Determination of valid R -curves for materials with large fracture toughness to yield strength ratios

Crack growth resistance curves are derived from a generalised theory of quasi-static crack propagation due to Gurney and Hunt. Both the subcritical and continuous cracking regions are investigated, where the fracture toughness of the material may depend on the cracking rate, the reacting environment at the crack tip and the mode of fracture. Precise conditions for stability of the spreading crack relative to chosen constraints of either a displacement- or load-controlled machine are formulated. Cracking of sheet materials with high fracture toughness and low yield stress, (e.g. ( K /σ y ) 2 > 200 mm), which do not satisfy certain size requirements, is often complicated by generalised yielding at regions remote from the crack tip. Complete R -curves for such materials cannot be established with conventional testpieces in the laboratory. The present paper adopts a new experimental technique [1] where a laboratory size reinforcement rig attached to the testpiece eliminates all irreversibilities caused by generalised yielding. Valid fracture toughness values and crack growth resistance curves are thereby determined, irrespective of the amount of elastic and plastic deformations occurring at the crack tip. Successful R -curve experiments are described for fracture in a few ductile and tough materials such as 7075-T3. and 1100-0 aluminium alloys, and a low carbon steel. Comparison is made with other published R -curves, and the influence of sheet thickness and ( K 1 c /σ y ) ratio on the geometry of R -curves is investigated. A simple relationship for R -curves is suggested, viz. : R = R 0 + (Δ L ) p , where, it seems, R 0 can be identified with the plane strain toughness (i.e. R 0 = G 1c = K 1c 2 / E (1 - v 2 )1/2). A possible reason for this unexpected result is given in the paper. Useful estimates of K lc may thus be available from thin sheet tests.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42760/1/10704_2004_Article_BF00032834.pd

Regulation of human renal adenocarcinoma cell growth by retinoic acid and its interactions with epidermal growth factor

Regulation of human renal adenocarcinoma cell growth by retinoic acid and its interactions with epidermal growth factor. Retinoic acid (RA) is a natural derivative of vitamin A which regulates the growth and differentiation of epithelia. We have previously proposed that RA participates in compensatory kidney growth and reported that RA inhibits rat mesangial cell growth. This paper describes the effects of RA on a human renal adenocarcinoma cell line (PAD) under different growth conditions, and its interactions with epidermal growth factor (EGF). PAD cells were shown to express RA receptors α and β by Northern blot analysis. In serum free cultures, addition of RA (10-7 M) markedly increased thymidine incorporation by PAD cells (155 ± 7% mean ± se vs. control in 6 separate experiments; P < 0.0001). RA also caused a significant increase in thymidine incorporation by PAD cells under conditions of rapid growth in serum supplemented medium (115 ± 2% vs. control; P < 0.001). RA by itself was unable to reverse contact inhibition of PAD cell growth (NS vs. control), but it synergistically enhanced the mitogenic effect of EGF on confluent monolayers (110 ± 0.6% vs. EGF alone; P < 0.05). Northern blot analysis demonstrated that PAD cells express EGF receptor mRNA, and this was not significantly modified by the addition of RA. Growth arrested (serum starved) PAD cells expressed RAR-α mRNA which was up-regulated eightfold at three hours following the addition of 10% FCS. Thus, our data show that RA is directly mitogenic for serum starved human renal adenocarcinoma cells and that it exerts complex modulation of cell growth in the presence of EGF and serum components

Reciprocating Compressors 101: The User's Perspective

Short CourseThis course will present the basic concepts of reciprocating compressor applications from a user’s perspective. There is an introductory section on application basics (why recips?), including selection criteria and industry standards (API 618, etc.). Compressor components, the basic compression cycle, capacity control, pistons, rings, rods and lubrication essentials are covered

Estimating Effect of Antiviral Drug Use during Pandemic (H1N1) 2009 Outbreak, United States

From April 2009 through March 2010, during the pandemic (H1N1) 2009 outbreak, ≈8.2 million prescriptions for influenza neuraminidase-inhibiting antiviral drugs were filled in the United States. We estimated the number of hospitalizations likely averted due to use of these antiviral medications. After adjusting for prescriptions that were used for prophylaxis and personal stockpiles, as well as for patients who did not complete their drug regimen, we estimated the filled prescriptions prevented ≈8,400–12,600 hospitalizations (on the basis of median values). Approximately 60% of these prevented hospitalizations were among adults 18–64 years of age, with the remainder almost equally divided between children 0–17 years of age and adults >65 years of age. Public health officials should consider these estimates an indication of success of treating patients during the 2009 pandemic and a warning of the need for renewed planning to cope with the next pandemic

The Lantern Vol. 47, No. 2, May 1981

• Festival • Ode to Old Tom • Living Room • Writing a Poem • Mission Impossible • The Hinge is Oiled • The Potter\u27s Field at Malvern • Points of Time • Attempted Autonomy • My Love • Love, not War • Death Comes Quickly • You Can\u27t Always Get What You Don\u27t Really Want • You See (Johnny\u27s Tale): An Elegy • Sanguine Hopeshttps://digitalcommons.ursinus.edu/lantern/1118/thumbnail.jp

Lower Bounds and Series for the Ground State Entropy of the Potts Antiferromagnet on Archimedean Lattices and their Duals

We prove a general rigorous lower bound for $W(\Lambda,q)=\exp(S_0(\Lambda,q)/k_B)$, the exponent of the ground state entropy of the $q$-state Potts antiferromagnet, on an arbitrary Archimedean lattice $\Lambda$. We calculate large-$q$ series expansions for the exact $W_r(\Lambda,q)=q^{-1}W(\Lambda,q)$ and compare these with our lower bounds on this function on the various Archimedean lattices. It is shown that the lower bounds coincide with a number of terms in the large-$q$ expansions and hence serve not just as bounds but also as very good approximations to the respective exact functions $W_r(\Lambda,q)$ for large $q$ on the various lattices $\Lambda$. Plots of $W_r(\Lambda,q)$ are given, and the general dependence on lattice coordination number is noted. Lower bounds and series are also presented for the duals of Archimedean lattices. As part of the study, the chromatic number is determined for all Archimedean lattices and their duals. Finally, we report calculations of chromatic zeros for several lattices; these provide further support for our earlier conjecture that a sufficient condition for $W_r(\Lambda,q)$ to be analytic at $1/q=0$ is that $\Lambda$ is a regular lattice.Comment: 39 pages, Revtex, 9 encapsulated postscript figures, to appear in Phys. Rev.

Phase II Study of Nivolumab and Salvage Nivolumab/Ipilimumab in Treatment-Naive Patients With Advanced Clear Cell Renal Cell Carcinoma (HCRN GU16-260-Cohort A)

PURPOSE To determine the value of tumor cell programmed death-ligand 1 (PD-L1) expression as a predictive biomarker of nivolumab monotherapy efficacy in treatment-naive patients with clear cell renal cell carcinoma (ccRCC) and the efficacy of salvage nivolumab/ipilimumab in patients with tumors unresponsive to nivolumab monotherapy. METHODS Eligible patients with treatment-naive ccRCC received nivolumab until progressive disease (PD), toxicity, or completing 96 treatment weeks (part A). Patients with PD before or stable disease at 48 weeks could receive salvage nivolumab/ipilimumab (part B). The primary end point was improvement in 1-year progression-free survival in patients with tumor PD-L1 expression > 20% versus 0%. RESULTS One hundred twenty-three patients were enrolled. The objective response rate (ORR) was 34.1% (95% CI, 25.8 to 43.2). ORR by International Metastatic RCC Database Consortium category was favorable-risk 57.1%, intermediate-risk/poor-risk 25.0%, and by sarcomatoid features 36.4%. The ORR was 26.9%, 50.0%, and 75.0% for patients with the tumor PD-L1 expression of 0, 1-20, or > 20%, respectively (trend test P value = .002). The median duration of response was 27.6 (19.3 to not reached) months, with 26 of 42 responders including 17 of 20 with favorable-risk disease remaining progression-free. The 1-year progression-free survival was 34.6% and 75.0% in the PD-L1 = 0% and > 20% categories, respectively (P = .050). Ninety-seven patients with PD or prolonged stable disease were potentially eligible for part B, and 35 were enrolled. The ORR for part B was 11.4%. Grade >= 3 treatment-related adverse events occurred in 35% of patients on nivolumab and 43% of those on salvage nivolumab/ipilimumab. CONCLUSION Nivolumab monotherapy is active in treatment-naive ccRCC. Although efficacy appears to be less than that of nivolumab/ipilimumab in patients with intermediate-risk/poor-risk disease, favorable-risk patients had notable benefit. Efficacy correlated with tumor PD-L1 status. Salvage nivolumab/ipilimumab was frequently not feasible and of limited benefit