommendations for optimal protein intake by older people, the European Union Geriatric Medicine Society (EUGMS), in cooperation with other scientific organizations, appointed an international study group to review dietary protein needs with aging (PROT-AGE Study Group). To help older people (>65 years) maintain and regain lean body mass and function, the PROT-AGE study group recommends average daily intake at least in the range of 1.0 to 1.2 g protein per kilogram of body weight per day. Both endurance-and resistance-type exercises are recommended at individualized levels that are safe and tolerated, and higher protein intake (ie, >= 1.2 g/kg body weight/d) is advised for those who are exercising and otherwise active. Most older adults who have acute or chronic diseases need even more dietary protein (ie, 1.2-1.5 g/kg body weight/d). Older people with severe kidney disease (ie, estimated GFR <30 mL/min/1.73m(2)), but who are not on dialysis, are an exception to this rule; these individuals may need to limit protein intake. Protein quality, timing of ingestion, and intake of other nutritional supplements may be relevant, but evidence is not yet sufficient to support specific recommendations. Older people are vulnerable to losses in physical function capacity, and such losses predict loss of independence, falls, and even mortality. Thus, future studies aimed at pinpointing optimal protein intake in specific populations of older people need to include measures of physical function. Copyright (C) 2013 - American Medical Directors Association, Inc

The curious role of sarcomeric proteins in control of diverse processes in cardiac myocytes

Introduction Relatively recent developments in our understanding of sarcomeric proteins have expanded their role from the home of molecular motors generating force and shortening to a cellular organelle fully integrated in the control of structural, electrical, mechanical, chemical, and metabolic homeostasis. Even so, in some cases these diverse functions of sarcomeric proteins appear to remain a curiosity, not fully appreciated in the analysis of major controllers of cardiac function. This attitude toward the function of sarcomeric proteins in cardiac myocytes is summarized in the following definition of “curiosity,” which seems particularly apropos: “meddlesome; thrusting oneself into and taking an active part in others’ affairs.” We focus in this Perspective on how sarcomeric proteins function in integration with membrane channels and transporters in control of cardiac dynamics, especially in adrenergic control of cardiac function. Understanding these mechanisms at the level of cardiac sarcomeres took on special significance with the identification of mutations in sarcomeric proteins as the most common cause of familial hypertrophic and dilated cardiomyopathies. These mutations commonly lead to structural, electrical, and metabolic remodeling and to sudden death. These disorders indicate a critical role of processes at the level of the sarcomeres in homeostatic control of cardiac energetics, dynamics, and structure. Yet, control of Ca2+ delivery to and removal from the myofilaments has dominated discussions of mechanisms regulating cardiac contractility. We first provide an alternative perspective in which rate processes at the level of the sarcomeres appear to be dominant during the rise and maintenance of systolic elastance and of isovolumic relaxation. A discussion of established adrenergic mechanisms and newly understood anti-adrenergic mechanisms controlling sarcomere response to Ca2+ follows and expands on this perspective

Randomised trial of glutamine and selenium supplemented parenteral nutrition for critically ill patients

Background: Mortality rates in the Intensive Care Unit and subsequent hospital mortality rates in the UK remain high. Infections in Intensive Care are associated with a 2–3 times increased risk of death. It is thought that under conditions of severe metabolic stress glutamine becomes "conditionally essential". Selenium is an essential trace element that has antioxidant and anti-inflammatory properties. Approximately 23% of patients in Intensive Care require parenteral nutrition and glutamine and selenium are either absent or present in low amounts. Both glutamine and selenium have the potential to influence the immune system through independent biochemical pathways. Systematic reviews suggest that supplementing parenteral nutrition in critical illness with glutamine or selenium may reduce infections and mortality. Pilot data has shown that more than 50% of participants developed infections, typically resistant organisms. We are powered to show definitively whether supplementation of PN with either glutamine or selenium is effective at reducing new infections in critically ill patients. Methods/design: 2 × 2 factorial, pragmatic, multicentre, double-blind, randomised controlled trial. The trial has an enrolment target of 500 patients. Inclusion criteria include: expected to be in critical care for at least 48 hours, aged 16 years or over, patients who require parenteral nutrition and are expected to have at least half their daily nutritional requirements given by that route. Allocation is to one of four iso-caloric, iso-nitrogenous groups: glutamine, selenium, both glutamine & selenium or no additional glutamine or selenium. Trial supplementation is given for up to seven days on the Intensive Care Unit and subsequent wards if practicable. The primary outcomes are episodes of infection in the 14 days after starting trial nutrition and mortality. Secondary outcomes include antibiotic usage, length of hospital stay, quality of life and cost-effectiveness. Discussion: To date more than 285 patients have been recruited to the trial from 10 sites in Scotland. Recruitment is due to finish in August 2008 with a further six months follow up. We expect to report the results of the trial in summer 2009. Trial registration: This trial is registered with the International Standard Randomised Controlled Trial Number system. ISRCTN87144826Not peer reviewedPublisher PD